Visual Migraines to Be Worried About Visual Migraines to Be Worried About

Total Page:16

File Type:pdf, Size:1020Kb

Visual Migraines to Be Worried About Visual Migraines to Be Worried About Dr Jo-Anne Pon Consultant Ophthalmologist and Oculoplastic Surgeon Southern Eye Specialists Christchurch 12:15 - 12:30 Visual Migraines to be Worried About Visual Migraines To Be Worried About Jo-Anne Pon Ophthalmologist Mr CS (57yo) • Right visual field loss RE only • Headaches – Like looking through water – Gets them intermittently (yrs) – Shimmering – Not severe – Lasted 60mins – No assoc nausea or need to lie down – Associated with headache – Assoc with tiredness • Started day before visual symptoms • lasted 48hrs • General ache/tension – Visual sx’s resolved • No further episodes • No history of migraine Mr CS • Normal ocular examination Management? • Neuro-imaging? • HVF 30-2 - normal • No investigations • Didn’t return with symptoms Outline • Visual Migraine symptoms – Typical – Red flags/ who needs neuro-imaging • Patterns of transient vision loss Perspective • Migraine with visual symptoms - • Which ones to worry about? common • Very few • Lifetime prevalence in general population 18% • Moorfields/St Thomas study – over 23 years, 9 cases • 1-3% of general population or – Literature 31 cases 1/3 of migraineurs will present 1950 to 2009 (59yrs) c/o visual aura International Classification of Headache Disorders – 3 (ICHD-3) • Prodromal phase • Aura • Headache • Postdromal phase Typical visual aura of migraine Biphasic aura 1. Positive visual phenomenon • Fortification spectra (Teichopsia) • Scintillations (flashing lights) • C-shape or semicircle surrounding scotoma 2. Negative symptoms minutes later • Blank scotoma • Hemianopia Visual symptoms Diagnostic criteria for typical migraine visual aura • Develops gradually over 5mins • Duration 5 to 60 mins • Headache begins during or follows aura Moorfields / St Thomas Hospital 9 cases Focal cerebral pathology Moorfields / St Thomas Hospital Literature 31 cases 9 cases 1950 to 2009 • Cavernous haemangioma (2) • AVM (16) • Subependymoma • Capillary haemangioma (1) • Intracranial calcification • Infarction (1) • Metastatic adenocarcinoma • Astrocytoma • Meningioma (3) • Unspecified mass • AVM (1) • Head injury • • Oligodendroglioma (1) Meningioma • Cavernous haemangioma • Aneurysm • Infarction (ICA dissection, occlusion) • Abscess Differentiate Migraine vs Structural Lesion ? Migraine vs Occipital lesion Both can have Occipital Lesion • Scintillating scotoma/teichopsia • Visual symptoms • Past history cannot reliably – Brief <5 mins, Unformed exclude occipital lesion • Photopsia • Duration 5-60mins in both – Flicker rapidly • Visual aura recurring in same – Remain stationery hemifield • Location – Same location in visual field, contralateral to lesion Migraine vs Occipital lesion Red Flags • > 40yo, esp no past history of migraine – DDx TIA • if < 50 yo, Acephalgic (Migraine-like visual aura without headache ) • Duration – brief (seconds) or < 5 mins (seizure related) – Prolonged (persist) • Symptoms exclusively negative e.g. hemianopia Mr MK 68yo • Left visual field loss with zigzag lines x 10 mins • No history of migraines • Went to Optometrist Left inferior quadrantanopia Visual Field Defects Luu, Lee, Daly Chen Visual field defects after stroke Australian Family Physician July 2010 Right Occipital CVA Who needs neuro-imaging? • Stereotypical visual aura: always in • Unexplained visual field defect same location in visual field • Subjective persistence of a scotoma following • Increase in frequency or change in pattern to longstanding visual aura typical visual aura – Daily = epileptic visual phenomena • Co-existence of seizures – Sudden alteration in aura characteristics – E.g. previous headache, now acephalgic – E.g. aura persisting