Radiological pathology of brain to brain metastasis: Pattern of spread of pri...Professor Yasser Metwally
Radiological pathology of brain to brain metastasis: Pattern of spread of primary brain tumors within the neural axis
http://yassermetwally.com
http://yassermetwally.net
Review of Nervous System, Unconsciousness, and CVA. The Nursing Core FunctionsAyinla Kazeem
This presentation was made at several sessions of Mandatory Continuing Professional Development Programme for Nigerian Nurses in Kwara State, and have undergone series of editing till date. While still working on the final editing to totally conform with global standard of practice, I deemed it necessary to share it in this forum.
Radiological pathology of brain to brain metastasis: Pattern of spread of pri...Professor Yasser Metwally
Radiological pathology of brain to brain metastasis: Pattern of spread of primary brain tumors within the neural axis
http://yassermetwally.com
http://yassermetwally.net
Review of Nervous System, Unconsciousness, and CVA. The Nursing Core FunctionsAyinla Kazeem
This presentation was made at several sessions of Mandatory Continuing Professional Development Programme for Nigerian Nurses in Kwara State, and have undergone series of editing till date. While still working on the final editing to totally conform with global standard of practice, I deemed it necessary to share it in this forum.
This is a series of Capacity Building documents that was prepared by the Sudanese Youth Leadership Development Program.
هذه مجموعة من المقالات في مجالات تدريبية متعددة مناسبة للجمعيات الطوعية تم تطويرها بين عامي 2003-2008 للبرنامج السوداني لإعداد القيادات الشبابية
The presentation that I gave during the Quantified Self Meetup in Amsterdam on November 19th, 2012. For more info and a detailed transcript, check http://www.okgo.nl
La guia Professional per a reunions del Baix Llobregat”, és una publicació adreçada a les empreses per a la organització de convencions, reunions o qualsevol altre tipus d’event, posant en relleu la disposició de la comarca per acollir i oferir un servei de qualitat d’aquest sector.
Estructurada en diverses seccions, s’ofereix informació relativa a “Fires, Auditoris i altres espais”, “Espais singulars”, “Gastronomia”, “Allotjament”, “Conference Services”, “Leisure Time” i “Activitats Outdoor (o teambuilding)”. La guia es completa amb una descripció dels principals atractius turístics del Baix Llobregat.
This is a series of Capacity Building documents that was prepared by the Sudanese Youth Leadership Development Program.
هذه مجموعة من المقالات في مجالات تدريبية متعددة مناسبة للجمعيات الطوعية تم تطويرها بين عامي 2003-2008 للبرنامج السوداني لإعداد القيادات الشبابية
The presentation that I gave during the Quantified Self Meetup in Amsterdam on November 19th, 2012. For more info and a detailed transcript, check http://www.okgo.nl
La guia Professional per a reunions del Baix Llobregat”, és una publicació adreçada a les empreses per a la organització de convencions, reunions o qualsevol altre tipus d’event, posant en relleu la disposició de la comarca per acollir i oferir un servei de qualitat d’aquest sector.
Estructurada en diverses seccions, s’ofereix informació relativa a “Fires, Auditoris i altres espais”, “Espais singulars”, “Gastronomia”, “Allotjament”, “Conference Services”, “Leisure Time” i “Activitats Outdoor (o teambuilding)”. La guia es completa amb una descripció dels principals atractius turístics del Baix Llobregat.
glucagon secretion via the stimulation of pancreatic GLP‐1 receptors in beta and alpha cells and by increasing insulin sensitivity [5]. GLP-1 and its analogues can also amplify insulin signaling in brain cells, leading to increased insulin sensitivity in neurons [7, 8]. Within the cardiovascular system, GLP-1 receptors are expressed on endothelial cells, monocytes, macrophages, and vascular smooth muscle cells (VSMCs) [9]. GLP-1 receptors are also widely expressed in the central nervous system, including the brainstem, cerebellum, hippocampus, cortex, hypothalamus, and amygdala [7, 10, 11]. There, the cellular expression of GLP-1 receptors is predominantly confined to neurons and dendrites [11]. GLP-1RAs are overall well-tolerated, with their most common adverse effects being nausea, vomiting, and diarrhea [7]. It has been recently shown that there are cholecystokinin-expressing neurons in the caudal brainstem, which are activated postprandially and are responsive to GLP-1RAs, explaining in part the body weight-lowering effects of GLP-1RAs but also their ability to induce nausea [12]. Based on similarities in their amino acid sequence, GLP-1RAs are peptide derivatives of either exendin-4 (exenatide, lixisenatide, and efpeglenatide) or human GLP-1 (albiglutide, dulaglutide, liraglutide, and semaglutide). Moreover, based on their pharmacokinetic/pharmacodynamic profile, GLP-1RAs can be classified into short-acting (exenatide and lixisenatide) and long-acting (albiglutide, dulaglutide, exenatide extended-release, liraglutide, semaglutide, and efpeglenatide) [5, 6]. T he main pharmacokinetic difference between shortacting (half-life of 2–5 h) and long-acting (half-life > 12 h) GLP-1RAs is that short-acting GLP-1RAs are subject to wide fluctuations in the plasma concentration of the active compound, while long-acting GLP-1RAs exert a more constant effect on the GLP-1 receptor [13]. Furthermore, short-acting GLP-1RAs predominantly affect postprandial glucose levels, mainly by reducing
glucagon secretion via the stimulation of pancreatic GLP‐1 receptors in beta and alpha cells and by increasing insulin sensitivity [5]. GLP-1 and its analogues can also amplify insulin signaling in brain cells, leading to increased insulin sensitivity in neurons [7, 8]. Within the cardiovascular system, GLP-1 receptors are expressed on endothelial cells, monocytes, macrophages, and vascular smooth muscle cells (VSMCs) [9]. GLP-1 receptors are also widely expressed in the central nervous system, including the brainstem, cerebellum, hippocampus, cortex, hypothalamus, and amygdala [7, 10, 11]. There, the cellular expression of GLP-1 receptors is predominantly confined to neurons and dendrites [11]. GLP-1RAs are overall well-tolerated, with their most common adverse effects being nausea, vomiting, and diarrhea [7]. It has been recently shown that there are cholecystokinin-expressing neurons in the caudal brainstem, which are activated postprandially and are responsive to GLP
V introduction anatomy head and neck for background infosiegfried van hoek
Replacing Medical Intitiation. Case: neurosurgicalo abuse with conspiracy of silence by others then direct offenders. Also by the Dutch government there is an active policy to keep abusive practises under the carpet, and cooperating in prevention cases would come up. Exposition with proof will follow.
