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  • 1. Volume 4 • 2005 Andreas Vesalius. Brain ventricles from his famous book De Humani Corporis Fabrica. TasciogluAO,TasciogluAB.Neuroanatomy2005(4)57-63 Indexed in EMBASE (Excerpta Medica), Directory of Open Access Journals (DOAJ), SCOPUS, and Index Copernicus.
  • 2. OwnedandPublishedby M. Mustafa Aldur, MD–PhD DepartmentofAnatomy HacettepeUniversity FacultyofMedicine 06100Ankara–Turkey e-Mail:mustafa@aldur.net Phone:+903123052466 Fax:+903124785200 www.neuroanatomy.org Aims and Scope Neuroanatomy is a journal in English, and publishes original research articles dealing with neuroanatomical sciences in animals (vertebrates and invertabrates) and humans. Papers in any of the following fields will be considered: molecular, cellular, histological and gross anatomical studies on normal and/or abnormal experimental animals and humans. Functional, morphological, biochemical, physiological and behavioral studies are considered if they include neuroanatomical analysis. Reports on techniques applicable to the above fields are also considered. Occasional reviews on subjects selected by the Editors will be published. Miscellaneous items, including essays, book reviews and commentaries may also be published on approval of the Editorial Board. Editorial Correspondence All material for publication should be sent to M. Mustafa Aldur, MD–PhD, Department of Anatomy, Hacettepe University, Faculty of Medicine, 06100, Ankara, Turkey; e-mail: editor@neuroanatomy.org. For detailed instructions concerning the submission of manuscripts, please refer to the Instructions to Authors at the back of the journal. Subscription Rates Both the electronic and the printed versions of Neuroanatomy are FREE. The printed version of journal (pISSN 1303-1783) is published annually. The electronic version of journal (eISSN 1303-1775) can be accessed on internet (http://www.neuroanatomy.org). Copyright and Photocopying 2002–2006 © neuroanatomy.org. No authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is required by the publisher. This consent does not extend to other kinds of copying such as copying for general distribution, for advertising or promotional purposes, for creating new collective works or for resale. Special requests should be addressed to the publisher (mustafa@ aldur.net). Disclaimer The Owner, Publisher and Editors can not be held responsible for errors or any consequences arising from the use of information contained in this journal; the views and opinions expressed do not necessarily reflect those of the Owner, Publisher and Editors, neither does the publication of advertisements constitute any endorsement by the Owner, Publisher and Editors of the products advertised. All responsibilities of the contents of articles belong to the authors. [5187 numaral› Bas›n Yasas› mucibince gösterilmesi zaruri bilgiler] Sahibi ve Sorumlu Müdürü: Doç. Dr. M. Mustafa Aldur Yönetim Yeri: Hacettepe Üniversitesi T›p Fakültesi Anatomi Anabilim Dal›, 06100 S›hhiye, Ankara. Telefon: 305 24 66 Faks: 478 52 00 Yay›n Türü: Yerel Süreli Yay›n Yay›n Dili: ‹ngilizce Yay›nlanma Biçimi: Y›ll›k Bas›m Yeri: Ankara Bas›m Tarihi: Ocak 2006 Bas›mc›: Hacettepe Üniversitesi Hastaneleri Bas›mevi, 06100 S›hhiye, Ankara. Telefon: 305 30 68 Ücretsiz olarak dağıtılır. Reklam kabul edilmez. Yazıların tüm yasal sorumluluğu yazarlarınındır. Printed by Hacettepe University Hospitals Printing House 06100, Ankara, Turkey +90 312 305 30 68 Ankara, December 2005 Honorary Editor Tuncalp Ozgen, MD Editors M. Dogan Aksit, DVM-PhD Ruhgun Basar, DDS-PhD Deputy Editor H. Hamdi Celik, MD-PhD Associate Editors Mustafa K. Baskaya, MD Safiye Cavdar, PhD Scott Lozanoff, PhD Erdogan Sendemir, MD Mustafa F. Sargon, MD-PhD Selcuk Surucu, MD-PhD A. Beliz Tascioglu, PhD Ibrahim Tekdemir, MD Engin Yilmaz, MD-PhD M. Ibrahim Ziyal, MD Ethics Editors  Robert Daroff, MD Sevket Ruacan, MD Section Editors Developmental Neuroanatomy Hakki Dalcik, PhD Structural Neuroanatomy Attila Dagdeviren, MD Neurobiology Reha S. Erzurumlu, PhD Functional Neuroanatomy Uner Tan, MD-PhD Chemical Neuroanatomy Turgay Dalkara, MD-PhD Clinical Neuroanatomy Bulent Elibol, MD-PhD Surgical Neuroanatomy O. Selcuk Palaoglu, MD Radiological Neuroanatomy Isil Saatci, MD Pathological Neuroanatomy Figen Soylemezoglu, MD Educational Neuroanatomy Selda Onderoglu, PhD Historical Neuroanatomy Recep Mesut, MD Variational Neuroanatomy Alaittin Elhan, PhD Terminology Sezgin Ilgi, PhD Comparative Neuroanatomy Orhan E. Arslan, DVM-PhD Language Editors Selma Yorukan, MD Emine Ozkul, PhD Ayberk Kurt, MD-PhD A. Kagan Karabulut, MD-PhD Muzaffer Seker, PhD Selcuk Tunali, MD Dogan Tuncali, MD Technical Editor M. Mustafa Aldur, MD-PhD Managing Editors Mustafa Aktekin, MD-PhD Alp Bayramoglu, MD-PhD M. Deniz Demiryurek, MD-PhD C. Cem Denk, MD-PhD A. Hakan Ozturk, MD-PhD Eray Tuccar, MD-PhD Associate Technical Editor Ilkan Tatar, MD Scientific Advisory Board Salih Murat Akkin, MD Mehmet Alikasifoglu, MD-PhD Ossama Al-Mefty, MD Kudret Aytemir, MD Mustafa Berker, MD-PhD Jacques Brotchi, MD-PhD Saruhan Cekirge, MD George Chaldakov, MD-PhD Ernesto Coscarella, MD Meserret Cumhur, PhD Michail S. Davidoff, MD-PhD D. Ceri Davies, PhD Aclan Dogan, MD Barbaros Durgun, MD Yaman Eksioglu, MD-PhD Vedat Evren, MD Ozhan Eyigor, MD-PhD Figen Govsa Gokmen, MD M. Oguz Guc, MD-PhD Erdem Gumusburun, PhD Gustav F. Jirikowski, PhD Tetsuo Kanno, MD Erkan Kaptanoglu, MD S. Tuna Karahan, MD Marios Loukas, MD-PhD Jacques Morcos, MD Akio Morita, MD-PhD Aytekin Oto, MD Wladimir Ovcharov, MD-PhD Hasan Ozan, MD Emin Oztas, MD Levent Ozturk, MD Tuncay Peker, MD Reinhard Putz, MD Kayihan Sahinoglu, MD Madjid Samii, MD-PhD Mustafa Sarsilmaz, MD Laligam N. Sekhar, MD Ahmet Sinav, MD Robert F. Spetzler, MD Ali Tascioglu, MD Ertugrul Tatlisumak, MD Ugur Ture, MD Ismail H. Ulus, MD Statistical Advisor Ergun Karaagaoglu, PhD Medical Illustrator Fikret Sen, MD
  • 3. See article Vucetic, p. 2 Neuroanatomy (2005) Volume 4 Table of Contents See article Kahilogullari et al., p. 16 See article Vollala et al., p. 35 See article Auluck et al., p. 28 1 Editorial Published online December 30, 2005 A brief evaluation of Neuroanatomy [2005] Aldur MM. 2 Original Article Published online April 15, 2005 The parasellar dura mater and adjacent dura: a microsurgical and light microscopic study in fetal materials Vucetic R. 8 Case Report Published online April 15, 2005 A rare origin of upper root of ansa cervicalis from vagus nerve: a case report Vollala VR, Bhat SM, Nayak S, Raghunathan D, Samuel VP, Rodrigues V, Mathew JG. 10 Original Article Published online July 13, 2005 Morphometric measurements of the thalamus and interthalamic adhesion by MR imaging Sen F, Ulubay H, Ozeksi P, Sargon MF, Tascioglu AB. 13 Case Report Published online July 20, 2005 An accessory branch of musculocutaneous nerve joining median nerve Kocabiyik N, Yalcin B, Yazar F, Ozan H. 16 Case Report Published online July 20, 2005 Caudal regression syndrome diagnosed after the childhood period: a case report Kahilogullari G, Tuna H, Aydin Z, Vural A, Attar A, Deda H. 18 Original Article Published online July 29, 2005 Centella asiatica (linn) induced behavioural changes during growth spurt period in neonatal rats Rao KGM, Rao SM, Rao SG. 24 Review Article Published online July 29, 2005 Brief review of vestibular system anatomy and its higher order projections Tascioglu AB. 28 Case Report Published online August 8, 2005 Anatomical variations in developing mandibular nerve canal: a report of three cases Auluck A, Ahsan A, Pai KM, Shetty C. 31 Original Article Published online August 9, 2005 Neuroanatomy in Tesrih-i Ebdan: a study on a book which is written in Ottoman era Ulucam E, Mesut R, Gokce N. 35 Case Report Published online August 11, 2005 Nerve compressions in upper limb: a case report Vollala VR, Raghunathan D, Rodrigues V. 37 Case Report Published online August 11, 2005 A rare variation in the formation of the upper trunk of the brachial plexus - a case report Nayak S, Somayaji N, Vollala VR, Raghunathan D, Rodrigues V, Samuel VP, Alathady Malloor P. 39 Case Report Published online October 26, 2005 Total fusion of atlas with occipital bone: a case report Nayak S, Vollala VR, Raghunathan D. 41 Case Report Published online November 14, 2005 Sciatic nerve entrapment in the popliteal fossa: a case report Paval J, Vollala VR, Nayak S. 43 Original Article Published online November 29, 2005 The effect of low protein diet on thalamic projections of hippocampus in rat Bayat M, Hasanzadeh GR, Barzroodipour M, Javadi M. See article Kocabiyik et al., p. 13 See article Sen et al., p. 10
  • 4. Neuroanatomy (2005) Volume 4 Table of Contents (continued) 49 Original Article Published online December 2, 2005 Three dimensional (3D) reconstruction of the rat ventricles Ozdemir MB, Akdogan I, Adiguzel E, Yonguc N. 52 Case Report Published online December 16, 2005 Clinical course and evaluation of meningocele lesion in adulthood: a case report Gok HB, Ayberk G, Tosun H, Seckin Z. 55 Case Report Published online December 20, 2005 Huge tumor of the intracranial cavity: a catastrophic imaging on USG and MRI Ziyal IM, Bilginer B, Bozkurt G. 57 Brief Review Published online December 26, 2005 Ventricular anatomy: illustrations and concepts from antiquity to Renaissance Tascioglu AO, Tascioglu AB. 64 Obituary Published online December 26, 2005 Remembrance of M. Atilla MUFTUOGLU, MD (1950–2005) Akkin SM. 65 Announcement Published online December 26, 2005 Scientific meetings Indexed in EMBASE (Excerpta Medica), Index Copernicus, Directory of Open Access Journals (DOAJ), and SCOPUS. You can download the articles from http://www.neuroanatomy.org address as Adobe PDF free full–text documents. You can check the table of contents from http://www.neuroanatomy.org/rss/rss.xml address as a RSS 2.0 XML feed regularly. M. Atilla Muftuoglu, MD Professor of Anatomy February 7, 1950 [Gaziantep–Turkey] • January 16, 2005 [Istanbul–Turkey] This volume of NEUROANATOMY is dedicated to Dr Muftuoglu. We are deeply sorry for his sudden death. Dr Muftuoglu will be in our thoughts and prayers. See article Nayak et al., p. 37 See article Nayak et al., p. 39 See article Ziyal et al., p. 55 See article Tascioglu and Tascioglu, p. 57 See article Bayat et al., p. 43 See article Ozdemir et al., p. 49
  • 5. Published online 30 December, 2005 © http://www.neuroanatomy.org Editorial Neuroanatomy (2005) 4: 1 A brief evaluation of Neuroanatomy [2005] M. Mustafa ALDUR Department of Anatomy, Hacettepe University, Faculty of Medicine, Ankara–Turkey. M. Mustafa ALDUR, MD–PhD Associate Professor of Anatomy Department of Anatomy, Hacettepe University, Faculty of Medicine, 06100 Ankara–TURKEY 90-312-305 24 66 90-312-478 52 00 mustafa@aldur.net Received 23 December 2005 eISSN 1303-1775 • pISSN 1303-1783 As the printing of this year’s volume of NEUROANATOMY is about to be achieved, I have personally undertaken the task of writing the Editorial which has become part of our tradition. The past year began with sadness. The President of the Turkish Society of Anatomy, Professor Atilla Müftüoğlu MD, whom I commemorate with much gratitude, passed away in mid January quite unexpectedly. Although it has been almost a year since this tragic loss, the vividness of his memory is for us, the proof that Dr Müftüoğlu is among the unforgettables of our society. I would like to take the opportunity to express my acknowledgment to the late Dr Müftüoğlu and to all those who have participated with their dedicated efforts in supporting our anatomical society. A short biography of Professor Müftüoğlu MD, is presented by his successor Professor Salih Murat Akkın MD in the ensuing pages of this volume. I wish to thank Professor Akkın for his participation. As will be noted by readers, compared to previous years, we have received many more international papers. We believe that our efforts have gained momentum and will continue to increase in the coming years. We wish to express our appreciation to our friends at home and abroad for their hearty support. We have been encouraged by the scientific papers submitted by our colleagues in India, Serbia-Montenegro, Iran and Greece and wish to expand our spectrum throughout the world. We hope that these connections and interrelations will form the core of shared works and the establishment of organized international scientific collaborations. We are also very pleased about the fact that the articles printed in NEUROANATOMY have started to receive citations on an international basis. This fact shows in an unbiased manner that the material we have been printing is being used by the international scientific community. Although we have been able to follow these citations only in the Science Citation Index (Thomson) until recently, we are now able to follow the citation reports of the articles and authors in SCOPUS (Elsevier) which is currently scanning our Journal. SCOPUS is an interdisciplinary, dynamic index which has a user panel similar to EMBASE interface through which it reaches 14.000 indexed continuous publications in the Elsevier Bibliographic Database and which can also be contacted electronically at the http://www.scopus. com address. The important hallmark of SCOPUS is that it encompasses not only articles printed in biomedical journals but also other related scientific fields. Because we support the open access journal concept as our publication policy, we are included in the Directory of Open Access Journal (DOAJ). DOAJ is an important source in which only the open access articles can be reached through a certain key word. Our readers will be able to reach this source easily through http://www.doaj.org. In2005,weattendedthe18thInternational Symposium on Morphological Science (Serbian Academy of Sciences and Arts, 5-8 June 2005) in Serbia-Montenegro in Belgrade within the scope of an international introductory program for our Journal where we have had the pleasure of meeting our colleague Professor Brasnilav Filipovic and wish to thank him and the organization committee for their kind hospitality. Additionally, my meeting with the Editor- in-Chief of Clinical Anatomy Professor Stephen Carmichael and the advices I have received from him for the scientific proliferation of NEUROANATOMY has proven to be invaluable. I wish to extend my appreciation to all the scientists who have participated in the publication of this volume: to all the authors who have sent their papers, to the referees who have evaluated them, to our Editors Professor M. Doğan Akşit PhD, Professor Ruhgün Başar PhD, and Professor Hamdi Çelik MD-PhD and to all the members of our publication and advisory boards who have made it possible to create this volume. Last but not least, we wish to thank Dr. Selçuk Tunalı MD and Professor A. Beliz Taşcıoğlu PhD for their language editing, the Hacettepe Hospitals Printing House and Coordinator Uğur Korkmaz for having printed the volume which was put on electronic media throughout the year, with impeccable timing in December 2005. Our special gratitude goes to the Rector of Hacettepe University and our Honorary Editor Professor Tunçalp Özgen MD for his everlasting support. I would like to conclude the Editorial with an invitation. The 10th National Anatomy Congress with international participation will be held in Bodrum, one of the most famous holiday sites of Turkey on September 6-10, 2006. We will be delighted to host our colleagues from all over the world. Information about the Congress can be obtained at the http://www.anatomy.web.tr/eng internet address. For correspondence, the congress@anatomy.web.tr address may be used. Wishing all Anatomists and their families a Happy New Year. Also hoping that 2006 will bring peace to the world… M. Mustafa Aldur, MD–PhD Technical Editor and Publisher
  • 6. Published online 15 April, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 2–7 Introduction The external membrane which invests the brain is called the cranial dura mater. It consists of a periosteal layer, which is rich in blood and lymphatic vessels and nerves, and an inner layer named the meningeal layer. At certain places the periosteal and meningeal layers are separated to form the dural venous sinuses. This is the typical description of the cranial dura mater [1–15]. As for localization, cranial dura mater may be roughly divided as the dura of the calvaria and the dura of the skull base, but concerning the adjacent structures it may be divided to the dura of the small wing, the dura of the clivus, the dura of the parasellar region etc. In literature, further attention was given to the parasellar dura mater than the other parts, and special interest was given to the cavernous sinus, as a part of the parasellar dura mater. In fact, many pathological processes are located in the parasellar region [14, 16–20]. In accordance with other authors [1, 7–14, 18–19, 21–22], we define the parasellar dura mater as the part which extends along to the lateral side of the body of the sphenoid bone. Also, it extends anteriorly to the superior orbital fissure, and to the level of the apex of the petrous bone posteriorly. The frontier between the parasellar dura mater and the adjacent dura mater is forms a line starting from the lateral end of the superior orbital fissure and passes through the lateral edge of the foramen rotundum, foramen ovale and foramen lacerum. The internal carotid artery and its sympathetic plexus use the parasellar dura mater as a milieu through which travel from the extradural space to the intradural space. On the other hand, some cranial nerves and some special venous canals use the parasellar dura mater as a milieu through which travel from the intradural space to the extradural space. In literature, we didn’t find any comparison between the description of the structure of the dura mater of the parasellar region and the dura mater of the middle cranial fossa, which is just near to the parasellar region. Is there any difference between the parasellar dura mater and the dura mater of the other cranial regions, or are they completely the same? The aim of this study is firstly to point out the difference between these two. Also, we would like to list and demonstrate our findings on the disposition of the components passing through the parasellar dura mater as the cranial nerves and their vessels, the internal carotid artery and its parasellar branches, which is very important in surgery. Especially, we would like to report our histological and dissection findings on the venous spaces which form the famous cavernous sinus. The parasellar dura mater and adjacent dura: a microsurgical and light microscopic study in fetal materials Radomir R. VUCETIC Medical Faculty of Nis, Serbia and Montenegro. Radomir R. Vucetic Professor of Anatomy and Neurosurgeon, Medical Faculty of Nis, Zorona Djindjica 81, 18000 Nis, SERBIA and MONTENEGRO 381-18-536 363 381-18-338 770 vuceticr@medfak.ni.ac.yu neuro_spine@yahoo.com Received 3 January 2005; accepted 29 March 2005 ABSTRACT The parasellar dura mater should be distinguished from the adjacent dura because the cavernous sinus, the internal carotid artery, and certain cranial nerves passes through it. The purpose of this study is to demonstrate the difference between the structure of the parasellar and the adjacent dura mater. The study was held with 80 fetuses at a gestational age of 20-40 weeks. Microdissection and histological investigation was performed without decalcification. The results are as follows: The meningeal layer of the parasellar dura mater was thicker from that of the adjacent dura, but their periosteal layers had similar thickness. The meningeal layer of the cranial dura mater had a multilayered structure, and also two types of lamellas have been found, the compact and the loose lamellas. Four compact and four loose lamellas of the meningeal layer of the parasellar dura mater have been shown by dissection and histological method. Through these lamellas are passing the cranial nerves III, IV, V1 , V2 , V3 , VI and their vessels. Through the fourth loose lamellae pass the parasellar portion of the internal carotid artery. In the third and fourth loose lamellas there are venous spaces arranged around the internal carotid artery, which form the cavernous sinus. The compact lamellas are thinner but firmer in comparison to loose lamellas. Ontheotherhand,threecompactandthreelooselamellashavebeenfoundinthemeningeallayeroftheadjacent dura mater. Neither evident vessels nor nerves have been noticed between these lamellas. Neuroanatomy; 2005; 4: 2–7. Key words [parasellar region] [dura mater] [cavernous sinus] [venous space] eISSN 1303-1775 • pISSN 1303-1783
  • 7. Parasellar duramater and adjacent dura Material and Methods The parasellar dura mater and the dura of the middle cranial fossa which is just near to the parasellar dura were examined in 80 fetuses at 20–40 weeks of gestational age, in accordance with the ethical standards. The fetuses were obtained from the Gynaecology and Obstetrics Clinic of the Medical Faculty of Nis. The arterial system of the fetuses were injected with Micropaque contrast medium. The fetuses were kept in 10% formaldehyde for 10 days and then the brains were removed from the skulls, and fetuses were returned to 10% formaldehyde for a period of five years to tan the connective tissue that forms the dura mater. After using the above described method, we studied the parasellar dura mater with micro dissection technique using an operating microscope. We started the micro dissection at the level of the apex of the petrous bone. We prepared the lamellar connective tissue of the parasellar dura mater and the middle cranial fossa dura, and the components passing through this region. In this study, in contrast to the other authors, the histologicalinvestigationwasheldwithoutdecalcification and staining. 10–15 microns thick frontal sections were prepared from the parasellar dura mater and the dura mater of the middle cranial fossa. Results We found that the parasellar dura mater and the dura mater near to the parasellar region were built up of two layers, a periosteal layer and an inner layer named the meningeal layer. The thickness of the periosteal layer of the parasellar dura mater, and the periosteal layer of the Figure 1.  Microphotography of the frontal section of the fetal dura mater of the floor of the middle cranial fossa, just near to the parasellar region [Unstained X40]. (1: great wing of the sphenoid bone, 2: periosteal layer of the dura mater, 3: compact lamellas of the meningeal layer of the dura mater, 4: loose lamellas of the meningeal layer of the dura mater) Figure 2.  Microphotography of the frontal section of the fetal parasellar dura mater [Unstained X20]. (1: hypophysis, 2: endosteal layer of the parasellar dura mater, 3: internal carotid artery, 4: venous space of the inferior group of the cavernous sinus, 5: abducent nerve, 6: ophthalmic division of the trigeminal nerve, 7: oculomotor nerve, 8: trochlear nerve, 9: second compact lamella, 10: first compact lamella) Figure 3.  The compact lamellas on the way to the fetal parasellar portion of the internal carotid artery [microdissection, superior-lateral view]. (1: posterior margin of the right small wing of the sphenoid bone, 2: first compact lamella, 3: superficial middle cerebral vein, 4: second compact lamella, 5: trochlear nerve, 6: third compact lamella, 7: oculomotor nerve, 8: fourth compact lamella, 9: parasellar portion of the internal carotid artery, 10: ophthalmic artery, 11: hypophysis) Figure 4.  Microphotography of the frontal section of the fetal meningeal layer of the parasellar dura mater [Unstained X40]. (1: first compact lamella, 2: first loose lamella, 3: second compact lamella, 4: trochlear nerve, 5: oculomotor nerve, 6: third compact lamella, 7: small venous space of the cavernous sinus, 8: ophthalmic division of the trigeminal nerve, 9: fourth compact lamella and the abducent nerve, 10: internal carotid artery, 11: large venous spaces of the cavernous sinus around the internal carotid artery)
  • 8.  Radomir R. Vucetic Figure 5.  Microphotography of the frontal section of the fetal parasellarduramater.Thefourthlooselamellaofthemeningeallayerof the parasellar dura mater, which is between the endosteal layer and the fourth compact lamella of the parasellar dura mater [Unstained X40]. (1: periosteal layer of the parasellar dura mater, 2: fourth compact lamella and the abducent nerve, 3: venous space of the medial group of the cavernous sinus, 4: internal carotid artery, 5: venous space of the lateral group of the cavernous sinus, 6: ophthalmic division of the trigeminal nerve, 7: trochlear nerve, 8: second compact lamella) Figure 6.  The lateral group of the venous spaces of the fetal cavernous sinus [microdissection, lateral view]. (1: supraclinoid portion of the internal carotid artery, 2: communicating opening of the venous space of the lateral group, 3: third compact lamella, 4: venous space of the lateral group, 5: infero-lateral trunk of the internal carotid artery, 6: venous space of the lateral group and its communicating openings, 7: parasellar portion of the abducent nerve, 8: venous space of the lateral group, 9: subarachnoid portion of the abducent nerve, 10: venous space of the lateral group, 11: venous space of the lateral group) Figure 7.  The medial group of the venous spaces of the cavernous sinus [microdissection, superior view]. (1: first compact lamella, 2: second compact lamella, 3: third compact lamella, 4: fourth compact lamella, 5: infero-lateral trunk, 6: parasellar portion of the internal carotid artery, 7: ophthalmic artery, 8: medial-anterior venous space, 9: inferior hypophyseal artery as a direct branch of the parasellar portion of the internal carotid artery, 10: medial-posterior venous space, 11: dominant type of the meningohypophyseal trunk) Figure 8.  The inferior group of the venous spaces of the cavernous sinus [microdissection, lateral view]. (1: supraclinoid portion of the internal carotid artery, 2: parasellar portion of the internal carotid artery, 3: anterior venous space of the superior group, 4: posterior venous space of the superior group, 5: parasellar portion of the abducent nerve, 6: posterior venous space of the inferior group, 7: infero-lateral trunk of the parasellar portion of the internal carotid artery, 8: anterior venous space of the inferior group, 9: third compact lamella) dura mater near to the parasellar region are same (about 0.4 mm). The thickness of the meningeal layer of the parasellar dura was about 4 mm and that of the meningeal layer of the dura mater adjacent to the parasellar region was about 1 mm (Figures 1–2, 4–5). Our examination demonstrated that the connective tissue of the meningeal layers of the parasellar dura mater and the adjacent dura were in a multilamellar structure. Essentially, we found two types of lamellae of the connective tissue of the meningeal layer as the compact and the loose lamellae. The compact lamellae were thinner than the loose lamellae (Figures 1–2, 4–5). We also found three compact and three loose lamellae in the meningeal layer of the middle cranial fossa dura adjacent to the parasellar region (Figure 1). Inside of these lamellae and between the compact lamellae we did not detect any large components, but a few branches of the accessory or middle meningeal artery may be found (Figure 1). On the other hand, we found four compact and four loose lamellae in the meningeal layer of the parasellar dura mater by dissection and histological examination (Figures 2–5, 7). The outer or superficial compact lamella of the connective tissue of the parasellar dura mater was