throughout or beyond headache – E.g. persistent darkening or dimming of homonymous region of visual field Mrs KO (76yo) c/o sparkly waves BE, worse in LE (amblyopia) • x 10 years, no change in nature of symptoms • Last 10-15mins (longest 30mins) • Symptoms also present with BE closed • No headache • Increase in frequency of symptoms – Previously occasionally – Now fortnightly – Recently a day – 3 episodes lasting 5mins each Mrs KO (76yo) • PMH: Normal ocular examination – HT • R 6/9, L CF – No CVA, IHD • No RAPD, normal optic discs 0.3 • POH: • IOP – Strabismus childhood – R 16mmHg, L 17mmHg – L Amblyopia • FH: Glaucoma (sister) HVF Not reliable Management? • Neuro-imaging? • Feb 2014 – Returned for R cataract management • CT and CTA Head: – Acephalgic migraines less frequent – Dec 2012 again – Normal Ms DC 52yo • PC: spinning propeller in R Superotemporal VF, expands, becomes colourful kaleidoscope obscuring VF • Resolves > 20mins • Originally lasted 1 min, but increased duration and frequency • Occurring every other day • Sees symptoms with eyes closed • No headache • 1 episode assoc with nausea and vomiting • Between episodes, back to normal, well, no neurological symptoms Ms DC 52yo Ms DC 52yo • PMH: Treatment for Breast • Presented Aug 2016 Cancer • Review 4 weeks with HVF – Surgery • If deterioration, MRI – Radiotherapy – Chemotherapy – Hormone treatment • 1 day before appointment – Found confused, headache, vomiting • CT scan with contrast 23/6/16 – (didn’t turn up at work) – No cause to explain symptoms Ms DC 52yo Acephalgic migraine vs retinal migraine •Usually young, well adults • Patchy fading vision over 5 min, then poor vision for 5-60mins •+/- headache •Choroidal circulation in spasm + •No neurologic symptoms No headache •Normal eye examination •Rx: Ca channel blocker to reduce frequency Patterns of vision loss • Monocular or binocular? – Patients can mistake monocular for binocular or vice versa • Other clinical /neurological signs Patterns of vision loss Monocular • Age? • Exercise or heat: – >50yo: Amaurosis fugax? Uhthoff’s phenomenon (cardiovascular workup) (optic neuritis/MS) – > 50yo & older: GCA? • Gaze evoked amaurosis: – All ages, <50yo orbital tumour? E.g. Carotid dissection (trauma, neck pain, Ipsilateral Horner’s syndrome, dysgeusia) Patterns of vision loss Transient Binocular Vision Loss Duration? Pattern of recovery? • Papilloedema – seconds, Transient Visual Obscurations (TVOs) • Vertebrobasilar insufficiency – onset sudden (seconds), then recovers over seconds to minutes • D’s: dysarthria, diplopa, dizziness (vertigo), drop attacks, • >50yrs, vasculopathic risk factors • All symptoms resolve < 1hour • TIA - < 15mins – Onset within seconds, lasts 1-10mins • Visual Aura of Migraine – 20 mins (5-60 mins) • Retrochiasmal disease < 5 mins (20-30mins) Migraine with visual symptoms Take home messages Who to refer for investigation? Pattern Recognition • Typical Migraine Visual Aura • Other patterns of vision loss – Unilateral – Bilateral Diagnostic criteria for typical migraine visual aura • Develops gradually over 5mins • Duration 5 to 60 mins • Headache begins during or follows aura Migraine vs Occipital lesion Red Flags • > 40yo, esp no past history of migraine – DDx TIA (can be acephalgic) • if < 50 yo, Acephalgic (Migraine-like visual aura without headache ) • Duration – brief (seconds) or < 5 mins (seizure related) – Prolonged • Symptoms exclusively negative e.g. hemianopia Who needs neuro-imaging? • Stereotypical visual aura: always in same location in visual field • Increase in frequency (daily = seizure activity?) • or change in pattern to longstanding visual aura – previous headache, now acephalgic – Persisting aura/ persisting scotoma – persistent darkening or dimming of homonymous region of visual field • Co-existence of seizures Thank you.