INTRODUCTION:
The recent use of ultrasound imaging in peripheral regional anesthesia allows the operator to see neural structures, guide the needle under real-time visualization, navigate away from sensitive anatomy, and monitor the spread of local anesthetic.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Pharynx and Clinical Correlations BY Dr.Rabia Inam Gandapore.pptx
Case record...Dilated Virchow-Robin spaces associated with leukoaraiosis
1. CASE OF THE WEEK
PROFESSOR YASSER METWALLY
CLINICAL PICTURE
CLINICAL PICTURE:
73 years old female patient, The patient is diabetic and hypertensive. The patient is presented clinically with mild
cognitive impairment. Apart from impairment of recent memory, clinical examination was normal. (To inspect the
patient's full radiological study, click on the attachment icon (The paper clip icon in the left pane) of the acrobat
reader then double click on the attached file) (Click here to download the attached file)
RADIOLOGICAL FINDINGS
RADIOLOGICAL FINDINGS:
Figure 1. Precontrast MRI T1. Virchow Robin spaces scattered in the region of the basal ganglia and thalamus. The
signal intensity of these spaces is identical to that of the CSF. (Type I VR spaces)
2. Figure 2. Precontrast MRI T2. Virchow Robin spaces scattered in the region of the basal ganglia and thalamus. The
signal intensity of these spaces is identical to that of the CSF. Also notice the periventricular white matter changes
(Leukoaraiosis) (Type I VR spaces)
Figure 3. Precontrast MRI FLAIR images. Virchow Robin spaces scattered in the region of the basal ganglia and
thalamus. The signal intensity of these spaces is identical to that of the CSF. Also notice the periventricular white
matter changes (Leukoaraiosis) (Type I VR spaces)
3. Figure 4. MRI T2 images showing
Vircho Robin spaces scsttered in the
region of the midbrain. (Type III VR
spaces)
Virchow-Robin (VR) spaces surround the walls of vessels as they course from the subarachnoid space through the
brain parenchyma. Small VR spaces appear in all age groups. With advancing age, VR spaces are found with
increasing frequency and larger apparent sizes. At visual analysis, the signal intensity of VR spaces is identical to
that of cerebrospinal fluid with all magnetic resonance imaging sequences. Dilated VR spaces typically occur in
three characteristic locations: Type I VR spaces appear along the lenticulostriate arteries entering the basal ganglia
through the anterior perforated substance. Type II VR spaces are found along the paths of the perforating
medullary arteries as they enter the cortical gray matter over the high convexities and extend into the white matter.
Type III VR spaces appear in the midbrain. Occasionally, VR spaces have an atypical appearance. They may
become very large, predominantly involve one hemisphere, assume bizarre configurations, and even cause mass
effect. Knowledge of the signal intensity characteristics and locations of VR spaces helps differentiate them from
various pathologic conditions, including lacunar infarctions, cystic periventricular leukomalacia, multiple sclerosis,
cryptococcosis, mucopolysaccharidoses, cystic neoplasms, neurocysticercosis, arachnoid cysts, and neuroepithelial
cysts.
Type I VR spaces Appear along the lenticulostriate arteries entering the basal ganglia through the anterior
perforated substance.
Type II VR spaces Are found along the paths of the perforating medullary arteries as they enter the cortical
gray matter over the high convexities and extend into the white matter.
Type III VR spaces Appear in the midbrain.
DIAGNOSIS:
DIAGNOSIS: ENLARGED VIRCHOW-ROBIN SPACES (PERIVASCULAR SPACES) ASSOCIATED WITH
MICROVASCULAR BRAIN DISEASE (LEUKOARAIOSIS)
DISCUSSION
DISCUSSION:
The Virchow-Robin (VR) space is named after Rudolf Virchow (German pathologist, 1821–1902) (1) and Charles
Philippe Robin (French anatomist, 1821–1885) (2). VR spaces, or perivascular spaces, surround the walls of vessels
as they course from the subarachnoid space through the brain parenchyma. VR spaces are commonly seen at
magnetic resonance (MR) imaging and may sometimes be difficult to differentiate from pathologic conditions.
4. Knowledge of their signal intensity characteristics and localization helps in this differentiation, which is important
for correct patient management.
Anatomy
VR spaces surround the walls of arteries, arterioles, veins, and venules as they course from the subarachnoid space
through the brain parenchyma (Fig 1) (1–5). Electron microscopy and tracer studies have given insight into the
location of VR spaces and clarified that the subarachnoid space does not communicate directly with the VR spaces
(3–5).
Figure 1. Photomicrograph (original magnification, x20; hematoxylin-
eosin stain) of a coronal section through the anterior perforated
substance shows two arteries (straight arrows) with surrounding VR
spaces (curved arrows).
Arteries in the cerebral cortex are coated by a layer of leptomeninges that is subtended from the pia mater; by this
anatomic arrangement, the VR spaces of the intracortical arteries are in direct continuity with the VR spaces
around arteries in the subarachnoid space (Fig 2). The lack of a similar coating of leptomeningeal cells around veins
in the cerebral cortex suggests that VR spaces around veins are in continuity with the subpial space (4).
Figure 2. Drawing shows a cortical
artery with a surrounding VR space
crossing from the subarachnoid and
subpial spaces through the brain
parenchyma. The magnified view
on the right shows the anatomic
relationship between the artery, VR
space, subpial space, and brain
parenchyma.