  • 9. Parasellar duramater and adjacent dura more compact and firm than the other lamellae of this region (Figures 2–4, 7). This lamella was spreading from the parasellar region along all over the middle cranial fossa. In the parasellar region, the middle cerebral superficial vein was piercing the anterior part of the lateral side of this lamella in about 30% of the cases, and going backwards along the inner side of this lamella to the venous spaces of the cavernous sinus (Figure 3). The second compact lamella was less compact and less firm than the outer or superficial compact lamella, and lying below the first one. At the level of the parasellar region, along the inner side of this lamella, the trochlear nerve and its arterial vessels were passing (Figures 3–4, 7). The third compact lamella was very close to the oculomotor, ophthalmic, maxillary, mandibular nerves, anterior parts of the trigeminal ganglion and to their arteries (Figures 3–4). In contrast to the first three compact lamellae, the fourth compact lamella was spreading only at the parasellar region (Figures 3–5). It was lying adjacent to the lateral side of the parasellar segment of the internal carotid artery. The abducent nerve and its arterial vessels were passing along the inferior margin of this lamella (Figures 4–6, 8). The loose connective tissue of the meningeal layer of the parasellar dura mater was lying between the compact lamellae, connecting them and forming the respective loose lamellae (Figures 2, 4–5). We found four loose lamellae in the meningeal layer of the parasellar dura mater. In about 30% of the cases, the middle superficial cerebral vein was piercing the anterior part of the lateral side of the first compact lamella and going backward through the first loose lamella (Figures 3–4). Through the second loose lamella were passing the trochlear nerve with its arterial vessels. This nerve was penetrating to the first two compact lamellae at the level of the posterior part of the oculomotor triangle and going ahead toward the superior orbital fissure, through the second loose lamella (Figures 3–5). In the third loose lamella we found the venous spaces of the lateral group of the cavernous sinus. Only one or two large venous spaces and several smaller venous spaces were presented in this loose lamella. The first three loose lamellae had the similar thickness (Figures 4–5). In contrast with the first three loose lamellae, the fourth loose lamella was slightly thicker than the first three loose lamellae (Figure 5). This lamella was lying between the fourth compact lamella and the periosteal layer of the parasellar dura mater. Through the fourth loose lamella was passing the parasellar segment of the internal carotid artery and within this lamella were the largest number of the venous spaces of the cavernous sinus (Figures 4–8). After piercing the periosteal layer of the parasellar dura mater at the level of the apex of the petrous bone, the internal carotid artery was immediately entering the fourth loose lamella and climbing to its first parasellar curve. Then it was turning abruptly forward to its horizontal portion, and was terminating by passing upwardonthemedialaspectoftheanteriorclinoidprocess, where it perforated all lamellae of the meningeal layer of the parasellar dura mater, and reached subarachnoid space. Also, we encountered its parasellar branches the meningohypophyseal trunk, the infero–lateral trunk, the McConnell’s capsular arteries and some of its variations (Figures 6–8). Our histological and dissection findings demonstrated that the venous spaces of the cavernous sinus were located mainly in the fourth and partly in the third loose lamella of the parasellar dura mater (Figures 2, 4–8). There were two types of venous spaces around the parasellar portion of the internal carotid artery as large and small ones. We did not find any small venous space on dissection but large ones were present (Figures 6–8). Histologicaly, the walls of the venous spaces were consisted of an endothelial layer and connective tissue layers of different thickness (Figures 4–5). 10 to 14 large venous spaces were found during dissection. In younger fetuses the venous spaces had smaller dimensions than the older fetuses. The venous spaces had an oval, triangular or a short canal form (Figures 4–8). Among the mentioned 10–14 large venous spaces we did not find wide communications. Small openings were present on the walls of the venous spaces, and we believe that these small openings regulate the anterograde and the retrograde circulation of the venous blood through the venous spaces of the cavernous sinus (Figure 6). Our findings suggest that the dissected large venous spaces were organized in five groups: around the internal carotid artery, lateral, medial, superior, inferior and posterior group (Table 1). The lateral group of the venous spaces was lateral to the parasellar portion of the internal carotid artery. We observed 3–6 venous spaces in this group (Figures 4–7). One or two of this venous spaces were located in the third loose lamella, but the others were located in the fourth. The medial group of the venous spaces were medially located to the parasellar portion of the internal carotid artery, in the fourth loose lamella (Figures 5, 7). We detected two venous spaces in this group, the anterior and the posterior ones. The superior group of the venous spaces was above the horizontal part of the internal carotid artery within the fourth loose lamella, and two venous spaces were present in this group, the anterior and the posterior ones (Figure 4). The inferior group of the venous spaces was below the horizontal part of the parasellar portion of the internal carotid artery, and medial to the parasellar portion of the abducent nerve, again in the fourth loose lamella. In this group 1–2 venous spaces were found, the anterior and posterior ones, or solitary one (Figures 4, 8). The posterior group of the venous spaces was in the form of canals; lying in the fourth loose lamella of the petro–clinoido–clival dura mater, behind the first curve and the first, or ascending part of the parasellar portion of the internal carotid artery (Figure 8). In this group two venous spaces were found as superior and inferior. The superior venous space or canal of this group was above the petro–clinoido–clival part of the abducent nerve and the corresponding part of the dorsal meningeal artery. Anteriorly, it was extending to thelevelofthemeningohypophysealtrunkandposteriorly,
  • 10.  Radomir R. Vucetic Table 1. Large venous spaces of the cavernous sinus. Group Number of large venous space Lateral 3–6 Medial 2 Superior 2 Inferior 1–2 Posterior 2 it was draining into the superior part of the basilar sinus, just below the posterior clinoid process. The inferior venous space or canal of this group was below the petro– clinoido–clival part of the abducent nerve. Anteriorly, it was narrow and extending to the posterior side of the first or ascending part of the parasellar portion of the internal carotid artery. Posteriorly, it was wider and draining to the inferior petrosal sinus, just below the apex of the petrous bone (Figure 8). Discussion Numerous pathological processes may appear in the parasellar and adjacent dura mater, such as various kinds of tumors, aneurysms, carotid–cavernous fistulas etc. A comprehensive understanding of the structure of the parasellar and adjacent dura mater is a prerequisite for successful surgical outcomes. In the available literature we did not find the parallel description of the structure of the parasellar dura mater and the middle cranial fossa dura, which is just adjacent to the parasellar region. All authors underline the fact that the cavernous sinus is a component which is inside of the parasellar dura mater. Some authors [4, 14, 23] underline the fact that Ridly and Winslow were the first authors who studied the parasellar dura mater, and Winslow’s finding (1732) were still convincing for a large number of authors of anatomical books in the second last half of the XXth century [1, 7, 9–11, 14]. It is commonly accepted that the cranial venous sinuses are located between the periosteal and meningeal layer of the dura mater, but Inoue et al. [20] believe that these sinuses are within the dural folds. It seems that the inferior sagittal sinus and the straight sinus are within the dural folds, because these sinuses do not have any periosteal layer. On the other hand, it seems that the superior sagittal sinus, the cavernous sinus and other sinuses are located between the periosteal and the meningeal layer of the dura mater. Many authors [1, 7–12, 14, 22–24] were able to show only schematic, phlebographic and one type of histological findings of the structure of the venous sinuses, but none of them had photographed of dissected cavities of these venous sinuses. Our findings are the same as many others, regarding the fact that the parasellar dura mater and adjacent dura were formed from the periosteal and the meningeal layers. We found that the thickness of the periosteal layer of the parasellarduramaterandoftheadjacentduraweresimilar, but they were thinner than the meningeal layer of the both mentioned regions. Also, our results demonstrated that the meningeal layer of the parasellar dura mater and of the adjacent dura were in a multilamellar structure and consisting of two type of lamellae, the compact and the loose lamellae. Four compact and four loose lamellae were found in the meningeal layer of the parasellar dura mater and three compact and three loose lamellae in the adjacent dura. From the surgical point of view the compact lamellae of the parasellar dura mater were lying on the way to the parasellar portion of the internal carotid artery. Umansky and Nathan [14] described only two layers on the way to the parasellar portion of the internal carotid artery. Several cranial nerves and some vessels use the loose lamellae of the meningeal layer of the parasellar dura mater as a milieu through which travel from the intradural space to the extradural space and reversally, but in the loose lamellae of the meningeal layer of the adjacent dura we did not find any evident vessels nor nerves. Our findings specified that in about 30% of cases, the middle superficial cerebral vein was traveling through the first loose lamella of the meningeal layer of the parasellar dura mater on the way to the cavernous sinus or into the middle meningeal vein. Also, we specified that the trochlear nerve and its vessels travel through the second loose lamella, and in the third loose lamella we found the venous spaces of the lateral group of the cavernous sinus. We specified that the thickness of the first three loose lamellae of the meningeal layer of the parasellar dura mater were similar, but the thickness of the fourth loose lamella was slightly thicker than the first three loose lamellae. We found that through the fourth loose lamella was passing the parasellar portion of the internal carotid artery. We specified that within the fourth loose lamella were the largest number of the venous spaces of the cavernous sinus, around the internal carotid artery, but not between the meningeal and periosteal layer as affirmed by many authors, and not into interperiosto–dural space of Taptas [12, 13]. The walls of the mentioned venous spaces were consisted of an endothelial layer and connective tissue layers of different thickness. We believe that these layers of the connective tissue of different thickness lying between the adjacent venous spaces represent famous trabeculae or ‘the cords of Willis’. Our findings suggest that the way of the venous blood through the meningeal layer of the parasellar dura mater is arranged in a few paths around the parasellar portion of the internal carotid artery, in the medial, lateral, superior et inferior path. In addition, the blood flow through the mentioned paths was not continuous, but segmented. The presence of large and small venous spaces around the parasellar portion of the internal carotid artery confirm that opinion. These results are the similar to that of Rhoton et al. [18, 19] and Kehrli et al. [4], but differs from the findings of Parkinson [17] who stated that the
  • 11. Parasellar duramater and adjacent dura References [1] Clemente CD. Gray’s Anatomy. 30th Ed., Philadelphia, Lea & Febiger. 1985; 682-703 and 799-816. [2] Carpenter BM. Core Text of Neuroanatomy. 4th Ed., Baltimore, Williams & Williams. 1996; 1-4 and 455-462. [3] Haines D. Fundamental Neuroscience. Churchill Livingstone. 1997; 99-111. [4] Kehrli P, Maillot C, Wolff MJ. The venous system of the lateral sellar compartment (cavernous sinus): an histological and embryological study. Neurol. Res. 1996; 18: 387-393. [5] Ros MH, Romrell LJ, Kaye GI. Histology. A Text and Atlas, 3rd Ed., Williams & Wilkins. 1995; 281- 283. [6] Krstic R. Human Microscopic Anatomy. Berlin, Springer-Verlag. 1991; 500-503. [7] Schaeffer JP. Morris’ Human Anatomy. 11th Ed., New York, Mc Graw-Hill. 1953; 752-757 and 1064- 1072. [8] Patouillard P, Vanneuville G. Les parois du sinus caverneux. Neurochirurgie. 1972; 18: 551-560. [9] Paturet G. Traite d’Anatomie Humaine. Paris, Masson. 1958; 3: 739-773. [10] Williams PL, Bannister LH. Gray’s Anatomy. 38th Ed., Edinburgh, Churchill Livingstone. 1995; 1210- 1212 and 1582-1589. [11] Rouviere H. Anatomie humaine, descriptive et topographique. Paris, Masson. 1959; 1: 209-216 and 3: 673-683. [12] Taptas JN. Must we still call cavernous sinus the parasellar vascular and nervous crossroad? Topographical description of the region. In: Dolenc VV, ed. The Cavernous sinus: a multidisciplinary approach to vascular and tumorous lesions. Wien, Springer-Verlag. 1987; 30-40. [13] Taptas JN. The so-called cavernous sinus: a review of the controversy and its implications for neurosurgeons. Neurosurgery. 1982; 11: 712-715. [14] Umansky F, Nathan H. The lateral wall of the cavernous sinus. With special reference to the nerves related to it. J. Neurosurg. 1982; 56: 228-234. [15] Kahle W, Leonhardt H, Platzer W. Color atlas and textbook of human anatomy. 4th Ed., Stuttgart, Thieme Verlag. 1993; 270-271. [16] Dolenc V. Direct microsurgical repair of intracavernous vascular lesions. J. Neurosurg. 1983; 58: 824-831. [17] Parkinson D. A surgical approach to the cavernous portion of the carotid artery. Anatomical studies and case report. J. Neurosurg. 1965; 23: 474 - 483. [18] Rhoton AL Jr, Hardy DG, Chambers SM. Microsurgical anatomy and dissection of the sphenoid bone, cavernous sinus and sellar region. Surg. Neurol. 1979; 12: 63-104. [19] Rhoton AL Jr, Harris FS, Renn WH. Microsurgical anatomy of the sellar region and cavernous sinus. Clin. Neurosurg. 1977; 24: 54-85. [20] InoueT,RhotonALJr,TheeleD,Barry ME. Surgicalapproachestothe cavernoussinus:amicrosurgical study. Neurosurgery. 1990; 26: 903-932. [21] Harris FS, Rhoton AL Jr. Anatomy of the cavernous sinus. A microsurgical study. J. Neurosurg. 1976; 45: 169-180. [22] Testut L, Latarjet A. Traite d’anatomie humaine. 9th Ed., Paris, Doin. 1948; 447-465 and 249-262. [23] Bedford MA. The cavernous sinus. Br. J. Ophthalmol. 1966; 50: 41-46. [24] Giudicelli G, Resche F, Louis R, Salamon G. Radioanatomie du sinus caverneux. Neurochirurgie. 1972; 18: 599-612. [25] Destrieux C, Velut S, Kakou MK, Lefranco T, Arbeille B, Santini JJ. A new concept in Dorello’s canal microanatomy: the petroclival venous confluence. J. Neurosurg. 1997; 87: 67-72. [26] Umansky Felix, Elidan J, Valarezo A. Dorello’s canal: a microanatomical study. J. Neurosurg. 1991; 75: 294-298. cavernous sinus is a plexus formed by several various– sized veins. The posterior group of the venous spaces were in form of canals, and lying in the fourth loose lamella of the petro– clinoido–clival dura mater, behind the ascending part of the parasellar portion of the internal carotid artery at the posterior end of the cavernous sinus. We see the superior and inferior venous canal of the posterior group as parts of the notion which is named as Dorello’s canal [25, 26]. We found small openings on the walls of the venous spaces serving for communication, but other authors did not have the similar findings. Conclusion Our findings demonstrated that the meningeal layer of the cranial dura mater is in a multilamellar structure, containing compact and loose lamellae in it. We confirmed that there are differences between the structures of the meningeal layers of the parasellar dura mater and of the adjacent dura. We specified that some cranial nerves and their vessels use the respective loose lamellae on their way through the meningeal layer of the parasellar dura mater. We confirmed that the venous spaces of the cavernous sinus are located in the third and mainly in the fourth loose lamella of the meningeal layer of the parasellar dura mater, but not between the meningeal and periosteal layer as affirmed by many authors. Our findings contribute to a better understanding of the dura mater and to successful microsurgical interventions in this area. Acknowledgements This study was supported by Gynaecology and Obstetrics Clinic of Nis. The collaboration of Prof.Dr. Dragomir Vucetic is gratefully acknowledged.
  • 12. Published online 15 April, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 8–9 Case Report During gross anatomy dissection of left side of neck of a 40-year-old male cadaver, we observed a variation in the origin of upper root of ansa cervicalis (Figures 1–2). The lower root of ansa cervicalis (Figure 1) was formed from the second and third cervical nerves, but the upper root came from the vagus. The muscular branches to sternohyoid, sternothyroid and inferior belly of the omohyoid were given by ansa cervicalis. The thyrohyoid and geniohyoid muscles were supplied by hypogossal nerve. However the ansa cervicalis nerve formation on the right side was normal. Discussion Normally the descending branch (descendens hypoglossi or upper root of the ansa cervicalis) leaves the hypoglossal nerve where it curves round the occipital artery and then descends in the anterior wall of the carotid sheath. After giving a branch to the superior belly of the omohyoid it is joined by the lower root of the ansa. Branches from the ansa supply the sternohyoid, sternothyroid and inferior belly of the omohyoid, another branch descends in to the thorax to join the cardiac and phrenic nerves [1]. The first cervical ventral ramus [1, 2] emerges above the posterior arch of atlas, passes forwards lateral to its lateral mass, descends anterior to its transeverse process, and joins the ascending branch of the second cervical ventral ramus. From this loop, communicating branches pass to the hypoglossal nerve, vagus nerve and sympathetic trunk. Fibres to hypoglossal nerve later leave it as a series of branches, viz. the meningeal, upper root of the ansa cervicalis, nerves to the thyrohyoid and geniohyoid. The hypoglossal nerve [1, 2] communicates with the sympathetictrunk,vagus,firstandsecondcervicalnerves, and lingual nerve. It emerges from the skull through the hypoglossal canal in the occipital bone, and then passes downwards and laterally forming a half-spiral turn round the inferior ganglion of vagus, to which it is united by connective tissue. The vagal connections occur between the hypoglossal nerve and the inferior vagal ganglion in the connective tissue uniting them. Close to its exit from the skull near the atlas the hypoglossal nerve is joined by branches from the superior cervical ganglion and a filament from the loop between the first and second cervical nerves which leaves the hypoglossal as the upper root of ansa cervicalis, nerve to the thyrohyoid, and nerve to the geniohyoid. Damage to the ansa can lead to change in voice quality after some time, the exact reason for this phenomenon is not known, it may be because of the loss of support provided by the strap muscles to the laryngeal cartilages during the movement of vocal folds. Inrecentyears,therehasbeenaproliferationoftechniques utilizing the ansa cervicalis nerve to reinnervate the paralyzed larynx such as neve-nerve anastomosis using ansa cervicalis nerve transfer to the recurrent laryngeal nerve [3]. The ansa cervicalis is used in reinnervation A rare origin of upper root of ansa cervicalis from vagus nerve: a case report Venkata Ramana VOLLALA Seetharama Manjunatha BHAT Satheesha NAYAK Deepthinath RAGHUNATHAN Vijay Paul SAMUEL Vincent RODRIGUES Jerry George MATHEW Department of Anatomy, Melaka Manipal Medical College (Manipal Campus), ICHS, Manipal 576104, Karnataka–India. Venkata Ramana Vollala, Department of Anatomy, Meleka Manipal Medical College (Manipal Campus), International Centre for Health Sciences, Manipal 576104, Karnataka–INDIA 91-820-257 12 01 (22516-22521) 91-820-257 19 05 ramana_anat@yahoo.co.in Received 17 February 2005; accepted 1 April 2005 ABSTRACT Ansa cervicalis is a loop of nerves in the carotid triangle of neck. Its upper root is the descending branch of hypoglossal nerve, which joins the lower root that is formed by branches from the second and third cervical nerves. The ansa cervicalis nerve formation is relatively complex, as its course and location along the great vessels of the neck vary. In the present case, on the left side of the neck of a 40-year-old male cadaver the upper root of ansa cervicalis came from vagus nerve. Neuroanatomy; 2005; 4: 8–9. Key words [ansa cervicalis] [upper root] [vagus nerve] [variation] eISSN 1303-1775 • pISSN 1303-1783
  • 13. A rare origin of upper root of ansa cervicalis of larynx because of its proximity to the larynx and it is quite active during phonation. Ansa cervicalis use is not limited to laryngeal reinnervation; the use of this nerve in preventing the morbidity associated with tongue hemiatrophy after facial-hypoglossal anastomosis has been reported [4]. Even though this nerve is sacrificed there is no serious functional disturbance. Therefore it is an ideal candidate for use in nerve reconstruction in the neck. The anatomic course and morphology of the ansa cervicalis are complicated by the variable course and location along the great vessels of the neck, as well as the significant differences observed in the arrangement of its contributing roots and regional branching patterns. The formation of the lower root varies greatly when compared with that of the upper root owing to the various cervical root contributions possible in its formations. In the present case, it appears that C1 fibres have joined the vagus nerve and leave as the upper root of the ansa cervicalis from the vagus nerve instead of hypoglossal nerve. Exact clinical significance of the present case cannot be postulated. There is no available literature on such variation. Figure 1.  Ansa cervicalis on left side. Note its upper root arising from the trunk of vagus nerve. (V: vagus nerve; H: hypoglossal nerve; U: upper root; L: lower root; A: ansa; T: nerve to thyrohyoids) References [1] Williams PL, Bannister LH, Berry MM, Collins P, Dyson M, Dussek JE, Ferguson MWJ. Gray’s Anatomy, 38th edn. Churchil & Livingstone, Baltimore. 1995; 1256-1263. [2] Chhetri DK, Berke GS. Ansa cervicalis nerve: review of the topographic anatomy and morphology. Laryngoscope. 1997; 107: 1366-1372. [3] Crumley RL, Izdebski K. Voice quality following laryngeal reinnervation by ansa hypoglossi transfer. Laryngoscope. 1986; 96: 611-616. [4] Kukwa A, Marchel A, Pietniczka M, Rakowicz M, Krajewski R. Reanimation of the face after facial nerve palsy resulting from resection of a cerebellopontine angle tumour. Br. J. Neurosurg. 1994; 8: 327-332. Figure 2.  Relation of ansa cervicalis to large vessels. (A: ansa; U: upper root; C: common carotid artery; J: internal jugular vein)
  • 14. Published online 13 July, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 10–12 Introduction The thalamus is a highly differentiated gray matter structure, comprising many subnuclei, each with specialized functional links to different cortical, subcorticalandcerebellarsitesandhasbeencharacterized as a dynamic conduit linking subcortical with cortical areas [1]. However, while normal ageing effects on thalamus have been studied in previous MRI studies, no report has covered normal ageing effect on both interthalamic adhesion (massa intermedia) and thalamus in the same sample. Some authors stated that in about 20% of cases it is even absent [2]. Human interthalamic adhesion except decussating, contains commissural fiber systems connecting some thalamic nuclei. The significance and eventual manifestation of its presence or absence is not known in humans. Knowledge of the morphology, size and position of interthalamic adhesion is important in neurosurgery as well as in neuroradiology and neuroanatomy. It is especially important because of its great variability in the human brain [3, 4]. The variability in presence and size of interthalamic adhesion is sexually dimorphic, with interthalamic adhesion being present more often in females, when compared with males [3]. Nopoulos at al. showed that female patients with schizophrenia had significantly higherincidenceofabsentinterthalamicadhesion(32.76%) compared with their healthy controls (13.50%) [5]. In this study, we compared the morphometric measurementsoftheinterthalamicadhesionandthalamus using MRI with regard to age and sex. Additionally, we analyzed the incidence of the absence of interthalamic adhesion. Material and Methods 161 patients (100 females and 61 males) without neuropathologic changes and symptoms being admitted to the Visart MRI center were included in this study. MR images (1.5 Tesla magnetom vision) were acquired in the axial and vertical planes by using flair T1-T2 weighted sequences. The patients were divided into six age groups. The groups were 19 years old and under, 20-29; 30-39; 40- 49; 50-59; 60 and over years. The transverse and vertical lengths of the interthalamic adhesion were measured in the coronal sections, while the anteroposterior and transverse length measurements of the thalami were obtained in the axial plane, and vertical length in the mid-sagittal plane. The anterior boundary of thalamus was defined as the posterior point of the interventicular foramen and the posterior boundary coincided with the section in which pulvinar thalami were seen. The lateral boundary of the thalamus was defined at the plane, where the posterior limb of the internal capsule was seen. The superior and inferior boundaries of thalamus was defined at the level of body of the fornix and hypothalamic sulcus respectively (Figures 1 and 2). Morphometric measurements of the thalamus and interthalamic adhesion by MR imaging Fikret SEN [1] Hakan ULUBAY [2] Pelin OZEKSI [1] Mustafa F. SARGON [1] A. Beliz TASCIOGLU [1] Department of Anatomy Hacettepe University Faculty of Medicine [1] and Visart Imaging Center [2] Ankara–Turkey. Dr. Fikret Sen Hacettepe University, Faculty of Medicine, Department of Anatomy, 06100 Ankara, TURKEY 90-312-305 21 01 90-312-310 71 69 fikret@hacettepe.edu.tr fikretsn@yahoo.com Received 4 March 2005; accepted 11 July 2005 ABSTRACT In this study, the morphometric measurements of the interthalamic adhesion and thalamus using MRI with regard to age and sex was assessed. Additionally, the incidence of the absence of the interthalamic adhesion was analysed. 161 patients (100 females and 61 males) without neuropathological changes and symptoms were included in this study. In the 60 and above age group, the transverse length of the interthalamic adhesion was measured as longest, while the vertical length was measured as the shortest. The anteroposterior and vertical lengths decreased gradually correlated with ageing, but the decrease in the anteroposterior length was not found related to the changes in thalamus sizes. No connection was found between the age groups and transverse, vertical and anteroposterior lengths of the thalamus. In the examination of the mean values of thalamus size with regard to age groups, the vertical length of thalamus was found to be shortest in the 60 and over years group. When investigating the mean values of the interthalamic adhesion size with regard to sex, the transverse lengthwasfoundlongerinmalesthaninfemales.Theverticalandanteroposteriorlengths,however,werelonger in females. When the mean values of the sizes of the thalami were evaluated according to sex, it was found that the transverse length was longer in males. The vertical and anteroposterior lengths were similar in both sexes. Additionally, the interthalamic adhesion was absent in 14 patients. Neuroanatomy; 2005; 4: 10–12. Key words [thalamus] [interthalamic adhesion] [morphometry] [MRI] eISSN 1303-1775 • pISSN 1303-1783
  • 15. 11Morphometric measurements of the thalamus and interthalamic adhesion Results In the 60 and over years group, the transverse length of the interthalamic adhesion was measured as longest, but the vertical length was measured as the shortest (Table 1). The anteroposterior and vertical lengths decreased gradually correlated with ageing, but the decrease in the anteroposterior length was not found parallel to the changes of thalamus sizes (Tables 1 and 2). No correlation was found between the age groups and transverse, vertical and anteroposterior lengths of the thalamus (p>0.05; Pearson correlation statistical test) (Table 2). In evaluation of the mean values of thalamus size with regard to age groups, the vertical length of thalamus was found to be shortest in 60 and over years group (Table 2). When investigating the mean values of interthalamic adhesion size with regard to sex, the transverse length Figure 1.  Measurement of the tranverse length of the thalamus. Figure 2.  Measurement of the anteroposterior length of the interthalamic adhesion. Table 1.  Mean values of the dimension of the interthalamic adhesion in age groups (mm). Age groups Transverse Vertical Anteroposterior 19 and under 2.41±0.89 5.66±2.44 9.52±3.24 20–29 2.67±0.73 4.81±2.21 8.05±2.85 30–39 3.22±1.03 4.51±2.63 7.61±3.28 40–49 3.11±1.00 3.87±2.22 7.95±3.04 50–59 3.09±1.00 4.61±2.74 7.95±3.15 60 and over 3.78±1.77 2.89±1.87 6.31±2.38 Table 2.  Mean values of the dimension of the thalamus in age groups (mm). Age groups Transverse Vertical Anteroposterior 19 and under 20.74±3.51 16.82±1.63 33.98±2.35 20–29 24.35±3.81 16.15±2.00 36.4±3.11 30–39 22.95±3.34 16.42±1.58 34.97±2.44 40–49 23.00±3.43 17.06±1.91 34.8±3.21 50–59 23.87±4.45 16.19±1.13 34.58±3.68 60 and over 23.98±4.70 14.55±1.73 35.72±4.17 was found longer in males than in females, however; the vertical and anteroposterior lengths were longer in females (Table 3). As the mean values of the thalamus sizes were assessed according to sex, it was found that the transverse length was longer in males than in females, while the vertical and anteroposterior lengths were similar in both sexes (Table 4). Additionally it was determined that the interthalamic adhesion was absent in 14 patients (8.7%). Discussion The incidence of the absence of interthalamic adhesion was found to be 13.3% [6], 13.79% [7] and 22% [3] in different studies. Additionally, it has been reported that the absence of the interthalamic adhesion was more frequent in patients with schizophrenia compared to healthy subjects [7]. In a study measuring the thalami,
  • 16. 12 Sen et al. it was concluded that the development of interthalamic adhesion did not depend on the size of the human thalamus. Next, it was also found that the volume of the interthalamic adhesion usually increased with age, probably caused by the widening of the third ventricle [3]. Rosales at al. showed that in elder persons, the interthalamic adhesion underwent atrophy and might disappear [8]. Absence of the interthalamic adhesion was found to be 8.7% in our study. In literature, we couldn’t find any data about the morphometric changes of interthalamic adhesion and thalamus with age examined within the same study. We found no correlation between size of thalamus and interthalamic adhesion with regard to age. Additionally we observed that as the anteroposterior and vertical lengths of the interthalamic adhesion decreases with age, the transverse length increases. This finding shows that the thalamus doesn’t undergo any significant changes with age, while the interthalamic adhesion becomes thin and lengthened. Table 3.  Mean values of the dimension of the interthalamic adhesion in sex groups (mm). Sex Transverse Vertical Anteroposterior Female 2.97±1.02 4.45±2,38 8.31±3.09 Male 3.26±1.40 4.19±2,66 6.98±2.88 Table 4.  Mean values of the dimension of the thalamus in sex groups (mm). Sex Transverse Vertical Anteroposterior Female 2.66±3.36 16.39±2.08 35.05±2.93 Male 24.31±4.67 16.00±1.37 35.23±3.71 References [1] Sullivan EV, Rosenbloom M, Serventi KL, Pfefferbaum A. Effects of age and sex on volumes of the thalamus,pons and cortex. Neurobiol. Aging. 2004; 25: 185-192. [2] Carpenter MB, Sutin J, Strong OS. Human neuroanatomy. Williams&Wilkins, Baltimore 1984; pp:52- 54. [3] Malobabic S, Puskas L, Blagotic M. Size and position of the human adhaesio interthalamica. Gegenbaurs Morphol. Jahrb. 1987; 133: 175-184. [4] Clarck DL, Boutros NN. The brain and behaviour. Blackwell Science, Massachusets. 1999; pp:121. [5] Nopoulos PC, Rideout D, Crespo-Facorro B, Adreasen NC. Sex differences in the absence of massa intermedia in patients with schizophrenia versus healthy controls. Schizophren. Res. 2001; 48: 177- 185. [6] MeisenzahlEM,FrodlT,ZetzscheT,LeinsingerG,HeissD,MaagK,HegeriU,HahnK,MöllerHJ. Adhesio interthalamica in male patients with Schizophrenia. Am. J. Psychiatry. 2000; 157: 823-825. [7] Erbagci H, Yildirim H, Herken H, Gumusburun E. A magnetic resonance imaging study of the adhesio interthalamica in schizophrenia. Schizophr. Res. 2002; 55: 89-92. [8] Rosales RK, Lemay MJ, Yakolev PI. The development and involution of massa intermedia with regard to age and sex. J. Neuropat. Exp. Neurol. 1968; 27: 166.
