This document discusses several types of complicated migraine syndromes including hemiplegic migraine, alternating hemiplegia of childhood, migraine with brainstem aura, retinal migraine, ophthalmoplegic migraine, and Alice in Wonderland syndrome. It provides details on symptoms, diagnostic criteria, potential causes or genetic factors, differential diagnoses, and treatment approaches for each type.
Headache Attributed to Nonvascular, Noninfectious
Intracranial Disorders
Headache Attributed to Trauma or Injury to the Head
and/or Neck
Headache Attributed to Infection
Headache Attributed to Cranial or Cervical Vascular
Disorders
Headache Associated with Disorders of Homeostasis
Headache Caused by Disorders of the Cranium, Neck,
Eyes, Ears, Nose, Sinuses, Teeth, Mouth, or Other
Facial or Cranial Structures
Headaches and the Cervical Spine
Migraine
Chronic Daily Headache
Cluster Headache
Other Trigeminal Autonomic Cephalalgias
Other Primary Headaches
Headache Attributed to Nonvascular, Noninfectious
Intracranial Disorders
Headache Attributed to Trauma or Injury to the Head
and/or Neck
Headache Attributed to Infection
Headache Attributed to Cranial or Cervical Vascular
Disorders
Headache Associated with Disorders of Homeostasis
Headache Caused by Disorders of the Cranium, Neck,
Eyes, Ears, Nose, Sinuses, Teeth, Mouth, or Other
Facial or Cranial Structures
Headaches and the Cervical Spine
Migraine
Chronic Daily Headache
Cluster Headache
Other Trigeminal Autonomic Cephalalgias
Other Primary Headaches
Neuropsychiatric manifestations of endocrine disordersDheeraj kumar
This is a subject seminar of neuropsychiatric manifesations of endocrine disorders.It took a lot of time to prepare,it helps fellow residents of Gen medicine to download and present as it is.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
Please find the power point on Tension Type Headache (TTH). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Neuropsychiatric manifestations of endocrine disordersDheeraj kumar
This is a subject seminar of neuropsychiatric manifesations of endocrine disorders.It took a lot of time to prepare,it helps fellow residents of Gen medicine to download and present as it is.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
Please find the power point on Tension Type Headache (TTH). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Isolated Cerebellar Stroke Masquerades as DepressionZahiruddin Othman
There are numerous reports on neurological conditions masquerading as psychiatric disorders. However, cerebellar
stroke is not established as one of it. The 2 case reports will highlight that this masquerade is possible and the physician's
high index of suspicion is the key to accurate diagnosis.
Suac Syndrome is an autoimmune endotheliopathy with about 304 cases described until 2013. It charaterized by the triad of E-H-V (Encephalopathy, Hearing loss and Vision - branch retinal artery occlusions/BRAO [3]. The case report early-onset autoimmune neuropsychiatric disorder in a pre-pubertal 12 year old girl innitialy presenting with behavioral and emotional manifestations
The following disorders are unique genetic neurological disorders .docxrhetttrevannion
The following disorders are unique genetic neurological disorders that result in varied clinical presentations and outcomes for patients.
Neurofibromatosis divided into type one (NF1) and type 2 (NF2) are autosomal dominant neurocutaneous disorders that results in altered genes that causes dysregulation of tumor suppression (Defendi, 2022). NF1 is more common and occurs in one out of every 3,500 births (Germanwala, n.d.). NF1, there is a deletion of the NF1 gene that produces neurofibromin 1 that activates the protein ras-GTPas which is involved with cellular signal transduction (Defendi, 2022). Without the NF1 gene there is an overactive ras-GTPas resulting in the activation of other proteins, in turn activating genes for cell growth and differentiation leading to benign or malignant tumors (Defendi, 2022). Common benign tumors include cutaneous neurofibromas, plexiform neurofibromas and optic nerve gliomas (Defendi, 2022). Patients with NF1 present with a family history of the disorder, six or more of the café-au-lait spots on the skin, freckling in the underarms and groin, presence neurofibromas (about pea-sized) on or just under skin, plexiform neurofibromas, Lisch nodules, skeletal abnormalities and have the potential for tumors on the optic nerve (Germanwala, n.d.). Additionally, these patients may present with macrocephaly, short stature, are at risk for seizures, learning disabilities, speech issues and hyperactivity (Germanwala, n.d.).