In contrast to arteries in the cerebral cortex, arteries in the basal ganglia are surrounded by not one but two distinct
coats of leptomeninges, separated by a VR space that is continuous with the VR space around arteries in the
subarachnoid space. The inner layer of leptomeninges closely invests the adventitia of the vessel wall. The outer
layer abuts on the glia limitans of the underlying brain and is continuous with the pia mater on the surface of the
brain and the anterior perforated substance. Veins in the basal ganglia have no outer layer of leptomeninges
(similar to cortical veins), which suggests that their VR spaces are continuous with the subpial space (5).
Interstitial fluid within the brain parenchyma drains from the gray matter of the brain by diffusion through the
extracellular spaces and by bulk flow along VR spaces. There is evidence from tracer studies and from pathologic
5. analysis of the human brain that VR spaces carry solutes from the brain and are, in effect, the lymphatic drainage
pathways of the brain (6).
Dilated VR Spaces
Dilatation of VR spaces was described by Durant-Fardel (7) in 1843. These dilatations are regular cavities that
always contain a patent artery. The mechanisms underlying expanding VR spaces are still unknown. Different
theories have been postulated: segmental necrotizing angiitis of the arteries or another unknown condition causing
permeability of the arterial wall (8–10), expanding VR spaces resulting from disturbance of the drainage route of
interstitial fluid due to cerebrospinal fluid (CSF) circulation in the cistern (11,12), spiral elongation of blood vessels
and brain atrophy resulting in an extensive network of tunnels filled with extracellular water (9,13), gradual leaking
of the interstitial fluid from the intracellular compartment to the pial space around the metarteriole through the
fenestrae in the brain parenchyma (14), and fibrosis and obstruction of VR spaces along the length of arteries and
consequent impedance of fluid flow (5).
Prevalence
Small VR spaces (<2 mm) appear in all age groups. With advancing age, VR spaces are found with increasing
frequency and larger apparent size (>2 mm) (15). Some studies found a correlation between dilated VR spaces and
neuropsychiatric disorders (16–19), recent-onset multiple sclerosis (MS) (20), mild traumatic brain injury (21), and
diseases associated with microvascular abnormalities (22).
The prevalence of VR spaces at MR imaging is also dependent on the applied technique. Heavier T2-weighted
imaging results in better visualization of VR spaces (23). In addition, the use of thinner sections will demonstrate
more VR spaces as well (15,24). Also, high-field-strength MR imaging is expected to have an increased clinical
impact in the near future; the current magnetic field (1.5 T) is likely to be switched to 3 or 4 T. The anticipated
higher signal-to-noise ratio at higher magnetic field strengths may successfully improve spatial resolution and image
contrast (25–27), leading to better visualization (and increased prevalence) of VR spaces on MR images.
Appearance at MR Imaging
Signal Intensity Characteristics
Visually, the signal intensities of the VR spaces are identical to those of CSF with all pulse sequences. However,
when signal intensities are measured, the VR spaces prove to have significantly lower signal intensity than the CSF-
containing structures within and around the brain (28), a finding consistent with the fact that the VR spaces
represent entrapments of interstitial fluid. This difference in signal intensity can also be explained by partial volume
effects, since a VR space with accompanying vessel is smaller than the contemporary volume of a voxel on MR
images. VR spaces show no restricted diffusion on diffusion-weighted images because they are communicating
compartments. T1-weighted images with substantial flow sensitivity may show high signal intensity due to inflow
effects, thereby helping confirm that one is indeed dealing with VR spaces (29). VR spaces do not enhance with
contrast material. In patients with small to moderate dilatations of the VR spaces (2–5 mm), the surrounding brain
parenchyma generally has normal signal intensity (30,31).
Locations and Morphology
Dilated VR spaces typically occur in three characteristic locations. The first type (type I) is frequently seen on MR
images and appears along the lenticulostriate arteries entering the basal ganglia through the anterior perforated
substance (Figs 3, 4) (15,32). Here, the tortuous lenticulostriate arteries change direction from a lateral to a
dorsomedial path and are grouped closely together. A proximal VR space, containing several vessels, is the resulting
physiologic finding (33).
6. Figure 3. Bilateral type I VR spaces in a 6-year-old boy. (a) Axial proton-density–weighted image (repetition time
msec/echo time msec = 2375/100) shows hyperintense areas (arrows) in the anterior perforated substance on both
sides. (b) Axial fluid-attenuated inversion-recovery (FLAIR) image (6606/100) obtained at the same level shows that
these areas have CSF-like content (arrows). The signal intensity of the surrounding brain parenchyma is normal. (c,
d) Diffusion-weighted image (2574/81; b factor = 1000 sec/mm2) (c) and corresponding apparent diffusion
coefficient map (d) show no restricted diffusion in these areas (arrows)..
Figure 4. Bilateral type I VR spaces in a 53-year-old woman. Coronal T1-
weighted image (500/30) shows symmetrical hypointense areas (arrows) in the
anterior perforated substance.
The second type (type II) can be found along the path of the perforating medullary arteries as they enter the cortical
gray matter over the high convexities and extend into the white matter (Figs 5, 6) (15,32).
7. Figure 5. Type II VR spaces in a 73-year-old woman. (a) Axial proton-density–weighted image (2376/100) shows
multiple hyperintense foci in the centrum semiovale in both hemispheres. (b) On an axial FLAIR image (6614/100)
obtained at the same level, the VR spaces are seen as hypointense dots without any surrounding high signal
intensity. Note the two small lesions with a hypointense center and a hyperintense rim (arrows) in the left
hemisphere; these lesions are not VR spaces but old lacunar infarctions.
Figure 6. Type II dilated VR spaces in a 6-year-old boy. (a) Axial T2-weighted image (2620/100) shows linear to
punctate hyperintense areas around the occipital horns, especially on the left side (arrow). (b) FLAIR image
(7572/100) obtained at the same level shows no abnormal signal intensity (arrow), in accordance with the fact that
these areas are true VR spaces..