Recommended publications
  • Advice for Floaters and Flashing Lights for Primary Care
    UK Vision Strategy RCGP – Royal College of General Practitioners Advice for Floaters and Flashing Lights for primary care Key learning points • Floaters and flashing lights usually signify age-related liquefaction of the vitreous gel and its separation from the retina. • Although most people sometimes see floaters in their vision, abrupt onset of floaters and / or flashing lights usually indicates acute vitreous gel detachment from the posterior retina (PVD). • Posterior vitreous detachment is associated with retinal tear in a minority of cases. Untreated retinal tear may lead to retinal detachment (RD) which may result in permanent vision loss. • All sudden onset floaters and / or flashing lights should be referred for retinal examination. • The differential diagnosis of floaters and flashing lights includes vitreous haemorrhage, inflammatory eye disease and very rarely, malignancy. Vitreous anatomy, ageing and retinal tears • The vitreous is a water-based gel containing collagen that fills the space behind the crystalline lens. • Degeneration of the collagen gel scaffold occurs throughout life and attachment to the retina loosens. The collagen fibrils coalesce, the vitreous becomes increasingly liquefied and gel opacities and fluid vitreous pockets throw shadows on to the retina resulting in perception of floaters. • As the gel collapses and shrinks, it exerts traction on peripheral retina. This may cause flashing lights to be seen (‘photopsia’ is the sensation of light in the absence of an external light stimulus). • Eventually, the vitreous separates from the posterior retina. Supported by Why is this important? • Acute PVD may cause retinal tear in some patients because of traction on the retina especially at the equator of the eye where the retina is thinner.
    [Show full text]
  • Fluids Hypertension Syndromes: Migraines, Headaches, Normal Tension Glaucoma, Benign Intracranial Hypertension, Caffeine Intolerance
    Fluids Hypertension Syndromes – Dr. Leonardo Izecksohn – page 1 Fluids Hypertension Syndromes: Migraines, Headaches, Normal Tension Glaucoma, Benign Intracranial Hypertension, Caffeine Intolerance. Etiologies, Pathophysiologies and Cure. Author: Leonardo Izecksohn. Medical Doctor, Ophthalmologist, Master of Public Health. We have no financial interest on any medicament, device, or technique described in this e-book. We authorize the free copy and distribution of this e-book for educational purposes. The 1st. edition was written at the year 1996, with 2 pages. There are other editions spread at the Internet. This is the enlarged and revised edition 65-f, updated on May 24, 2016. ISBN 978-85-906664-1-7 DOI: 10.13140/2.1.3074.5602 www.izecksohn.com/leonardo/ [email protected] Fluids Hypertension Syndromes – Dr. Leonardo Izecksohn – page 2 Abstract A – Migraines, Headaches and Fluids Hypertension Syndromes – What are they? - Answer: Migraines and most primary headaches are the aches of the pressure increase in the fluids: - Intraocular Aqueous Humor, - Intracranial Cerebrospinal Fluid, and - Inner ear’s Perilymph and Endolymph. We denominate the fluids’ pressure rises and their consequent migraines, signs, symptoms and sick- nesses as the Fluids Hypertension Syndromes. Migraines and headaches are not sicknesses: they are symptoms of the sicknesses. B – How many Fluids Hypertension Syndromes do exist? - Answer: There are three Fluids Hypertension Syndromes: 1- Ocular, due to raises of the intraocular Aqueous Humor pressure. 2- Cerebrospinal, due to raises of the intracranial Cerebrospinal Fluid pressure. 3- Inner Ears, due to raises of the inner ears' Perilymph and Endolymph pressures. Each patient can present one, two, or all the three Fluids Hypertension Syndromes in the same time.
    [Show full text]
  • Visual Perception in Migraine: a Narrative Review
    vision Review Visual Perception in Migraine: A Narrative Review Nouchine Hadjikhani 1,2,* and Maurice Vincent 3 1 Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA 2 Gillberg Neuropsychiatry Centre, Sahlgrenska Academy, University of Gothenburg, 41119 Gothenburg, Sweden 3 Eli Lilly and Company, Indianapolis, IN 46285, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-617-724-5625 Abstract: Migraine, the most frequent neurological ailment, affects visual processing during and between attacks. Most visual disturbances associated with migraine can be explained by increased neural hyperexcitability, as suggested by clinical, physiological and neuroimaging evidence. Here, we review how simple (e.g., patterns, color) visual functions can be affected in patients with migraine, describe the different complex manifestations of the so-called Alice in Wonderland Syndrome, and discuss how visual stimuli can trigger migraine attacks. We also reinforce the importance of a thorough, proactive examination of visual function in people with migraine. Keywords: migraine aura; vision; Alice in Wonderland Syndrome 1. Introduction Vision consumes a substantial portion of brain processing in humans. Migraine, the most frequent neurological ailment, affects vision more than any other cerebral function, both during and between attacks. Visual experiences in patients with migraine vary vastly in nature, extent and intensity, suggesting that migraine affects the central nervous system (CNS) anatomically and functionally in many different ways, thereby disrupting Citation: Hadjikhani, N.; Vincent, M. several components of visual processing. Migraine visual symptoms are simple (positive or Visual Perception in Migraine: A Narrative Review. Vision 2021, 5, 20. negative), or complex, which involve larger and more elaborate vision disturbances, such https://doi.org/10.3390/vision5020020 as the perception of fortification spectra and other illusions [1].