Cri-du-chat syndrome is a chromosomal disorder, also known as 5p minus syndrome where there is a deletion of the variable size on the short arm of chromosome 5 (Mainardi, 2006). Since this disorder is a syndrome, there are several clinical features that are common in the presentation of this disorder including microcephaly, large nasal bridge, hypertelorism, epicanthal folds, downward slanting palpebral fissures, down-turned corners of the mouth, low-set ears, micrognathia, abnormal dermatoglyphics and the hallmark high-pitched cry (Mainardi, 2006). The cry is a result of structural abnormalities of the larynx caused by laryngeal hypoplasia and central nervous system (Lal, 2021). The central nervous system deficit is noted in the “…clivus region of the cranial base with the laryngeal region from which the characteristic cry derived” (Lal, 2021). Neurologically, these patients have developmental and psychomotor delay, with varied levels of abilities. Patients also present with hypotonia which progresses to hypertonia with age. On magnetic nuclear resonance imaging, brainstem atrophy has been noted including the pons, cerebellum, median cerebellar peduncles and cerebellar white matter” (Mainardi, 2006).
Tay-Sachs Disease also known as GM2 gangliosidosis, is a fatal autosomal recessive disorder caused by the HexA gene found on chromosome 15 (McCance & Huether, 2014). The deficiency in the lysosomal enzyme hexosaminidase A (HexA) results in decreased degradation in GM2 gangliosi.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
4. Hemiplegic Migraine
A form of migraine with aura that includes motor weakness
Aura consists of fully reversible motor weakness and visual, sensory, and/or
speech/language symptoms
“stroke-like”
The onset of attacks is in the teen years and early twenties
Beginning with a hemiparesis or motor deficit that precedes the headache and
may persist throughout the duration of the episode
These neurologic disturbances may occasionally persist for days or weeks after the
conclusion of the headache phase
Davidoff RA: Clinical manifestations of migraine. In: Reinhardt RW, editor. Migraine: Manifestations, pathogenesis, and management. Philadelphia, PA: F.A. Davis Company; 1995; p. 60-6.
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
Winner P, Rothner AD, Lewis DW: Migraine, migraine variants, and other primary headache syndromes. In: Headache in children and adolescents. Hamilton, Ontario: BC Decker Inc; 2001; p. 60.
5. Familial Hemiplegic Migraine
Familial hemiplegic migraine (FHM) is an autosomal dominant form of migraine in
which at least one of the patient’s first or second-degree relatives has migraine
aura with motor weakness
A distinct diagnosis of sporadic hemiplegic migraine (SHM) exists, which is
clinically the same as FHM, but lacks a family history. SHM cases often require
neuroimaging, lumbar puncture and/or additional tests to rule out other potential
causes
Davidoff RA: Clinical manifestations of migraine. In: Reinhardt RW, editor. Migraine: Manifestations, pathogenesis, and management. Philadelphia, PA: F.A. Davis Company; 1995; p. 60-6.
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
6. Familial Hemiplegic Migraine Type 1
FHM type 1 (FHM1) is due to a mutation of the CACNA1A gene in the
chromosome 19p32 region and accounts for approximately 50% of all FHM cases
This missense mutation creates defective neuronal-gated calcium channels
(channelopathy)
This mutation causes calcium channel opening at a more negative membrane
potential, lowering the channel activation threshold, and delaying its inactivation,
therefore creating cortical and subcortical hyper excitability
Kazemi H, Speckmann EJ, Gorji A: Familial hemiplegic migraine and spreading depression. Iran J Child Neurol 8:6-11, 2014
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
Winner P, Rothner AD, Lewis DW: Migraine, migraine variants, and other primary headache syndromes. In: Headache in children and adolescents. Hamilton, Ontario: BC Decker Inc; 2001; p. 60.
7. Familial Hemiplegic Migraine Type
2
FHM Type 2 (FHM2) is secondary to a
mutation on the ATP1A2 gene in the
chromosome 1q23 region, which codes for
a Na/K-ATPase
Familial Hemiplegic Migraine Type
3
FHM type 3 (FHM3) presents with a
sodium channel defect secondary to
mutation on the SCN1A gene.