The third type (type III) appears in the midbrain. In the lower midbrain, VR spaces at the pontomesencephalic
junction surround the penetrating branches of the collicular and accessory collicular arteries (Figs 7, 8). They are
mainly located between the cerebral peduncles in the axial plane and correspond to the level of the tentorial margin
as seen in coronal sections. In the upper midbrain, where the VR spaces are visible at the mesencephalodiencephalic
junction, they appear along the posterior (interpeduncular) thalamoperforating artery or the paramedian
mesencephalothalamic artery and short and long circumferential arteries originating from the upper basilar artery
or proximal posterior cerebral artery (23,34,35).
8. Figure 7. Type III VR space in a 25-year-old man. (a) Axial proton-density–weighted image (2620/100) shows a
hyperintense spot in the brainstem (arrow). (b) Axial FLAIR image (7292/120) obtained at the same level shows that
the spot has CSF-like content without abnormal surrounding signal intensity (arrow). These findings confirm that
the spot is a VR space.
Figure 8. Type III VR spaces in a 68-year-old man. (a) Axial proton-density–weighted image (2382/100) shows
multiple punctate hyperintense areas in the brainstem (arrow). (b) Close-up T2-weighted image (4615/120) clearly
shows the fine punctate pattern. (c) Axial FLAIR image (6609/100) shows the CSF-like content of the dots (arrow).
No surrounding high signal intensity is seen. The typical configuration and the fact that no high signal intensity is
seen on the FLAIR image confirm that the dots are VR spaces.
VR spaces are mostly seen as well-defined oval, rounded, or tubular structures, depending on the plane in which
they are intersected. They have smooth margins, commonly appear bilaterally, and usually measure 5 mm or less
(32).
Atypical VR Spaces
It is reported that clusters of type II enlarged VR spaces may predominantly involve one hemisphere (36). There are
even reports that describe the solely unilateral appearance of enlarged VR spaces in the high convexity (37,38).
Occasionally, VR spaces appear markedly enlarged, cause mass effect, and assume bizarre cystic configurations that
9. may be misinterpreted as other pathologic processes, most often a cystic neoplasm. As most of these giant VR spaces
border a ventricle or subarachnoid space, reports of such cases (39–41) have offered an extensive differential
diagnosis that includes cystic neoplasms, parasitic cysts, cystic infarctions, nonneoplastic neuroepithelial cysts, and
deposition disorders such as mucopolysaccharidosis. Salzman et al (42) presented a series of 37 patients with giant
VR spaces. These spaces most often appear as clusters of variably sized cysts and are most common in the
mesencephalothalamic region (Fig 9), in the territory of the paramedial mesencephalothalamic artery, and in the
cerebral white matter. Giant VR spaces in the mesencephalothalamic region may cause hydrocephalus by direct
compression of the third ventricle or the sylvian aqueduct (Fig 9), requiring surgical intervention (8,11,42–47).
Figure 9. Giant VR spaces in the mesencephalothalamic region in a 19-year-old
man. (a, b) Axial (a) and sagittal (b) T2-weighted images (5970/120) show a
multicystic lesion in the mesencephalothalamic region. The lesion extends from
the left cerebral peduncle to the left thalamus. The content of the cysts is CSF-
like. The adjacent brain parenchyma has normal signal intensity. No solid
components are identified. (c) Axial gadolinium-enhanced T1-weighted image
(478/18) shows no enhancement. The process has caused obstruction of the
sylvian aqueduct, resulting in hydrocephalus. The size of the lesion and the
degree of hydrocephalus were unchanged compared with the appearance on
MR images obtained 2 years earlier
In one-half of cases, giant VR spaces that occur in the white matter may have surrounding signal intensity
abnormality on T2-weighted or FLAIR images (42). This may be viewed as a worrisome finding and in some cases
has prompted the performance of tissue biopsy. However, the abnormal signal intensity stems from reactive gliosis
surrounding the enlarged VR spaces and is not an ominous finding (47).
Dilated Virchow-Robin spaces as a marker of microvascular brain disease
Virchow-Robin spaces (VRSs) are perivascular spaces that surround the perforating arteries that enter the brain.
The spaces are normally microscopic, but when dilated, they may be seen on MR images. Even in the normal brain,
some VRSs are usually seen in the area of the substantia innominata at the level of the anterior commissure, and a
small number of dilated spaces may also be seen in the basal ganglia (BG) in up to 60% of individuals. Virchow-
Robin Spaces can be identified by a combination of their typical location and their signal intensity characteristics.
They are classically described as isointense to CSF on images obtained with all pulse sequences, and they are round
10. or linear depending on the imaging plane, although their characteristics may vary from this pattern for a number of
reasons. First, the small size of the Virchow-Robin Spaces makes partial-volume effects common; therefore,
measured signal intensities seldom equal those seen in pure CSF, although the changes in signal intensity between
sequences are closely correlated. In addition, T1-weighted images with substantial flow sensitivity may show high
signal intensity due to inflow effects. Even if we allow for these effects, the measured signal intensity in the VRS
often slightly differs from that of true CSF. This finding has been attributed to the fact that Virchow-Robin Spaces
around intracerebral arteries may represent interstitial fluid trapped in the subpial or interpial space.
Pathologic dilatation of Virchow-Robin Spaces is most commonly associated with arteriolar abnormalities that arise
due to aging, diabetes, hypercholesterolemia, smoking, and hypertension and other vascular risk factors. This
dilatation forms part of a histologic spectrum of abnormalities, which include old, small infarcts (type 1 changes);
scars from small hematomas (type 2 changes); and dilatations of Virchow-Robin Spaces (type 3 changes) (74). The
presence of these abnormalities on histologic examination is believed to result from moderate-to-severe
microangiopathy characterized by sclerosis, hyalinosis, and lipid deposits in the walls of small perforating arteries
50 – 400 `im in diameter (74, 75). As the severity of the microangiopathy increases, microvessels demonstrate
increasingly severe changes, with arterial narrowing, microaneurysms and pseudoaneurysms, onion skinning, mural
calcification, and thrombotic and fibrotic luminal occlusions (74–76) Although microvascular disease is common,
few reliable surrogate imaging markers of its presence have been described. The extent and severity of deep white
matter (WM) and periventricular hyperintensity on T2-weighted images have been widely studied as potential
surrogate markers for small-vessel disease. However, the correlation between these abnormalities and clinical
characteristics, such as diagnosis, vascular risk factor, or neuropsychological deficit, is often poor (77).
