Migraine Visual Aura: A discussion with Nobel Laureate David H. Hubel

Update item information
Identifier 947-2
Title Migraine Visual Aura: A discussion with Nobel Laureate David H. Hubel
Ocular Movements Normal
Creator Shirley H. Wray, M.D., Ph.D., FRCP, Professor of Neurology Harvard Medical School, Director, Unit for Neurovisual Disorders, Massachusetts General Hospital
Contributor Primary Shirley H. Wray, MD, PhD, FRCP, Professor of Neurology, Harvard Medical School; Director, Unit for Neurovisual Disorders, Massachusetts General Hospital
Subject Migraine Visual Aura; Occipital Lobe; Visual Phenomena; David H. Hubel, Nobel Laureate
Supplementary Materials View Case ID 41-1 Migraine/PET Study: http://content.lib.utah.edu/u?/ehsl-shw,292
Presenting Symptom Scintillating scotoma
History I am greatly indebted to the Nobel Laureate, David Hubel for his permission to publish his description of his migraine aura. The recording was made fortuitously at the time that I invited David to the Unit for Neuro-Visual Disorders to record an audio clip describing the experiments in the cat that led him and Torsten Wiesel to win the 1981 Nobel Prize in Medicine or Physiology. Hubel and Wiesel used microelectrodes and modern electronics to detect the activity of individual visual neurons, using cats as their subjects. (The cats were not harmed by these experiments; indeed, their purring created vibration problems.) Thanks to the work of Hubel and Wiesel, the visual cortex has become the best known part of the brain. Review ID 947-3 The Prize, David Hubel, Nobel Laureate Physiology or Medicine 1981.
Clinical In this recording, you will hear David Hubel describing his migraine visual aura. He had no history of migraine headache. All the episodes of visual aura were headache free The interview is unique and remarkable because the world's most expert visual physiologist and Nobel Laureate found it difficult to describe what he sees during an aura. Hubel speculates on what may be happening in the visual cortex to generate the characteristic spread of the arc of a scintillating scotoma. We also briefly discussed an observation by Woods et al who described a patient who, during positron emission tomography (PET), fortuitously had an attack of migraine. The PET study showed a reduction in blood flow that started in the occipital cortex and spread slowly forward to the temporal and parietal lobes bilaterally. The observed pattern of "spreading oligemia", is illustrated on video tape courtesy of J.C. Mazziotto, M.D., Ph.D. et al (ID41-1).
Neuroimaging Functional MRI (fMRI) performed during spontaneous visual aura in migraineurs has shown moderate focal reductions in cerebral blood flow and volume in the occipital lobe during the aura. The occipital lobe perfusion deficit corresponded anatomically with the reported visual field disturbance and with the side of the subsequent headache.
Anatomy Review ID 41-1
Pathology Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Data from functional MRI studies in the visual cortex strongly suggest that an electrophysiological event such as CSD does in fact generate visual aura in migraine. Visual aura are characterized by a wave of cerebral hypoperfusion-oligemia that passes across the cortex at the characteristically slow rate of 2 to 6 mm per minute. Richards suggested that in migraineurs the cortical neurons activated by the leading edge of CSD are sensitive ‘line detectors'. His reasoning was based on Hubel and Wiesel's concept of neurons as ‘feature detectors', which in turn was suggested by the results of recording the intracellular activity of single neurons in the primary visual cortex of the cat and monkey brain in response to specific visual stimuli. Richards calculated that the cortical distance for each teichoptic line was 1.2 mm, five times larger than the known diameter of individual orientation columns in the monkey and so he argued that the scale discrepancy suggested that the orientation columns alone were not responsible for the phenomena. Increased activity within lattice-like, long range excitatory connections in different layers of V1, V2 and V4 are considered better anatomical candidates for the generation of visual aura. The trigger to provoke visual aura is unknown. In a study of visual processing in migraine subjects with aura, Wray et al found that the migraineurs response time in the low-level tasks was better than normal controls. The data suggests that migraineurs process visual signals to the primary visual cortex [Area V1] more rapidly than non-migraineurs and that Area V1, between attacks of visual aura, may be hypersensitive to visual stimuli.
Etiology In a related disorder, known as hemiplegic migraine, linkage analysis studies have localized the responsible gene to chromosome 19 in one third of families; in other families the gene has localized to chromosome 1; and yet in other families no linkage has been found. The gene on chromosome 19 codes for a voltage-gated calcium channel protein, which raises the provocative possibility that other forms of migraine are also due to an ion channel disorder. In migraine with and without aura, an underlying genetic factor is implicated, although it is expressed in a recognizable mendelian pattern (autosomal dominant) in a relatively small number of families. The puzzle is how this genetic fault is translated periodically into a regional neurologic deficit, unilateral headache or both.