Both are associated with recurrent seizures
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
8. Diagnosis & Treatment
Diagnosis: MRI/MRA brain & EEG
Treatment:
- NSAIDS and triptans as abortive therapy
- Verapamil as preventive and abortive therapy
- Other treatments: acetazolamide, intranasal ketamine, ergotamine
Snow V, Weiss K, Wall EM, Mottur-Pilson C, American Academy of Family Physicians, American College of Physicians-American Society of Internal Medicine: Pharmacologic management of acute attacks of migraine and prevention of migraine headache.
Ann Intern Med 137:840-849, 2002
Artto V, Nissila M, Wessman M, et al: Treatment of hemiplegic migraine with triptans. Eur J Neurol 14:1053-1056, 2007
Yu W, Horowitz SH: Treatment of sporadic hemiplegic migraine with calcium-channel blocker verapamil. Neurology 60:120-121, 2003
Black DF: Sporadic and familial hemiplegic migraine: Diagnosis and treatment. Semin Neurol 26:208-216, 2006
Davidoff RA: Clinical manifestations of migraine. In: Reinhardt RW, editor. Migraine: Manifestations, pathogenesis, and management. Philadelphia, PA: F.A. Davis Company; 1995; p. 60-6.
10. Alternating Hemiplegia of Childhood
a rare, sporadic neurodevelopmental syndrome with an incidence of 1 in 1,000,000
children
Recurrent bouts of intermittent, often migratory, alternating hemiplegic episodes
associated with other neurological features such as dystonia, choreoathetosis and
developmental delay
Onset as early as 3-6 months of age
The duration of the episodes varies and some may last up to three weeks
Paroxysmal eye movements, such as nystagmus, are the most frequent and
earliest symptoms.
Sweney MT, Silver K, Gerard-Blanluet M, et al: Alternating hemiplegia of childhood: Early characteristics and evolution of a neurodevelopmental syndrome. Pediatrics 123:e534-541, 2009
Tenney JR, Schapiro MB: Child neurology: Alternating hemiplegia of childhood. Neurology 74:e57-59, 2010
11. Alternating Hemiplegia of Childhood
Environmental stress such as temperature extremes and odors, water exposure,
physical activity, lighting and food may be triggering factors, and neurologic
deficits can improve or resolve with sleep
ATP1A3 mutation
Associated with epilepsy and cognitive symptoms
Sweney MT, Silver K, Gerard-Blanluet M, et al: Alternating hemiplegia of childhood: Early characteristics and evolution of a neurodevelopmental syndrome. Pediatrics 123:e534-541, 2009
Tenney JR, Schapiro MB: Child neurology: Alternating hemiplegia of childhood. Neurology 74:e57-59, 2010
Sweney MT, Newcomb TM, Swoboda KJ: The expanding spectrum of neurological phenotypes in children with ATP1A3 mutations, alternating hemiplegia of childhood, rapidonset dystonia-parkinsonism, CAPOS and beyond. Pediatr Neurol 52:56-64, 2015
Wagener-Schimmel LJJC, Nicolai J: Child neurology: Benign nocturnal alternating hemiplegia of childhood. Neurology 79:e161-163, 2012
Panagiotakaki E, Gobbi G, Neville B, et al. Evidence of a non-progressive course of alternating hemiplegia of childhood: Study of a large cohort of children and adults. Brain 133:3598-3610, 2010
12. Diagnosis
Metabolic screening to exclude mitochondrial disorders
Neuroimaging to rule out stroke and/or vasculopathy
CSF analysis for neurotransmitters, pterin metabolites and methyltetrahydrofolate
to exclude dopamine biosynthesis disorders
EEG may be needed to diagnose epilepsy
Sweney MT, Silver K, Gerard-Blanluet M, et al: Alternating hemiplegia of childhood: Early characteristics and evolution of a neurodevelopmental syndrome. Pediatrics 123:e534-541, 2009
13. Treatment
Removing inciting triggers and facilitating sleep early on
Benzodiazepines as abortive therapy
Flunarizine as prophylactic therapy
Sweney MT, Silver K, Gerard-Blanluet M, et al: Alternating hemiplegia of childhood: Early characteristics and evolution of a neurodevelopmental syndrome. Pediatrics 123:e534-541, 2009
Tenney JR, Schapiro MB: Child neurology: Alternating hemiplegia of childhood. Neurology 74:e57-59, 2010
15. Migraine with Brainstem Aura