Figure 10. MRI T2 (A), MRI FLAIR (B) and precontrast
MRI T1 (C) images showing dilated Virchow-Robin
Spaces associated with diffuse white matter changes
(leukoaraiosis)
More details about etiology and pathogenesis of dilatation of Virchow-Robin Spaces
Virchow-Robin Spaces are potential perivascular spaces covered by pia that accompany arteries and arterioles as
they perforate the brain substance. Deep in the brain, the Virchow-Robin Spaces are lined by the basement
membrane of the glia limitans peripherally, while the outer surfaces of the blood vessels lie centrally. These pial
layers form the Virchow-Robin Spaces as enclosed spaces filled with interstitial fluid and separated from the
11. surrounding brain and CSF . Dilatation of Virchow-Robin Spaces results in fluid filled perivascular spaces along the
course of the penetrating arteries.
Abnormal dilatation of Virchow-Robin Spaces is clinically associated with aging, dementia, incidental WM lesions,
and hypertension and other vascular risk factors (73). Pathologically, this finding is most commonly associated with
arteriosclerotic microvascular disease, which forms a spectrum of severity graded from 1 to 3 on the basis of
histologic appearances (74, 76). Grade 1 changes include increased tortuosity and irregularity in small arteries and
arterioles (74) Grade 2 changes include progress sclerosis, hyalinosis, lipid deposits, and regional loss of smooth
muscle in the vessel wall associated with lacunar spaces that are histologically seen to consist of three subtypes. Type
1 lacunes are small, old cystic infarcts; type 2 are scars of old hematomas; and type 3 are dilated Virchow-Robin
Spaces (79). Grade 3 microangiopathy represents the most severe stage and is especially related to severe chronic
hypertension. Typical changes described in lower grades are accompanied by fibrotic thickening vessel wall with
onion skinning, loss of muscularis and elastic lamina, and regional necrosis in the vessel walls. The brain
parenchyma contains multiple lacunae, and diffuse abnormality of myelin is present in the deep hemispheric white
matter.
Several mechanisms for abnormal dilatation of Virchow-Robin Spaces have been suggested (80,81). These include
mechanical trauma due to CSF pulsation or vascular ectasia (83), fluid exudation due to abnormalities of the vessel
wall permeability (82), and ischemic injury to perivascular tissue causing a secondary ex vacuo effect (83).
In the Western world, ischemic vascular dementia is seen in 8 –10% of cognitively impaired elderly subjects (84)
and commonly associated with widespread small ischemic or vascular lesions throughout the brain, with
predominant involvement of the basal ganglia, white matter, and hippocampus (84). Several groups have shown that
a severe lacunar state and microinfarction due to arteriolosclerosis and hypertensive microangiopathy are more
common in individuals with IVD than in healthy control subjects, and they have emphasized the importance of
small vascular lesions in the development of dementia (84, 85). On CT or MR imaging, white matter lesions are
commonly used as potential biomarkers of vascular abnormality. Many groups have suggested that simple scoring
schemes for white matter lesion load and distribution are useful in the diagnosis of vascular dementia (86,87,88,89).
Although white matter lesions are more severe in patients with vascular dementia (86), they are more prevalent in
all groups with dementia than in healthy control subjects.
Dilation of Virchow-Robin Spaces provides a potential alternative biomarker of microvascular disease (small vessel
disease). Virchow-Robin Spaces in the centrum semiovale were significantly more frequent in patients with fronto-
temporal dementia (FTD) than in control subjects (P .01). This finding is not associated with increases in basal
ganglionic Virchow-Robin Spaces and is closely correlated with measures of forebrain atrophy, suggesting that
these changes are probably representative of atrophy, which is more marked in this patient group than in those with
other dementing conditions (78).
SUMMARY
SUMMARY
Pathologic Findings
Enlarged perivascular spaces, also known as Virchow-Robin spaces, are pial-lined interstitial fluid-filled structures
that accompany penetrating arteries and veins. They do not communicate directly with the subarachnoid space.
They are common, incidental, "leave me alone" lesions that should not be mistaken for more ominous disease. They
frequently appear in the inferior basal ganglia, clustering around the anterior commissure and surrounding the
12. lenticulostriate arteries as they superiorly course through the anterior perforated substance. Other common
locations include the midbrain, deep white matter, and subinsular cortex. They can also be found in the region of the
thalami, dentate nuclei, corpus callosum, and cingulate gyrus .
Microscopically, perivascular spaces consist of a single or double layer of invaginated pia. They are typically very
small or inapparent as they pass through the cortex, enlarging in the subcortical white matter. They are typically
not associated with gliosis in the surrounding parenchyma.
Imaging
Prominent perivascular spaces are considered a normal variant. Most appear as smoothly demarcated fluid-filled
cysts, typically less than 5 mm in diameter, and often occur in clusters in the basal ganglia or midbrain. They are
isointense to CSF at all sequences, including FLAIR. Most show normal signal intensity in the adjacent brain; 25%
may have a small rim of slightly increased signal intensity. They do not enhance, cause focal mass effect, or restrict
on diffusion-weighted images. In older patients, basal ganglia perivascular spaces sometimes become prominent and
sievelike, a condition known as état criblé, or cribriform state.
Occasionally perivascular spaces may become very large and appear bizarre. They are probably caused by the
accumulation of interstitial fluid between the penetrating vessels and the pia. If interstitial fluid egress is blocked,
fluid accumulates and the perivascular spaces dilate . These lesions cause focal mass effect and occasionally even
hydrocephalus. Rarely, so-called giant or tumefactive perivascular spaces may be mistaken for more ominous
disease.
Differential Diagnosis
Enlarged perivascular spaces are often mistaken for multiple lacunar infarcts, cystic neoplasms, and infectious
cysts. Lacunar infarcts can usually be distinguished from perivascular spaces since many exhibit adjacent
parenchymal hyperintensity (so-called état lacunaire). Cystic neoplasms rarely exhibit signal intensity exactly like
the CSF. Neurocysticercosis cysts may have a scolex (parasite head), and the cyst walls often enhance.