    [Show full text]
  • Read PDF Edition
    REVIEW OF OPTOMETRY EARN 2 CE CREDITS: Positive Visual Phenomena—Etiologies Beyond the Eye, PAGE 58 ■ VOL. 155 NO. 1 January 15, 2018 www.reviewofoptometry.comwww.reviewofoptometry.com ■ ANNUAL CORNEA REPORT JANUARY 15, 2018 ■ CXL ■ EPITHELIAL DEFECTS How to Heal Persistent Epithelial Defects PAGE 38 ■ TRANSPLANTS Corneal Transplants: The OD’s Role PAGE 44 ■ INFILTRATES Diagnosing Corneal Infiltrative Disease PAGE 50 ■ POSITIVE VISUAL PHENOMENA CXL: Your Top 12 Questions —Answered! PAGE 30 001_ro0118_fc.indd 1 1/5/18 4:34 PM ĊčĞĉėĆęĊĉĆĒēĎĔęĎĈĒĊĒćėĆēĊċĔėĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊĘ ĊđĎĊċĎēĘĎČčę ċċĊĈęĎěĊ Ȉ 1 Ȉ 1 ĊđđǦęĔđĊėĆęĊĉ Ȉ Ȉ ĎĒĕđĊĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊ Ȉ Ȉ ĔēěĊēĎĊēę Ȉ͝ Ȉ Ȉ Ƭ 1 ǡ ǡǡǤ͚͙͘͜Ǥ Ȁ Ǥ ͚͙͘͜ǣ͘͘ǣ͘͘͘Ǧ͘͘͘ ĕĕđĎĈĆęĎĔēĘ Ȉ Ȉ Ȉ Ȉ Ȉ čĊĚėĎĔē̾ėĔĈĊĘĘ Ȉ Ȉ Katena — Your completecomplete resource forfor amniotic membrane pprocedurerocedure pproducts:roducts: Single use speculums Single use spears ͙͘͘ǡ͘͘͘ήĊĞĊĘęėĊĆęĊĉ Forceps ® ,#"EWB3FW XXXLBUFOBDPNr RO0118_Katena.indd 1 1/2/18 10:34 AM News Review VOL. 155 NO. 1 ■ JANUARY 15, 2018 IN THE NEWS Accelerated CXL Shows The FDA recently approved Luxturna (voretigene neparvovec-rzyl, Spark Promise—and Caution Therapeutics), a directly administered gene therapy that targets biallelic This new technology is already advancing, but not without RPE65 mutation-associated retinal dystrophy. The therapy is designed to some bumps in the road. deliver a normal copy of the gene to By Rebecca Hepp, Managing Editor retinal cells to restore vision loss. While the approval provides hope for patients, wo new studies highlight the resulted in infection—while tradi- the $425,000 per eye price tag stands as pros and cons of accelerated tional C-CXL has a reported inci- a signifi cant hurdle.