~ Basilar migraine, Bickerstaff migraine, and/or basilar artery migraine
Aura symptoms for this disorder are specifically referable to the brainstem, and
are not ischemic in etiology
This disorder is characterized by fully reversible speech/language, sensory or visual
auras that are not accompanied by retinal or motor symptoms and, by definition,
spread over five or more minutes, last from 5 to 60 minutes, and may be followed
by a headache within one hour
There must be at least two of the following “brainstem” features present:
dysarthria, vertigo, tinnitus, hypoacusis, diplopia, ataxia, and decreased level of
consciousness
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
16. Migraine with Brainstem Aura
This disorder typically involves both the left and right visual fields and may begin
with unilateral or bilateral visual symptoms
Visual symptoms are typically followed by bilateral paresthesias of arms and legs
and are frequently associated with a combination of the aforementioned
“brainstem” symptoms
Seizures especially in pediatric population
Migraine with brainstem aura typically presents in adolescence but may occur at
any age and affects both sexes
3-19 % of all migraines
Blumenfeld AE, Victorio MC, Berenson FR. Complicated migraines. InSeminars in pediatric neurology 2016 Feb 1 (Vol. 23, No. 1, pp. 18-22). WB Saunders.
17. Differential Diagnosis
Vertebral dissection or thrombosis
TIA
Arteriovenous malformations / cavernous angiomas
Chiari malformations
Platybasia
Basilar impression
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
19. Retinal Migraine
~ Ophthalmic, ocular, or anterior visual pathway migraine
A rare disorder that generally presents with scotoma or visual loss
1 in 200 migraineurs
At least two attacks of fully reversible monocular visual disturbance, with either
positive and/or negative visual phenomena. An associated migraine headache
occurs either during or within 60 minutes of onset of the visual phenomena, and
typically lasts for less than 30 minutes
Normal ophtalmological examination between attacks
Vascular risk factors need to be evaluated
International Headache Society: Headache classification committee of the international headache society (IHS). The international classification of headache disorders, 3rd edition (beta version) Cephalalgia 33:629-808, 2013
Troost T, Tomsak R: Opthalmoplegic migraine and retinal migraine. In: Olesen J, Tfelt-Hansen P, Welch K, editors. The headaches. New York: Raven Press; 1993; p. 421.
Carroll D: Retinal migraine. Headache 10:9-13, 1970
Corbett JJ: Neuro-ophthalmic complications of migraine and cluster headaches. Neurol Clin. 1:973-995, 1983
20. Differential Diagnosis
Transient ischemic attack
Retinal detachment
Optic neuropathy
Amaurosis Fugax (abrupt onset with narrowing retinal vessels)
Migraine with visual aura (hemifield)
Corbett JJ: Neuro-ophthalmic complications of migraine and cluster headaches. Neurol Clin.1:973-995, 1983
Kline LB, Kelly CL: Ocular migraine in a patient with cluster headaches. Headache 20:253-257, 1980
Killer HE, Forrer A, Flammer J: Retinal vasospasm during an attack of migraine. Retina 23:253-254, 2003
Russell MB, Olesen J: A nosographic analysis of the migraine aura in a general population. Brain 119:355-361, 1996
22. Ophtalmoplegic Migraine
Is a rare condition, occurring in 0.7 of 1 million people and presents as headache
associated with unilateral partial or complete oculomotor palsy
Cranial neuralgia; often identifiable 2nd cause
Two attacks of migrainous headaches accompanied or followed by partial or
complete 3rd, 4th, 6th, or occasionally 5th cranial nerve palsies within 4 days of
headache that lack another identifiable etiology
Onset: children < 10 years old of age, rare in infants
~ Tolosa-Hunt syndrome in adults
Thought to be secondary to ischemic, compressive or inflammatory processes
Blumenfeld AE, Victorio MC, Berenson FR. Complicated migraines. InSeminars in pediatric neurology 2016 Feb 1 (Vol. 23, No. 1, pp. 18-22). WB Saunders.