Neurocysticercosis cysts may be multiple but do not typically occur in clusters within the brain parenchyma.
Addendum
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13. REFERENCES
References
1. Virchow R. Ueber die Erweiterung kleinerer Gefaesse. Archiv Pathol Anat Physiol Klin Med 1851; 3:427–462.
2. Robin C. Recherches sur quelques particularités de la structure des capillaires de l’encephale. J Physiol
Homme Anim 1859;2:537–548.
3. Hutchings M, Weller RO. Anatomical relationships of the pia mater to cerebral blood vessels in man. J
Neurosurg 1986;65:316–325.
4. Zhang ET, Inman CB, Weller RO. Interrelationship of the pia mater and the perivascular (Virchow-Robin)
spaces in the human cerebrum. J Anat 1990;170:111–123.
5. Pollock H, Hutchings M, Weller RO, Zhang ET. Perivascular spaces in the basal ganglia of the human brain:
their relationship to lacunes. J Anat 1997;191:337–346.
6. Schley D, Carare-Nnadi R, Please CP, Perry VH, Weller RO. Mechanisms to explain the reverse perivascular
transport of solutes out of the brain. J Theor Biol 2006;238:962–974.
7. Durant-Fardel M. Traite du ramollissement du cerveau. Paris, France: Balliere, 1843.
8. Poirier J, Barbizet J, Gaston A, Meyrignac C. Thalamic dementia: expansive lacunae of the thalamo-
paramedian mesencephalic area—hydrocephalus caused by stenosis of the aqueduct of Sylvius [in French].
Rev Neurol (Paris) 1983;139:349–358.
9. Benhaiem-Sigaux N, Gray F, Gherardi R, Roucayrol AM, Poirier J. Expanding cerebellar lacunes due to
dilatation of the perivascular space associated with Binswanger’s subcortical arteriosclerotic encephalopathy.
Stroke 1987;18:1087–1092.
10. Hughes W. Origin of lacunes. Lancet 1965;2:19–21.
11. Homeyer P, Cornu P, Lacomblez L, Chiras J, Derouesne C. A special form of cerebral lacunae: expanding
lacunae. J Neurol Neurosurg Psychiatry 1996;61:200–202.
12. Mascalchi M, Salvi F, Godano U, et al. Expanding lacunae causing triventricular hydrocephalus: report of
two cases. J Neurosurg 1999;91:669–674.
13. Awad IA, Johnson PC, Spetzler RF, Hodak JA. Incidental subcortical lesions identified on magnetic resonance
imaging in the elderly. II. Postmortem pathological correlations. Stroke 1986;17: 1090–1097.
14. Adachi M, Hosoya T, Haku T, Yamaguchi K. Dilated Virchow-Robin spaces: MRI pathological study.
Neuroradiology 1998;40:27–31.
15. Heier LA, Bauer CJ, Schwartz L, Zimmerman RD, Morgello S, Deck MD. Large Virchow-Robin spaces: MR-
clinical correlation. AJNR Am J Neuroradiol 1989;10:929–936.
16. Rollins NK, Deline C, Morriss MC. Prevalence and clinical significance of dilated Virchow-Robin spaces in
childhood. Radiology 1993;189:53–57.
17. Machado MA Jr, Matos AS, Goyanna F, Barbosa VA, Vieira LC. Dilatation of Virchow-Robin spaces in
patients with migraine [in Portuguese]. Arq Neuropsiquiatr 2001;59:206–209.
18. MacLullich AM, Wardlaw JM, Ferguson KJ, Starr JM, Seckl JR, Deary IJ. Enlarged perivascular spaces are
14. associated with cognitive function in healthy elderly men. J Neurol Neurosurg Psychiatry 2004;75:1519–1523.
19. Taber KH, Shaw JB, Loveland KA, Pearson DA, Lane DM, Hayman LA. Accentuated Virchow-Robin spaces
in the centrum semiovale in children with autistic disorder. J Comput Assist Tomogr 2004;28:263–268.
20. Achiron A, Faibel M. Sandlike appearance of Virchow-Robin spaces in early multiple sclerosis: a novel
neuroradiologic marker. AJNR Am J Neuroradiol 2002;23:376–380.
21. Inglese M, Bomsztyk E, Gonen O, Mannon LJ, Grossman RI, Rusinek H. Dilated perivascular spaces:
hallmarks of mild traumatic brain injury. AJNR Am J Neuroradiol 2005;26:719–724.
22. Patankar TF, Mitra D, Varma A, Snowden J, Neary D, Jackson A. Dilatation of the Virchow-Robin space is a
sensitive indicator of cerebral microvascular disease: study in elderly patients with dementia. AJNR Am J
Neuroradiol 2005;26: 1512–1520.
23. Saeki N, Sato M, Kubota M, et al. MR imaging of normal perivascular space expansion at midbrain. AJNR
Am J Neuroradiol 2005;26:566–571.
24. Song CJ, Kim JH, Kier EL, Bronen RA. MR imaging and histologic features of subinsular bright spots on T2-
weighted MR images: Virchow-Robin spaces of the extreme capsule and insular cortex. Radiology
2000;214:671–677.
25. Takahashi M, Uematsu H, Hatabu H. MR imaging at high magnetic fields. Eur J Radiol 2003;46: 45–52.
26. Uematsu H, Dougherty L, Takahashi M, et al. A direct comparison of signal behavior between 4.0 and 1.5 T: a
phantom study. Eur J Radiol 2003; 45:154–159.
27. Sasaki M, Inoue T, Tohyama K, Oikawa H, Ehara S, Ogawa A. High-field MRI of the central nervous system:
current approaches to clinical and microscopic imaging. Magn Reson Med Sci 2003; 2:133–139.
28. Ozturk MH, Aydingoz U. Comparison of MR signal intensities of cerebral perivascular (Virchow-Robin) and
subarachnoid spaces. J Comput Assist Tomogr 2002;26:902–904.