  • 17. Published online 20 July, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 13–15 Introduction Weobservedanaccessorybranchofthemusculocutaneous nerve. This variation has clinical importance in median nerve lesions and its distinctive diagnosis. The coracobrachialis muscle is usually supplied by the musculocutaneous nerve. Its innervation pattern exhibits a considerable variation [1]. The change in the innervation of the coracobrachialis muscle is reported to be closely correlated with the change of course of the musculocutaneous nerve [2, 3]. The musculocutaneous nerve usually arises from the lateral cord of the brachial plexus, pierces and innervates the coracobrachialis muscle [2, 4]. However, the course and branching anomalies of the musculocutaneous nerve and its relation to the coracobrachialis muscle have been documented in the literature by Koizumi [2], Buch [5], Flatow et al. [6], and Le Minor [7]. On the other hand, the distribution, course and branching of the musculocutaneous nerve is important from the clinical point of view, especially in compression neuropathies due to vigorous activity and stretch injuries seen in various surgical interventions [8–10]. Case Report During the educational gross anatomy dissections of the right axilla and brachium of a 50-years-old male cadaver in our laboratory, we encountered neuroanatomical variation. The lateral cord of brachial plexus and its branches had a different configuration. The nerves forming the letter ‘M’ were normal on the right side under the pectoralis minor muscle. The musculocutaneous nerve passed through the coracobrachialis muscle, and gave branches to biceps brachii and brachialis muscles. The abnormal branch of the musculocutaneous nerve originated approximately at the mid point level of the brachial region, and 2.8 cm above the distal end of the deltoid tuberosity. It coursed inferiorly between the biceps brachii and brachialis muscles for about 12.6 cm and joined the median nerve 5.6 cm superior to the interepicondillary line. Giving its accessory branch and the nerve to the biceps brachii and brachialis muscle, the musculocutaneous nerve coursed normally as a lateral antebrachial cutaneous nerve (Figure 1). The course of the musculocutaneous nerve was normal in the forearm region. Other branches originating from the brachial plexus were also normal (Figure 2). In the left brachial region of the same cadaver, the nerve to the coracobrachialis muscles was seen to originate from the musculocutaneous nerve which arose normally from the lateral cord of the brachial plexus and pierced the coracobrachialis muscles as usual. Discussion The musculocutaneous nerve usually arises from the lateral cord of the brachial plexus (C5, C6 and C7), pierces the coracobrachialis muscles and then passes downward between the biceps and the brachialis muscle. It appears at the lateral margin of the biceps tendon and runs down the lateral aspect of the forearm as the lateral cutaneous An accessory branch of musculocutaneous nerve joining median nerve Necdet KOCABIYIK Bulent YALCIN Fatih YAZAR Hasan OZAN Department of Anatomy Gulhane Military Medical Academy (GATA), Etlik Ankara–Turkey. Necdet Kocabiyik, MD Department of Anatomy, Gulhane Military Medical Academy (GATA), 06018 Etlik Ankara–TURKEY 90-312-304 35 08 90-312-304 21 50 nkocabiyik@gata.edu.tr Received 7 April 2005; accepted 19 July 2005 ABSTRACT During the educational gross anatomy dissections of the axilla and brachium of a 50-year-old male cadaver in our laboratory, we encountered a neuroanatomical variation. The lateral cord of brachial plexus and its branches, had a different configuration. The nerves forming the letter ‘M’ was normal right under the pectoralis minor muscle. The musculocutaneous nerve passed through the coracobrachialis muscle, and gave branches to biceps brachii and brachialis muscles. The anomalous branch of the musculocutaneous nerve originated approximately at the mid point level of the brachial region, and 2.8 cm above the distal end of deltoid tuberosity. It coursed inferiorly between the biceps and brachialis muscles about 12.6 cm and joined the median nerve 5.6 cm superior to the interepicondillary line. Giving its accessory branch and the nerve to the biceps brachii and brachialis muscle, the musculocutaneus nerve coursed normally as a lateral antebrachial cutaneous nerve. This variation has clinical importance in median nerve lesions and its distinctive diagnosis. Lesions of the median nerve, If lesion was proximal to this accessory branches, muscles and cutaneous innervations related to this branch was normal. Neuroanatomy; 2005; 4: 13–15. Key words [coracobrachialis muscle] [musculocutaneous nerve] [brachial plexus] [median nerve] [communicating branch] eISSN 1303-1775 • pISSN 1303-1783
  • 18. 14 Kocabiyik et al. nerve of the forearm after piercing the fascia just above the elbow. It sometimes shows wide distribution to the skin. Appleton [11] showed a case of complete absence of the cutaneous branch of the radial nerve, to the hand, and replacement by the musculocutaneous nerve. The distribution and the course and the branching of the musculocutaneous nerve is important from the clinical viewpoint. Linell [12] advised that for clinical investigation and the surgical treatment of peripheral nerve injury, a more precise knowledge than that found in classical anatomical texts was necessary, because the musculocutaneous nerve sometimes runs a different course and supplies some branches to the median nerve, a communicating branch. According to Hollinshead [13], this is usually interpreted as meaning that fibers that should have run through the lateral root of the median nerve failed to do so, but entered the musculocutaneous and rejoined the median nerve. Iwamoto [14] analyzed the root of communicating branch with the median nerve, and described the communicating branch, consisting of fibers arising from C5 and C6. There have been many reports of the occurrence of a communication between the musculocutaneous nerve and the median nerve [3, 5, 14–17]. Communication between the musculocutaneous and the median nerve was considered as a remnant from the phylogenic or comparative anatomical view point. The median nerve has two roots from the lateral and medial cords. The medial root of the median nerve crosses the axillary artery at an oblique angle to join the lateral root, thus forming the median nerve. The nerve to coracobrachialis muscle lies close to the axillary artery but than usually pierces the coracobrachialis muscle and passes laterally and obliquely to lie between the biceps brachii and brachialis. The variations of the musculocutaneous and median nerve may be classified in five types [7] (Figure 2). Type I: there are no connecting fibers between the musculocutaneous and median nerve as described in classic textbooks [18, 19]. The musculocutaneous nerve pierces the coracobrachialis muscle and innervates the coracobrachialis, the biceps brachii and brachialis muscle. Figure 1.  Showing the accessory branch from the musculocutaneous nerve to the median nerve. (1: lateral cord; 2: medial cord; 3: lateral root of median nerve; 4: medial root of median nerve; 5: musculocutaneous nerve; 6: median nerve; 7: ulnar nerve; 8: nerve to biceps brachii; 9: nerve to brachialis; 10: lateral cutaneous antebrachial nerve; 11: accessory branch; 12: coracobrachialis muscle, 13: biceps brachii muscle, 14: brachialis muscle.) Figure 2.  Showing illustrations of five types of the musculocutaneous and the median nerves (I-V) and our case (*). (LF: lateral cord; MF: medial cord; MC: musculocutaneous nerve; M: median nerve; U: ulnar nerve; CB: coracobrachialis muscle; BB: biceps brachii muscle; B: brachialis muscle; LR: lateral root of median nerve; MR: medial root of median nerve)
  • 19. 15An accessory branch of musculocutaneous nerve Type II: although some fibers of the medial root of the median nerve unite with the lateral root of the median nerveandformthemaintrunkofmediannerve,remaining medial root fibers run in the musculocutaneous nerve leaving it after a distance to join the main trunk of median nerve. Type III: the lateral root of the median nerve from the lateral cord runs in the musculocutaneous nerve and leaves it after a distance to join the main trunk of median nerve. Type IV: the fibers of the musculocutaneous nerve unite with the lateral root of the median nerve. After some distance, the musculocutaneous nerve arise from the median nerve. Type V: the musculocutaneous nerve is absent. The fibers of the musculocutaneous nerve run within the median nerve along its course. In this type the musculocutaneous nerve does not pierces the coracobrachialis muscle. According to Le Minor, the variation of Type V was described by Broca in 1888 and its incidence ranged 0.3-2% [7]. Kerr in his study covering 175 brachial plexuses found this variation in only 3 cases (1.7%) [1]. Watanabe et al. Found 2 cases (1.4%) of fusion of the musculocutaneous and median nerve among 140 upper limbs [3]. Although our case is similar to Type II, the accessory branch of musculocutaneous nerve united with the lateral root of the median nerve, and joined the median nerve 5.6 cm superior to the interepicondillary line. References [1] Kerr AT. The brachial plexus of nerves in man, the variations in its formation and branches. Am. J. Anat. 1918; 23: 285-395. [2] Koizumi M. A morphological study on the coracobrachialis muscle. Kaibogaku Zasshi. 1989; 64: 18- 35. [3] Watanabe M, Takatsuji K, Sakamoto N, Morita Y, Ito H. Two cases of fusion of the musculocutaneous and median nerves. Kaibogaki Zasshi. 1985; 60: 1-7. [4] Kosugi K, Shibata S, Yamashita H. Supernumerary head of biceps brachii and branching pattern of the musculocutaneous nerve in Japanese. Surg. Radiol. Anat. 1992; 14: 175-185. [5] Buch C. On the variation in the method of innervation of the biceps muscle of the arm with special reference to branches from the musculocutaneous nerve and the median nerve. Anat. Anz. 1964; 114: 131-140. [6] Flatow EL, Bigliani LU, April EW. An anatomic study of the musculocutaneous nerve and its relationship to the coracoid process. Clin. Orthop. Relat. Res. 1989; 244: 166-171. [7] Le Minor JM. A rare variation of the median and musculocutaneous nerves in man. Arch. Anat. Histol. Embryol. 1990; 73: 33-42. [8] Braddom RL, Wolfe C. Musculocutaneous nerve injury after heavy exercise. Arch. Phys. Med. Rehabil. 1978; 59: 290-293. [9] Caspi I, Ezra E, Nerubay J, Horoszovski H. Musculocutaneous nerve injury after corocoid process transfer for clavicle instability. Acta Orthop. Scand. 1987; 58: 294-295. [10] Pecina M, Bojanic I. Musculocutaneous nerve entrapment in the upper arm. Int. Orthop. 1993; 17: 232-234. [11] Appleton AB. A case of abnormal distribution of the musculocutaneous nerve, with complete absence of the ramus cutaneous nervus radialis. J. Anat. Physiol. 1912; 46: 89-94. [12] Linell EA. The distribution of nerves in the upper limb, with reference to variabilities and their clinical significance. J. Anat. 1921; 55: 79-112. [13] Hollinshead WH. Anatomy for surgeons. The back and limbs. 3rd Ed., Harper & Row, Philadelphia, 1982. [14] Iwamoto S, Kimura K, Takahashi Y, Konishi M. Some aspects of the communicating branch between the musculocutaneous and median nerves in man. Okajimas Folia Anat. Jpn. 1990; 67: 47-52. [15] Fujita T. Complete fusion of the musculocutaneous and median nerve in a human arm, with some anomalies of the biceps brachii muscle. Kaibogaku Zasshi. 1957; 32: 257-262. [16] Monden M. The communication between the median nerve. Juzen Med. 1942; 47: 2045-2055. [17] Serisawa M, Hagura N, Eto M. On the third head of the biceps brachii muscle and its relation to the lateral cutaneous nerve of the forearm. Dokkyo J. Med. Sci. 1978; 5: 303-312. [18] Arinci K, Elhan A. Anatomi. Gunes Kitapevi, Ankara. 1997; p. 210-220. [19] Williams PL, Bannister LH, Berry MM, Collins P, Dyson M, Dussek JE, Ferguson MWJ. Gray’s anatomy 38th Ed., Churchill Livingstone, Edinburgh. 1995; pp: 842, 1269, 1924. [20] Spinner M, Winkelman MA. Variant branch of median nerve. Bull. Hosp. Joint Dis. 1973; 34: 161-196. The musculocutaneous nerve has rather constant anatomical features, that is, originating from the lateral cord of the brachial plexus and piercing the coracobrachialis muscle. However, Buch [5] reported that, in his cadaveric study, the musculocutaneous nerve originated from the median nerve in 3-6% and from the posterior cord in 1-5% of cases. Le Minor [7], Spinner and Winkelman [20] observed in their case that the lateral cord, without giving off the lateral root of the median nerve, passed through the coracobrachialis muscle and innervated the coracobrachialis, biceps brachii and brachialis muscles. On the other hand, the musculocutaneous nerve does not pierce the coracobrachialis muscle in some instances (according to Buch, up to (14%) or even might be absent in rare cases because to musculocutaneous nerve joins the median nerve [2]. In our case, the musculocutaneous nerve pierced the coracobrachialis muscle. In conclusion, the presence of this variation should be considered when a high median nerve paralysis exists in the axilla or proximal arm in a patient presenting weakness of forearm flexion and supination. The variant course of the musculocutaneous nerve should be kept in mind as a possible way of treatment in recurrent compression neuropathies. This variation has clinical importance in median nerve lesions and its distinctive diagnosis. In median nerve lesions proximal to the accessory branches, motor and sensory innervation remains normal.
  • 20. Published online 20 July, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 16–17 Introduction Caudal regression syndrome is a pathology caused by anomaly of spinal trunk ‘ending’, and encompasses a wide range of anomalies of the hind end of the trunk, including partial agenesis of the thoracolumbosacral spine, imperforate anus, malformed genitalia, bilateral renal dysplasia or aplasia, pulmonary hypoplasia, and in the most severe deformities, extreme external rotation and fusion of the lower extremities (sirenomelia). The syndrome is significantly associated with several systems, including congenital cardiac disease (24%), genito-urinary disease like hydronephrosis, renal agenesis, epispadias and hypospadias (24%), orthopedic anomalies like gluteal anomalies, scoliosis, and talipes deformities (12%), and progressive deficits like back and leg pain (30%). Tethered cord, dermoid cyst, lipoma and diastematomyelia may emerge in the central nervous system [1-3]. Examination and clinical follow-up are important for the decision of operation if these anomalies are suspected to cause neurological deficits. Myelography and myelo- computerized tomography (CT) have been replaced today by magnetic resonance imaging (MRI) as the gold standard for diagnosis [1, 2, 4-6]. There is a definite but incomplete association of the syndrome with diabetes mellitus; 1% of the offspring of diabetic mothers will have a form of this syndrome. Genetic changes caused by teratogens and pathologies 7q have been suggested as other factors [2]. Caudal regression syndrome has been reported only rarely after the childhood period in the literature. Case Report A 16-year-old female was examined for back pain while on follow-up forneurogenicbladder by theUrology Clinic. There was no symptom other than urinary incontinence, and no history of another illness. Family history revealed that the mother of the patient had diabetes mellitus before and during her pregnancy. Lumbosacral MRI scan demonstrated termination of the spinal cord at the T11-T12 level and narrowing of the canal at the L4-L5 level, and the patient was diagnosed as caudal regression syndrome. No fracture lines were found at bone structures, but the partial sacral agenesis was shown on direct films (Figure 1). The spinal cord fit the classic caudal regression syndrome imaging by lumbar MRI (Figure 2). Detrusorhyperreflectionwasshownwithcystometrogram (CMG) and minimal residue was observed on voiding cystourethrogram (VCUG). The patient’s complaints significantly improved with anticholinergic medication. No operation was planned because the patient improved with medications and because no other pathological signs were determined. There has been no progression of the patient’s complaints after three years of follow-up. Discussion Caudal regression syndrome is generally diagnosed in the early years of life and requires surgical intervention Caudal regression syndrome diagnosed after the childhood period: a case report Gokmen KAHILOGULLARI [1] Hakan TUNA [1] Zafer AYDIN [1] Ahmet VURAL [2] Ayhan ATTAR [1] Haluk DEDA [1] Department of Neurosurgery [1] and Radiology [2], Ankara University, Faculty of Medicine, Ankara–Turkey. Gokmen Kahilogullari, MD Department of Neurosurgery, Ankara University, Faculty of Medicine, 06100 Ankara–TURKEY 90-312-310 33 33 (Ext:2598) 90-312-309 43 40 gokmenkahil@hotmail.com Received 17 February 2005; accepted 19 July 2005 ABSTRACT Caudal regression syndrome is a congenital syndrome that presents with pathology of spinal tract migration during the embryologic period. In this paper, we report a 16–year-old caudal regression syndrome case. This syndrome is very rare, especially after the childhood period. In this patient, caudal regression syndrome was demonstrated by imaging techniques. The patient was planned to be followed without operation. Treatment methods and the follow- up period in caudal regression syndrome are discussed. Neuroanatomy; 2005; 4: 16–17. Key words [caudal regression] [spinal cord] [abnormality] [disease] eISSN 1303-1775 • pISSN 1303-1783
  • 21. 17Caudal regression syndrome in the case of neurological deficits. The signs on neurological examination may range from a variety of minimal deficits to severe paralysis. Motor deficits are generally more severe than sensory deficits. The syndrome has been shown to occur more frequently in the offspring of diabetic versus non-diabetic mothers. Although hyperglycemia in the early stages has been implicated, the pathogenesis remains unknown. Trauma, nutritional problems, toxic agents and genetics are the other factors suggested in the etiology [3, 4]. Myelography and myelo-CT were previously used for diagnosis. Sacral agenesis and vertebrae anomalies that are shown by direct films may give information about the syndrome. Distal vertebral anomalies and fetal spine anatomy may be seen by obstetric ultrasonography (USG), and in the intrauterine period, amniofusion may be important, especially in cases associated with oligohydramnios. The superiority of lumbosacral MRI is generally accepted today [2, 5, 6]. Patients may require surgical intervention for decompression and vertebral anomalies, especially in caudal regression syndrome with neurological deficits. Some authors have advised that in tethered cord cases in caudal regression syndrome, cutting of the filum terminale would be useful to prevent secondary infection caused by residual urine in the bladder [7]. We suggest clinical follow-up after the childhood period for those patients with no severe or progressive neurological deficit, as in our case. However, patients with severe or progressive neurological deficits should be operated. Figure 1.  Lateral radiograph revealing a partial sacral agenesis. References [1] Pappas CT, Seaver L, Carrion C, Rekate H. Anatomical evaluation of the caudal regression syndrome (lumbosacral agenesis) with magnetic resonance imaging. Neurosurgery. 1989; 25: 462-465. [2] Atlas SW. Magnetic resonance imaging of the brain and spine. 3rd Ed., Philadelphia, Lippincott Williams & Wilkins, 2002; 1589-1595. [3] Towfighi J, Housman C. Spinal cord abnormalities in caudal regression syndrome. Acta Neuropathol. (Berl). 1991; 81: 458-466. [4] Adra A, Cordero D, Mejides A, Yasin S, Salman F, O’Sullivan MJ. Caudal regression syndrome: etiopathogenesis, prenatal diagnosis, and perinatal management. Obstet. Gynecol. Surv. 1994; 49: 508-516. [5] Nievelstein RA, Valk J, Smit LM, Vermeij-Keers C. MR of the caudal regression syndrome: embryologic implications. Am. J. Neuroradiol. 1994; 15: 1021-1029. [6] Hirano H, Tomura N, Watarai J, Kato T. Caudal regression syndrome: MR appearance. Comput. Med. Imaging and Graph. 1998; 22: 73-76. [7] Selcuki M, Unlu A, Ugur HC, Soygur T, Arikan N, Selcuki D. Patients with urinary incontinence often benefit from surgical detethering of tight filum terminale. Childs Nerv. Syst. 2000; 16: 150-154. Figure 2.  Caudal regression syndrome. Sagittal T1-weighted (left) and T2-weighted (right) midsagittal MRIs. Partial sacral agenesis, with only S1, S2 and a portion of S3 present. The conus lies at T12 and shows bulbous angulated termination (arrows). The distal bony canal and thecal sac are narrow.
  • 22. Published online 29 July, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 18–23 Introduction A characteristic feature of animals and particularly of humans is the ability to alter their behaviour on the basis of experience or learning. Learning is an acquisition and storage of information as a consequence of experience. Memory is a relatively permanent storage form of the learned information [1]. The hippocampus and amygdala are two important regions involved in learning and memory. In the ayurvedic system of medicine “Medhya drugs” are a group of medicines known to act on the nervous system. In the texts of Ayurveda, many medhya drugs have been claimed to improve mental ability [2]. Some of the drugs, which act on the nervous system, include Bacopa monnieri, Ashwagandha (Withania somnifera), Jyotishmati (Celastrus panniculatus) Shankapushpi (Clitoria ternatea), Jatamansi (Nardostachys jatamansi), Vacha (Acorus calamus) and Mandukaparni (Brahmi, Centella asiatica) [3–6]. Among these, Centella asiatica (CeA) is a herb growing in wet and marshy places throughout the country. It has been used in ayurvedic preparations either in the fresh or in the extract form [2]. Centella asiatica is shown to be very useful in improving learning and memory [4–6]. It is also used as a brain tonic for promoting brain growth and improving memory [7]. In addition, the plant is also used in mentally retarded children to improve general mental ability [5, 8–10]. Though the fresh juice of CeA has been claimed to improve learning and memory in different clinical studies, there are no direct neurological studies to show the action of fresh leaf juice of this plant on improvement of behaviour especially learning and memory in neonatal rats. Thus this study was designed to find the effect of CeA fresh leaf juice treatment on learning and memory in neonatalrats.Thisexperimentwascarriedoutonneonatal rats, since, active brain growth occurs in them during pre and post-weaning period (growth spurt period) [11]. Materials and Methods Animals and experimental groups 7 days old Wistar rats of both sexes maintained under 12 hours dark and 12 hours light cycle, provided with food and water ad libitum were used in the experiments. Rat pups were divided into three major groups: 1) two weeks, 2) four weeks, 3) six weeks treatment groups. In each of these groups there were subgroups: a.  Normal control (NC): These animals remained undisturbedintheirhomecagetillothergroupscompleted their saline/CeA fresh leaf juice treatment, b.  Saline control (SC): These animals received equivolume of saline, c.  2ml/kg CeA group: These animals received 2ml/kg CeA fresh leaf juice every day, Centella asiatica (linn) induced behavioural changes during growth spurt period in neonatal rats K. G. Mohandas RAO [1] S. Muddanna RAO [2] S. Gurumadhva RAO [3] Departments of Anatomy [1] and Pharmacology [3], Meleka Manipal Medical College, Manipal–India; Department of Anatomy [2], Kasturba Medical College, Manipal–India. Dr. K. G. Mohandas Rao Assistant Professor in Anatomy, Meleka Manipal Medical College, 576 104 Manipal–INDIA 91-820-257 12 01 (Extn:22519) 91-820-257 19 05 babbarao@yahoo.com Received 19 April 2005; accepted 26 July 2005 ABSTRACT Neonatal rat pups (7 days old) were given different doses of fresh leaf juice of Centella asiatica (CeA) orally for different periods of time. These rats were then subjected to spatial learning (T- Maze) and passive avoidance tests along with the age matched normal and saline control rats. The results showed improvement in spatial learning performance and enhanced memory retention in neonatal rats treated with higher doses. These results indicate that treatment with CeA fresh leaf juice during growth spurt period of neonatal rats enhances memory retention. Neuroanatomy; 2005; 4: 18–23. Key words [centella asiatica] [growth] [spatial learning] [passive avoidance] [memory] eISSN 1303-1775 • pISSN 1303-1783
  • 23. 19Centellia asiatica induced behavioural changes in neonatal rats d.  4ml/kg CeA group: These animals received 4ml/kg CeA fresh leaf juice every day, e.  6ml/kg CeA group: These animals received 6ml/kg CeA fresh leaf juice every day. The experiments were carried out after the approval from the animal ethical committee. Extraction and administration of Centella asiatica leaf juice The plant, CeA was identified by Mr. P. Venugopal Tantry, Professor of Botany, Department of Botany, Vijaya College, Mulky, Karnataka, India and has been entered in and given the voucher specimen number “525PP” by the department of Pharmacognosy, Manipal College of pharmaceutical Sciences, Manipal, India. These plants were specially grown in uniform soil and water conditions. Fresh leaves of CeA were collected in the morning. Care was taken to collect the leaves of uniform growth (15–20 days old). After washing, air drying and homogenizing by grinding, the juice was extracted by squeezing the paste like homogenate using a piece of clean cloth. The fresh juice so obtained was administered as such or after appropriate dilution with saline by gastric intubation, using a capillary tube attached to a tuberculin syringe. The volume of juice to be given to the individual rat was calculated based on their body weight. Behavioural tests Following treatment, all the groups (NC, SC and CeA) of rats were subjected to behavioural tests. The behavioural tests included, 1) spatial learning (T- Maze) test and 2) passive avoidance test. Spatial learning (T–maze) tests The purpose of this test was to assess the spatial learning ability of the rats. This test included spontaneous alternation and rewarded alternation tests. The wooden T–maze apparatus consisted a stem (35x12cm), a choice area (15x12 cm) and two arms (35x12cm). The start box (15x12 cm) was located at the beginning of the stem. The goal areas were at the ends of the two arms (each 15x12 cm) containing the food well. The stem and start box were separated by a sliding door. A cloth curtain separated the arm and goal areas. The height of the sidewall of the apparatus was about 40 cm. The apparatus was kept in a sound attenuated normally lit room. Spontaneous alternation test [12]. Two days prior to the starting of the test, the rats were deprived of food in order to motivate them for the food reward. Subsequently, the food was restricted so that the animal’s body weight was maintained at 85% of pre-test weight. This was followed by orientation, which was done to familiarize the rats with the T–maze. During orientation, the rats subjected for food restriction were placed in the start box for sixty seconds. The sliding door was then opened to allow the rat to explore the T–maze for thirty minutes, and to eat fifteen pellets (10 mg each) in each goal area. After thirty minutes the rat was returned to the start box. This procedure was carried out for two consecutive days for all rats of the group. After the orientation, six trials were given daily for the following four days. In each trial, the rat was first placed in the start box. By opening the sliding door it was allowed to enter into the stem and allowed to choose any one of the arms. A rat was considered to have entered into a particular arm only when it entered that arm with all its limbs. Once the rat ate the pellet in the goal area of that arm, it was replaced back in the start box for the next trial. The intertrial interval was one minute. In each trial, the arm chosen by the rat was noted. At the end of four days i.e. twenty-four trials, the total number of alternations were also noted. The percentage bias was calculated for each rat using the following formula. Percentage bias = Total number of choices of more frequently chosen side x 100 Total number of trials More number of alternations and less percentage bias was considered as an index for improved learning ability. Rewarded alternation test [2]. This test was started on the day after the completion of spontaneous alternation test. During this test, six trials per day were conducted for four days. Each trial had two runs namely, a forced run and a choice run. In the forced run, the animal was forced to one of the arms by blocking the other arm and was allowed to consume the pellet in the goal area. Once the animal ate the pellet in the goal area, it was placed back in the start box for a choice run. In the choice run, the goal area of the forced arm was kept empty and pellets were placed in the goal area of the opposite arm. But both the arms were kept free for the rat to choose. Between each forced run and the choice run, a gap of one minute was given. Similarly there was a gap of one minute between the two trials again. The sequence of the forced arm was predetermined and was same for all the rats for a given day. On subsequent days it was alternatively changed. For example on the first day of the test, if the animals were forced to the right arm of the T–maze, on the second day they were forced to enter the left arm. On the third day, again forced to the right arm and on the fourth day to the left arm. During the choice run, if the rat entered the arm opposite to the forced arm, then that response was considered as “correct response”. If it entered the same arm to which it was forced during forced run, it was considered as “wrong response”. Percentage of correct responses was calculated for each rat by using the following formula. Percentage of correct responses = Total number of correct responses x 100 Total number of trials Increase in percentage of correct response was considered as an index of improved learning and memory. Passive avoidance test (Modified from Bures et al. [13]) The passive avoidance apparatus was fabricated locally. It had two compartments, a rectangular larger compartment with a 50x50 cm grid floor and wooden
  • 24. 20 Rao et al. walls of 35 cm height. It had a roof, which could be opened or closed. In the centre, one of the walls had a 6x6 cm opening connecting the larger compartment to a dark smaller compartment. The smaller compartment had 15x15 cm electrifiable grid connected to a constant current stimulator, wooden walls of 15 cm height and a ceiling, which could be opened or closed. The connection between the two compartments could be closed with a sliding door. The larger compartment was illuminated with a 100 W bulb placed 150 cm above the centre. The experiment included three parts, 1) exploration test, 2) an aversive stimulation and learning (passive avoidance acquisition), and 3) retention test. During exploration test each rat was kept in the centre of the larger compartment facing away from the entrance to the dark smaller compartment. The door between the two compartments was kept open. The rat was allowed to explore the apparatus (both larger and smaller compartments) for 3 minutes. In each trial, the total time spent by the animal in the smaller compartment was noted. At the end of the trial, the rat was replaced in the home cage, where it remained during inter-trial interval of five minutes. After the last exploration trial, the rat was forced into the smaller compartment and the sliding door between the two compartments of the apparatus was closed. Three strong foot shocks (50 Hz, 1.5 mA, 1 sec duration) were given at approximately five-second intervals. The ceiling was then opened and the rat was returned to its home cage. Retention test was carried out after twenty-four hours of acquisition test. The rat was kept in the centre of the larger compartment facing away from the entrance to the smaller compartment. The sliding door between the two compartments was kept open. The rat was allowed to explore the apparatus for three minutes. After three minutes the rat was kept back in the home cage. With a gap of five minutes the trial was repeated for three times. In each trial, the time spent by the rat in the smaller compartment was noted. Decrease in the time spent in the smaller compartment during retention test was considered as good memory retention performance Data analysis. Data was analyzed using analysis of variance (ANOVA) followed by Bonferroni’s test (post- test) using Graph Pad In Stat (GPIS) software, version 1.13. Results Spatial learning (T-Maze tests) Table-1 shows results of the T-Maze tests. In 2 weeks treatment group, during spontaneous alternation test, animals treated with 2ml of CeA fresh leaf juice did not show any significant difference in their performance. However, animals treated with higher doses of CeA fresh leaf juice (4 and 6 ml) showed significantly higher number of alternations when compared to normal control group of rats (10.1 ± 3.66 in normal control vs. 17.85 ± 2.34 in CeA 4 ml group, P< 0.01 and 17.95 ± 3.0 in CeA 6 ml, P<0.01). Similarly, rats treated with higher doses (4 and 6 ml) of CeA showed significantly lesser percentage bias in comparison with normal control rats (69.59 ± 13.32 in normal control group vs. 51.18 ± 2.02 in CeA 4 ml group, P<0.05 and 50.56 ± 2.87 in CeA 6 ml group, P<0.05). During rewarded alternation test also, only rats treated with higher doses (4 and 6 ml) of CeA fresh leaf juice showed a significant increase in the percentage of correct response when compared to the normal control group rats (63.68 ± 19.79 in normal control vs. 87.49 ± 9.62 in CeA 4 ml group, P< 0.01 and 90.47 ± 6.68 in CeA 6 ml group, P<0.01). In 4 weeks treatment group, during spontaneous alternation test, the animals treated with 2, 4 and 6ml of CeA fresh leaf juice showed significantly higher number of alternations when compared to the normal control group of rats (12.62 ± 2.13 in normal control vs. 15.85 ± 0.89 in CeA 2 ml group, P<0.05, 19.0 ± 0.70 in CeA 4 ml group, P<0.001 and 16.37 ± 2.13 in CeA 6 ml group, P<0.01). Table 1. Results of spatial learning (T-maze) tests Groups n 2 weeks treatment group 4 weeks treatment group 6 weeks treatment group Spont. alt. test % Bias Rew. alt. test Spont. alt. test % Bias Rew. alt. test Spont. alt. test % Bias Rew. alt. test No. of alternations % of correct response No. of alternations % of correct response No. of alternations % of correct response Normal control (NC) 8 10.1±3.66 69.59±13.32 63.68±19.79 12.62±2.13 66.24±5.89 69.78±16.02 12.0±2.88 69.48±4.64 65.1±5.29 Saline control (SC) 8 15.0±1.00 57.49±4.56 76.66±11.25 13.37±1.76 56.24±4.45 76.03±9.38 15.16±2.31 64.85±5.52 66.1±6.26 CeA-2ml 8 14.71±2.62 55.35±2.03 82.13±8.9 15.85# ±0.89 50.14## ±3.96 92.85# ±9.22 18.42## ±2.69 56.51## ±5.8 93.42### ±5.3 CeA-4ml 8 17.85** ±2.34 51.18* ±2.02 87.49** ±9.62 19.0*** ±0.7 52.49*** ±2.27 92.49* ±15.43 19.5*** ±2.07 55.2** ±6.58 95.83*** ±5.89 CeA-6ml 8 17.95$$ ±3.0 50.56$ ±2.87 90.47$$ ±6.68 16.37$$ ±2.13 50.12$$$ ±4.31 90.14$ ±9.22 18.62$$$ ±2.06 55.2$$ ±4.85 88.01$$$ ±10.55 Each value represents Mean±SD. (NC vs. CeA 2ml: # P< 0.05, ## P<0.01, ### P<0.001; NC vs. CeA 4ml: * P<0.05, ** P<0.01, *** P<0.001; NC vs. CeA 6ml: $ P<0.05, $$ P<0.01, $$$ P<0.001; CeA: Centella asiatica; n: Number of rats)
  • 25. 21Centellia asiatica induced behavioural changes in neonatal rats Similarly, the rats treated with 2, 4 and 6 ml of CeA fresh leaf juice showed significantly lesser percentage bias in comparison with the normal control group of rats (66.24 ± 5.89 in normal control vs. 50.14 ± 3.96 in CeA 2 ml group, P<0.01, 52.49 ± 2.27 in CeA 4 ml group, P<0.001 and 50.12 ± 4.31 in CeA 6 ml group, P<0.001). During rewarded alternation test, rats treated with three different doses (2, 4 and 6 ml) of CeA fresh leaf juice showed a significant increase in the percentage of correct response when compared to the normal control group rats (69.78 ± 16.02 in normal control vs. 92.85 ± 9.22 in CeA 2 ml group, P<0.05, 92.49 ± 15.43 in CeA 4 ml group, P<0.05 and 90.14 ± 9.22 in CeA 6 ml group, P<0.05). In 6 weeks treatment group, during spontaneous alternation, test animals treated with all the 3 doses (2, 4 and 6 ml) of CeA fresh leaf juice showed significantly higher number of alternations when compared to normal control group of rats (12.0 ± 2.88 in normal control vs. 18.42 ± 2.69 in CeA 2 ml group, P< 0.01, 19.5 ± 2.07 in CeA 4 ml group, P< 0.001 and 18.62 ± 2.06 in CeA 6 ml group, P<0.001). However, all the three groups of rats treated with CeA (2, 4 and 6 ml) showed significantly lesser percentage bias in comparison with normal control group (69.48 ± 4.64 in normal control vs. 56.51 ± 5.8 in CeA 2 ml group, P<0.01, 55.2 ± 6.58 in CeA 4 ml group, P<0.01 and 55.2 ± 4.85 in CeA 6 ml group, P<0.01). During rewarded alternation test, rats treated with all the three different doses (2, 4 and 6 ml) of CeA fresh leaf juice showed a significant increase in the percentage of correct response when compared to normal control group (65.10 ± 5.29 in normal control vs. 93.42 ± 5.3 in CeA 2 ml group, P<0.001, 95.83 ± 5.89 in CeA 4 ml group, P<0.001 and 88.01 ± 10.55 in CeA 6 ml group, P<0.001). Passive avoidance test Results of passive avoidance exploration and retention performance are shown in figures 1, 2 and 3. All the CeA treatment groups showed good memory retention. In 2 weeks treatment group (Figure 1) during exploration, there was no significant difference between animals treated with the CeA fresh leaf juice (2, 4 and 6 ml) and normal control animals in total time spent in small compartment. However, during retention test, it was seen that animals treated with CeA fresh leaf juice spent significantly less time in the smaller compartment (218.16 ± 20.94 sec in normal control vs. 77.66 ± 12.35 sec in CeA 2 ml group, P<0.001, 59.0 ± 5.28 sec in CeA 4 ml group, P<0.001 and 18.28 ± 2.88 sec in CeA 6 ml group, P<0.001). In 4 weeks treatment group (Figure 2) during exploration, there was no significant difference between the animals treated with CeA fresh leaf juice (2, 4 and 6 ml) and the normal control animals in total time spent in small compartment. However, during retention test, it was observedthattheanimalstreatedwithCeAfreshleafjuice spent significantly less time in the small compartment (287.0 ± 74.35 sec in normal control vs. 39.0 ± 14.24 sec in CeA 2 ml group, P<0.001, 48.6 ± 18.95 sec in CeA 4 ml group, P<0.001 and 25.14 ± 18.77 sec in CeA 6 ml group, P<0.001). In 6 weeks treatment (Figure 3) group during exploration, there was no significant difference between the animals treated with CeA fresh leaf juice (2, 4 and 6 ml) and the normal control animals in total time spent in small compartment. However, during the retention test, animals Figure 1.  Graph showing the time spent in small compartment in 2 weeks treatment group. (Normal control (n= 8), Saline control (n= 8), CeA 2 ml (n= 8), CeA 4 ml (n= 8), CeA 6 ml (n= 8). Each bar represents Mean + SD. NC vs. CeA 2 ml: ### P<0.001; NC vs. CeA 4 ml: *** P<0.001; NC vs. CeA 6 ml: $$$ P<0.001) Figure 2.  Graph showing the time spent in small compartment in 4 weeks treatment group. (Normal control (n= 8), Saline control (n= 8), CeA 2 ml (n= 8), CeA 4 ml (n= 8), CeA 6 ml (n= 8). Each bar represents Mean + SD. NC vs. CeA 2ml: ### P<0.001; NC vs. CeA 4 ml: *** P<0.001; NC vs. CeA 6 ml: $$$ P<0.001) Figure 3.  Graph showing the time spent in small compartment in 6 weeks treatment group. (Normal control (n= 8), Saline control (n= 8), CeA 2ml (n= 8), CeA 4ml (n= 8), CeA 6ml (n= 8). Each bar represents Mean + SD. NC vs. CeA 2 ml: ### P< 0.001; NC vs. CeA 4 ml: *** P<0.001; NC vs. CeA 6 ml: $$$ P< 0.001)
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Neurol. 1988; 100: 1–15. [19] Rao BS, Desiraju T, Raju TR. Neuronal plasticity induced by self-stimulation rewarding experiences in rats-astudyonalterationindendriticbranchinginpyramidalneuronsofhippocampusandmotorcortex. Brain Res. 1993; 627: 216–224. [20] Kempermann G, Kuhn HG, Gage FH. More hippocampal neurons in adult mice living in an enriched environment. Nature. 1997; 386: 493–495. [21] Nilsson M, Perfilieva E, Johansson U, Orwar O, Eriksson PS. Enriched environment increases neurogenesis in the adult rat dentate gyrus and improves spatial memory. J. Neurobiol. 1999; 39: 569–578. [22] Moser MB. Making more synapses: a way to store information. Cell Mol. Life Sci. 1999; 55: 593–600. of all the three groups treated with CeA fresh leaf juice spent significantly less time in the small compartment (297.3 ± 71.94 sec in normal control vs. 37.71 ± 12.31 sec in CeA 2 ml group, P<0.01, 10.1 ± 1.92 sec in CeA 4 ml group, P<0.001 and 15.28 ± 22.69 sec in CeA 6 ml group, P<0.001). Discussion In the present study the results of T-Maze tests of rats treated with lower doses of CeA (2 ml) for shorter duration (2 weeks) were not significantly different than the normal rats. However animals of higher dose groups (4 and 6 ml) showed significant improvement in the learning behaviour even in shorter (2 weeks) duration of treatment. Rats when treated for longer duration (4 and 6 weeks) showed significant improvement in the learning behaviour in all (2, 4 and 6 ml) dose groups. In the passive avoidance tests, there was no significant change in behaviour during exploration. However, during retention test, animals of all the three dose groups (2, 4 and 6 ml) spent less time in the smaller compartment suggesting improved memory retention. This enhanced memory retention was observed in the animals treated with CeA for 2, 4 and 6 weeks. These results clearly indicate that oral administration of fresh leaf juice of CeA improved learning and memory in neonatal rats. This effect was marked in animals treated with higher doses of CeA. Use of CeA in preventing radiation induced behavioural changes during clinical radiotherapy has been reported before [14]. Asiatic acid, a triterpine of CeA is used in the treatment of dementia and as an enhancer of cognition. Three derivatives obtained from CeA are found to be efficacious in protecting neurons from oxidative damage caused by exposure to excess glutamate [15]. Aqueous extract of CeA has an enhancing effect on cognitive functions [16]. Centella asiatica is also reported to improve general mental ability and behavioural pattern in mentally retarded children [5, 8–10]. Nalini et al. [17] have reported the memory enhancing effect of aqueous extract of CeA in adult rats. But the results of present study is the first experimental evidence regarding the memory enhancing property of CeA fresh leaf juice during growth spurt period of rats. Treatment with Clitoria ternatea root extract has been shown to enhance memory in neonatal rats [3]. The exposure to the new learning experiences [18], intracranial self stimulation [19], living in enriched environment [20–22] and environment within pyramid model [23] has been shown to alter the cytoarchitecture of hippocampus which is a part of the brain concerned with learning and memory. Similarly fresh leaf juice of CeA has been shown to improve dendritic arborisation of amygdala and hippocampus [24–27]. Improved learning behaviour and enhanced memory retention in the present study is probably because of the structural changes in these brain regions [18, 28, 29]. It has been observed that CeA treatment increases the level of neurotransmitter GABA that is known to act on hippocampus [30, 31]. Similarly CeA may also affect the biosynthesis of other neurotransmitters involved in learning and memory like Ach, noradrenaline, 5HT, dopamine [32–34]. However these morphological, neurophysiological and neurochemical changes need to be investigated. We conclude by saying that oral administration of CeA fresh leaf juice in neonatal rats (during growth spurt period) enhances their memory, which is probably due to the structural, neurochemical and neurophysiological changes in the brains of these rats.