    [Show full text]
  • Migraine Triggered Seizures and Epilepsy Triggered Headache and Migraine Attacks: a Need for Re-Assessment
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central J Headache Pain (2011) 12:287–288 DOI 10.1007/s10194-011-0344-2 COMMENTARY Migraine triggered seizures and epilepsy triggered headache and migraine attacks: a need for re-assessment Paul T. G. Davies • C. P. Panayiotopoulos Received: 5 April 2011 / Accepted: 8 April 2011 / Published online: 24 April 2011 Ó The Author(s) 2011. This article is published with open access at Springerlink.com In this issue of the Journal, Belcastro and associates review Migralepsy terminology and classification issues for migralepsy, hem- icrania epileptica, post-ictal and ictal headache [1]. They According to the ICHD-II 1.5.5, ‘‘migraine-triggered sei- raise key points such as ictal headache and visual seizures zure (sometimes referred to as migralepsy)’’ denotes an are often misdiagnosed as migraine, ‘‘migralepsy’’ is unli- epileptic seizure that occurs ‘‘during or within one hour kely to exist and an ‘‘epilepsy-migraine sequence’’ is much after a migraine aura’’ [3]. However, the evidence of this more common and well documented than the dominant ‘‘migraine-seizure’’ sequence is weak and the proposed view of a ‘‘migraine-epilepsy sequence’’. Their relevant criterion of 1 h gap between the end of the ‘‘aura’’ and the proposals need appropriate attention by the committee of start of an epileptic seizure is entirely arbitrary the international classification of headache disorders Migralepsy is an old term derived from migra(ine) and (ICHD) as well as the physicians in their clinical practice (epi)lepsy, coined by Dr Douglas Davidson, but mainly because of the consequences that misdiagnosis may have on attributed to Lennox and Lennox, which we quote, ‘‘a patients.
    [Show full text]
  • Migraine: Spectrum of Symptoms and Diagnosis
    KEY POINT: MIGRAINE: SPECTRUM A Most patients develop migraine in the first 3 OF SYMPTOMS decades of life, some in the AND DIAGNOSIS fourth and even the fifth decade. William B. Young, Stephen D. Silberstein ABSTRACT The migraine attack can be divided into four phases. Premonitory phenomena occur hours to days before headache onset and consist of psychological, neuro- logical, or general symptoms. The migraine aura is comprised of focal neurological phenomena that precede or accompany an attack. Visual and sensory auras are the most common. The migraine headache is typically unilateral, throbbing, and aggravated by routine physical activity. Cutaneous allodynia develops during un- treated migraine in 60% to 75% of cases. Migraine attacks can be accompanied by other associated symptoms, including nausea and vomiting, gastroparesis, di- arrhea, photophobia, phonophobia, osmophobia, lightheadedness and vertigo, and constitutional, mood, and mental changes. Differential diagnoses include cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoenphalopathy (CADASIL), pseudomigraine with lymphocytic pleocytosis, ophthalmoplegic mi- graine, Tolosa-Hunt syndrome, mitochondrial disorders, encephalitis, ornithine transcarbamylase deficiency, and benign idiopathic thunderclap headache. Migraine is a common episodic head- (Headache Classification Subcommittee, ache disorder with a 1-year prevalence 2004): of approximately 18% in women, 6% inmen,and4%inchildren.Attacks Recurrent attacks of headache, consist of various combinations of widely varied in intensity, fre- headache and neurological, gastrointes- quency, and duration. The attacks tinal, and autonomic symptoms. Most are commonly unilateral in onset; patients develop migraine in the first are usually associated with an- 67 3 decades of life, some in the fourth orexia and sometimes with nausea and even the fifth decade.
    [Show full text]
  • Elementary Visual Hallucinations, Blindness, and Headache in Idiopathic Occipital Epilepsy: Diverentiation from Migraine
    536 J Neurol Neurosurg Psychiatry 1999;66:536–540 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.66.4.536 on 1 April 1999. Downloaded from SHORT REPORT Elementary visual hallucinations, blindness, and headache in idiopathic occipital epilepsy: diVerentiation from migraine C P Panayiotopoulos Abstract also fundamental symptoms often with the This is a qualitative and chronological same sequence of events in occipital seizures.1−9 analysis of ictal and postictal symptoms, This is a systematic prospective qualitative frequency of seizures, family history, study of the characteristics of elementary visual response to treatment, and prognosis in hallucinations, blindness, and headache in nine patients with idiopathic occipital epi- idiopathic occipital epilepsy. lepsy and visual seizures. Ictal elementary visual hallucinations are stereotyped for Methods each patient, usually lasting for seconds. These are detailed elsewhere.910 Patients with They consist of mainly multiple, bright occipital seizures were prospectively evaluated coloured, small circular spots, circles, or and followed up from 1973. Nine patients with balls. Mostly, they appear in a temporal idiopathic occipital epilepsy with visual halluci- hemifield often moving contralaterally or nations (IOEVH) had: in the centre where they may be flashing. (a) Incontrovertible clinical evidence of oc- They may multiply and increase in size in cipital seizures with or without secondarily the course of the seizure and may progress generalisation. to other non-visual occipital seizure (b) Normal physical, neurological, and men- symptoms and more rarely to extra- tal states and high resolution MRI. They all had detailed interviews, seven com- occipital manifestations and convulsions. 9 Blindness occurs usually from the begin- pleted a purposely designed questionnaire, ning and postictal headache, often indis- and eight provided drawings of their visual hal- tinguishable from migraine, is common.