23. Diagnosis and Treatment
Diagnosis: MRI brain and orbits with and without contrast
Treatment: corticosteroids
Ostergaard JR, Moller HU, Christensen T: Recurrent ophthalmoplegia in childhood: Diagnostic and etiologic considerations. Cephalalgia 16:276-279, 1996
Carlow TJ: Oculomotor ophthalmoplegic migraine: Is it really migraine? J Neuroophthalmol 22:215-221, 2002
Prats JM, Mateos B, Garaizar C: Resolution of MRI abnormalities of the oculomotor nerve in childhood ophthalmoplegic migraine. Cephalalgia 19:655-659, 1999
Wong V, Wong WC: Enhancement of oculomotor nerve: A diagnostic criterion for ophthalmoplegic migraine? Pediatr Neurol 17:70-73, 1997
25. Alice in Wonderland Syndrome
Altered body perceptions is cortical in nature and characterized by variations in
size and shape and distorted body images
Patients often describe bizarre visual illusions, spatial distortions, micropsia,
macropsia, metamorphopsia, and teleopsia
These strange experiences may precede or accompany the headache or may occur
without headache at all
Not migraine specific and may occur in a variety of disorders including epilepsy,
drug intoxication, delirium of fever, cerebral lesion, schizophrenia, or hypnagogic
states
The most common etiologies are migraine and Epstein-Barr viral infections
Davidoff RA: Clinical manifestations of migraine. In: Reinhardt RW, editor. Migraine: Manifestations, pathogenesis, and management. Philadelphia, PA: F.A. Davis Company; 1995; p. 60-6.
Winner P, Rothner AD, Lewis DW: Migraine, migraine variants, and other primary headache syndromes. In: Headache in children and adolescents. Hamilton, Ontario: BC Decker Inc; 2001; p. 60.
Todd J. The syndrome of alice in wonderland. Can Med Assoc J 73:701-704, 1955
Losada-Del Pozo R, Cantarin-Extremera V, Garcia-Penas JJ, et al: Characteristics and evolution of patients with alice in wonderland syndrome. Rev Neurol 53:641-648, 2011
27. Acute Confusional Migraine
A rare condition, first described by Gascon and Barlow
Acute onset of confusion manifesting as agitation, memory deficit, disorientation,
increased alertness, dysarthria or perceptual disturbance
Childhood and adolescence
50 % have migraine attacks; family history
Headache may occur prior to, during or after the confusional state, may last for
minutes to hours, usually resolves within 24 hours, and may be associated with
retrograde amnesia.
During the confusional state, the neurological examination is otherwise normal. Mild
trauma appears to be a trigger.
The pathophysiology is unclear
Blumenfeld AE, Victorio MC, Berenson FR. Complicated migraines. InSeminars in pediatric neurology 2016 Feb 1 (Vol. 23, No. 1, pp. 18-22). WB Saunders.
28. Diagnosis and Treatment
The diagnosis requires exclusion of encephalitis, seizure, stroke, CNS vasculitis,
metabolic encephalopathy, toxic ingestion, or other causes of acute confusional
state
During an episode, EEG often shows diffuse slowing and, occasionally, frontal
intermittent rhythmic delta activity (FIRDA)
Neuroimaging and CSF findings are normal
Prochlorperazine and intravenous valproate have been reported to be effective
treatments during the episodes.
Valproate has also been shown to be effective as preventative treatment
Shaabat A: Confusional migraine in childhood. Pediatr Neurol 15:23-25, 1996
Avraham SB, Har-Gil M, Watemberg N:Acute confusional migraine in an adolescent: Response to intravenous valproate. Pediatrics 125:e956-959, 2010
Gantenbein AR, Riederer F, Mathys J, et al: Confusional migraine is an adult as well as a childhood disease. Cephalalgia 31:206-212, 2011
Pietrini V, Terzano MG, D'Andrea G, et al: Acute confusional migraine: Clinical and electroencephalographic aspects. Cephalalgia 7:29-37, 1987
Khatri R, Hershey AD, Wong B: Prochlorperazine--treatment for acute confusional migraine. Headache 49:477-480, 2009
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29. Summary
Complicated migraines present as variable neurological conditions, and must be
carefully differentiated from more serious CNS pathologies
Careful diagnosis and appropriate treatments