  • 27. 23Centellia asiatica induced behavioural changes in neonatal rats [23] Bharathi H, Rao MS, Murthy KD. Pyramid environment enhances learning and memory–a behavioural and morphological study. Paper presented in International congress on frontiers in Pharmocology and Therapeutics in 21st century, All India Institute of Medical Sciences, New Delhi, India, 1-4 December, 1999. [24] Rao Mohandas KG, Rao Muddanna S, Rao Gurumadhva S. Effect of Centella asiatica on the dendritic morphology of hippocampal neurons in adult rats. Paper presented in 36th National Conference of Indian Pharmacological Society, Vallabha Bai Chest Institute, New Delhi, 5-7 December, 2003. [25] Rao Mohandas KG, Rao Muddanna S, Rao Gurumadhva S. Effect of Centella asiatica on the dendritic morphology of amygdaloid neurons in adult rats. Paper presented in 35th National Conference of Indian Pharmacological Society, DRDE, Gwalior, India, 26-29 November, 2002. [26] Rao Mohandas KG, Rao Muddanna S, Rao Gurumadhva S. Effect of Centella asiatica on dendritic morphology of amygdaloid neurons in neonatal rat pups. Paper presented in National Conference of Association of Physiologists and Pharmacologists of India, Armed Force Medical college, Pune, India, 21-25 December, 2001. [27] Rao Mohandas KG, Rao Muddanna S, Rao Gurumadhva S. Role of Centella asiatica leaf extracts in enhancing the dendritic arborization and memory retention in rats. Paper presented in 33rd National Conference of Indian Pharmacological Society, K B Institute of Pharmaceutical Education and Research, Gandhi Nagar, India, 28-30 December, 2000. [28] Maren S. Long-term potentiation in the amygdala: a mechanism for emotional learning and memory. Trends Neurosci. 1999; 22: 561–567. [29] O’Keefe J, Nadel L. Hippocampus as a cognitive map. Oxford Clarendon Press, London/New York. 1978. [30] Chatterjee TK, Chakraborthy A, Pathak M, Sengupta GC. Effects of plant extract Centella asiatica (Linn.) on cold restraint stress ulcer in rats. Indian J. Exp. Biol. 1992; 30: 889–891. [31] Ji WQ, Zhang CC, Zhang GH. Effect of somatostatin and GABA on long term potentiation in hippocampal CA1 area in rats. Zhongguo Yao Li Xue Bao. 1995; 16: 380–382. [32] Hatfield T, McGaugh JL. Norepinephrine infused into the basolateral amygdala posttraining enhances retention in a spatial water maze task. Neurobiol. Learn Mem. 1999; 71: 232–239. [33] Farr SA, Banks WA, Morley JE. Estradiol potentiates acetylcholine and glutamate-mediated post-trial memory processing in the hippocampus. Brain Res. 2000; 864: 263–269. [34] Cho YH, Friedman E, Silva AJ. Ibotenate lesions of the hippocampus impair spatial learning but not contextual fear conditioning in mice. Behav. Brain Res. 1999; 98: 77–87.
  • 28. Published online 29 July, 2005 © http://www.neuroanatomy.org Review Article Neuroanatomy (2005) 4: 24–27 Introduction The vestibular system provides orientation in three dimensional space, modification of muscle tone and balance [1]. It is essential for the coordination of motor responses, eye movement and posture. However, compared to other sensory modalities, the sense of balance appears to be rather poorly represented in centers of consciousness. To maintain balance and body posture, there has to be a continuous flow of information about position and movement from every part of the body, including head and eyes. The vestibular system detects motion of the head and maintains stability of images on the fovea of the retina as well as postural control during movements of the head. Signals representing angular and translational motion of the head as well as the tilt of the head relative to gravity are translated by the peripheral vestibular organs in the inner ear. This sensory information is used in turn to control reflexes used for maintaining the stability of the images on the retina during movements of the head. Feedback information from the head and eyes must be independent from each other since the eyes can be fixed on a target when the head is moving [2]. Vestibular information is also important for posture and gait. When vestibular function is normal these reflexes operate with exquisite accuracy and, in the case of eye movements, at very short latencies [3]. The peripheral part of the vestibular system is located in the labyrinth, the inner ear. The vestibule and semicircular canals which are dilations and carvings within the petrous temporal, form a large part of the bony labyrinth. They contain the membranous labyrinth which is similar in shape, but much smaller. Between the bony and membranous labyrinth circulates a fluid called perilymph which in composition is similar to the cerebrospinal fluid. The membranous labyrinth on the other hand is filled with a fluid called endolymph with a high concentration of K+ and a low concentration of Na+ . The stria vascularis in the cochlear duct and secretory cells in the transitional epithelium surrounding sensory epithelia are probably responsible for the production of endolymph. The part of the membranous labyrinth related to vestibular function consists of three semicircular ducts (superior, lateral or horizontal, posterior) and the utricle and saccule. Within these structures are areas containing neuroepithelial cells which form the peripheral receptors of the vestibular system. The Semicircular Ducts The semicircular ducts open into the utricle. The posterior limbs of the superior and posterior ducts unite before opening into the utricle, thus forming a common limb. One end of each duct is dilated and is called the ampulla and epithelial cells here thicken to form the ampullary crest. This zone contains neuroepithelial hair cells covered by a gelatinous substance, the cupula, which extends to the roof of the ampulla. These receptor cells Brief review of vestibular system anatomy and its higher order projections A. Beliz TASCIOGLU Department of Anatomy, Hacettepe University, Faculty of Medicine, Ankara–Turkey. A. Beliz Tascioglu, PhD Associate Professor in Anatomy, Department of Anatomy, Hacettepe University, Faculty of Medicine, 06100 Ankara–TURKEY 90-312-305 21 01 90-312-310 71 69 btasciog@hacettepe.edu.tr Received 16 March 2005; accepted 25 July 2005 ABSTRACT The vestibular system is one of the most complex systems of the human brain. A very small peripheral organ in the inner ear, the labyrinth, forms the peripheral receptor. This receptor forms connections with centers at all levels within the central nervous system. These centers in turn, will project back to vestibular structures in the brain stem who will control the geography of the body providing balance and an accuracy in visual movements as well as posture and gait. This review aims to give the readers a brief overview as to what the vestibular system is; its related structures and defined anatomical pathways. Neuroanatomy; 2005; 4: 24–27. Key words [vestibular system] [anatomy] [review] [connections] eISSN 1303-1775 • pISSN 1303-1783
  • 29. 25Brief review of vestibular system anatomy are innervated by afferent peripheral processes from the vestibular ganglion. Hair cells contain a kinocilium arising from the cytoplasmic surface of the cell and stereocilia, their numbers varying between 40-70. The longest stereocilium is the one nearest to the kinocilium gradually decreasing in length with accordance to their distance to the kinocilium [2]. The semicircular ducts respond to angular acceleration (rotation of the head). When the head is rotated, movement of the endolymph causes displacement of the cupula resulting in deflection of the hair cells. Movement towards the kinocilium depolarizes the hair cells causing stimulation, whereas movement away from the kinocilium hiperpolarizes the hair cell decreasing firing of the afferent fibers [2]. The superior duct of one side lies approximately in the same plane as the posterior of the opposite side forming a functional pair. Similarly, the horizontal ducts of the two sides lie in the same plane again forming a functional pair. Movement of the endolymph on one side will cause excitation of hair cells on same side while inhibiting hair cells of its partner on the opposite side. The Utricle And Saccule The utricle and saccule on the other hand are related to static equilibrium (position of the head in space which is very important for the control of posture) and to changes in gravitational forces. Hence they are also sensitive to linear acceleration. Saccular neurons appear to detect vertical acceleration while utricular neurons are sensitive to dorsoventral acceleration and sideways movement. The utricle and saccule also contain an area of neuroepithelial cells, in this instance called the macula. Here, hair cells come into contact with a gelatinous substance containing particles of calcium carbonate. This structure is called the otolithic membrane. All hair cells have their kinocilium at one end but they are not oriented in the same direction. Hair cells that come from all directions are oriented towards a curved border on the surface of the macula called the striola. When the head is bent in any direction a group of cells is stimulated while another group is inhibited, having no effect on yet a different group. This complicated pattern sends accurate messages to the brain related to the position of the head at any given time [2]. Diseases of the labyrinth produce severe symptoms such as vertigo, nausea, vomiting, nystagmus. Following lesions, the static deficits usually disappear in a few days, whereas recuperation of the dynamic, vestibular-related synergies is much slower and merely partial [4]. Vestibular Ganglion [Scarpa’s Ganglion] The vestibular ganglia, one on each side, lie in the lateral part of the internal auditory meatus, near the fundus. The vestibular ganglia contain the cell bodies of afferents innervating the peripheral vestibular apparatus. Each ganglion contains about 20,000 cells [2]. The vestibular ganglion appears to be divided into a superior and inferior part united by an isthmus. Peripheral processes from the superior ganglion innervate the ampullary crests of the superior and lateral semicircular ducts and macula of utricle, while peripheral fibers from the inferior ganglion innervate the macula of the saccule. Some peripheral fibers from the inferior ganglion pass through the singular foramen at the bottom of the internal auditory meatus and innervate the ampullary crest of the posterior semicircular duct [1]. Central processes from the vestibular ganglion form the vestibular nerve. Together with the cochlear nerve, the vestibular nerve courses in the internal auditory meatus as the vestibulocochlear nerve in close relation with the facial nerve and passes through the cerebellopontine angle and enter the pons to terminate in the vestibular nuclear complex. Few fibers however pass directly to the flocculo-nodular lobe of the cerebellum. These fibers coming from the vestibular apparatus to be relayed to the vestibular nuclei or directly to the cerebellum are called primary vestibular fibers. Thevestibularcomplexanduvula-nodulusareresponsible for the initial processing of vestibular information by the central nervous system [5]. Vestibular Nuclear Complex Thevestibularnucleilieinthelateralrecessoftherhomboid fossa extending from a level rostral to the hypoglossal nucleus to a level slightly above the abducens nucleus. There are four vestibular nuclei: superior, lateral, medial and inferior (descending) vestibular nuclei. The lateral nucleus contains the largest cells and the inferior nucleus has the smallest cells [6]. The vestibular nuclei form two distinct cell columns. The medial vestibular nucleus which is the largest forms the medial cell column while the superior, lateral and inferior vestibular nuclei form the lateral cell column [1]. There is evidence that most of the vestibular nuclei are topographically interconnected through a commissural system. However, commissural connections are not restricted to homologous nuclei [5]. Electrical stimulation of the utricular macula evokes excitation in ipsilateral secondary vestibular neurons and inhibition in more than 50% of the contralateral secondary vestibular neurons excited by ipsilateral utricular stimulation. Only 10% of ipsilaterally saccular- sensitive secondary vestibular neurons are inhibited by contralateral saccular stimulation [7]. Interconnections within the vestibular complex have also been shown. Besides the main vestibular nuclear complex other nuclei related to the vestibular system are present. One is the nucleus prepositus hypoglossi which recieves scarce primary vestibular afferents but has its main input from secondary vestibular projections as well as projections fromtheflocculo-nodularlobe.Anotheristheparasolitary nucleus located between the medial vestibular and inferior vestibular nuclei. Two smaller nuclei adjacent to the vestibular complex are thought to have vestibular connections: Nucleus x, lateral to the caudal part of the inferior vestibular nucleus and nucleus z, located rostral to the anterior pole of the nucleus gracilis [5]. Secondary Vestibular Fibers Secondary vestibular fibers are fibers that arise mainly: 1)  from the medial and inferior vestibular nuclei destined for the flocculo-nodular lobe and uvula, 2)  from all vestibular nuclei travelling within the medial longitudinal fasciculus to reach cranial nerve motor nuclei innervating extraocular muscles and axial musculature of the neck,
  • 30. 26 Tascioglu 3)  from the lateral vestibular nucleus to all spinal levels forming the lateral vestibulospinal tract to regulate extensor muscle tone. 4)  Outputs of vestibular nuclei not only evoke reflexes mediated by skeletal muscles, they evoke autonomic reflexes as well. Vestibulo-sympathetic reflexes modulate local changes in blood flow, respiration and heart rate. These reflexes are abolished in lesions of certain parts of the vestibular nuclei in cats. The circuit which induces these vestibulo-autonomic effects, includes projections from the inferior, medial vestibular nuclei and parasolitary nucleus to the solitary nucleus. The solitary nucleus recieves afferents from the heart, oesophagus and stomach, mediated mainly by branches of the glossopharyngeal and vagus nerves. Additionally, stimulation of certain nuclei in the cerebellum causes changes in blood pressure, heart rate and respiration [5]. With all these main projections the vestibular system controls eye movements, reflex postural head and neck movements and balance during stance and gait as well as modulation and modification of autonomic function to maintain homeostasis during changes in body posture. Radtke et al., in their study of vestibulo-autonomic control in man in normal control and labyrithine-defective subjects exposed to abrupt head acceleration, concluded that a delayed increase of heart rate in response to postural challenge occurred in patients with vestibular loss. These authors postulated that this condition could be the reason of the autonomic distress experienced by these patients [8]. It is a fact that the vestibular system is a complex system involving not only the posterior labyrinth and cerebellum but also central structures such as striatum, thalamus, frontal and prefrontal cortex to assure balance, movements and gait. Information reaching the vestibular system are not purely vestibular but also from visual and somatosensory origins. Equilibrium is equally a complex physiological function needing harmony of vestibular, visual and somatosensory information together with an integrity of the central nervous system [9]. Vestibular projections to higher order neurons appear to be very complex and not very clearly defined. However some connections of the vestibular system with these higher centers have been established. Vestibular Projections To Thalamus Vestibular projections to the thalamus originate from the rostral part of the vestibular nuclear complex and are destined to the VPL (ventral posterolateral), VPM (ventral posteromedial) and VPI (ventral posteroinferior) nuclei (ventrobasal thalamus). Neurons in the ventrobasal nuclei respond to stimulation of deep proprioceptors and joint receptors as well as vestibular inputs [1, 5]. Vestibular-hippocampal Interactions The hippocampus is thought to be important for spatial representation processes that depend on the integration of both self-movement and allocentric cues. The vestibular system is an important source of self- movement information that may contribute to this spatial representation [10]. This system contributes to spatial information processing and the development of spatial memory in the hippocampus. Anatomical studies have suggested that various parts of the thalamus are likely to transmit vestibular information to the hippocampus perhaps via the parietal cortex; however, it is possible that more direct pathways exist. In recent years, electrophysiological studies have shown that vestibular stimulation affects cells in the anterior thalamic nuclei and the hippocampus. These studies demonstrate the importance of vestibular-hippocampal interaction for hippocampal function but also suggests that the hippocampus may be an important site for compensation of vestibular function following peripheral or central vestibular lesions [11]. Does A Vestibular Cortex Exist? Different areas of the primate cortex have been named ‘vestibular’. Guldin and Gurusser [12] have defined in three different primate series the existence of a vestibular cortical system. Based on the verification of their study in three different species of primates, they postulate that a similar pattern exists in the human. There is considerable evidence from studies on cats and monkeys that several cortical areas such as area 2v at the tip of the intraparietal sulcus, area 3av in the central sulcus, the parietoinsular vestibular cortex next to the posterior insula (PIVC) and area 7 in the inferior parietal lobule are involved in the processing of vestibular information. Recordings from these areas have shown that: 1)  these cortical neurons are connected to the vestibular labyrinth, 2)  they receive converging vestibular, visual and somatosensory inputs. In humans, positron emission tomography (PET) scans and functional magnetic resonance imaging (fMRI) have shown these data to be correct [13]. It is stated by some authors that vestibular thalamo- cortical projections end in areas 3av and T3, parietal visual cortex and parietoisular cortex. These areas in humans are involved mainly in percieving both verticality and self-motion [14]. Humans with damage to parietal cortex do not recognize true vertical. Deprived of surrounding visual cues, they cannot align a disk with a line on it so that the line has a true vertical orientation [5]. Corticofugal connections in the macaque monkey where cortical vestibular areas project back to vestibular nuclei have been shown [15]. Vestibular System And Aging Falling and loss of balance among the geriatric population is a frequent and serious problem. The reason has been attributed to the progressive deterioration of the anatomical components of the vestibular system. In a study investigating quantitative differences in the number, density or types of hair cells or the length of the crista ampullaris in young and aged gerbils, no difference was found, suggesting that the cause of vestibular dysfunction during aging should be looked for elsewhere [16]. On the other hand, a study regarding age-related change in the
  • 31. 27Brief review of vestibular system anatomy References [1] Truex RC, Carpenter MB. Human Neuroanatomy. 6th Ed., Williams & Wilkins, Baltimore. 1969; p: 347–356. [2] Kandel ER, Schwarz JH, Jessell TM. Principles of Neuroscience. 3rd Ed., Appleton & Lange, Norwalk. 1991; p: 500–511. [3] Schubert MC, Minor LB. Vestibulo-ocular physiology underlying vestibular hypofunction. Phys. Ther. 2004; 84: 373–85. [4] Vidal PP, de Waele C, Vibert N, Muhlethaler M. Vestibular compensation revisited. Otolaryngol. Head Neck Surg. 1998; 119: 34–42. [5] Barmack NH. Central vestibular system: vestibular nuclei and posterior cerebellum. Brain Res. Bull. 2003; 60: 511–541. [6] Suarez C, Diaz C, Tolivia J, Alvarez JC, Gonzalez del Rey C, Navarro A. Morphometric analysis of the human vestibular nuclei. Anat. Rec. 1997; 247: 271–288. [7] Uchino Y, Sato H, Zakir M, Kushiro K, Imagawa M, Ogawa Y, Ono S, Meng H, Zhang X, Katsuta M, Isu N, Wilson VJ. Commissural effects in the otholith system. Exp. Brain Res. 2001; 136: 421–430. [8] Radtke A, Popov K, Bronstein AM, Gresty MA. Vestibulo-autonomic control in man: short- and long- latency vestibular effects on cardiovascular function. J. Vestib. Res. 2003; 13: 25–27. [9] Sakka L, Vitte E. Anatomy and physiology of the vestibular system: review of the literature. Morphologie. 2004; 88: 117–126. [10] Russell NA, Horii A, Smith PF, Darlington CL, Bilkey DK. Long-term effects of permanent vestibular lesions on hippocampal spatial firing. J. Neurosci. 2003; 23: 6490–6498. [11] Smith PF. Vestibular-hippocampal interactions. Hippocampus. 1997; 7:465–471. [12] Guldin WO, Grusser OJ. Is there a vestibular cortex? Trends Neurosci. 1998; 21: 254–259. [13] De Waele C, Baudonniere PM, Lepecq JC, Tran Ba Huy P, Vidal PP. Vestibular projections in the human cortex. Exp. Brain Res. 2001; 141: 541–551. [14] Dieterich M, Brandt T. Vestibular system: anatomy and functional magnetic resonance imaging. Neuroimaging Clin. N. Am. 2001; 11: 263–273. [15] Akbarian S, Grusser OJ, Guldin WO. Cortico-fugal connections between the cerebral cortex and brainstem vestibular nuclei in the macaque monkey. J. Comp. Neurol. 1994; 339: 421–439. [16] Kevetter GA, Zimmerman CL, Leonard RB. Hair cell numbers do not decrease in the crista ampullaris of the geriatric gerbils. J. Neurosci. Res. 2005; 80: 279–285. [17] Park JJ, Tang Y, Lopez I, Ishiyama A. Age-related change in the number of neurons in the human vestibular ganglion. J. Comp. Neurol. 2001; 431: 437–443. [18] Enrietto JA, Jacobson KM, Baloh RW. Aging effects on auditory and vestibular responses: a longitudinal study. Am. J. Otolaryngol. 1999; 20: 371–378. number of neurons in the human vestibular ganglion, proved that age-related decline in primary neurons existed, providing an anatomical basis for the increased incidence of imbalance seen with age [17]. Another interesting finding is that although the auditory and vestibular apparatus are closely related anatomically, age-related changes are not correlated. In the same individual, the two systems may age at different rates [18].
  • 32. Published online 8 August, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 28–30 Introduction Chavez et al. [1] suggested that during embryonic development three canals fuse to form a single nerve canal. Failure of these canals to fuse can explain presence of multiple canals in some individuals. In case-1 and case- 2 there are bifid canals, one nerve canal is supplying the developing permanent tooth bud while the other branch is following its coarse into the mandible. To the best of our knowledge case-3 is the first reported case of a trifid mandibular nerve canal. Case Reports Case 1 A 9-year-old girl reported at our department with a request for panoramic radiograph to evaluate eruption status of permanent teeth. Panoramic radiograph (Fig-1 and Fig-2) indicated presence of bifid canals on the both the sides. Bilaterally, one canal is supplying the developing tooth bud of permanent third molar while the other branch is extending its coarse into the mandible. Case 2 A 10-year-old boy underwent a routine panoramic radiographic examination. Panoramic radiograph (Fig- 3) revealed bifid canal on the right side with a branch supplying the developing tooth bud of third permanent molar while the other branch followed its coarse in the mandible. Case 3 A 20-year-old female patient reported with a request for a panoramic radiograph for evaluation of orthodontic treatment and pain in the lower left molar teeth. Panoramic radiograph (Fig-4) revealed presence of bilateral lower impacted third molars and multiple nerve canals on the left side. Patient was made aware of presence of multiple mandibular canals and after her consent, a CT scan was advised. Coronal CT scan of 2 mm slice thickness revealed presence of multiple canals on the left side. Coronal section in the mandibular ramus region showed presence of a canal perforating the lingual cortex, innervating and terminating after supplying the left lower third molar (Fig-5). The coronal section at the second molar region revealed presence of two canals on left side but only one canal on the right side (Fig-6). Based on the findings on the panoramic radiograph and CT scan a final diagnosis of a trifid mandibular canal was made. Discussion Chavez et al. [1] suggested that during embryonic development there might be three inferior dental nerves innervating three groups of mandibular teeth. The canal to the incisors appeared first followed by the canal to the primary molars and subsequently canal to the permanent molars. These canals are directed from the lingual surface of mandibular ramus towards different tooth groups. During rapid prenatal growth and remodeling Anatomical variations in developing mandibular nerve canal: a report of three cases Ajit AULUCK [1] Ausaf AHSAN [1] Keerthilatha M. PAI [1] Chandrakant SHETTY [2] Oral Medicine and Radiology [1], Manipal College of Dental Sciences, Manipal–India; Department of Radiodignosis [2], Kasturba Medical College, Manipal–India. Dr. Ajit Auluck, Department of Oral Medicine and Radiology, Manipal College of Dental Sciences, Manipal 576104, Karnataka–INDIA 91-820-257 12 01 (22210) 91-820-257 19 66 drajitauluck@yahoo.co.in Received 30 May 2005; accepted 1 August 2005 ABSTRACT Anatomical variations in the known pattern and coarse of inferior alveolar nerve are of considerable interest to a dentist. We report three cases, two paediatric cases with bifid canals and a case of 20-year-old female patient with trifid mandibular nerve canal and discuss in brief about the development of mandibular nerve canal. Neuroanatomy; 2005; 4: 28–30. Key words [mandibular] [nerve] [canal] [anatomy] [variation] eISSN 1303-1775 • pISSN 1303-1783
  • 33. 29Anatomical variations in developing mandibular nerve canal Figure 1.  Panoramic radiograph of case-1 (left side) showing a branch supplying the developing third molar and another branch following its coarse in the mandible. Figure 2.  Panoramic radiograph of case-1 (right side) showing a branch supplying the developing third molar and another branch following its coarse in the mandible. Figure 3.  Panoramic radiograph of case-2 (right side) showing a branch supplying the developing third molar and another branch following its coarse in the mandible. Figure 4.  Panoramic radiograph of case-3 showing trifid mandibular canal on the left side. Figure 5.  Coronal CT scan section at the ramus region showing a trifid canal with perforation of lingual cortex. Figure 6.  Coronal CT scan at molar region showing two canals.