    [Show full text]
  • Textbook of Ophthalmology, 5Th Edition
    Textbook of Ophthalmology Textbook of Ophthalmology 5th Edition HV Nema Former Professor and Head Department of Ophthalmology Institute of Medical Sciences Banaras Hindu University Varanasi India Nitin Nema MS Dip NB Assistant Professor Department of Ophthalmology Sri Aurobindo Institute of Medical Sciences Indore India ® JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD. New Delhi • Ahmedabad • Bengaluru • Chennai Hyderabad • Kochi • Kolkata • Lucknow • Mumbai • Nagpur Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110 002 I ndia Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672 Rel: +91-11-32558559 Fax: +91-11-23276490 +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094, e-mail: [email protected] 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001, Phones: +91-80-22285971, +91-80-22382956, 91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897 Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] No. 41/3098, B & B1, Kuruvi Building, St.
    [Show full text]
  • NEUROLOGY in TABLE.Pdf
    ZAPORIZHZHIA STATE MEDICAL UNIVERSITY DEPARTMENT OF NEUROLOGY DISEASES NEUROLOGY IN TABLE (General neurology) for practical employments to the students of the IV course of medical faculty Zaporizhzhia, 2015 2 It is approved on meeting of the Central methodical advice Zaporozhye state medical university (the protocol № 6, 20.05.2015) and is recommended for use in scholastic process. Authors: doctor of the medical sciences, professor Kozyolkin O.A. candidate of the medical sciences, assistant professor Vizir I.V. candidate of the medical sciences, assistant professor Sikorskaya M.V. Kozyolkin O. A. Neurology in table (General neurology) : for practical employments to the students of the IV course of medical faculty / O. A. Kozyolkin, I. V. Vizir, M. V. Sikorskaya. – Zaporizhzhia : [ZSMU], 2015. – 94 p. 3 CONTENTS 1. Sensitive function …………………………………………………………………….4 2. Reflex-motor function of the nervous system. Syndromes of movement disorders ……………………………………………………………………………….10 3. The extrapyramidal system and syndromes of its lesion …………………………...21 4. The cerebellum and it’s pathology ………………………………………………….27 5. Pathology of vegetative nervous system ……………………………………………34 6. Cranial nerves and syndromes of its lesion …………………………………………44 7. The brain cortex. Disturbances of higher cerebral function ………………………..65 8. Disturbances of consciousness ……………………………………………………...71 9. Cerebrospinal fluid. Meningealand hypertensive syndromes ………………………75 10. Additional methods in neurology ………………………………………………….82 STUDY DESING PATIENT BY A PHYSICIAN NEUROLOGIST
    [Show full text]
  • Permanent Central Scotoma Caused by Looking at the Sun During an Eclipse, and Complicated by Uniocular, Transi- Ent, Revolving Hemianopsia
    PERMANENT CENTRAL SCOTOMA CAUSED BY LOOKING AT THE SUN DURING AN ECLIPSE, AND COMPLICATED BY UNIOCULAR, TRANSI- ENT, REVOLVING HEMIANOPSIA. From Dr. Knapp’s Practice, Reported by Dr. A. DUANE, New York. Reprinted from the Archives of Ophthalmology, Vol. xxiv., No. i, 1895 PERMANENT CENTRAL SCOTOMA CAUSED BY LOOKING AT THE SUN DURING AN ECLIPSE, AND COMPLICATED BY UNIOCULAR, TRANSI- ENT, REVOLVING HEMIANOPSIA. From Dr. Knapp’s Practice, Reported by Dr. A. DUANE, New York, instances of central scotoma after expos- ALTHOUGHure to sunlight are by no means rare, the subjoined case seems worthy ofrecord, because of the persistence of the scotoma twelve years afterwards, and because of the pres- ence of a peculiar hemiopic and scotoma scintil- lans, which apparently was likewise the result of the action of the sun’s rays. The patient, P. W., a man twenty-four years of age, consulted Dr. Knapp on Feb. 5, 1895, and gave the following history: Twelve years previous he had, on the occasion of the transit of Venus, 1 looked directly at the sun through the tube formed by the nearly closed fist. Soon after, he found that when both eyes were open, but not when the left was closed, a greenish cloud hid com- pletely the centre of every object looked at. This had exactly the shape of the illuminated portion of the sun at the time of the transit, i. e., was a circle with a crescentic defect at the upper part corresponding to the spot occupied by the planet at the time. It was then of considerable size, covering an area 5 inches in width when projected upon a surface 15 or 20 inches off.