29. Hirabuki N, Fujita N, Fujii K, Hashimoto T, Kozuka T. MR appearance of Virchow-Robin spaces along
lenticulostriate arteries: spin-echo and two-dimensional fast low-angle shot imaging. AJNR Am J Neuroradiol
1994;15:277–281.
30. Braffman BH, Zimmerman RA, Trojanowski JQ, Gonatas NK, Hickey WF, Schlaepfer WW. Brain MR:
pathologic correlation with gross and histopathology. 1. Lacunar infarction and Virchow-Robin spaces. AJR
Am J Roentgenol 1988;151: 551–558.
31. Demaerel P, Wilms G, Baert AL, Van den Bergh V, Sainte T. Widening of Virchow-Robin spaces. AJNR Am J
Neuroradiol 1996;17:800–801.
32. Jungreis CA, Kanal E, Hirsch WL, Martinez AJ, Moossy J. Normal perivascular spaces mimicking lacunar
infarction: MR imaging. Radiology 1988; 169:101–104.
33. Pullicino PM, Miller LL, Alexandrov AV, Ostrow PT. Infraputaminal ‘lacunes’: clinical and pathological
correlations. Stroke 1995;26:1598–1602.
34. Elster AD, Richardson DN. Focal high signal on MR scans of the midbrain caused by enlarged perivascular
spaces: MR-pathologic correlation. AJR Am J Roentgenol 1991;156:157–160.
35. Duvernoy HM. Human brainstem vessels. Berlin, Germany: Springer-Verlag, 1978; 16–66.
15. 36. Ogawa T, Okudera T, Fukasawa H, et al. Unusual widening of Virchow-Robin spaces: MR appearance. AJNR
Am J Neuroradiol 1995;16:1238–1242.
37. Sawada M, Nishi S, Hashimoto N. Unilateral appearance of markedly dilated Virchow-Robin spaces. Clin
Radiol 1999;54:334–336.
38. Shiratori K, Mrowka M, Toussaint A, Spalke G, Bien S. Extreme, unilateral widening of Virchow-Robin
spaces: case report. Neuroradiology 2002; 44:990–992.
39. Davis G, Fitt GJ, Kalnins RM, Mitchell LA. Increased perivascular spaces mimicking frontal lobe tumor. J
Neurosurg 2002;97:723.
40. Romi F, Tysnes OB, Krakenes J, Savoiardo M, Aarli JA, Bindoff L. Cystic dilation of Virchow-Robin spaces
in the midbrain. Eur Neurol 2002; 47:186–188.
41. Cakirer S. MR imaging findings in tumefactive perivascular spaces. Acta Radiol 2003;44:673–674.
42. Salzman KL, Osborn AG, House P, et al. Giant tumefactive perivascular spaces. AJNR Am J Neuroradiol
2005;26:298–305.
43. Kanamalla US, Calabro R, Jinkins JR. Cavernous dilatation of mesencephalic Virchow-Robin spaces with
obstructive hydrocephalus. Neuroradiology 2000;42:881–884.
44. Papayannis CE, Saidon P, Rugilo CA, et al. Expanding Virchow Robin spaces in the midbrain causing
hydrocephalus. AJNR Am J Neuroradiol 2003;24:1399–1403.
45. Rohlfs J, Riegel T, Khalil M, et al. Enlarged perivascular spaces mimicking multicystic brain tumors: report
of two cases and review of the literature. J Neurosurg 2005;102:1142–1146.
46. Longatti PL, Fiorindi A, Carteri A, Caroli F, Martinuzzi A. Expanding cerebral cysts (lacunae): a treatable
cause of progressive midbrain syndrome. J Neurol Neurosurg Psychiatry 2003;74:393–394.
47. House P, Salzman KL, Osborn AG, MacDonald JG, Jensen RL, Couldwell WT. Surgical considerations
regarding giant dilations of the perivascular spaces. J Neurosurg 2004;100:820–824.
48. Fisher CM. Lacunes: small, deep cerebral infarcts. Neurology 1965;15:774–784.
49. Fisher CM. Lacunar strokes and infarcts: a review. Neurology 1982;32:871–876.
50. Bokura H, Kobayashi S, Yamaguchi S. Distinguishing silent lacunar infarction from enlarged Virchow-Robin
spaces: a magnetic resonance imaging and pathological study. J Neurol 1998;245: 116–122.
51. Regli L, Regli F, Maeder P, Bogousslavsky J. Magnetic resonance imaging with gadolinium contrast agent in
small deep (lacunar) cerebral infarcts. Arch Neurol 1993;50:175–180.
52. Baker LL, Stevenson DK, Enzmann DR. End-stage periventricular leukomalacia: MR evaluation. Radiology
1988;168:809–815.
53. Flodmark O, Lupton B, Li D, et al. MR imaging of periventricular leukomalacia in childhood. AJR Am J
Roentgenol 1989;152:583–590.
54. Pretorius PM, Quaghebeur G. The role of MRI in the diagnosis of MS. Clin Radiol 2003;58:434–448.
55. Mathews VP, Alo PL, Glass JD, Kumar AJ, McArthur JC. AIDS-related CNS cryptococcosis: radiologic-
pathologic correlation. AJNR Am J Neuroradiol 1992;13:1477–1486.
16. 56. Tien RD, Chu PK, Hesselink JR, Duberg A, Wiley C. Intracranial cryptococcosis in immunocompromised
patients: CT and MR findings in 29 cases. AJNR Am J Neuroradiol 1991;12:283–289.
57. Wehn SM, Heinz ER, Burger PC, Boyko OB. Dilated Virchow-Robin spaces in cryptococcal meningitis
associated with AIDS: CT and MR findings. J Comput Assist Tomogr 1989;13:756–762.
58. Miszkiel KA, Hall-Craggs MA, Miller RF, et al. The spectrum of MRI findings in CNS cryptococcosis in
AIDS. Clin Radiol 1996;51:842–850.
59. Lee C, Dineen TE, Brack M, Kirsch JE, Runge VM. The mucopolysaccharidoses: characterization by cranial
MR imaging. AJNR Am J Neuroradiol 1993;14:1285–1292.