  • 34. 30 Auluck et al. in the ramus region there is coalescence of canal entrances that are obvious at birth. These observations are consistent with panoramic radiographic findings in case-1 and case-2 in which there are different branches supplying the developing tooth buds of permanent third molars and extending into the mandible. This theory also explains the occurrence of trifid mandibular canals in some patients secondary to incomplete fusion of these three nerves as observed in case-3. It is suggested that two canals showed a relatively parallel coarse but there were variations in the orientation of the third canal with distribution towards the molar crypt [1]. In case-3, CT scan showed a branch that has perforated the lingual cortex to supply the third molar (Fig-5) while two branches are following their coarse in the mandible (Fig-6). The incidence of bifid canals is considered to be very low and reported to be 0.08%, 0.4% and 0.9% in various studies [2, 3]. It is important for dentisits to identify the presence of bifid canals to modify anesthetic techniques to avoid pain and discomfort to patients [4, 5]. Therefore identification of such variations in patterns of mandibular nerve canal are of considerable interest to dentists. It is reported that inferior alveolar nerve is a single canal in 60% cases while in other specimens the canal was less defined and the nerves and vessels were spread out to occupy a space within the bone rather than a tunnel [6]. This can explain the absence of complete coarse of nerve canal in case-1 and case-2. With further growth and remodeling of the mandible follow up radiographs in case-1 and case-2 may show the complete path of nerve canal in the mandible. As different nerve branches supply different teeth groups, congenital absence of some teeth can be attributed to lack of development of different nerve branches. References [1] Chavez Lomeli ME, Mansilla Lory J, Pompa JA, Kajer I. The human mandibular canal arises from three separate canals innervating different tooth groups. J. Dent. Res. 1996; 75: 1540–1544. [2] DeSantis JL, Liebow C. Four common mandibular nerve anomalies that lead to local anesthesia failures. J. Am. Dent. Assoc. 1996; 127: 1081–1086. [3] Sanchis JM, Penarrocha M, Soler F. Bifid manidbular canal. J. Oral Maxillofac. Surg. 2003; 61: 422–424. [4] Langlais RP, Broadus R, Glass BJ. Bifid mandibular canals in panoramic radiographs. J. Am. Dent. Assoc. 1985; 110: 923–926. [5] Meechan JG. How to over come failed local anaesthesia. Br. Dent. J. 1999; 186: 15–20. [6] ClaeysV,WackensG.Bifidmandibularcanal:literaturereviewandcasereport.Dentomaxillofac.Radiol. 2005; 34: 55–58.
  • 35. Published online 9 August, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 31–34 Introduction The writer of the first pictorial Turkish Anatomy handwritten book “Tesrih-i ebdan ve Tercuman-i kibale- i feylesufan” that was written during the period of Murat the IVth was Sirvanlı Semseddin Itaki. This book must have been written between the years 1623-1632. The most important characteristic of the book whose seven copies are available today is that it has so many defining pictures and explanations in it. It is thought that some of the pictures were drawn by the writer himself and the others with the help of the pictures in “De Humani Corporis Fabrica” of Andreas Vesalius [1-4]. In this study, we aimed to review the neuroanatomy subject in the anatomy book of Itaki and show the relations between that book and the anatomy knowledge that we have today. In his book, Itaki had analysed the neuroanatomy subject in two parts. Although in today’s anatomy books, the peripheral and central nervous systems are hold and studied together within the human nervous system, in Itaki, the peripheral and cranial nerves were analysed in the part of the general structure of the organs. The peripheral nerves were described like the distribution of the skeleton and the muscles. Besides, the subject of central nervous system was described with internal organs. So he studied these two subjects separately [1]. Material and Methods We mainly studied the book which is written by Prof Dr Esin Kahya named “Şemseddin-i İtaki’nin Resimli Anatomi Kitabı”. We worked on the Ottoman text of “Teşrih-i ebdan ve tercüman-ı kibale-i feylesufan” given at the end of this book. The translation text in the book was not used, it was retranslated to current Turkish by the researchers. The text consists of 241 pages. The nervous system is between pages 78–97. The subjects in the text were compared with two anatomy books that instructed in medical faculties today. Results The anatomy of peripheral nerves He studied this subject in the section “the anatomy of nerves”. First he mentioned the cranial nerves and then the spinal nerves. He started the topic with some general information about nerves. According to Itaki, the nerves were sending sensation and motion to the organs. He said that some of the nerves came out of the brain and some came out of spinal cord which is called “nuha” in Arabic. He mentioned the spinal cord as the caliph of the brain [1]. Just as we do today, Itaki also divided the nerves into two parts as sensitive and motor fibers. He stated that all the nerves were paired except the one that came out of the tip of “kavimec” (coccyx). Neuroanatomy in Tesrih-i Ebdan: a study on a book which is written in Ottoman era* Enis ULUCAM [1] Recep MESUT [1] Nilufer GOKCE [2] Departments of Anatomy [1], Deontology and History of Medicine [2], Trakya University, Faculty of Medicine, Edirne–Turkey. Enis Ulucam, MD–PhD Department of Anatomy, Trakya University, Faculty of Medicine, 22030 Edirne–TURKEY 90-284-235 59 35 90-284-235 59 35 eulucam@trakya.edu.tr Received 3 January 2005; accepted 8 August 2005 ABSTRACT The writer of the first pictorial Turkish Anatomy handwritten book (Tesrih-i ebdan ve Tercuman-i kibale-i feylesufan) is Sirvanlı Semseddin Itaki. In our study, we aimed to review the neuroanatomy topics in his book, and to show the relationship between the book and the current anatomy knowledge that we have today. One of the main characteristic of the book is the availability of numerous illustrated explanations. Itaki studied neuroanatomy in two parts in his book. He considered peripheral and cranial nerves in the common structure of organ related structures in the book. He considered the topic, cerebrum in internal organs. He combined the illustrations and schemes he used for considering the neuroanatomy topics with pretty good and explanatory notes. Different sides were seen in addition to similarities to nowadays knowledge. Neuroanatomy; 2005; 4: 31–34. Key words [anatomy] [neuroanatomy] [Ottoman] [medical history] [Semseddin Itaki] eISSN 1303-1775 • pISSN 1303-1783 * This study was presented as a poster presentation in VII. National Anatomy Congress (2003, Diyarbakir–Turkey).
  • 36. 32 Ulucam et al. The anatomy of the cranial nerves As Galen and Ibni Sina had done, Itaki gave the number of the cranial nerves as seven pairs. The explanations of Itaki about the cranial nerves which he called head pairs are as stated below. The first cranial nerve. While explaining this nerve, Itaki mentioned two nipples like prolongations in front of the brain. He stated that this place was called “halamet-u’s- sudi” (olfactory tract) in Arabic and was also the reason for the human to smell but Itaki did not realize that it was a different cranial nerve. Then he explained that from each of those prolongations a single nerve came out and in a place near to the eye it made a crosswise. He said that this crosswise was called “mecma’en-nur” (optic chiasm). And he also wrote that after those nerves got into a crosswise, they came to the eye and got into the circumference of lens and enabled the eye to see. He reported that inside of the nerve was perforated so it was called “mucevvef” which means “nerve with holes”. Itaki thought that optic nerve was a part of prolongation of the olfactory nerve and he explained those two as a single nerve. He also gave some information about the useful features of the optic chiasma. First of all, when damage occurred in one of the eyes, it increased the power of the healthy one by enabling all the light to go into it. Secondly, optic chiasma prevented diplopia. Thirdly, by the help of that crosswise, the nerves were becoming stronger and stronger [1]. The second cranial nerve. He said that this cranial nerve went out of the front part of the first one and started from the hole in the eyelid and then came to the muscles of the apple of the eye and divided into six branches. He also told that eye movements were enabled by those nerves which were thick [1]. Here we can see that those nerves are occulomotor nerve, trochlear nerve and abducent nerve. Itaki explained those three as a single nerve. The third cranial nerve. He said that it started in the middle of the brain and then was mixed with the fourth pair and then again separated into four branches. He also reported that one of the branches spread to the interior organs through the neck and diaphragm by going out of the hole (carotid canal) where “uruk-u sibati” (internal carotid artery) went in. He wrote that the second branch mixed with the branches of the fifth pair by going out of the temple bone’s hole. The third branch went out through the hole of the second cranial nerve and again divided into three branches. The first of those branches spread through the auricular, temporal, frontal and orbital regions. The second branch spread inside the nasal cavity. The third branch innervated the upper part of mental and oral regions; the fourth branch went to the tongue and the lower part of mental and oral regions. And he also added that the tongue could feel bitter and sweet objects with the help of that branch [1]. As understood from these explanations, the first branch of the nerve that is mentioned as the third cranial is vagus nerve, the second branch is facial nerve, the third branch is ophthalmic and maxillary branches of trigeminal nerve, and the fourth branch is mandibular nerve. The fourth cranial nerve. He gave less information about this cranial nerve. He said that this one came out from the behind of the third cranial nerve and mixed with the third pair and reached the nasal fossa [1]. This nerve is mandibular nerve which is the motor branch of trigeminal nerve. The fifth cranial nerve. He wrote that this nerve which came out of the two sides of the brain was composed of two branches. One of the branches spread in the ear and went into the tympanic membrane. He added that the ability of hearing was held with that nerve. The other branch came out of the hole called as “a-ver” or “a’ma” and mixed with the third pair and innervated the face and the flat muscle on the face [1]. It can be understood that the structures that Itaki mentioned here are facial and vestibulocochlear nerves. The sixth cranial nerve. Itaki said that this nerve was originated from the backside of the brain, and then divided into three branches and these three came out of the hole at the end of lomboid suture in the neck. The first branch reached the pharyngeal muscles and the root of the tongue. The second branch went to the shoulder girdle muscles and to the flat muscle behind them (trapezius). He added that the third branch was bigger than the other two. It innervated the organs in abdomen and chest, and at the same time it reached the carotid artery and the laryngeal muscles. Itaki described recurrent laryngeal nerve here. While third branch went to the organs of chest, a subbranch of it returned and went to “tircihali” cartilage (arytenoid cartilage). He defined that branch as “asab-i ric” (recurrent laryngeal nerve). He wrote that the rest of the nerve went to heart, lung and liver, then spread into the internal organs in abdomen by passing through the diaphragm and conjoined with the third pair [1]. As understood, the first branch of the nerve that Itaki mentioned as the sixth cranial nerve is glossopharyngeal nerve. The second branch is accessory nerve. The third branch he mentioned is vagus nerve. It is interesting that he mentioned vagus nerve both in the third and in the sixth head pairs. The seventh cranial nerve. As for that nerve, he said that it came out of the top of the spinal cord and went to the tongue muscles, neck muscles which were between hyoid bone and thyroid cartilage [1]. The anatomy of the spinal nerves Itaki stated that the number of the spinal nerve pairs arising from the cervical part of the spinal cord was eight. He added that these nerves generally spread to the head muscles and enabled head to sense. The explanations of Itaki about the cervical spinal nerves were as follows: The first cervical spinal nerve. It was thinner than the others and it was not able to reach the head completely. The second cervical spinal nerve. It reached the outer skin behind the ear, the muscles behind the neck. The third cervical spinal nerve. It divided into two branches. The branch going forwards spread to the ear region and to the neck muscles. He added that this branch was responsible for ear movements in animals.
  • 37. 33Neuroanatomy in Tesrih-i Ebdan The second branch went to the cheek and the flat muscle located there. The fourth cervical spinal nerve. It divided into two branches. The branch going forwards went to the muscles between head and neck after uniting with the fifth cervical spinal nerve. The second branch reached the muscles of the face. The fifth cervical spinal nerve. It divided into two parts. The branch on the front side went to the shoulder muscles, the flat muscle in the face, and to the muscle that bends the head and the neck forward. Some of its branches reached the diaphragma by uniting with the sixth and seventh cervical spinal nerves. The sixth cervical spinal nerve. It divided into two parts. Some of its branches spread to the head muscles, lumbar muscles and at the lumbar bone, some of the fibres came to the top of the shoulder. The seventh cervical spinal nerve. It divided into two branches. Some of them reached until the head muscles and lumbar muscles and diaphragma after uniting with the fifth and the sixth cervical spinal nerves and also some of them reached the arms. The eighth cervical spinal nerve. It divided into two branches. The first branch went to the head and neck muscles and the second branch to the arm, wrist and to the palm of the hand [1]. Thoracal spinal nerves. Itaki told that the number of the thoracal spinal nerves was twelve in number. While talking about those nerves, he analysed the first two pairs separately, and after explaining the outlets of the others, he accepted that their destinations were the same. According to him, after the first two parts divided into two branches, the branch at the front side spread in rib muscles and back muscles. The branch on the backside reached the wrist after uniting with the eighth pair of the neck nerves. The second pair went to the skin of the arm and the palm of the hand. Then the ten pairs of back nerve went to the inside of the hand, muscles in wrist, girdle muscles and rib muscles respectively. The bottom back nerve lines also gave branches that go to the abdomen muscles [1]. Lumbar spinal nerves. According to Itaki, the nerves in the “katan” (lumbar) section were in five pairs. The branches coming out of those nerves went to the abdomen muscles. Itaki said that the first three lumbar nerves unite with the nerves coming from the brain. He also added that some branches of the third, fourth and fifth lumbar nerves unite in each other and mix with the nerves of “aciz” section (sacrum, rump bone) and reach the coccyx, the groin section and also the calf and the knee [1]. Sacral spinal nerves. Itaki said that the number of the nerves coming out of “aciz” (sacrum) and “usus” (coccyx) was six. Three pairs were separated from the sacral and three pairs were separated from coccyx. The branches coming out of those nerves united with the nerves that were going down to calf, end went to the muscles there and to the leg muscles. The second sacral and the third sacral reached the penis, urinary bladder and anus muscles and the muscles starting from the sacrum [1]. When Itaki counted the nerves coming out between vertebras, he found 32 pairs but he said that the nerve coming out of coccyx was a single nerve. Today the number of spinal nerves is stated as 31 pairs [5, 6]. When Itaki said that all the nerves that come out divided into two branches, he makes us consider that he was talking about ramus anterior and ramus posterior. Here the nerve that he said which came out of coccyx as a single should probably be filum terminale. Itaki didn’t mention the plexus concept but he said that some branches united with each other [1]. Brain anatomy Firstly, Itaki gave some information about the structure of the brain and then he explained the brain-membranes, ventricles, and the canals of the ventricles respectively. He didn’t give any information about the brainstem, cerebellum and the spinal cord. According to him, brain had the capacity for the power of spirits of the thinking power that human beings need. It provided the way for the vapours in the stomachs of the human to go out. The nerves whose duties were to make the human stand up in a controlled way came out of the brain. Some important activities like hearing, memory, seeing took place here. The human brain was in front of the head, and was divided into two parts. Those two parts were united with membranes and spaces [1]. After that introduction, Itaki gave some information about the temperament of the brain. According to him, brain was cold. The movements of the nerves and souls coming out of it were cold in order to modify that movement. The brain is humid. A part of the brain is soft, and it has to be soft so as to provide the ability of understanding. The brain is oily. The muscles that are responsible to sense began from the front of the brain, because the front side is soft. The behind of the brain is harder and the muscles responsible for the movement began from there. There was a thin membrane between the soft part of the brain and the hard part of it. Here Itaki talked about a soft and a hard part of the brain. That soft part is cerebrum and the hard one is cerebellum. But Itaki didn’t mention cerebellum separately [1]. Itaki said that there were two types of brain membranes. He wrote that the one which is thin and adhered to the brain was called as “ummu’l-rakik” (pia mater) and the hard and thick one was called as “ummu’l-cafiye” (dura mater). Itaki didn’t mention arachnoidea mater [1]. Itaki emphasized the ventricles of the brain. According to him, there were three spaces in brain. He added that the doctors were calling those as “batn-i dimag”. The one on the front side was called as “batn-i mukaddes” (lateral ventricle), and the one on the backside was called as “batni muahhar” (the fourth ventricle). And the one between those was called as “batn-i evsat” (the third ventricle). The first ventricle is big, the second is smaller than the first one, and the one between these two is riddled. The three spaces were connected to each other with the one in the middle which functioned as a tunnel. He said that between the ventricles there were three canals. Two of those were between the front space and the backspace. As the endings of those canals were
  • 38. 34 Ulucam et al. References [1] Kahya E. Semseddin-i Itaki’nin Resimli Anatomi Kitabi. 1st Ed., Ankara, Ataturk Kultur Merkezi Yay. 1996; 156-163, 199-204. [2] Mesut R. Osmanlı Doneminde Turk Anatomi Bilimi ve Anatomi Ogretimi. Morfoloji Derg. 1999; 7: 11-14. [3] Sehsuvaroglu B. Bizde Anatomi Ogretimine Dair. Istanbul Tip Mecmuasi. 1952; 15: 365-412. [4] Unver SA. Uc Asirlik Resimli Bir Tesrih Kitabimiz “Risalei Tesrihi Ebdan” Sirvanlı Semsettin (Itaki) 1622-1648. Tedavi Notları. 1934; 9: 189-192. [5] Arinci K, Elhan A. Anatomi. Cilt 2, Ankara, Gunes Kitabevi. 1995; 69-70. [6] Gokmen FG. Sistematik Anatomi. Izmir, Guven Kitabevi. 2003; 783-846. like a funnel, they were called as “kam” (infundibulum). He said that after that funnel there was a gland and this gland is probably the hypophysis. Itaki especially gave his attention to the middle space. He said that inside of the space was a lining of the brain membranes and added that it continued to the back ventricle [1]. Discussion Itaki was influenced by the doctors of his time and the past in subjects about nervous system. He was especially influenced by Ibn–i Sina and Ali bin Abbas. He also made use of the ideas of Galen and Vesalius. Itaki especially mentioned the peripheral nervous system in a more detailed way. Even though he said that the number of the cranial nerves was seven pairs, he explained the twelve pairs of cranial nerves we know today [1, 5, 6]. The fact that he mentioned the existing points of the nerves in a very detailed way shows that he probably made dissection. Considering that dissection was forbidden in those times, it is understood that he knew the anatomy writers before him really well. It is also possible to think that he understood the spinal nerves very well. But it is also obvious that Itaki did not have enough information about brain. And the information that was provided by the doctors of those times was not enough either; however, it may makes us think that it was enough because of the fact that some examinations which were being done on animals in those times were applied to human. Itaki did not talk about the concept of the brain. But he mentioned the membranes of the brain, optic chiasm and the ventricles elaborately. He showed optic chiasm in his schema. His schema about nervous system are relatively good and explanatory.
  • 39. Published online 11 August, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 35–36 Case Report During the gross anatomy dissection of a 50-year-old male cadaver, we observed persistent median artery piercing median nerve (Figure 1). The median artery was long and slender. It arose from the ulnar artery, just above the origin of the common interosseous artery. Immediately after its origin, it pierced the median nerve and terminated before reaching the wrist. The cadaver also showed an accessory belly of abductor digiti minimi muscle crossing ulnar nerve and ulnar vessels (Figure 2). These variations were bilateral. Discussion Entrapment or compressive neuropathies are important and wide spread debilitating clinical problems. They are caused frequently as the nerve passes through a fibrous tunnel, or an opening in fibrous or muscular tissue. The most common is the median nerve entrapment in the wrist leading to carpal tunnel syndrome. There are reports of median nerve compression by persistent median artery [1], large superficial palmar branch of the radial artery [2]. In some cases, the median nerve splits, forming a cleft in the forearm and allowing the ulnar artery or one of its branches. The median nerve may be perforated by median artery when present [3]. In the present report, the median artery, arose from the ulnar artery, pierced the median nerve and terminated before reaching the wrist. This could be a cause for pronator syndrome. As a result of median artery piercing median nerve, the median nerve may be compressed. This variation may be clinically important because symptoms of median nerve compression arising from similar variations are often confused with more common causes such as radiculopathy and carpal tunnel syndrome. The ulnar nerve, after descending in the forearm between the flexor digitorum profundus and flexor carpi ulnaris muscles, pierces the deep fascia and enters the wrist through the Guyon’s canal. The walls of this canal consist of the pisiform medially and the hook of the hamate laterally; the floor is formed by the flexor retinaculum, and the roof is formed by the palmar carpal ligament and the palmaris brevis muscle. The Guyon tunnel houses the ulnar nerve, ulnar artery, and ulnar vein. In the distal canal, the ulnar nerve bifurcates into a superficial sensory branch and a deep motor branch, which supplies the hypothenar muscles and then passes across the palm, distributing to other intrinsic hand muscles. The ulnar nerve may be compressed in the guyon’s canal by the presence of an anomalous muscle of hypothenar eminence [4]. In the present case there was an accessory belly of abductor digiti minimi muscle which took origin from the deep forearm fascia, traversed Guyon’s canal superficial to the ulnar nerve and vessels and inserted into the lateral side of abductor digiti minimi. The nerve supply arose from the ulnar nerve. Its course through Guyon’s canal could be a cause for ulnar tunnel syndrome. The accessory belly of the abductor digiti minimi muscle may compress the ulnar nerve when grasping objects with the Nerve compressions in upper limb: a case report Venkata Ramana VOLLALA Deepthinath RAGHUNATHAN Vincent RODRIGUES Department of Anatomy, Melaka Manipal Medical College (Manipal Campus), ICHS, Manipal 576104, Karnataka–India. Venkata Ramana Vollala, Department of Anatomy, Meleka Manipal Medical College (Manipal Campus), International Centre for Health Sciences, Manipal 576104, Karnataka–INDIA 91-820-257 12 01 (22516-22521) 91-820-257 19 05 ramana_anat@yahoo.co.in Received 27 April 2005; accepted 10 August 2005 ABSTRACT Entrapment of a peripheral nerve may lead to painful tingling, numbness and weakness. These entrapment or compressive neuropathies are important and wide spread debilitating clinical problems. During a routine dissection of an adult male cadaver we found median artery arising from the ulnar artery and piercing the median nerve. This variation may be clinically important because symptoms of median nerve compression arising from similar variations are often confused with more common causes such as radiculopathy and carpal tunnel syndrome. We also observed an accessory belly of abductor digiti minimi muscle. The accessory belly was found to take origin from the deep forearm fascia, traversed Guyon’s canal superficial to the ulnar nerve and vessels to reach the hypothenar eminence. Its course through Guyon’s canal could be a cause for ulnar tunnel syndrome. The ulnar nerve trunk innervated the muscle. Accessory fasciculi of the hypothenar muscles have been involved in vascular and nerve compressions. Neuroanatomy; 2005; 4: 35–36. Key words [median nerve] [ulnar nerve] [entrapment] [median artery] [muscle] eISSN 1303-1775 • pISSN 1303-1783
  • 40. 36 Vollala et al. hand leading to sensory or motor abnormalities of ulnar nerve. Compression of ulnar nerve by accessory belly of abductor digiti minimi is reported [4, 5, 6]. Compressive neuropathies of the ulnar nerve in the canal of Guyon are less common, but they can also result in significant disabilities. Compression can occur in 1 of 3 zones. Zone 1 is in the most proximal portion of the canal, where the nerve is a single structure consisting of motor and sensory fascicles, and zone 2 and 3 are distal where the ulnar nerve has divided into motor and sensory branches. The clinical picture correlates with the zone in which compression occured [7]. This knowledge can assist the surgeon in the diagnosis and treatment of conditions associated with the ulnar aspect of the hand. The crossing of accessory belly of the abductor digiti minimi muscle over the ulnar nerve and compressing it remind physicians that not every instance of numbness and tingling in the hand represents carpal tunnel syndrome. Careful clinical examination may not only localize compression of the ulnar nerve at wrist level but also may reveal its etiology. Figure 1.  The Median artery arising from the ulnar artery and piercing the median nerve. (B: brachial artery; U: ulnar artery; Mn: median nerve; Ma: median artery) References [1] Jones NF, Ming NL. Persistent median artery as a cause of pronator syndrome. J. Hand Surg. (Am). 1988; 13: 728–732. [2] Widder S, Shons AR. Carpal tunnel syndrome associated with extra tunnel vascular compression of the median nerve motor branch. J. Hand Surg. (Am). 1988; 13: 926–927. [3] Bergman RA, Thompson SA, Afifi AK, Saadeh FA. Compendium of human anatomic variations. Urban & Schwarzenberg, Baltimore-Munich. 1988; p:141–142. [4] Luethke R, Dellon AL. Accessory abductor digiti minimi muscle originating proximal to the wrist causing symptomatic ulnar nerve compression. Ann. Plast. Surg. 1992; 28: 307–308. [5] Sheppard JE, Prebble TB, Rahn K. Ulnar neuropathy caused by an accessory abductor digiti minimi muscle. Wis. Med. J. 1991; 90: 628–631. [6] Al-qattan MM. Ulnar nerve compression at the wrist by the accessory abductor digiti minimi muscle: wrist trauma as a precipitating factor. Hand Surg. 2004; 9: 79–82. [7] Posner MA. Compressive neuropathies of the ulnar nerve at the elbow and wrist. Instr. Course Lect. 2000; 49: 305–317. Figure 2.  Accessory belly of abductor digiti minimi crossing ulnar nerve and ulnar vessels. (ABADM: accessory belly of abductor digiti minimi; ADM: abductor digiti minimi; Un: ulnar nerve; Ua: ulnar artery)
  • 41. Published online 11 August, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 37–38 Introduction Brachial plexus is the plexus of nerves that supplies the structures in the upper limb. It is formed by the union of ventral rami of C5, C6, C7, C8 and T1 spinal nerves. The brachial plexus has roots, trunks, cords, divisions and branches. Variations are common in the branches of brachial plexus but the variations in the roots and trunks are very rare. The knowledge of such rare variations in the roots and trunks is very useful in the practice of orthopedics and anesthesia. We present one such rare variation of the trunks of brachial plexus in this report. Case Report Duringtheroutinedissectionsformedicalundergraduates, a variation in the formation of upper trunk of the brachial plexus was found unilaterally on the right side of a male cadaver aged approximately 55 years. The upper trunk was formed by the union of ventral rami of C5, C6 and C7 spinal nerves (Fig 1). The middle trunk was absent and the lower trunk was formed by the union of ventral rami of C8 and T1 spinal nerves. The abnormal upper trunk was cleaned thoroughly to rule out the fascial connection betweentheupperandmiddletrunks.Theabnormalupper trunk passed laterally between the scalenus anterior and medius muscles (Fig 2). After giving the two branches, suprascapular nerve and nerve to subclavius, the trunk divided into two divisions (Fig 2). These two divisions divided again into anterior and posterior division, which further coursed like the divisions of normal upper and middle trunks. The rest of the parts of the brachial plexus were normal. Discussion The brachial plexus variations could fail the brachial plexus loco-regional anesthesia. In the surgical treatment of brachial plexus lesions, the surgeon must know brachial plexus anatomical variations perfectly. Common variations in the formation, prefixed and postfixed plexuses have been well documented [1–4]. Variations in the formation of the trunks of the brachial plexuses have been reported [4]. An extensive study by Uysal et al., (2003) showed superior trunk not being formed in 1% of cases, inferior trunk not being formed in 9% of cases and formation of superior trunk by C4 and C5 roots and formation of inferior trunk by T1 and T2 roots [5]. Formation of upper trunk of brachial plexus by C5, C6 and C7 roots is very rare. This will be associated with absence of the middle trunk. We can also put this case as anatomical fusion of upper and middle trunks. One such case has been reported so far where the fusion between upper and middle trunks was bilateral [4]. In the previous studies, the variations in the supra or infraclavicular part of brachial plexus were more frequent in the left side [4] but in our case, the variation found was on the right side. The knowledge of variations in the formation of brachial plexus is very useful for the neurosurgeons. It will help in the surgical treatment of tumors of nerve sheaths such as schwannomas and neurofibromas. This knowledge A rare variation in the formation of the upper trunk of the brachial plexus - a case report Satheesha NAYAK Nagabhooshana SOMAYAJI Venkata Ramana VOLLALA Deepthinath RAGHUNATHAN Vincent RODRIGUES Vijay Paul SAMUEL Prasad ALATHADY MALLOOR Department of Anatomy, Melaka Manipal Medical College (Manipal Campus), Madhav Nagar, Manipal 576104, Karnataka State–India. Dr. Satheesha Nayak B, Department of Anatomy, Meleka Manipal Medical College (Manipal Campus), Madhav Nagar, Manipal Udupi District 576104, Karnataka–INDIA 91-820-292 25 19 91-820-257 19 05 nayaksathish@yahoo.com Received 13 June 2005; accepted 10 August 2005 ABSTRACT Brachial plexus is the plexus of nerves that supplies the upper limb. Variations in the origin and distribution of the branches of brachial plexus are common but variation in the roots and trunks are very rare. Here, we report one of such rare variations in the formation of the upper trunk of the brachial plexus. In this case, the upper trunk was formed by the union of ventral rami of C5, C6 and C7 nerves. The middle trunk was absent and lower trunk was normal. Neuroanatomy; 2005; 4: 37–38. Key words [brachial plexus] [upper trunk] [variation] [Erb’s point] [spinal nerve] eISSN 1303-1775 • pISSN 1303-1783
  • 42. 38 Nayak et al. might also help in treating the non-neural tumors like lipoma. Orthopedic treatments of the cervical spine also need a thorough knowledge of the normal and abnormal formation of brachial plexus. Though the variation that we are reporting here may not alter the normal functioning of the limb of the person, it is very important in clinical neurosurgery and orthopedic procedures. Figure 1.  Formation of abnormal upper trunk of the brachial plexus. (ABUT: abnormal upper trunk; C5, C6, C7, C8, T1: roots of brachial plexus; LT: lower trunk) References [1] Matejcik V. Aberrant formation and clinical picture of brachial plexus from the point of view of a neurosurgeon. Bratisl. Lek. Listy. 2003; 104: 291–299. [2] Matejcik V. Variations of nerve roots of the brachial plexus. Bratisl. Lek. Listy. 2005; 106: 34–36. [3] Lee HY, Chung IH, Sir WS, Kang HS, Lee HS, Ko JS, Lee MS, Park SS. Variations of the ventral rami of the brachial plexus. J. Korean Med. Sci. 1992; 7:19–24. [4] Matejcik V. Anatomic variations in the brachial plexus trunks and nerve roots. Rozhl. Chir. 2003; 82: 456–459. [5] Uysal II, Seker M, Karabulut AK, Buyukmumcu M, Ziylan T. Brachial plexus variations in human fetuses. Neurosurgery. 2003; 53: 676–684. Figure 2.  Abnormal upper trunk with its branches and relations. (ABUT: abnormal upper trunk; SSN: suprascapular nerve; UT: upper trunk; NS: nerve to subclavius; SA: scalenus anterior; SM: scalenus medius; PN: phrenic nerve; CCA: common carotid artery; VN: vagus nerve; SV: subclavian vein, SCA: subclavian artery)
  • 43. Published online 26 October, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 39–40 Introduction Atlas is the first cervical vertebra. It is ring shaped, without a body. It has an anterior arch, a posterior arch and two lateral masses. The lateral masses articulate with the occipital condyles to form ellipsoid type of synovial joints. The anterior arch articulates with the dens of the axis vertebra to form a pivot type of synovial joint. The posterior arch is grooved by the third part of the vertebral artery. In rare cases the lateral masses of the atlas vertebra fuse with the occipital bone. Case Report During the routine osteology demonstration class for medical undergraduates, a total fusion of the atlas vertebra with the skull was seen (Figs 1–4). The lateral masses had fused completely with the occipital condyles. The anterior arch was fused with the basilar part of the occipital bone. The hypoglossal canals were absent. There was a median foramen between the anterior arch of atlas and the basilar part of the occipital bone (Fig 3). The posterior arch was also fused with the squamous part of the occipital bone. There were some perforations between the posterior arch of atlas and the occipital bone (Fig 2). The gap for the vertebral artery to enter the cranial cavity was very small. Discussion Fusion, either partial or complete, of the atlas with the occipital bone may occur in about 1% of cases so-called atlas assimilation [1]. Two cases of occipitalization with spina bifida of atlas vertebra have been reported recently [2]. Individuals with occipitalization of the atlas may have low hairline, torticollis, restricted neck movements and/ or abnormal short neck [3]. The clinical findings may be the headache, neck pain, numbness and pain in the limbs, weakness, abnormal head posture, posteriorly located dull aching headache. Cranial nerve findings associated may include tinnitus, visual disturbances and lower cranial nerve palsies leading to dysphagia and dysarthria [3]. The neurological symptoms and signs of atlanto- occipital fusion can not be distinguished from those of the Arnold Chiari malformation as the pathophysiology of both is essentially the same. Fusion between atlas and occiput usually occurs anteriorly between the arch and rim of the foramen with some segment of the posterior arch of C1 present in some cases. The fusion of posterior arch frequently constricts the spinal canal causing intermittent symptoms depending on the position of the head [4]. The onset of neurological symptoms is usually in the third or fourth decade. Younger patients are commonly asymptomatic. Atlanto occipital fusion reduces the foramen magnum dimension leading to neurological complications due to compression of spinal cord [2]. The knowledge of total occipitalization may be of importance to orthopedic surgeons dealing with the pathologies of upper cervical spine. It may be the cause of failure of a cisternal puncture and thus may be of importance for the anesthetist. Neurosurgeons dealing Total fusion of atlas with occipital bone: a case report Satheesha NAYAK Venkata Ramana VOLLALA Deepthinath RAGHUNATHAN Department of Anatomy, Melaka Manipal Medical College (Manipal Campus), Madhav Nagar, Manipal 576104, Karnataka State–India. Dr. Satheesha Nayak B, Department of Anatomy, Meleka Manipal Medical College (Manipal Campus), Madhav Nagar, Manipal Udupi District 576104, Karnataka–INDIA 91-820-292 25 19 91-820-257 19 05 nayaksathish@yahoo.com Received 11 August 2005; accepted 24 October 2005 ABSTRACT Atlas is the first cervical vertebra. It does not have a body like other cervical vertebrae. It forms ellipsoidal synovial joints with the condyles of the occipital bone. Rarely, it gets occipitalized, where the condyles of the occipital bone fuse with the lateral masses of the atlas vertebra. In this article, a total fusion of the atlas vertebra has been reported and the knowledge of such a fusion may be of importance for radiologists, anesthesiologists, orthopedic and neurosurgeons because skeletal abnormalities at the craniocervical junction may result in sudden unexpected death. It can result in dysphagia, disarthria or torticollis because of compression of cranial nerves. Neuroanatomy; 2005; 4: 39–40. Key words [atlas] [cervical vertebra] [fusion] [occipitallization] [condyles] eISSN 1303-1775 • pISSN 1303-1783
  • 44. 40 Nayak et al. with the tumours of cerebellum, physiotherapist dealing with the neck pain and the radiologists dealing with the Figure 1.  Base of the skull with totally fused atlas vertebra. References [1] Bergman RA, Afifi AK, Miyauchi R. Compendium of human anatomical variations. Baltimore: Urban and Schwarzenberg. 1988; 197. [2] Jayanthi V, Kulkarni R, Kulkarni RN. Atlanto-occipital fusion: report of two cases. J. Anat. Soc. India. 2003; 52: 71–73. [3] Mc Rae DL, Barnon AS. Occipitalization of atlas. Am. J. Roentgenol. Radium Ther. Nucl. Med. 1953; 70: 23–46. [4] Bailey RW, Sherk HH, Don EJ, Fielding JW, Martin Long D, Uno K, Fening L, Staufer ES. The cervical spine: occipitalization of atlas. Philadelphia: Lippincott. 1983; 150. Figure 2.  Posterior view of the skull with atlas vertebra. (IF: incomplete fusion of posterior arch with the occipital bone) Figure 3.  Anterobasal view of the skull showing anterior aspect of fused atlas vertebra. (MF: median foramen) Figure 4.  Posteroinferolateral view of the skull with totally fused atlas vertebra. abnormalities of cervical spine must also be aware of this total occipitalization of the atlas vertebra.