    [Show full text]
  • The Neuro-Ophthalmology of Cerebrovascular Disease*
    The Neuro-Ophthalmology of Cerebrovascular Disease* JOHN W. HARBISON, M.D. Associate Professor, Department of Neurology, Medical College of Virginia, Health Sciences Division of Virginia Commonwealth University, Richmond The neuro-ophthalmology of cerebrovascular however, are important pieces to the puzzle the disease is a vast plain of neuro-ophthalmic vistas, patient may present. A wide variety of afflictions encompassing virtually all areas of disturbances of of the eye occur by virtue of its arterial dependence the eye-brain mechanism. This paper will be re­ on the internal carotid artery. It is also logical to stricted to those areas of the neuro-ophthalmology assume that changes in the distribution of the of cerebrovascular disease which one might con­ ophthalmic artery may reflect changes taking place sider advances in its clinical diagnosis and treatment. in other channels of the internal carotid artery­ Most practitioners of medical and surgical neu­ the middle cerebral, the anterior cerebral, and de­ rology give little thought to that aspect of medicine pending upon anatomic variations, the posterior generally accepted as the ideal approach to any cerebral artery. This paper will discuss these afflic­ disease-prevention. Usually when one is presented tions, those common as well as rare, those well with an illness of the central nervous system, it recognized, and those frequently overlooked. seems to be a fait accompli. Although prevention Historically, the recognition of the eye as an is by no means new, certain aspects of it qualify index of cerebrovascular disease presents an inter­ as advances. There is one advance in cerebrovascu­ rupted course. Virchow is credited with the first lar disease in which prevention plays a significant autopsy correlation of ipsilateral blindness with role.
    [Show full text]
  • Home>>Common Retinal & Ophthalmic Disorders
    Common Retinal & Ophthalmic Disorders Cataract Central Serous Retinopathy Cystoid Macular Edema (Retinal Swelling) Diabetic Retinopathy Floaters Glaucoma Macular degeneration Macular Hole Macular Pucker - Epiretinal Membrane Neovascular Glaucoma Nevi and Pigmented Lesions of the Choroid Posterior Vitreous Detachment Proliferative Vitreoretinopathy (PVR) Retinal Tear and Detachment Retinal Artery and Vein Occlusion Retinitis Uveitis (Ocular Inflammation) White Dot Syndromes Anatomy and Function of the Eye (Short course in physiology of vision) Cataract Overview Any lack of clarity in the natural lens of the eye is called a cataract. In time, all of us develop cataracts. One experiences blurred vision in one or both eyes – and this cloudiness cannot be corrected with glasses or contact lens. Cataracts are frequent in seniors and can variably disturb reading and driving. Figure 1: Mature cataract: complete opacification of the lens. Cause Most cataracts are age-related. Diabetes is the most common predisposing condition. Excessive sun exposure also contributes to lens opacity. Less frequent causes include trauma, drugs (eg, systemic steroids), birth defects, neonatal infection and genetic/metabolic abnormalities. Natural History Age-related cataracts generally progress slowly. There is no known eye-drop, vitamin or drug to retard or reverse the condition. Treatment Surgery is the only option. Eye surgeons will perform cataract extraction when there is a functional deficit – some impairment of lifestyle of concern to the patient. Central Serous Retinopathy (CSR) Overview Central serous retinopathy is a condition in which a blister of clear fluid collects beneath the macula to cause acute visual blurring and distortion (Figure 2). Central serous retinochoroidopathy Left: Accumulation of clear fluid beneath the retina.
    [Show full text]