60. Matheus MG, Castillo M, Smith JK, Armao D, Towle D, Muenzer J. Brain MRI findings in patients with
mucopolysaccharidosis types I and II and mild clinical presentation. Neuroradiology 2004;46:666–672.
61. Takahashi Y, Sukegawa K, Aoki M, et al. Evaluation of accumulated mucopolysaccharides in the brain of
patients with mucopolysaccharidoses by (1)H-magnetic resonance spectroscopy before and after bone marrow
transplantation. Pediatr Res 2001;49:349–355.
62. Tien RD, Felsberg GJ, Friedman H, Brown M, MacFall J. MR imaging of high-grade cerebral gliomas: value
of diffusion-weighted echoplanar pulse sequences. AJR Am J Roentgenol 1994;162: 671–677.
63. Noguchi K, Watanabe N, Nagayoshi T, et al. Role of diffusion-weighted echoplanar MRI in distinguishing
between brain abscess and tumour: a preliminary report. Neuroradiology 1999;41:171–174.
64. Desprechins B, Stadnik T, Koerts G, Shabana W, Breucq C, Osteaux M. Use of diffusion-weighted MR
imaging in differential diagnosis between intracerebral necrotic tumors and cerebral abscesses. AJNR Am J
Neuroradiol 1999;20:1252–1257.
65. do Amaral LL, Ferreira RM, da Rocha AJ, Ferreira NP. Neurocysticercosis: evaluation with advanced
magnetic resonance techniques and atypical forms. Top Magn Reson Imaging 2005;16: 127–144.
66. Dumas JL, Visy JM, Belin C, Gaston A, Goldlust D, Dumas M. Parenchymal neurocysticercosis: follow-up
and staging by MRI. Neuroradiology 1997;39:12–18.
67. Noujaim SE, Rossi MD, Rao SK, et al. CT and MR imaging of neurocysticercosis. AJR Am J Roentgenol
1999;173:1485–1490.
68. Van Tassel P, Cure JK. Nonneoplastic intracranial cysts and cystic lesions. Semin Ultrasound CT MR
1995;16:186–211.
69. Andrews BT, Halks-Miller M, Berger MS, Rosenblum ML, Wilson CB. Neuroepithelial cysts of the posterior
fossa: pathogenesis and report of two cases. Neurosurgery 1984;15:91–95.
70. Guermazi A, Miaux Y, Majoulet JF, Lafitte F, Chiras J. Imaging findings of central nervous system
neuroepithelial cysts. Eur Radiol 1998;8:618–623.
71. Sherman JL, Camponovo E, Citrin CM. MR imaging of CSF-like choroidal fissure and parenchymal cysts of
the brain. AJNR Am J Neuroradiol 1990;11:939–945.
72. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD
agency for electronic publication, version 11.4a. October 2010
73. Heier LA, Bauer CJ, Schwartz L, Zimmerman RD, Morgello S, Deck MD. Large Virchow-Robin spaces: MR-
clinical correlation. AJNR Am J Neuroradiol 1989;10:929 -936
17. 74. Hommel M, Gray F. Microvascular pathology. In: Caplan L, ed. Brain Ischaemia: Basic Concepts and
Clinical Relevance. New York: Springer-Verlag Berlin; 1995:215-223
75. Furuta A, Ishii N, Nishihara Y, Horie A. Medullary arteries in aging and dementia. Stroke 1991;22:442- 446
76. Brun A, Fredriksson K, Gustafson L. Pure subcortical arterioscle- rotic encephalopathy (Binswanger’s
disease): a clinicopathological study. Part 2: Pathological features. Cerebrovasc Dis 1992;2:87-92
77. Thomas AJ, O’Brien JT, Davis S, et al. Ischemic basis for deep white matter hyperintensities in major
depression: a neuropatho- logical study. Arch Gen Psychiatry 2002;59:785-792
78. Thacker NA, Varma AR, Bathgate D, et al. Dementing disor- ders: volumetric measurement of cerebrospinal
fluid to distin- guish normal from pathologic findings: feasibility study. Radi- ology 2002;224:278 -285
79. Poirier J, Derouesne C. Cerebral lacunae: a proposed new classi- fication [letter]. Clin Neuropathol
1984;3:266
80. Fazekas F, Kleinert R, Offenbacher H, et al. The morphologic correlate of incidental punctate white matter
hyperintensities on MR images. AJNR Am J Neuroradiol 1991;12:915-921
81. Ogawa T, Okudera T, Fukasawa H, et al. Unusual widening of Virchow-Robin spaces: MR appearance. AJNR
Am J Neuroradiol 1995;16:1238 -1242
82. Hughes W. Origin of lacunes. Lancet 1965 1:19 -21
83. Benhaiem-Sigaux N, Gray F, Gherardi R, Roucayrol AM, Poirier J. Expanding cerebellar lacunes due to
dilatation of the perivascular space associated with Binswanger’s subcortical arteriosclerotic en-
cephalopathy. Stroke 1987;18:1087-1092
84. Derouesne C, Gray F, Escourolle R, Castaigne P. "Expanding cerebral lacunae" in a hypertensive patient
with normal pressure hydrocephalus. Neuropathol Appl Neurobiol 1987;13:309 -320
85. Pullicino PM, Miller LL, Alexandrov AV, Ostrow PT. Infrapu- taminal "lacunes": clinical and pathological
correlations. Stroke 1995;26:1598 -1602
86. Jellinger KA. The pathology of ischemic-vascular dementia: an update. J Neurol Sci 2002; 203-204:153-157
87. Hulette C ND, McKeel D, Morris K, Mirras SS, Sumi SM, et. a. Clinical-neuropathologic findings in multi-
infarct dementia: a re- portof six autopsied cases. Neurology 1997;48:668 – 672
88. Erkinjuntti T. Diagnosis and management of vascular cognitive impairment and dementia. J Neural Transm
Suppl 2002:91-109
89. Hentschel F, Kreis M, Damian M, Krumm B. Microangiopathic lesions of white matter: quantitation of
cerebral MRI findings and correlation with psychological tests. Nervenarzt 2003;74:355-361