  • 45. Published online 14 November, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 41–42 Introduction Variationsamongtheposteriorcompartmentmusclesofthe thigh are uncommon. In 1998, Somayaji et al [1] reported a muscle which originated from the semimembranosus and biceps femoris muscles and then inserted in to the superficial surface of the tendo calcaneous. According to Barry and Bothroyd [2] extra slips of origin associated with gastrocnemius and soleus usually join those muscles or the tendo calcaneus. Parsons [3], reported about a muscle slip that passed transversely between the two heads of origin of gastrocnemius. Insertion of muscle slips from biceps femoris into gastrocnemius and into the tendo calcaneus have been reported [4]. In this report, we discuss an anomalous muscle in the popliteal fossa with a difference in its origin and insertion from the muscles mentioned above. We also discuss in this context, the possible compressive neuropathies caused by such variant muscles. Case Report During the routine dissection we found an anomalous muscle in the popliteal fossa bilaterally in a male cadaver. It originated from two narrow tendinous slips, one from lateral intermuscular septum and the other from the posterior intermuscular septum of the thigh. These two slips then united and formed a narrow muscular belly in front of the sciatic nerve at its division into tibial and common peroneal nerve. The muscle crossed the popliteal fossa superficial to the tibial nerve and then inserted into both the heads of the gastrocnemius muscle. This anomalous muscle derived its nerve supply from the tibial nerve and the blood supply from the popliteal artery (Figs 1–2). Discussion Compressive neuropathy involving sciatic nerve within the popliteal fossa is very rare [5]. In this case report we speculate that the muscle variations in the popliteal fossa such as the anomalous muscle we found in the popliteal fossa may cause the compression of sciatic nerve. This may results in mimicking the manifestations shown by the compressive neuropathy involving the common peroneal or tibial nerve or both of them as they pass through the popliteal fossa. Although tibial nerve entrapment can be seen anywhere along the course of the nerve, the most common location is distal to the ankle [6]. Entrapments above the ankle have been reported in the popliteal fossa, where the nerve is compressed by the tendinous arch of origin of the soleus muscle, a Baker’s cyst, or other masses that may occur in this region [7]. Compression of the tibial nerve or one of its branches can occur because of intrinsic neural abnormalities or can be a result of external compression. External compression etiologies reported in the literature have included fibrosis, neurilemomas, ganglion cysts, lipomas, osteochondromas, varicosities, other benign and malignant tumors, tight tarsal canal, hypertrophic abductor hallucis, anomalous artery, and anomalous Sciatic nerve entrapment in the popliteal fossa: a case report Jaijesh PAVAL Venkata Ramana VOLLALA Satheesha NAYAK Department of Anatomy, Melaka Manipal Medical College (Manipal Campus), Manipal 576104, Karnataka–India. Jaijesh Paval, Department of Anatomy, Meleka Manipal Medical College (Manipal Campus), Manipal 576104, Karnataka–INDIA 91-820-257 12 01 (ext 22519–21) 91-820-257 19 05 jaijesh@yahoo.co.in Received 28 August 2005; accepted 11 November 2005 ABSTRACT During the routine dissection we found an anomalous muscle in the popliteal fossa bilaterally in a male cadaver. This muscle had tendinous origin from the lateral and posterior intermuscular septum of the thigh as separate slips. These two slips united in front of the sciatic nerve and formed a narrow muscular belly which enclosed the sciatic nerve and the tibial nerve in its downward course and then inserted in to both the heads of gastrocnemius muscle. Sciatic entrapment in the popliteal region is uncommon and in this report we discuss the possible nerve entrapment due to the aforesaid kind of muscle variants which may confuse the surgeons. Neuroanatomy; 2005; 4: 41–42. Key words [sciatic nerve] [entrapment] [popliteal fossa] eISSN 1303-1775 • pISSN 1303-1783
  • 46. 42 Paval et al. extra muscles such as the flexor digitorum accessorius longus [6] or the muscle mentioned in this report. Local trauma is the most common underlying cause of entrapment of the superficial peroneal nerve. Nontraumatic causes of entrapment are commonly due to anatomical variations such as fascial defects, with or without muscle herniation at the upper part of the lateral side of the leg, where the nerve is entrapped as it emerges into the subcutaneous tissue [8]. Deep pernoeal Figure 1.  Popliteal fossa. (A: The anomalous muscle; B: Sciatic nerve; C: Common peroneal nerve) References [1] Somayaji SN, Vincent R, Bairy KL. An anomalous muscle in the region of the popliteal fossa: case report. J. Anat. 1998; 192: 307–308. [2] Barry D, Bothroyd JS. Tensor fasciae suralis. J. Anat. 1924; 58: 382–390. [3] Parsons FG. Note on an abnormal muscle in the popliteal space. J. Anat. 1920; 54: 170–178. [4] Moore AT. An anomalous connection of the piriformis and biceps femoris muscles. Anat. Rec. 1922; 23: 307–314. [5] Tani JC. Fibrous band compression of the tibial nerve branch of the sciatic nerve. Am. J. Orthop. 1995; 24: 910–912. [6] Reichner DR, Evans GRD. Tibial and common peroneal nerve compression in the popliteal fossa: a case report and literature review. The Internet Journal of Plastic Surgery. 2004; 2: 1. [9] Sansone V, Sosio C, da Gama Malcher M, de Ponti A. Two cases of tibial nerve compression caused by uncommon popliteal cysts. Arthroscopy. 2002; 18: E8. [8] Mastaglia FL. Tibial nerve entrapment in the popliteal fossa. Muscle Nerve. 2000; 23: 1883–1886. [9] Fabre T, Piton C, Andre D, Lasseur E, Durandeau A. Peroneal nerve entrapment. J. Bone Joint Surg. Am. 1998; 80: 47–53. Figure 2.  Popliteal fossa. (A: Tibial nerve; B: Anomalous muscle) nerve entrapment is most commonly due to the repetitive mechanical irritation of the nerve at the ankle beneath the extensor retinaculum [9]. In case of sciatic nerve entrapment, surgeons have to be vigilant in considering the possible muscle variants in the popliteal fossa which may be one of the reasons of the compressive neuropathies when the symptoms persist or recovery remains incomplete.
  • 47. Published online 29 November, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 43–48 Introduction Hippocampal formation is a part of limbic system that consists of dentate gyrus, proper hippocampus, subicular complex and entorhinal cortex [1]. Proper hippocampus consists of three parts in transverse section: CA1, CA2 and CA3. Each part has three cellular layers. Middle layers consist of pyramidal cells that are the chief cells of hippocampus. Efferent projections from proper hippocampus are axons of these pyramidal cells [2]. Hippocampus converts short term memory into long term memory. Without hippocampus, symbolic type of long term memory is not stabilized [3]. Hippocampus has connections with the entorhinal area such that efferents of entorhinal area synapse with pyramidal cells of CA3. The entorhinal area connects with extensive areas of neocortex. In this manner all types of sensory inputs reach the hippocampal formation [2]. Hippocampal formation receives afferent fibers from septal area, supramammillary area cholinergic cells of medial septal and Broca nucleus, anterior thalamus, lateral dorsal and midline thalamic nuclei and medial part of pulvinar. Activity of hippocampal formation is modified with afferents that come from the brainstem [2, 4]. Thalamus is the largest part of diencephalon and contains numerous nuclei. Each thalamic nucleus except for the reticular nucleus, sends efferents to the cortex, so that each part of cortex has reciprocal connections with the thalamus. Internal medullary lamina consists of axons that enter or leave the thalamus, dividing it into three masses of gray matter: anterior, lateral and medial thalamic nuclear groups. Anterior thalamic nucleus is enclosed by the bifurcation of the lamina [5]. The principal afferent of anterior thalamus comes from mammilary bodies through the mammillothalamic tract. These nuclei also receive direct and massive fibers from pyramidal cells of the hippocampus. Cortical efferents of anterior thalamus are sent to the cingulate gyrus through the anterior limb of internal capsule [2]. Also, projections from anterior and midline thalamic nuclei and nucleus reuniens are sent to the hippocampus [6]. Connections between hippocampus and diencephalon have an important role in memory. An experimental study on monkeys showed that thalamic lesions cause disorder of recent memory [3]. Protein malnutrition is a common type of malnutrition troughout the world [7]. It is evident that this type of malnutrition has effects on some parts of the brain such as the hippocampal formation [8]. Protein malnutrition causes decrease in the number of synapses in some cortical areas and changes of behavior in animals. It can also reduce the serotonergic afferents of hippocampus [9]. Based on the physiological importance of connections between thalamus and hippocampus in memory and learning, and effects of protein malnutrition on hippocampal formation, we decided to study the effect of protein malnutrition on the thalamic efferent projections to the hippocampus. The effect of low protein diet on thalamic projections of hippocampus in rat Mohammad BAYAT [1] Gholam Reza HASANZADEH [2] Mitra BARZROODIPOUR [1] Maryam JAVADI [3] Department of Anatomy [1] and Department of Social Medicine [3], Qazvin University of Medical Science, Qazvin–Iran; Department of Anatomy [2], Tehran University of Medical Science, Tehran–Iran. Mohammad Bayat, MS of Anatomy, Department of Anatomy, Qazvin University of Medical Science, Shahid Bahonar Boulevard, Qazvin–IRAN 98-281-333 60 01-6 98-281-332 49 70 mohamad_bayat@yahoo.com Received 28 August 2005; accepted 24 November 2005 ABSTRACT Recent investigations show that protein malnutrition alters the structure and function of some areas of the hippocampal formation. We investigated therefore the effect of protein malnutrition on thalamic projections to the CA1 hippocampal area. In this study, the efferent projections from the thalamus to hippocampus in rat by horseradish peroxidase (HRP) neural tract tracing was investigated in two groups. The control group was fed with regular diet (18% protein) whereas the study group was fed with low protein diet (8% protein). In the control group we found that the whole anterior thalamic nuclei and nucleus reuniens send projections to the CA1 hippocampal region. Among these nuclei, the anteroventral nucleus (AV) had the highest amount of labelled neurons which sent projection to the CA1 hippocampal region. Anterior thalamus projected to both hippocampus. Number of HRP labelled neurons in the contralateral thalamus were less than the ipsilateral thalamus. As a result of the influence of low protein diet, efferent projection from the anterior thalamus and nucleus reuniens to the CA1 region of hippocampus had decreased (p<0.05) in the study group. The reason may be due to reduction of neuronal activity of thalamus and hippocampal formation under the influence of protein restriction or the affected progression of developmental programmes controlling synaptogenesis. Neuroanatomy; 2005; 4: 43–48. Key words [thalamus] [CA1] [hippocampal area] [protein malnutrition] [efferent projection] eISSN 1303-1775 • pISSN 1303-1783
  • 48. 44 Bayat et al. Material and Methods Thalamus is made up of several nuclei that individually form specific connections. In this experiment we used HRP to study the effects of protein malnutrition on the connections between thalamus and CA1 hippocampal area. Following injection, HRP is absorbed by axonal endings and is transferred retrogradely to perikaria that send projections to the injection site. It accumulates in several vesicles, which are HRP labelled cells. In this study, after injection of HRP into CA1 hippocampal area, we counted the number of labeled cells and studied their topography in thalamic nuclei bilaterally both in study and control groups. Wistar rats of male sex were used (103±2 gr; n=22). Prior to the study they were divided into two groups (study and control) in simple randomized manner. During a 7 months period the control group was fed with regular (18% protein) and the study group was fed with low protein (8% protein) diet. The rats were kept in a 12 hours light/dark cycle. All of the experimental procedures was approved by the Animal Ethics Committee of Qazvin Medical University. Animals were anesthesized after an intraperitoneal injection of ketamin (40 mg/kg) and zylazin (5mg/kg). We performed a stereotaxic injection of HRP (Sigma) enzyme into the CA1 hippocampal region of the two groups. After surgery, rats were allowed to recover for 48 to 72 hours and were then anesthesized deeply with ketamin and zylazin. The animals were perfused intracardiacly with fixative solution (glutaraldehyde 1.25% and paraformaldehyde %1 in 0.2 mol buffer phosphate at pH=7.4) followed by sucrose buffer 10%. After removal, the rat brains were cut using freezing microtome (Cryocut 1800) in coronal sections at a thickness of 40 μm and stored in phosphate buffer. Sections were reacted with tetra methyl benzidin (Sigma, Mo.,USA) following the procedure of Mesolam et al [10]. Sections were then mounted onto gelatinized slides, air- dried and counterstained with neutral red. After assessment of the injection site, we examined slides with light microscope and took digital photographs from all thalamic areas. Selected slices were traced with reference to the atlas of Paxinos and Watson (1986) and the injection site (Fig. 1) and retrogradely labeled cells were plotted with the use of a microprojectore. Topographical study on dispersion of labelled cells with HRP was performed by Adobe Photoshop 7.0 software; we used Image tool 2.0 and SPSS 11.0 (Mann-Whitney and t test) softwares for the analysis of findings. Results The results of our study are summarized in Chart 1. Anterodorsal (AD) thalamic nucleus In the control group we observed that the ipsilateral AD sends numerous projections to CA1, which appears with the presence of numerous labelled cells in the slices (Fig. 2). These cells were scattered throughout the nucleus. The contralateral AD also send projections to CA1. The number of labeled cells in the contralateral nucleus was lesser than ipsilateral AD but the topography was similar. In the study group meaningful difference (P<0.05) was present between study and control groups in the number of labeled cells in the ipsilateral AD with no difference in topography. There were no labeled cells in the controlateral AD of the study group (Fig 3). Anteroventral (AV) thalamic nucleus This nucleus is divided into ventrolateral (AVVL) and dorsomedial (AVDM) parts. In the control group ipsilateral AVVL sent numerous projections to CA1. In the anterior (rostral) part of AVVL, the labelled cells located in the dorsal part of the nucleus, and in the posterior (caudal) part the labelled cells were in the ventral part. In ipsilateral AVDM labelled cells had more density in rostroventral part of nucleus. The number of labelled cells in the contralateral AVVL and AVDM were less than those of the ipsilateral side, but the topography was similar. In the study group that was fed with low protein diet we found that the amount of projections from AVVL and AVDM were lesser than (P<0.05) the control group. In the ventral parts of AVVL and AVDM there were no labelled cells with few labelled cells in the dorsal part. Anteromedial (AM) and interanteromedial (IAM) thalamic nuclei In the study group the lateral part of the AM sent projections to CA1 region of both sides. Fibers that reached the contralateral hippocampus were fewer. More labelled cells were seen in the middle sections of AM. In the study group, we observed that the number of projections sent to the hippocampus were reduced (p<0.5) and the density of labelled cells were more anterolaterally located. The ipsilateral AMV (ventral part of AM) was found to send fibers to CA1 with no difference between the number and topography of labelled cells in the control and study groups. In the rostral slices, AM nuclei of both sides were fused. In the control group we observed few labelled cells rostrally in the midline. There were no labelled cells in the IAM of the study group. Lateral dorsal (LD) thalamic nucleus In the ipsilateral thalamus of the control group, the ventrolateral part of LD (LDVL) had labelled cells. These cells were located in the ventromedial part of anterior sections, in the ventrolateral part of posterior sections of the LDVL. Contralateral LDVL had no labelled cells in control and study groups. In the ipsilateral thalamus of the control group, dorsomedial part of LD (LDDM) had labelled cells in the medial part. Contralateral LDDM of control group had few labelled cells medially. Comparing the number and topography of labelled cells in the ipsilateral LDVL and LDVM, there was no significant difference between the study and control groups, with no labelled cell in the contralateral LDDM.
  • 49. 45The effect of low protein diet on thalamic projections of hippocampus Figure 2.  Labeled cells in ipsilateral AD of control group. Figure 3.  Labeled cells in ipsilateral AD of study group. Figure 4.  Labeled cells in anterior part of Re in control group. Figure 5.  Labeled cells in anterior part of Re in study group. Figure 1.  Photograph of the injection site of HRP. (Bregma: -3.60; Lateral: 1.80; Depth: 3.20) Chart 1.  Comparison of the total number of labeled cells in ipsilateral thalamus of the study (red) and the control groups (blue).
  • 50. 46 Bayat et al. Midline thalamic nuclei Inthisgroupwefoundthatthereuniens(Re)andrhomboid (Rh) nuclei send projections to CA1 hippocampal area. Nucleus Reuniens (Re) This nucleus was divided into right and left halves in rostral slices. After injection of tracer into CA1, labelled cells were observed in the rostral and caudal sections of Re (Fig 4). In this area, labelled cells were scattered between other cells. Rostral part of nucleus Re had no labelled cells. The number of labelled cells in the Re of the study group was also lesser than the control group (p<0.05). Figure 6.  Drawing of dispersions of labeled cells in control group. Figure 7.  Drawing of dispersions of labeled cells in study group.
  • 51. 47The effect of low protein diet on thalamic projections of hippocampus Topography of dispersion of the labelled cells was similar in both groups (Fig. 5). Rhomboid nucleus In the study and control groups there was no difference in the number and topography of dispersion of labelled cells. Labelled cells in this nucleus were located in the lateral part of the caudal slices. Ventrolateral (VL) and ventromedial (VM) thalamic nuclei On the side of injection of HRP, nucleus VL projected to CA1. Cells that sent fibers to hippocampus were in the anterodorsal part of VL. In the VL nucleus of study group we found no labelled cells. More rostral parts of the VM in the control and study groups was found to send few projections to CA1. These were dispersed in the anterior sections of this nucleus. Lateral posterior (LP) nucleus We found that in the study and control groups on the side of injection there were few dispersed labelled cells througout the nucleus. Posterior (Po) and ventral posterolateral (VPL) thalamic nuclei In the dorsal part of the middle sections of the ipsilateral Po of the control group a few labelled cells were seen. This shows that this part of the Po sends projections to the hippocampus. In the study group, labelled cells in the Po were similar those of the control group. Labelled cells were seen in the control group in the lateral part of the VPL adjacent to reticular thalamic nucleus. Labelled cells were in the ipsilateral and contralateral VPL. The number of labelled cells in the contralateral VPL were fewer than the ipsilateral side. We compared number and topography of connections between VPL and CA1 in the two groups and found that the number of labelled cells were reduced in the study group with no change in the topography of their connections. Parataenial (Pt) thalamic nucleus In the dorsal part of Pt, we found a few labelled cells on both sides in the control group. Controlateral Pt sent fewer projections to CA1 compared to the ipsilateral. Examinations of Pt in the study group revealed no labelled cells on both sides. The topographical organization of the labeled cells for the control and study groups are given in Figure 6–7. Discussion In this study it was found that all anterior thalamic nuclei (AM, AV and AD) sent their projections to the hippocampus. Among these nuclei, the AV was found to have the most efferent projections to CA1. Anterior thalamic nuclei of both sides sent efferents to CA1, but the connection of ipsilateral anterior thalamic nuclei with the hippocampus was more profuse. It was also found that Re and Rh nuclei project to CA1 hippocampal area. Connection of Re to hippocampus was dominant to that of Rh to hippocampus, and labelled cells were scattered in the anterior and middle sections of the nucleus showing that the anterior and middle sections of nucleus send projections to CA1. It was seen that LD thalamic nucleus on the side of the injection site sends projection to CA1. We also found that ipsilateral VPL, Po, LPMR, VM, VL and Pt send a few fibers to CA1 area. Paxinos reports that all anterior thalamic nuclei and nucleus Reuniens send projections to the hippocampus [2]. Swanson and Wyss in their study on the subcortical afferents of the hippocampus using HRP as a tracer and tetramethylbebenzidin histochemical reaction found that all anterior thalamic nuclei, Re, PV and Pt send projection to the hippocampus. They concluded that AD sends more efferents to the ipsilateral hippocampus and found labelled cells of AM on both sides with ipsilateral predominancy [6]. Van Groen et al stated that AM sends projections to the entorhinal area and subiculum. There was no information about the hippocampus as a target of efferents [11]. Bokor et al found that the neurons of nucleus Re thalami sendprojectiontotheCA1hippocampalsubfield.Itisalso reported that these cells are located in the dorsolateral part of the nucleus Re [12]. Su and Bentivoglio described efferents of Re and stated that Re sends projections to hippocampus, amygdala and nucleus accumbens [13]. Herkenham found in his study with autoradiography and HRP tracing that there is a direct connection between Re and hippocampus in which those efferents pass through the genu of internal capsule and terminate in the stratum lacunosom moleculare of CA1 [14]. In the examination of the number and dispersion of labelled cells in animals fed with low protein diet (8%), we found that the amount of efferent projections from all anterior thalamic nuclei, Re, Rh, VPL, Po, VL, VA, and Pt was lower than the control group. According to Mokler et al [15] protein malnutrition causes changes in the hippocampal formation. Viana et al [16] reported that protein-energy malnutrition tends to cause significant decreases in muscarinic receptors in the hippocampus and basal ganglia. However, no significant differences in acethylcholinesterase activity or protein content were observed between control and undernutritioned animals in any of the brain areas studied. Granados-Rojas et al [17] stated that prenatal protein malnutrition induces long-lasting deleterious effects on the progression of developmental programs controlling synaptogenesis and/or synaptic consolidation, likely by affecting a myriad of cellular progresses. Andrade et al [18] found that protein deprivation experienced in adult rats causes reduction in the volume of the subiculum and the total number of its neurons. They reported that protein malnutrition causes a marked regressive change in the basal dendritic trees of the pyramidal subicular neurons. However, the spine density was increased in malnourished rats. They concluded that the effects of long-term protein deprivation are region specific and that the resulting structural alternations are confined to the three-layered components of the
  • 52. 48 Bayat et al. hippocampal region. Andrade et al [8] also showed that among hippocampal neurons, dentate granule cells are selectively vulnerable to food restriction. Nonetheless the reorganization which takes place in their dendrites and synapses is capable of minimizing the functional importance that were expected to occur following changes in the hippocampal neuronal circuitry induced by this type of dietary restriction. Results of these experiments show that the hippocampal formation is vulnerable to protein malnutrition. Due to this type of restriction, significant functional and morphological changes have been reported. Our findings show that under the influence of protein malnutrition efferent projections from anterior nuclear group and midline thalamic nuclei to the CA1 hippocampal area had decreased. According to our results, it was assessed that in protein malnourished rats after injection of a retrograde tracer in CA1 hippocampal area, the number of labelled cells in the anterior and midline thalamic nuclei is reduced compared to normal animals. We conclude that neuronal activity of the thalamus and hippocampal formation may be affected by the influence of protein restriction or the progression of developmental programs controlling synaptogenesis, or axonal transport may be reduced. Acknowledgement This study was supported by Qazvin University of Medical Science Research Unit. References [1] Amaral DG, Witter MP. The three dimensional organization of the hippocampal formation. A review of anatomical data. Neuroscience. 1989; 31: 571–591. [2] Paxinos G. The rat nervous system. 2nd Ed., San Diego, Academic Press. 1995; 629–648. [3] Guyton AC. Textbook of medical physiology. 9th Ed., Philadelphia, Saunders. 1998; 841–843. [4] Carpenter MB. Core text of neuroanatomy. 4th Ed., Baltimore, Williams and Wilkins. 1991; 370–373. [5] Kiernan JA, Barr ML. The human nervous system. 7th Ed., Philadelphia, Lippincott-Raven. 1998; 324–350. [6] Wyss JM, Swanson LW, Cowan WM. A study of subcortical afferents to the hippocampal formation in the rat. Neuroscience. 1979; 4: 463–476. [7] Pitkanen A, Maria Pikkarainen M, Nurminen N, Ylinen A. Reciprocal connections between the amygdala and hippocampal formation, perirhinal cortex and postrhinal cortex in rat. A review. Ann. N. Y. Acad. Sci. 2000; 911: 369–391. [8] Andrade JP, Lukoyanov NV, Paula-Barbosa MM. Chronic food restriction is associated with subtle dendretic alternations in granule cells of the rat hippocampal formation. Hippocampus. 2002; 12: 149–164. [9] Krause MV, Mahan LK, Escott-Stump S. Krause’s food, nutrition and diet therapy. 10th Ed., Philadelphia, Saunders. 2000; 242. [10] Mesulam MM, Van Hoesen GW, Pandya DN, Geschwind N. Limbic and sensory connections of the inferior parietal lobule (area PG) in the rhesus monkey: a study with a new method for horseradish peroxidase histochemistry. Brain Res. 1977; 136: 393–414. [11] van Groen T, Kadish I, Wyss JM. Efferent connections of anteromedial nucleus of the thalamus of the rat. Brain Res. Brain Res. Rev. 1999; 30: 1–26. [12] Bokor H, Csaki A, Kocsis K, Kiss J. Cellular architecture of the nucleus reuniens thalami and its putative aspartatergic/glutamatergic projection to the hippocampus and medial septum in the rat. Eur. J. Neurosci. 2002; 16: 1227–1239. [13] Su HS, Bentivoglio M. Thalamic midline cell populations projecting to the nucleus accumbens, amygdala, and hippocampus in the rat. J. Comp. Neurol. 1990; 297: 582–593. [14] Herkenham M. The connections of nucleus Reuniens thalami: evidence for a direct thalamo-hippocampal pathway in the rat. J. Comp. Neurol. 1978; 177: 589–610. [15] Mokler DJ, Bronzino JD, Galler JR, Morgane PJ. The effects of median raphe electrical stimulation on serotonin release in the hippocampal formation of the prenatally protein malnourished rats. Brain Res. 1999; 838: 95–103. [16] Viana GS, Figueiredo RM, Bruno JA. Effect of protein-energy malnutrition on muscarinic receptor density and acetylcholinesterase activity in rat brain. Ann. Nutr. Metab. 1997; 41: 52–59. [17] Granados-Rojas L, Larriva-Sahd J, Cintra L, Gutierrez-Ospina G, Rondan A, Diaz-Cintra S. Prenatal protein malnutrition decreases mossy fibers-CA3 thorny excrescences asymmetrical synapses in adult rats. Brain Res. 2002; 933: 164–171. [18] Andrade JP, Madeira MD, Paula-Barbosa MM. Differential vulnerability of the subiculum and entorhinal cortex of the adult rat to prolonged protein deprivation. Hippocampus. 1998; 8: 33–47.