Disease/Diagnosis Migrain Visual Aura
Treatment Patients with episodic migraine visual aura without headache do not require treatment.
References 1. Afridi SK, Giffin NJ, Kaube H, Friston KJ, Ward NS, Frackowiak RSJ, Goadsby PJ. A Positron Emission Tomographic Study in Spontaneous Migraine. Arch Neurol 2005;62:1270-1275. http://www.ncbi.nlm.nih.gov/pubmed/16087768 2. Afridi SK, Matharu MS, Lee L, Kaube H, Friston KJ, Frackowiak RSJ, Goadsby PJ. A PET study exploring the laterality of brainstem activation in migraine using glyceryl trinitrate. Brain 2005;128:932-939. http://www.ncbi.nlm.nih.gov/pubmed/15705611 3. Afridi SK, Goadsby PJ. Neuroimaging of migraine. Curr Pain Headache Rep 2006;10:221-224. Review. http://www.ncbi.nlm.nih.gov/pubmed/18778577 4. Cutrer FM, Sorensen AG, Weisskoff RM, Ostergaard L, Sanchez del Rio M, Lee EJ, Rosen BR, Moskowitz MA.. Perfusion-weighted imaging defects during spontaneous migraine aura. Ann Neurol 1998, 43:25-31. http://www.ncbi.nlm.nih.gov/pubmed/9450765 5. Goadsby PJ, Hargreaves R. Refractory migraine and chronic migraine: pathophysiological mechanisms. Headache 2008;48:1399-1405. http://www.ncbi.nlm.nih.gov/pubmed/19006557 6. Goadsby PJ. Calcitonin gene-related peptide (CGRP) antagonists and migraine: is this a new era? Neurology 2008;70:1300-1301. http://www.ncbi.nlm.nih.gov/pubmed/18413584 7. Hadjikhani N, Sanchez del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, Kwong KK, Cutrer FM, Rosen BR, Tootell RBH, Sorensen AG, Moskowitz MA. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci USA 2001;98:4687-4692. http://www.ncbi.nlm.nih.gov/pubmed/11287655 8. Hubel DH, Wiesel TN. Receptive fields and functional architecture of monkey striate cortex. J Physiol (Lond) 1968; 195:215-243. http://www.ncbi.nlm.nih.gov/pubmed/4966457 9. Hubel DH, Wiesel TN. Sequence regularity and geometry of orientation columns in the monkey striate cortex. J Comp Neurol 1974a; 158:267-293. http://www.ncbi.nlm.nih.gov/pubmed/4436456 10. Hubel DH, Wiesel TN. Uniformity of monkey striate cortex: a parallel relationship between field size, scatter and magnification factor. J Comp Neurol 1974b; 158:295-305. http://www.ncbi.nlm.nih.gov/pubmed/4436457 11. Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psychiatry 1941; 46:331-339. 12. Lauritzen M. Pathophysiology of the migraine aura: the spreading depression theory. Brain 1994;117:199-210. http://www.ncbi.nlm.nih.gov/pubmed/7908596 13. Leao AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 1944, 7:379-390. http://www.ncbi.nlm.nih.gov/pubmed/20268874 14. Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol 1981;9:344-352. http://www.ncbi.nlm.nih.gov/pubmed/6784664 15. Richards W. The fortification illusions of migraines. Sci Am 1971; 224(5): 88-96. http://www.ncbi.nlm.nih.gov/pubmed/5552581 16. Woods RP, Jacoboni M and Mazziotta JC. Bilateral spreading cerebral hypoperfusion during spontaneous migraine headache. New Eng J Med 1994; 331:1689-1692. http://www.ncbi.nlm.nih.gov/pubmed/7969360 17. Wray SH, Mijovic-Prelec D, Kosslyn SM. Visual processing in migraineurs. Brain. 1995 Feb;118 ( Pt 1):25-35. http://www.ncbi.nlm.nih.gov/pubmed/7895008
Relation is Part of 932-5, 939-4, 947-1
Contributor Secondary Ray Balhorn, Video Compressionist; Steve Smith, Videographer
Publisher Spencer S. Eccles Health Sciences Library, University of Utah
Date 2002
Type Image/MovingImage
Format video/mp4
Source 3/4" Umatic master videotape
Rights Management Copyright 2002. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah, 10 N 1900 E, SLC, UT 84112-5890
Collection Neuro-ophthalmology Virtual Education Library: NOVEL http://NOVEL.utah.edu
Language eng
ARK ark:/87278/s6cg2mpx
Setname ehsl_novel_shw
Date Created 2008-10-07
Date Modified 2017-11-22
ID 188651
Reference URL https://collections.lib.utah.edu/ark:/87278/s6cg2mpx
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