Original Articles Migraine Patients Exhibit Abnormalities in the Visual Evoked Potential M. Gawel, M.A., M.B., M.R.C.P., * J.F. Connolly, Ph.D. ** and Dr. F. Clifford Rose, F.R.C.P. *** * Assistant Professor University of Toronto, Consultant Neurologist, Sunnybrook Medical Centre. ** Lecturer in Neuropsychology, Department of Psychiatry, Charing Cross Hospital, London, England. *** Physician in Chief, Department of Neurology, Charing Cross Hospital, London W6, England. Accepted for Publication: April 26, 1982 SYNOPSIS An experiment is described which compared visual evoked potential (VEP) amplitudes and latencies in normal subjects and migraine patients. Several VEP abnormalities were found: at vertex and to a lesser extent at temporal sites, P100-N120 amplitudes were larger in patients; at vertex and temporal sites N120 amplitudes were larger in patients; at temporal sites patients had larger N120-P200 amplitudes but smaller P100 amplitudes. Peak latencies of the VEP were also found to be abnormal in patient s. At vertex, patients had delayed N120 peak latencies while at temporal sites delays were found in the P200 latencies. Patients were subdivided according to side of headache. Right-sided headache patients showed larger temporal P100 amplitudes and l arger left temporal P100-N120 amplitudes than bilateral headache patients. ( Headache 23:49-52, 1983) Visual evoked potentials (VEP) have been used in clinical neurology for the diagnosis of lesions in the optic pathway, and more specifically in the diagnosis of multiple sclerosis. 8 Although alterations in evoked potentials can be due to marked anato mical changes, other factors are abnormalities in neurotransmitters (e.g. Parkinsonism, 7 phenylketonuria 17 ) and ischaemic damage to the nervous system, 2 and the changes, in general, correlate with the severity of the clinical condition. More subtle a bnormalities have been reported in conditions not usually associated with signs of overt neurological damage such as migraine 10 and following the ingestion of a number of psychoactive drugs. It has been proposed that there is a failure of some input modulation mechanism in migraine. Wolff's 4 early experiment suggested that migraineurs had a low pain threshold and Sicuteri 18 postulated that they have a central deficiency of some sensation modulatory substance. His experiment concentrated initially on 5 hydroxy-tryptamine (5 HT) metabolism and he showed that hallucinogenic responses of migraineurs to lysergic acid diethylamide, a 5 HT antagonist, were present at much lower dose levels than those of controls. More recently, Sicuteri 19 has proposed that substance P as well as 5HT are important in maintaining the "anti nociceptive system." The sympotomatology of migraine is mediated by vascular events, the neurological signs and symptoms possibly being related to focal ischaemia, while the pain is related to but not caused by extra cerebral vasodilatation. The studies of cerebral blood flow by Sakai and Meyer 26 suggest that there are areas of focal ischaemia surrounded by hyperaemia in the brain during a migraine attack, and Welch's 20 finding of elevation of gamma amino butyric acid (GABA) and cyclic AMP following an attack sugges ts that cerebral ischaemia does occur. The ischaemic processes during the attack have been studied by Maclean and Appenzeller (1975) 12 and Regan and Heron (1970) 15 who both found alteration of the VEP amplitude over the hemisphere presumed to be suffering from ischaemia. Kennard et al 10 s tudied visual evoked potentials in migraine patients between attacks using a checkerboard stimulus and found that the latency of the major positive wave was greater, and the amplitude larger, than in a group of age-matched controls; they interpreted their results as being indicative of a neurotransmitter abnormality resulting in either a lack of inhibition or an increase in excitation. There was also evidence of an asymmetry of response depending on the role of the headache, patients with left f rontal headache having larger amplitudes. We undertook the present study in order to evaluate this phenomenon further and to assess the nature of the VEP abnormalities in migraine patients. METHODS The control group consisted of 22 healthy volunteers (11 men and 11 women) from the staff of Charing Cross Hospital. The age range was from 21 to 48 years. The patient group consisted of 16 migraineurs (15 women and 1 man) ranging in age from 16 to 6 1 years. All patients and controls were