  • 53. Published online 2 December, 2005 © http://www.neuroanatomy.org Original Article Neuroanatomy (2005) 4: 49–51 Introduction Ventricular system is a brain area that can be effected by numerousdisorderslikepsychiatricdisorders,particularly schizophrenia and Alzheimer [1, 2]. Furthermore, some changes during the biologic course of aging are also seen [3]. Nowadays, many studies are being done on the ventricular system. In these studies, the most preferable animal is rat, because of the similarity of the histological structure of the ventricles to that of human. It is important to determine the exact border of this area pertinent to basic and clinical sciences. To improve the understanding of the ventricles’ anatomy, we created three-dimensional (3D) models of rat ventricular system. This 3D model helps to understand the complex anatomic structure with ease. At the same time, 3D images may be used as a tool for virtual reality modeling of the ventricular system on planning the stereotaxic trial formerly. We are of opinion that this study will be useful for the neuroscientists in studies on ventricular system morphology and quantitative analysis. Material and Methods This experimental study was performed in a 6-month-old male Wistar rat, weighting 240 g and fed in a pathogen- free environment. The animal was anaesthetized with ketamine hydrochloride (Ketalar, Parke-Davis, Istanbul, Turkey) 30 mg/kg intramuscularly. For muscle relaxation 2% xylazine hydrochloride (Rompun, Bayer, Istanbul, Turkey) 6 mg/kg was used. The animal was decapitated, the brain was removed by craniotomy and frozen in cryostat (Leica CM3050) at –50°C. The frozen brain was cut in horizontal plane at a thickness of 60 μm with the cryostat at –15°C. Sections were stained with [4–6] hematoxylin-eosin (Fig. 1). After the staining, we examined the preparations in light microscope (Fig. 2). We scanned all the preparations. After the scanning of each slice, the images were imported to the computer [7]. Lazonoff and his co-workers [8] developed Surf Driver, a commercially distributed PC and Mac based program is used for reconstructing the 3D coordinate models from serial sections. Results Ventricular system of rat were like “Y” in shape, similar to human ventricles mentioned in textbooks (Fig. 3). Basically, the lateral venrtricles were the first and second ventricles. They were connected to the third ventricle of the diencephalon by the interventricular foramina. Continuing caudally, the cerebral aqueduct of the midbrain opened into the fourth ventricle. The fourth ventricle occupied the space dorsal to the pons and medulla and ventral to the cerebellum. It can be said that rat ventricular system was similar to human’s one (Fig. 4). Additionally, we also reconstructed brain hemispheres, and cerebellum. So, the 3D position of the ventricular system relative to the brain is observed. With computer aid, it was possible to rotate all the figures at 360 degrees, Three dimensional (3D) reconstruction of the rat ventricles Mehmet Bulent OZDEMIR Ilgaz AKDOGAN Esat ADIGUZEL Nilufer YONGUC Department of Anatomy, Pamukkale University, Faculty of Medicine, Denizli–Turkey. Dr. Mehmet Bulent Ozdemir, Department of Anatomy, Pamukkale University, Faculty of Medicine, Denizli–TURKEY 90-258-213 40 30 90-258-213 28 74 bulento@hacettepe.edu.tr Received 4 March 2005; accepted 30 November 2005 ABSTRACT The aim of this study is to investigate the normal three dimensional (3D) shape of the ventricular system of rat brain. The shape and volume of ventricles can be correlated with clinical or other characteristics of illness. Recently, many diagnostic imaging techniques allow to get the 3D images of anatomical structures easily. So it is possible to determine the correlation between subjects and pattern of the structures. In this study, we constructed a 3D model of the rat ventricles and their related structures. It is possible to say that, ventricular system of rat brain was similar to the human’s completely. Understanding such patterns may eventually help to improve rat experiments’ vision. Furthermore, these 3D models can be used for virtual animations and stereotaxic trials in further studies. Neuroanatomy; 2005; 4: 49–51. Key words [rat brain] [ventricular system] [anatomy] [computer] [3D reconstruction] eISSN 1303-1775 • pISSN 1303-1783
  • 54. 50 Ozdemir et al. thus we saw all the structure from different angles. It was also possible to magnify or zoom out the figures. Furthermore, the software allowed one to delete or add any structure to the image; also to view the complete model. These images were basic for advanced search. But, they contributed to improve the understanding of the ventricles of the brain and related organs of rat. Discussion In human, the central canal of the embryo differentiates into the ventricular system of adult brain. The ventricular cavities are filled with cerebrospinal fluid (CFS), which is produced by vascular tufts called choroid plexus. The ventricular cavity of the telencephalon is represented by the lateral ventricles. The lateral venrtricles are the first and second ventricles. They connect to the third ventricle of the diencephalon by the interventricular foramina (of Monro). Continuing caudally, the cerebral aqueduct of the midbrain opens into the fourth ventricle. The fourth ventricle occupies the space dorsal to the pons and medulla and ventral to the cerebellum. Cerebrospinal fluid flows from the fourth ventricle to the subarachnoid space trough the median aperture (of Magendie) and the Figure 2.  3D view of rat ventricles. (LV: lateral ventricle; 3V: 3th ventricle; CA: cerebral aqueduct; 4V: 4th ventricle; C: cerebellum) Figure 3.  A 3D reconstruction view of the rat ventricles from left antero-infero-lateral angle. Figure 4.  Reconstruction of the ventricles with brain. Figure 1.  Sections taken from a 6-month-old male Wistar rat brain stained with hematoxylin-eosin. Preparations were examined in light microscope, then the serial images were imported to computer.
  • 55. 51Three dimensional (3D) reconstruction of the rat ventricles lateral apertures (of Luschka). Most of the cerebrospinal fluid is produced by the choroid plexus of the lateral ventricles, although tufts of choroid plexus are found in the third and fourth ventricles as well [9]. The structures that construct the ventricular system of the rat were similiar to human in this study. This result was more comprehensible with the 3D model by the means of the possibility to rotate, zoom in or zoom out the 3D images. Thus, one can easily examine the structures from different angles. This model contributed to a new vision to the rat ventricular system, as well as to human. In human, results of ventricular system shape and volume examination are used in diagnosis; the lateral as well as the third ventricles have been noted to be enlarged in a number of psychiatric disorders, particularly in schizophrenia [10, 11]. Enlargement of the ventricles usually reflects atrophy of surrounding brain tissue. The term hydrocephalus is used to describe abnormal enlargement of ventricles. In the condition known as normal pressure hydrocephalus, the ventricles enlarge in the absence of brain atrophy or obvious obstruction to the flow of the CSF. Normal pressure hydrocephalus is classically characterized by progressive dementia, ataxia, and incontinence [12]. In addition, ventricular system changes in Alzheimer disease [13]. In human, with the imaging techniques like computed tomography (CT), magnetic resonance imaging (MRI) and others, we can easily demonstrate the ventricular system and related organs. So, it is possible to follow up the changes in the shape or functions of the ventricular system. Physicians usually correlate the outline with the disease. This is also done in rat experiments, and became the subject of many investigations. Consequently, there have been many studies of the ventricular system both on human and rats. Therefore, it is important to improve the understanding of the hippocampus of rat, as well as the one of human. Furthermore, 3D models that developed in this study can be used in creating virtual simulations, and volumetric studies. Because of the surgical interventions can be hard in small animal brains like rat, surgeons can practice on this computer assisted models, especially in stereotaxic trials. This study may also contribute to a new vision in rat studies. References [1] Shenton ME, Dickey CC, Frumin M, McCarley RW. A review of MRI findings in schizophrenia. Schizophr. Res. 2001; 49: 1–52. [2] Holodny AI, Waxman R, George AE, Rusinek H, Kalnin AJ, de Leon M. MR differential diagnosis of normal- pressure hydrocephalus and Alzheimer disease: significance of perihippocampal fissures. AJNR Am. J. Neuroradiol. 1998; 19: 813–819. [3] Resnick SM, Goldszal AF, Davatzikos C, Golski S, Kraut MA, Metter EJ, Bryan RN, Zonderman AB. One-year age changes in MRI brain volumes in older adults. Cereb. Cortex. 2000; 10: 464–472. [4] Gartner LP, Hiatt J. Color textbook of histology. 2nd Ed., Philadelphia, Saunders Company. 2001; 504–505. [5] Junqueira LCU, Carneiro J. Basic histology text and atlas. 10th Ed., Newyork, McGraw-Hill. 2003; 444–445. [6] Ross MH, Kaye GI, Pawlina W. Histology: a text and atlas. 4th. Ed., Philadelphia, Lippincott Williams. 2003; 662–663. [7] Spitzer VM, Whitlock DG. The Visible Human Dataset: the anatomical platform for human simulation. Anat. Rec. 1998; 253: 49–57. [8] Trelease RB. Anatomical informatics: millenial perspectives on a newer frontier. Anat. Rec. 2002; 269: 224–235. [9] Clark DL, Boutros NN. The brain and behavior: an introduction to behavioral neuroanatomy. Malden, Blackwell Science. 1999; 143–154. [10] Daniel DG, Goldberg TE, Gibbons RD, Weinberger DR. Lack of bimodal distribution of ventricular size in schizophrenia: a Gaussian mixture analysis of 1056 cases and controls. Biol. Psychiatry. 1991; 30: 887–903. [11] Elkis H, Friedman L, Wise A, Meltzer HY. Meta-analysis of studies of ventricular enlargement and cortical sulcal prominence in mood disorders. Comparisons with controls or patients with schizophrenia. Arch. Gen. Psychiatry. 1995; 52: 735–746. [12] Friedland RP. Normal-pressure hydrocephalus and the saga of the treatable dementias. JAMA. 1989; 262: 2577–2581. [13] Abbruzzese M, Scarone S, Colombo C. Obsessive-compulsive symptomatology in normal pressure hydrocepalus: a case report. J. Psychiatry Neurosci. 1994; 19: 378–380.
  • 56. Published online 16 December, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 52–54 Introduction Surgical management of spinal dysraphism is an important area of neurosurgery. Spinal dysraphism defines incomplete fusion the neuronal arch, varying from the occult to more severe open neural tube defects. Meningocele, the simplest form of open neural tube defects, is characterized by cystic dilatation of meninges, which contain cerebrospinal fluid without any neuronal tissue. The natural course of meningocele has not entirely explored. Adult patients with spinal dysraphism may give some evidences about the clinical progression of malformations. Small series or few cases have been reported on dyplastic malformations in adults [1–5]. In this report, we present a 48 years-old patient with meningocele who has developed urinary and fecal incontinence in adulthood. The clinical course of this congenital malformation and the pathophysiology of the adult onset of symptoms are discussed. Case Report 48 years old male ambulance driver presented with low back pain without radiating to legs for nearly 8 years and a 5 years history of progressive loss of sensation of bladder fullness, loss of ability to develop erection, decreased penile sensation and constipation. From puberty until age of 43, he had no difficulty with bladder function. For the past 5 years, he has realized increased effort in initiating urination and decreased force of urination. Over the past 5 years, he experienced decreased firmness and duration of erection. His difficulty with bowel movements was one of chronic constipation, increasing over 5 years. He did not have any systemic disease. During the inspection, a dorsal midline cystic lesion, measuring 4x3 cm, covered with skin, was noticed (Fig. 1). The lesion was tender to touch. The neurological examination of the patient revealed intact strength in all muscle groups and no sensory abnormality was evident. Straight leg raising test were negative bilaterally. Deep tendon reflexes were diminished and no fasciculation accompanied. There was decreased touch sensation over the perianal area and over the shaft of penis corresponding to S3-S5 spinal cord segment. The patient had a very weak anal sphincter although it was capable of voluntary contraction. The anal wink reflex and the bulbocavernous reflex were markedly decreased. Urological evaluation with abdominal and urogenital ultrasonographyshowednoabnormality.Theurodynamic evaluation with pressure flow studies and sphincter electromyographic studies demonstrated a flaccid neurogenic bladder with evidence of internal sphincter denervation. The blood chemistry was normal including blood glucose and prostate specific antigen levels. X-ray images of lumbosacral region demonstrated L5 sipina bifida. Sagittal T1-weighted magnetic resonance (MR)imagingoflumbosacralregionrevealedamyelocele sac originated from L5 spina bifida. It was also observed Clinical course and evaluation of meningocele lesion in adulthood: a case report H. Beril GOK Giyas AYBERK Hakan TOSUN Zekai SECKIN Ankara Ataturk Education and Research Hospital, Department of Neurological Surgery, Ankara–Turkey. H. Beril Gok, MD Umit Mahallesi, Beril Sitesi, 436. Sok. No:8 06800 Umitkoy, Ankara–TURKEY 90-505-501 13 27 90-312-291 27 05 beryl_gok@yahoo.com Received 19 October 2005; accepted 14 December 2005 ABSTRACT Theprogressivecourseofspinaldysraphismhasnotyetbeenunderstood.Adultpatientswithspinaldysraphisms may give some evidences about the clinical progression of the malformations. In the present study we discussed a 48 years old patient with meningocele who has developed adult onset of impairment of sacral functions. The radiological, electrophysiological and urodynamic evaluations and pathophysiology of the adult onset of sypmtoms are also discussed. Neuroanatomy; 2005; 4: 52–54. Key words [meningocele] [adulthood] [surgery] [spinal dysraphism] [neurosurgery] eISSN 1303-1775 • pISSN 1303-1783
  • 57. 53Clinical course and evaluation of meningocele lesion in adulthood Figure 2.  Sagittal T1-weighted MR images demonstrated myelocele sac originated from L5 spina bifida. Notice that conus medullaris reached L5 level and extension of the filum terminale terminated within the meningocele. Figure 3.  Sagittal T2-weighted MR images demonstrated tethering of spinal cord with no hydromyelia nor myelomalacia. Figure 4.  Axial T2-weighted MR images demonstrated associated lipoma and no neurological tissue involved in the meningocele cavity. Figure 1.  Patient with lumbosacral meningocele.
  • 58. 54 Gok et al. that conus medullaris reached L5 level and extension of the filum terminale terminated within the meningocele, causing tethering of the spinal cord (Fig. 2). Sagittal T2-weighted MR images demonstrated tethering of spinal cord with no hydromyelia nor myelomalacia (Fig. 3). With T1-weighted axial MR images an associated lipoma was detected and no neurological tissue involved in meningocele cavity (Fig. 4). Somatosensory evoked potential (SSEP) was in normal range. Since the patient had progressive neurological symptoms, surgical treatment was suggested. The patient did not accept the operation and he has been under control of both neurosurgery and urology departments. He has been followed up with intermittent urinary catheterization. Discussion Any meningocele patient has deteriorating clinical symptoms such as progressive orthopedic deformities, lower extremity weakness or urinary and fecal incontinence associated with low back pain, should be considered as tethered cord [4]. The degree of traction of the conus is thought to determine the age of onset of symptoms [3–4]. In cases of marked tethering and severe stretching of the conus, neurological symptoms appear in infancy or early childhood [6]. Minimal tethering may remain subclinical until adulthood [3]. 29% of patients with symptomatic tethered cord, have been found to be older than 35 years [7]. The mechanism of late onset of symptoms has not yet been well understood, however the mechanism is explained by the cumulative effect of repeated cord traction by various postures [3–5, 8]. Yamada et al. stated that neurological dysfunction in patients with tethered cord correlates with mitochondrial anoxia within the conus [9]. The narrowing of the spinal canal by lumbar spinal stenosis and disc prolapsus and resultant increased tension in spinal cord may also precipitate symptoms [7–9]. It has been suggested that the longitudinal stress within the spinal cord may be transmitted more distally along the lateral columns as they are fixed by dentate ligaments [3–5, 8]. Direct trauma to the lumbosacral region may precipitate the symptoms causing deformation of the marginally functioning neuronal elements within the stretched cord [3–5]. In our patient, conus situated at L5 and extension of the filum terminale terminated in meningocele at the level of S1. The precipitating factors in the appearance of symptoms that are the momentary stretching of the tight conus with sudden flexion of the neck and hip, may be related to his occupation since driving often predispose to these conditions. MR is a useful technique for evaluation of patients with spinal dysraphisms. Direct X-ray and computed tomography may give information about the associated bone defects, while MR is a superior diagnostic tool for verifying the cystic lesion in the sagittal plane, its relation with the spinal cord and associated spinal cord anomalies [7]. In the present case, direct X-ray shown L5 sipina bifida and MRI studies demonstrated low lying conus associated with lumbosacral meningocele. SSEP was reported as more sensitive than clinical testing for detection of neurological deficits in patients with spinal cord lesion [10]. Abnormal SSEP is a clear indication of spinal pathology. However, not all spinal pathologies are associated with abnormalities in SSEP [4, 10]. In the reported patient, SSEP was found to be within normal range. Pre-operative urodynamic investigation is strongly recommended, especially if the patient seems continent [2]. In our patient, urodynamic evaluation demonstrated non-functioning internal sphincter and detrusor hyporeflexia indicating flaccid neurogenic bladder. It was demonstrated that tethering of the conus usually causes mixed abnormalities of parasympathetic, sympathetic and somatic pathways [2]. Sympathetic innervation was often impaired first, resulting in non-functioning internal urethral sphincter, which characteristically causes post- voiding dripping and stress incontinence [2]. Although conflictions are present about the surgical indication of asymptomatic patients, it has been suggested that, each adult or child should be operated as soon as symptoms appeared or progressed because in the majority of patients only stabilization of the disease is achieved [1, 4–5]. Because of the progressive neurological symptoms, the patient was suggested to surgical treatment. Since the patientdidnotaccepttheoperation,wecouldnotcomment on the results of surgical intervention. This patient may give some evidences about the relation between the untreated intradural abnormalities and progressive neurological deficits. Further investigations are necessary on the natural history of spinal dysraphism. References [1] Klekamp J, Raimondi AJ, Samii M. Occult dysraphism in adulthood: clinical course and management. Childs Nerv. Syst. 1994; 10: 312–320. [2] Kondo A, Kato K, Kanai S, Sakakibara T. Bladder dysfunction secondary to tethered cord syndrome in adults: is it curable? J. Urol. 1986; 135: 313–316. [3] Pang D, Wilberger JE Jr. Tehtered cord syndrome in adults. J. Neurosurg. 1982; 57: 32–42. [4] Satar N, Bauer SB, Shefner J, Kelly MD, Darbey MM. The effects of delayed diagnosis and treatment in patients with an occult spinal dysraphism. J. Urol. 1995; 154: 754–758. [5] Gupta SK, Khosla VK, Sharma BS, Mathuriya SN, Pathak A, Tewari MK. Tethered cord syndrome in adults. Surg. Neurol. 1999; 52: 362–370. [6] Roy MW, Gilmore R, Walsh JW. Evaluation of children and young adults with tethered spinal cord syndrome. Surg. Neurol. 1986; 26: 241–248. [7] Raghavan N, Barkovich AJ, Edwards M, Norman D. MR imaging in the tethered spinal cord syndrome. Am. J. Roentgenol. 1989; 152: 843–852. [8] Schmidt DM, Robinson B, Jones D. The tethered spinal cord. Etiology and clinical manifestations. Orthop. Rev. 1990; 19: 870–876. [9] Yamada S, Zinke DE, Sanders D. Pathophysiology of ‘tethered cord syndrome’. J. Neurosurg. 1981; 54: 494–503. [10] Nadeem RD, Brown JK, Macnicol MF. Somatosensory evoked potentials as a means of assessing neurological abnormality in congenital talipes equinovarus. Dev. Med. Child. Neurol. 2000; 42: 525–530.
  • 59. Published online 20 December, 2005 © http://www.neuroanatomy.org Case Report Neuroanatomy (2005) 4: 55–56 Introduction Fetal intracranial tumors are often associated with hydrocephalus, polyhydramnios and macrocephaly. The most common location is supratentorial compartment [1– 3]. Focal neurological changes are absent in most cases of neonatal brain tumors despite the large head size and the hydrocephalus. These tumors do not interfere severely with normal gestation and parturition. Several histologic types of congenital intracranial tumors have been described, including teratoma, choroid plexus papilloma, craniopharyngioma, meningeal sarcoma, lipoma of the corpus callosum and oligodendroglioma [1–4]. Here, a tumor occupying 76.19% of the intracranial cavity is presented. Our literature review revealed no intracranial tumor with such huge volume ratio. Case Report A two month old girl was born to a 35 years old gravida 5, para 3, aborta 2 mother at 38th week gestation via cesarean section. Prenatal ultrasonography at 35th week revealed an enlarged head. An intracranial tumorlike mass without obviously normal intracranial structures was evident on ultrasonography. Because of severe macrocephaly, an elective cesarean section was performed at 38th week of gestation. The infant’s Apgar score was low. Her weight was 3045 g, length was 45 cm and head circumference was 47 cm at birth. She was admitted to our hospital because of increase in her head circumstance and unconsciousness. Physical examination revealed a huge head with wide bulging fontanels and a bossing forehead. She was extremely hypotonic with widely separated cranial sutures. No other congenital anomaly was observed. Transcranial ultrasonographic examination revealed a heterogeneous intracranial mass without normal brain structure (Fig. 1). Magnetic resonance imaging demonstrated a huge intracranial mass lesion occupying 76.19% of the intracranial cavity (Fig. 2). A subtotal tumor removal was performed. During surgery it was observed that the tumor was excessively vascular. Short after the operation the patient was deceased. Discussion Congenital brain tumors are rare entities which are nowadays often recognised during pregnancy by ultrasound and magnetic resonance imaging [5]. In literature, first report of a massive congenital intracranial teratomawaspublishedin1864byBreslauandRindfleisch [6]. Giant pediatric tumors may present with seizures due to irritation of the cortical gray matter. In more rapidly growing tumors, signs of increased intracranial pressure such as papilledema may occur. Bulging fontanels and macrocephaly may be evident in infants [7]. Nerve and glial cells are derived from a specialized portion of the ectoderm termed the neural plate. The edges of the neural plate fold, ultimately appose, and form the neural tube. The cerebral hemispheres and the brain stem develop from the rostral and intermediate portions of the neural tube, and the spinal cord develops from the caudal portions. The neuroepithelium lines the Huge tumor of the intracranial cavity: a catastrophic imaging on USG and MRI Ibrahim M. ZIYAL Burcak BILGINER Gokhan BOZKURT Hacettepe University, Faculty of Medicine, Department of Neurosurgery, Ankara–Turkey. Ibrahim M. Ziyal, MD Associate Professor of Neurosurgery, Department of Neurosurgery, Hacettepe University, Faculty of Medicine, 06100 Ankara–TURKEY 90-312-305 26 27 90-312-311 11 31 ibrahimziyal@yahoo.com Received 27 October 2005; accepted 19 December 2005 ABSTRACT In this case, we report a tumor occupying 76.19% of the intracranial cavity which is diagnosed with magnetic resonance imaging. This tumor is inspected as one of the biggest intracranial mass lesions in literature. In such cases, the postoperative survival rate is low due to several factors such as perioperative bleeding, sudden volume changes in the intracranial cavity and intracranial hypotension. The surgical excision is open to question. Neuroanatomy; 2005; 4: 55–56. Key words [huge] [tumor] [intracranial cavity] [USG] [MRI] eISSN 1303-1775 • pISSN 1303-1783
  • 60. 56 Ziyal et al. Figure 2.  Post-contrast T1- weighted coronal (A), sagittal (B) and axial (C) magnetic resonance images showing the extension of huge intracranial mass occupying 76.19% of the intracranial cavity and the distortion and compression of neural structures. Figure 1.  A huge intracranial mass with heterogeneous echogenicity and multilobulated cysts associated with obstructive hydrocephalus is observed in ultrasonography of a 2 months old girl. neural tube and forms the cellular constituents of the central nervous system. Immature neurons arise from the neuroepithelium. The neural tube has two additional layers: the mantle layer, which becomes the gray matter of the central nervous system, and the marginal layer, which becomes the white matter. The cavity within References [1] Horton D, Pilling DW. Early antenatal ultrasound diagnosis of fetal intracranial teratoma. Br. J. Radiol. 1997; 70: 1299–1301. [2] Palo P, Penttinen M, Kalimo H. Early ultrasound diagnosis of fetal intracranial tumors. J. Clin. Ultrasound. 1994; 22: 447–450. [3] Chien YH, Tsao PN, Lee WT, Peng SF, Yau KI. Congenital intracranial teratoma. Pediatr. Neurol. 2000; 22: 72–74. [4] Wakai S, Arai T, Nagai M. Congenital brain tumors. Surg. Neurol. 1984; 21: 597–609. [5] Mazouni C, Porcu-Buisson G, Girard N, Sakr R, Figarella-Ballanger D, Guidicelli B, Bonnier P, Gamerre M. Intrauterine brain teratoma: a case report of imaging (US, MRI) with neuropathologic correlations. Prenat. Diagn. 2003; 23: 104–107. [6] Breslau, Rindfleisch E. Geburtsgeschichte und Untersuchung eines Falles von Foetus in Foetu. Virchows Arch. Pathol. Anat. 1864; 30: 406–417. [7] Winn HR, Youmans JR. Youmans neurological surgery. 5th Ed., Philadelphia, Saunders. 2004; 3697. [8] Martin JH. Neuroanatomy text and atlas. 2nd Ed., New York, McGraw-Hill. 1996; 57. A B C the neural tube forms the ventricular system [8]. These tumors are most commonly localized to supratentorial region and generally arised from the cortical gray-white matter or from the ventricules. In this case the congenital tumor prohibit development of normal neural structures. Instead of gray and white matter, corpus callosum, internal-external capsule, thalamus, nucleus caudatus and basal ganglions, there was a huge tumor distorting and compressing the brain. As far as we know, this case was the biggest intracranial tumor in literature, regarding the ratio of the tumor volume to the intracranial cavity. Such cases may be called “Pandora’s box”. The prognosis is usually fatal in these cases because of rapid, invasive growth of the tumors and the destruction of regular cerebral structures [1]. Surgical excision may be curative at smaller benign intracranial lesions. But in such cases like ours, if the intracranial cavity is opened, control of bleeding is extremely diffucult because of large surface of bleeding area in the tumor. On the other hand, sudden intracranial hypotension after removing the tumor may also be fatal. Because of poor prognosis we have to think twice before operating such cases.
  • 61. Published online 26 December, 2005 © http://www.neuroanatomy.org Brief Review Neuroanatomy (2005) 4: 57–63 Introduction The localization of motor and sensory activities, the “rete mirabile” and the localization of the mental processes – the seat of the soul – in the ventricles or “cells” of the brain were ancient Greek concepts which were handed down to the middle ages. Although this last concept had not fully matured during classical antiquity its basic elements can be traced to Galen’s works. Even though there were dissections (mostly animal) and enough visual material, the concepts were passed through writings with rare medical illustrations. With the death of Galen in 199 anatomical dissection of either scientific or medical reasons was absent in both Europe and Islam for over a thousand years. It began again in thirteenth century Italy, first for forensic purposes and then as a way of illustrating Galen’s anatomical works for medical students [1]. As the Renaissance men began doing their own dissections, medieval physiology, passed through translations of Arab scholars, confronted with their anatomical dissections. Being not able to totally rid themselves from medieval learning there became a transitional period in which medieval physiology was superimposed upon Renaissance anatomy [2]. In this article we shall narrate ventricular anatomy from “the Alexandrian series” to the Renaissance transitional period; touching some other medieval concepts when relevant. The functional role of the ventricles began with Herophilus of Alexandria (ca 270). The uniqueness of the Alexandrian anatomy nexus is revealed by the fact that not only was human dissection first practiced in that city, but this was the first and virtually the only place where human vivisection was systematically carried out for scientific purposes. Both Herophilus and Erasistratus (ca 260) were particularly interested in the brain. They provided the first accurate and detailed description of the human brain including the ventricles [3–4]. Like Alcmaeon and the Hippocratic doctors before them, they had no question about the brain’s dominant role in sensation, thought, and movement. Herophilus claimed that the fourth ventricle was the “command center” and compared the cavity in the posterior floor of the fourth ventricle with the cavities in the pens that were in use in Alexandria at the time, and it is still called calamus scriptorius or sometimes calamus Herophili [5]. Anatomical illustrations were also first produced in Hellenistic Alexandria about 300 BC. The tradition, owing much to Herophilus and to Erasistratus has been traced by way of Byzantium to the medieval west. Figure 1 is a unique drawing around 1250 AD which according to Sudhoff may have originated in Salerno [6]. It is most probably a copy of original Alexandrian series and depicts the venous system. The text written Ventricular anatomy: illustrations and concepts from antiquity to Renaissance Ali Oguz TASCIOGLU [1] Ayse Beliz TASCIOGLU [2] Department of Neurosurgery [1], Ankara University, Faculty of Medicine, Ankara–Turkey; Department of Anatomy [2], Hacettepe University, Faculty of Medicine, Ankara–Turkey. Ali O. Tascioglu, MD Professor of Neurosurgery, Department of Neurosurgery, Ankara University, Faculty of Medicine, 06100 Ankara–TURKEY 90-312-310 33 33 / 3138 90-312-310 71 69 btasciog@hacettepe.edu.tr Received 17 November 2005; accepted 19 December 2005 ABSTRACT In this article we have tried to narrate ventricular anatomy from its start in antiquity to the transitionalists of the Renaissance. The crude drawings of the Alexandrian series can hardly be called “anatomical“. The accompanying texts consisted mostly of concepts unrelated to sketches. With the Renaissance there came an era where true knowledge, through dissections, revealed the actual structures of the ventricles and ended the unfounded arguments of ventricular function. Neuroanatomy; 2005; 4: 57–63. Key words [brain ventricles] [anatomy] [antiquity] [Renaissance] [history] eISSN 1303-1775 • pISSN 1303-1783
  • 62. 58 Tascioglu and Tascioglu Figure 1.  A unique drawing of around 1250. Salerno. Part of Alexandrian Series [12]. in Catalan describes three chambers in the brain thus referring to the cell doctrine of ventricular localization of mental functions although it is not apparent where these are sited other than possibly between the worm like structures. Since the figure is essentially of the venous system, the brain is most probably added at this later copy. Galen (129–199 AD) was the most important figure in ancient medical science. He provided a detailed and accurate account of anatomy in general and anatomy of the brain in special. But, it was not until recently that historians realized his descriptions being remarkably accurate when applied to the monkey or ox (his usual subjects of dissection) but not on humans [7–8]. More curiously, Galen never mentioned that his anatomical descriptions were almost always based on non humans. He described the ventricles in considerable detail as four cavities and their connections. He described the two lateral (anterior), the third and the fourth ventricle and addressed them as crucial in his physiological system where the ventricles were the site of storage of psychic pneuma. The psychic pneuma (animal spirit) was the active principle of both sensory and motor nerves and the central nervous system. Although the ventricles, particularly the anterior ventricle, were important as a source of psychic pneuma he located the soul and higher cognitive functions not in the ventricles but in the solid portions of the brain around the ventricles. For that, he argued on the basis of his extensive clinical experience as a doctor at the gladiatorial school in Pergamon. He claimed that when brain lesions penetrated to the ventricles, death did not invariably result even if both sensation and movement were lost. Imagination, reason and memory were the three constituents of intellect and they could be affected separately. Being the greatest anatomist of antiquity, he did not, however, encourage his students to rely on illustrations, believing that direct visualization and handling of the structures was the only way to appreciate their form and relationship. Cell Doctrine The cell doctrine developed out of a curious amalgam of Greek medical theory and practice and ideological concerns of early Christian church authorities. In the fourth century Poseidonus of Byzantinum developed Galen’s ideas of cerebral localization further [9]. He is, probably, the first to report in detail on the effects of localized brain damage in humans. He said that the lesions of the anterior brain substance impaired imagination, lesions of the posterior brain impaired memory, and damage to the middle ventricle produced deficit in reasoning. The early church authorities, in particular Nemesius, Bishop of Emesia (ca 390) and St Augustine (350–430) were very much concerned with the nonmaterial nature of the soul. Therefore, rather than localise the soul, they localized Aristotle’s classification of its functions such as sensation and memory. They believed that soul cannot be localized in the heart as Aristotle did, and placed it in a much higher place at the temple, to encephalon. Furthermore they believed that the brain tissue was too earthy, too dirty to act as an intermediary between the body and soul; so Nemesius put all the faculties of the soul into the ventricles following the same antero-posterior pattern as his contemporary Poseidonus [10]. Besides the desire for a suitable intermediary between the body and non corporeal soul another desire was to make it match to trinity, so they reduced the four ventricles of Galen to three. The lateral ventricles were considered as one cavity, the first cell or the small room or the vestibulum of the temple. It received impulses from the special senses and from the rest of the body and thus accommodated “sensus communis”thecommonsense.Sinceimageswerecreated from these sensations so “imaginativa” imagination and “fantasia” fantasy were also in the posterior part of the first cell. The second cell (our third ventricle) or middle cell was the seat of the cognitive process: “ratio” reason, “aestimativa” judgement or “cogitativa” thought. For the posterior third cell (our fourth ventricle) Galen’s original thought of motor function was changed to “memorativa” memory. The three stages of processing postulated for the three cells were also rationalized by a comparison with the spatial division of function in classical law courts. The quotation from the Anatomia Nicolai Physici, a twelfth- century text of Nemesius and Poseidonus [11]:
  • 63. 59Ventricular anatomy: illustrations and concepts from antiquity to Renaissance Figure 2.  From an 11th century manuscript. The earliest known illustration of brain Function [12]. “On the account of the three divisions of the brain the ancient philosophers called it the temple of the spirit, for the ancients had three chambers in their temples: first the vestibulum, then the consistorium, finally the apotheca. In the first, the declarations were made in law cases, in the second, the statements were sifted in the third, final sentence was laid down. The ancients said that the same process occur in the temple of the spirit, that is the brain. First, we gather ideas into the cellular phantisca, in the second cell We think them over, in the third, we lay down our thought, that We commit to memory” [9]. The cell doctrine, though discussed a lot in the texts was not pictured in figures. As we see, there are no ventricles in figure 1. Figure 2 is from eleventh-century and is the earliest known western illustration of brain function. The design is reminiscent of the Celtic stone cross found in Anglo-Saxon diagrams. The figure shows four principle human members, which are the liver, heart, testes, and cerebrum in a clockwise sequence from 12 o’clock. The last, in fact, is a drawing of skull facing inwards and seen from above. Coronal, sagittal, and lambdoid sutures are presented by double lines. The mental faculties fantasia, intellectus, and memoria are inscribed on it centrifugally. Around the circle “there are present four principle human members” is written. In the text, the brain is labelled cold and moist where as the heart is hot and dry in accordance with the ancient Greek theory of qualities. Since these designations were given great prominence by Aristotle and his followers, the illustration transmits traditional Greek ideas as well as the concept of ventricular localization of mental functions. The initial form of cell doctrine was liable to variations and more complicated rearrangements. The first cell could have two separate parts (sensus communis and imaginativa) or the second might be doubled (aestimativa and cognitiva) or, occasionally the third cell can be in control of both motiva and memoria. Variations from the central theme was determined by the master teaching, whether it be Galen or Avicenna or the church fathers. For example, Avicenna, being a non Christian, did not feel obliged to stick to three cells and favoured a five cell scheme. The diagram shown in Figure 3 is at the end of a treatise by Avicenna copied in 1347 as “De Generatione Embryonis” [12]. There is no legend other than the statement “this is the anatomy of the head for physicians”. It is a crude profile of a human head. There are five cells in the brain. Fivesenses – tactus (touch), gustus(taste), olfactus (smell), auditus (hearing) and visus (vision) – are connected to the first cell sensus communis, and other cells fantasia, imaginativa, cogitativa, seu estimativa and memorativa are shown separately and interconnected. Besides this classification, the head is also divided to three cells from anterior to posterior as first, second, and third. This may be original or, more likely, a contribution of the copier. Avicenna is neither the only nor the first of this variation of five compartments. About 100 years before this diagram Roger Bacon (1219–1292) prepared a similar manuscript “De scientia perspectiva”. Figure 4 is a 1428 copy of this manuscript [12]. It is very similar to Avicenna’s description showing five interconnected circles with much the same labelling. But in the accompanying text there is an interesting and unique discussion of brain function. The four humors of ancient Greek medicine, blood, phlegm, yellow bile and black bile are said to be excreted from cranial apertures: blood from the mouth, phlegm from the nose, yellow bile from the ears as ear wax and black bile from the eyes as tears. On the drawing these functions are recorded, close to each special sense organ. Crude drawings similar to figure 3 later became the basis of Leonardo’s first anatomical drawings of the brain about 140 years later. Transitionists With the advent of Renaissance learning, the medieval cell doctrine began to lose ground. This gradual transition was brought about by a group of men who stand between the medieval period and the Renaissance. Men who, having learned the old ways, had begun to assimilate and adopt the new. Leonardo de Da Vinci (1472–1519) is the first of these pioneers. His powerful, insatiable, and extraordinary visual curiosity drove him to seek meaning in the structure and pattern of the body. Looking at the crude drawings before him it can easily be said that he was probably, the first great medical illustrator. His drawings are the earliest naturalistic drawings of the internal structure of the human body. He introduced a number of powerful techniques for potraying anatomical structures such as the use of transparencies, cross sections and three dimensional shading. Leonardo’s studies on anatomy can be roughly divided into an early (from 1478), middle, (1506–1510) and a late (after 1510) phase. As in other areas of his investigations, Leonardo’s understanding of the brain showed a progression from unrefined images clouded
  • 64. 60 Tascioglu and Tascioglu Figure 3.  Avicenna’s De Generatione Embryonis. Copied probably in 1347 [16]. is an uncritical amalgam of Arabic and medieval sources with minor discovery and some new techniques thrown in [2, 13–15]. At that stage Leonardo probably did not do much dissection of the brain and relies on Avicenna through Mondino’s text. The terms for the layers from hair to brain are from Avicenna and portrayal of the ventricles as three connected spheres are from medieval cell doctrine. There, he did not even follow Galen, as the first (lateral) ventricles are not paired. Drawn by red chalk and two shades of brown ink, the figure is more artistic than the previous ones. What Leonardo shows and discusses is the visual input, not the ventricles. At the bottom of the figure we can see an axial section at the eye level showing the visual and auditory inputs into the first cell. For an artist like Leonardo who could draw the axial section of the brain, it is highly unlikely that he would miss the cross sectional anatomical structure of the ventricles. At this level of his drawings it was not clear whether Leonardo was drawing the brain observed, the brain remembered, the brain read about or the brain dissected. This is a typical figure of the early transition period artist, putting his art to half observed facts and half accepted false knowledge. To stress this argument further, we can look at his later works. A few years later Leonardo turned to the ventricles with brilliant success. Using the sculptural technique of wax injection he revealed the shape of the ventricles. As he instructed: “Make two vent-holes in the horns of great ventricles, and insert melted wax with a syringe, making a hole in the ventricle of memoria. Then when the wax has set, take away the brain and you will see the shape of the ventricles. But first put narrow tubes into the vents so that the air which is in the ventricles can escape and make room for the wax which enters into the ventricles”. Wax injection is a technique Leonardo learned from his artistic craft. He was genius enough to apply it to the ventricles of the brain. This technique was not used again until Frederic Ruysch in the eighteenth century. French Academy of Science thought it to be an achievement equal to Newton’s [9, 14]. The results of Leonardo’s wax studies stands out in Figure 6. In the figure there is a sagittal and axial sectional anatomical drawing of the ventricles. In the axial view, posterior horns of the lateral ventricles cannot be seen. It was probably due to the absence of air vents in the posterior horns and the use of unpreserved brain. At this point we think that Leonardo deserves extra credit for his anatomical studies, for at his time corpses were not fixed and began to putrefy within hours and especially organs like the brain lost shape and consistency. It took fast, meticulous and uninterrupted work of several  Anatomia of Mordino de Luzzi (Mondinus) written in 1316 was the first European anatomy textbook. It was essentially a 40 page dissection guide for learning Arab accounts of Galen’s words, not for learning about the actual body. Mondino’s work went through many manuscripts editions before it was finally printed in 1478, but remained unillustrated until the 1521 edition [16–18]. It was known to Leonardo at the beginning of his dissections around 1490 and was an important source of anatomical nomenclature for him [15–17, 19]. Figure 4.  Manuscript copy of De scientia perspectiva by Roger Bacon, 1428 [16]. with medieval knowledge to the refined illustrations conveying first hand knowledge through dissections. One of Leonardo’s earliest anatomical drawings shows the visual input to the brain (Figure 5). Drawn in 1490 it
  • 65. 61Ventricular anatomy: illustrations and concepts from antiquity to Renaissance Figure 6.  Leonardo da Vinci. Drawings after his wax injection studies 1504–1507 [22]. corpses to reveal even one muscle leave alone the brain. Most probably these frustrations made Leonardo seek techniques like wax injection. At the top right of the figure there is a faint drawing of the cortex seen from above. This is the most accurate cortex drawing up to that time. The base of the brain at the bottom left shows the “rete mirable” and is probably drawn from an ox brain. Lastly at the middle right there is an axial section showing the senses and cells. Here Leonardo, typical of an early transitionist, is trying to adopt his old knowledge to his new findings, to see whether they match. At the text he is mentioning the horns of great ventricles, yet he is putting the ox brain and cell doctrine side by side with the human brain. About 20 years after Leonardo’s wax studies Berengario da Carpi (1460–1530) published his book “Isagoge Breves” in 1522. His anatomical illustrations were more like pictures and were much improved compared to Leonardo’s. Figure 7 is from the second edition of Isagore Breves published in 1523. It shows the brain from above with, at first one ventricle opened to show the vermis. In this figure vermis is shown as the sitting place of the choroid plexus where as in the dynamic cell doctrine it acted as a valve between cells one and two. The lower view reveals both lateral ventricles at their anterior venter, two veins in the midline and the “embotum”. Embotum may be, either the opening into the aqueduct of Sylvius or the hypothetical exit by way of the pituitary for ventricular wastes. With our present knowledge and due Figure 5.  Leonardo da Vinci’, sagittal section of head. The early drawings 1490 [22]. Figure 7.  Berengario da Carpi. Anatomical illustration from Isagoge breves 1522 [12].
  • 66. 62 Tascioglu and Tascioglu Figure 9.  Andreas Vesalius. Brain ventricles from his famous book De Fabrica 1543 [21]. Figure 8.  Berengario da Carpi. Cover of his famous book. Tractatus de fractura calve Sive cranei a carpo editus 1518 [12]. to its anterior localization the second hypothesis seems more plausible. In a statement at the text Berengario discusses the aim of his anatomical studies and illustrations as “… so that the matter discussed may be better understood I have accommodated below such figures of the brain as I was able in which some of the matters previously described can be understood as you see”. Though his visuals were much removed from medieval cell doctrine, he was still a transition man under the influence of medieval knowledge. When it came to argument in the text of his Isagoge, he accepted some of the cell doctrine, for he located all the mental functions in the lateral ventricles. He argued that the other ventricles dealt with excretion, motion and sensation. His most famous book “Tractatus ed Fractua Calve Sive Cranei” is a surgical text on cranial fractures. On the cover of his book there is a head in profile showing the three cells. This cover figure (Figure 8) is a reproduction of another famous Renaissance anatomist of Bologna, Alessandro Achilini (1460–1512) without the namings of the ventricles. Andreas Vesalius of Pauda (1514–1564), is known as the greatest of the Renaissance Anatomists and also, maybe, the last man of transition with regard to brain function. He rekindled anatomical science and virtually broke Galen’s stranglehold on the field. In his remarkable book “De Humani Corporis Fabrica” 1543 [20], he tells how he was taught the cell doctrine and although he describes its basic tenets, referring to one of the most popular portrayals of cell doctrine by Gregor Reich (1467–1525) – a Carthusian prior of Freiburg and Confessor to Emperor Maximillian I – he implicates his rejection for church sanctified authority for knowledge and casts doubt upon its veracity. Figure 9 is from the seventh book of the De Humani Corporis Fabrica VIII. Vesalius says: “We have resected all the portions of the dural and the thin membranes which occurred in previous figures. Then we have removed in the sequence of dissection the right and left portions of the brain so that the cerebral ventricles now begin to come into view. First, we made a long incision along the right side of corpus callosum where the sinus denoted by one of the M’s exists, which was led into the right cerebral ventricle. Next we removed the right part of the brain lying above the section where we cut the skull in circular fashion with a saw. When we have finished the same on the left side, we placed here the left part of the brain so as to show to some extent the upper aspect of the left ventricle, while the corpus callosum still remains in the head” [21]. This is a clear scientific description of brain dissection that requires no more comment. As to their function, Vesalius argued against placing the functions of the soul in the ventricles. He argued that many animals have ventricles similar to those of humans and yet they were denied a reigning soul. He said that he believed nothing ought to be said of the locations of the faculties, of the principal soul in the brain even though they are so assigned by those who today rejoice in the name of theologians. Although cell doctrine persisted into the seventeenth century by transmission through the writings of certain authors, with the work of Renaissance artists and, mainly, Vesalius, the true anatomy of the ventricular system was established. The crude medieval conceptual sketches were no longer accepted. It was shown that the ventricles contained a fluid, a what is now called “cerebrospinal” fluid and it was highly unlikely that mental functions took place within it.
  • 67. 63Ventricular anatomy: illustrations and concepts from antiquity to Renaissance References [1] Gross CG. Brain, vision, memory: tales in the history of neuroscience. Cambridge, MIT Press. 1998; 94. [2] Keele KD. Leonardo da Vinci’s influence on Renaissance anatomy. Med. Hist. 1964; 8: 360–370. [3] Von Staden H. Herophilus : the art of medicine in early Alexandria. New York, Cambridge University Press. 1989; 146. [4] Dopson JF. Erasistratus. Proc. B. Soc. Med. 1927; 20: 835–832. [5] Longrigg J. Anatomy in Alexandria in the third century BC. Br. J. Hist. Sci. 1988; 21: 455–488. [6] Sudhoff K. Ein beitrag zur geschicte der anatomie dre mittelalter speziel der anatomischen graphik. Leipzig, JA Barth, Studien zur Geschichte der Medizin, hft 4. 1908; 11–23. [7] Singer CJ. A short history of anatomy from the Greeks to Harvey; the evolution of anatomy. New York, Dover. 1957; 23–94. [8] Woolam DMH. Concepts of the brain and its functions in classical antiquity. In: Poynter FNL Ed. The history and philosophy of knowledge of the brain and its function. Sprigfield, Thomas, 1958; 48–75. [9] Gross CG. Brain, vision, memory: tales in the history of neuroscience. Cambridge, MIT Press. 1998; 253. [10] Nemesius. On the nature of man. In: Tefler W, ed. Cyric of Jerusalem and Nemesius of Emesa. Philadelphia, Westminister Press. 1955; 84. [11] Corner GW. Anatomical texts of the earlier middle ages: a study in the transmission of cultures. Washington DC, Carnegie Institute of Washington. 1927; 74. [12] Clarke E, Dewhurst K. An illustrated history of brain function. Berkley California, University of California Press. 1972; 149. [13] McMurrich JP. Leonardo da Vinci the anatomist. Baltimore, Williams and Wilkins. 1930; 93–98. [14] O’Malley CD, Saunders JB. Leonardo da Vinci on the human body. New York, Henry Schuman. 1952; 99. [15] Clayton M. Leonardo da Vinci: the anatomy of man. Boston, Little Brown. 1992; 51. [16] Herrlinger R. History of medical illustrations from antiquity to AD 1600. London, Ditman Medical. 1970; 227. [17] Roberts KB, Tomlinson JDW. The fabrics of the body: European traditions of anatomical illustrations. New York, Charledon Press. 1992; 376. [18] Lucy WA. Anatomical illustrations before Vesalius. J. Morp. 1911; 22: 945–988. [19] Singer CJ. A study in early Renaissance anatomy, with a new text: The anatomia of Hieronymo Manfredi (1490). Oxford, Claredon Press, Studies in the History and Method of Science, Vol I, 1917; 79–164. [20] O’Malley CD. Andreas Vesalius of Brussels 1514-1564. Berkley, University of California Press. 1964; 37. [21] Saunders JB, O’Malley CD. The anatomical drawings of Andreas Vesalius. New York, Bonanza Books. 1982; Plt 68, 190. [22] Zolner F. Leonardo da Vinci: the complete paintings and drawings. Koln, Taschen, 2003; 353–357.
  • 68. Published online 26 December, 2005 © http://www.neuroanatomy.org Obituary Neuroanatomy (2005) 4: 64 Remembrance of M. Atilla MUFTUOGLU, MD (1950–2005) Salih Murat AKKIN Department of Anatomy, Istanbul University, Cerrahpasa Faculty of Medicine, Istanbul–Turkey. Salih Murat AKKIN, MD Professor of Anatomy President of the Turkish Society of Anatomy Department of Anatomy, Cerahpasa Faculty of Medicine, Istanbul University, K.M.Pasa 34303 Istanbul–TURKEY 90-212-414 30 57 90-212-414 30 59 sma@deomed.com Received 30 November 2005 eISSN 1303-1775 • pISSN 1303-1783 M. Atilla Müftüoğlu, M.D., professor of anatomy at the Department of Anatomy, Cerrahpaşa Faculty of Medicine (CFM), Istanbul University and President of the Turkish Society of Anatomy (TSA) died unexpectedly Sunday, January 16, 2005 at the age of 54 in Istanbul at the faculty hospital where he had been working as a lecturer for more than 20 years. Atilla had been under treatment with the diagnosis of bone marrow dysplasia (myelodysplastic syndrome) and had undergone bone marrow transplantation approximately two months prior to his death. Atilla was born in Gaziantep, Turkey on 7th of February 1950. He completed his elementary and secondary school education between 1957–1969 in Gaziantep and started his university education in 1970 in the CFM. In 1977 he graduated from CFM and became an anatomy specialist after finishing his education at the Department of Anatomy in the same institution. He contributedgreatlytotheestablishment and development of the Department of Anatomy Gülhane Military School of Medicine (Ankara) where he worked during his military service between 1982–1983. He worked as an assistant professor in the Department of Anatomy at CFM between 1984–1987. He became associate professor in 1987. Additional to his lectures in the DepartmentofAnatomyinCFMwhere he had worked as an academician since 1984, he gave anatomy lessons in the Nişantaşı Private Faculty of Dentistry between 1987–1989 and in the Faculty of Art of the Mimar Sinan University, Istanbul from 1984 to 1992. He was the member of the Executive Board of CFM between 1986–1988 and the director of Blood Bank between 1988– 1989. He worked also as the Head Physician of CFM between 1990–1994. Additionally he gave anatomy lectures in Florence Nightingale High School of Nursing, Istanbul University in the academic year of 1993–1994. Atilla who became full professor in 1994 had worked as the president of TSA since 2002. The importance of anatomy education, especially clinical anatomy was a passion for Atilla. He mostly published articles on morphometry and clinical anatomy emphasizing especially on the anatomy of the femoral and sublingual regions. Atilla educated many students during his lectureship lasting over 20 years. He had very good relations with his students, and was much loved by them. He had a special talent for explaining even very complicated anatomical issues in the simplest way and loved to prepare explanatory drawings for his lectures. He payed attention to the demeanor and attire of the students both in class and in the dissection laboratory. He would talk with his students about general culture so that he could add on their education in every way. Atilla was a very social man and had warm relations with the faculty and his students and liked to relate to everyone of any age. He worked as the president of the Eminönü Service Foundation, of which he was one of the founders for more than 10 years. He contributed greatly to the development of the foundation and also in the organisation of scientific activities in its historical building in Istanbul. The TSA, which was established in 1991, showed great improvement during the presidency of Atilla. The number of members and scientific activities increased and it became socially more powerful. It was a very important project for him to visit all departments of anatomy in Turkey one by one and to determine the support that could be given to anatomy departments especially in recently established faculties. However, he unfortunately did not get to finish the project. Luckily, he had visited about 80% of the anatomy departments in some steps together with the executive committee of the society; suggestions and experiences having been shared. He married Gülipek Büyükgebiz, MD in 1980. His daughter Gizem and his son Atacan were born in 6 year intervals. He was a very good, loving father being very close to his children. We will remember him and his contributions with love and miss him very much. After his death the Executive Committee of the TSA has decided to give an Atilla Müftüoğlu Memorial Award for his dear memory and the first of these were awarded during the IV. Asian-PacificInternationalCongressof Anatomists and IX. National Congress of TSA, which were held in September 2005 in Kuşadası, Turkey.
  • 69. Published online 26 December, 2005 © http://www.neuroanatomy.org Announcement Neuroanatomy (2005) 4: 65 Scientific meetings eISSN 1303-1775 • pISSN 1303-1783 •  10th National Anatomy Congress   Date : September 6–10, 2006   Venue : Bodrum–Turkey   Deadline for submission of abstracts : June 15, 2006   Scientific Secretariat : Prof.Dr. H. Hamdi Celik, Hacettepe University Faculty of Medicine Department of Anatomy, 06100 Ankara–Turkey.   Mailing Address : Bodrum Congress, Hacettepe University Faculty of Medicine Department of Anatomy, 06100 Ankara–Turkey.   Telephone : +90 312 305 21 01   Fax : +90 312 310 71 69   E-mails : congress@anatomy.web.tr   Website : http://www.anatomy.web.tr •  5th National Neuroscience Congress   Date : April 10-14, 2006   Venue : Zonguldak–Turkey   Deadline for submission of abstracts : Not mentioned   Scientific Secretariat : Doc.Dr. Emine Yilmaz Sipahi, Zonguldak Karaelmas University, Faculty of Medicine, Department of Pharmacology, 67600 Zonguldak–Turkey.   Mailing Address : 5th National Neuroscience Congress, Zonguldak Karaelmas University, Faculty of Medicine, Department of Pharmacology, 67600 Zonguldak–Turkey.   Telephone : +90 372 261 02 43 and +90 372 261 43 17   Fax : +90 372 261 02 65   E-mails : bilgi@sinirbilim.karaelmas.edu.tr   Website : http://sinirbilim.karaelmas.edu.tr •  28th Congress of the Yugoslav Association of Anatomists – 1th Congress of Serbian Anatomical Society   Date : September 12–15, 2006   Venue : Novi Sad–Serbia and Montenegro   Deadline for submission of abstracts : Not mentioned.   Scientific Secretariat : Prof.Dr. Radmila Gudovic, Department of Anatomy, Faculty of Medicine, Hajduk Veljkova 3, 21000 Novi Sad–Serbia and Montenegro.   Mailing Address : Department of Anatomy, Faculty of Medicine, Hajduk Veljkova 3, 21000 Novi Sad–Serbia and Montenegro.   Telephone : +90 224 442 92 42   Fax : +90 372 261 02 65   E-mails : anatomi@uns.ns.ac.yu   Website : Not mentioned. — announcement@neuroanatomy.org —
  • 70. http://www.anatomy.web.tr Contact Information 10th National Anatomy Congress Hacettepe University Faculty of Medicine Department of Anatomy 06100, Ankara–TURKEY +90 312 310 21 01 (telephone) +90 312 310 71 69 (fax) congress@anatomy.web.tr http://www.anatomy.web.tr Honorary Board Dr.Tunçalp Özgen President of Hacettepe University Dr. İskender Sayek Hacettepe Faculty of Medicine, Dean Dr. M. Doğan Akşit Honory President of TSA Congress President Dr. Ruhgün Başar Head of Department, HU Dept of Anatomy Executive Committee of the Turkish Society of Anatomy President – Dr. Salih Murat Akkın Vice president – Dr. H. Hamdi Çelik Secretary – Dr. Mustafa F. Sargon Member – Dr. Muzaffer Şeker Member – Dr. M. Ali Malas Member – Dr. M. Mustafa Aldur Member – Dr. Mehmet Uzel Organization Committee Chairman – Dr. H. Hamdi Çelik Financial Member– Dr. Mustafa F. Sargon Correspondance – Dr. H. Selçuk Sürücü Correspondance – Dr. BelizTaşçıoğlu Inrormatics– Dr. M. Mustafa Aldur Member – Dr. Cem Denk Member – Dr. Alp Bayramoğlu Member – Dr. Deniz Demiryürek Correspondance – Dr. SelçukTunalı Correspondance– Dr. İlkanTatar Member – Dr. Samet Kapakin The 10th National Anatomy Congress with international participation, organized and hosted by the Hacettepe University Faculty of Medicine Department of Anatomy and the Turkish Society of Anatomy will be held in Bodrum, on September 6–10, 2006. Our aim is to present to our colleagues a congress that together with its scientific and social programs, will be one to be remembered for many years to come. We are planning to hold the congress fee under 100 Euro and would like to thank all participants in advance for giving us the honor of hosting such a congregation. Final deadline for the abstracts will be June 15, 2006; and the accepted English summaries will be printed as a supplement of the NEUROANATOMY journal which is scanned by many international scientific indexes [http://www.neuroanatomy.org]. Awards will be given to selected oral presentations and posters. The fact that this congress is organized together with the Turkish Society of Anatomy will make it possible to discuss Education in Anatomy for a duration of half a day. Congress language will be Turkish and English. Colleagues who wish to take part in the scientific evaluation boards should contact us by March 31, 2006 at congress@anatomy. web.tr e-mail address. With the hope of getting together in a very pleasant congress in Bodrum... 10th NATIONAL ANATOMY CONGRESS with international participation September6–10,2006 Bodrum TURKEY Photographs: Dr. H. Hamdi ÇELİK • Design: Dr. M. Mustafa ALDUR
  • 71. NEUROANATOMY annually publishes original articles related to the central and peripheral nervous system morphology and structure. The content of the NEUROANATOMY is determined by the Editors. The manuscript which is submitted to the journal must not contain previously published material or material under consideration for publication elsewhere. Accepted manuscripts become the property of NEUROANATOMY and may not be republished. All manuscripts will undergo peer review. A final review and a subsequent decision relative to publication will then be made by a NEUROANATOMY editor. Manuscripts and all correspondence should be addressed to M. 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  • 72. IndexedinEMBASEExcerptaMedica, IndexCopernicus,DirectoryofOpen AccessJournals(DOAJ),andSCOPUS. TABLE OF CONTENTS 1 A brief evaluation of Neuroanatomy [2005] Aldur MM. 2–7 The parasellar dura mater and adjacent dura: a microsurgical and light microscopic study in fetal materials Vucetic R. 8–9 A rare origin of upper root of ansa cervicalis from vagus nerve: a case report Vollala VR, Bhat SM, Nayak S, Raghunathan D, Samuel VP, Rodrigues V, Mathew JG. 10–12 Morphometric measurements of the thalamus and interthalamic adhesion by MR imaging Sen F, Ulubay H, Ozeksi P, Sargon MF, Tascioglu AB. 13-15 An accessory branch of musculocutaneous nerve joining median nerve Kocabiyik N, Yalcin B, Yazar F, Ozan H. 16–17 Caudal regression syndrome diagnosed after the childhood period: a case report Kahilogullari G, Tuna H, Aydin Z, Vural A, Attar A, Deda H. 18–23 Centella asiatica (linn) induced behavioural changes during growth spurt period in neonatal rats Rao KGM, Rao SM, Rao SG. 24–27 Brief review of vestibular system anatomy and its higher order projections Tascioglu AB. 28–30 Anatomical variations in developing mandibular nerve canal: a report of three cases Auluck A, Ahsan A, Pai KM, Shetty C. 31–34 Neuroanatomy in Tesrih-i Ebdan: a study on a book which is written in Ottoman era Ulucam E, Mesut R, Gokce N. 35–36 Nerve compressions in upper limb: a case report Vollala VR, Raghunathan D, Rodrigues V. 37–38 A rare variation in the formation of the upper trunk of the brachial plexus - a case report Nayak S, Somayaji N, Vollala VR, Raghunathan D, Rodrigues V, Samuel VP, Alathady Malloor P. 39–40 Total fusion of atlas with occipital bone: a case report Nayak S, Vollala VR, Raghunathan D. 41–42 Sciatic nerve entrapment in the popliteal fossa: a case report Paval J, Vollala VR, Nayak S. 43–48 The effect of low protein diet on thalamic projections of hippocampus in rat Bayat M, Hasanzadeh GR, Barzroodipour M, Javadi M. 49–51 Three dimensional (3D) reconstruction of the rat ventricles Ozdemir MB, Akdogan I, Adiguzel E, Yonguc N. 52–54 Clinical course and evaluation of meningocele lesion in adulthood: a case reports Gok HB, Ayberk G, Tosun H, Seckin Z. 55–56 Huge tumor of the intracranial cavity: a catastrophic imaging on USG and MRI Ziyal IM, Bilginer B, Bozkurt G. 57–63 Ventricular anatomy: illustrations and concepts from antiquity to Renaissance Tascioglu AO, Tascioglu AB. 64 Remembrance of M. Atilla MUFTUOGLU, MD (1950–2005) Akkin SM. 65 Scientific meetings (Announcement) Volume 4 • December 2005 ISSN 1303-1783 9 7 7 1 3 0 3 1 7 8 0 0 0 0 1