Neurophysiological and Biochemical Changes of Migraine

The present study aims at evaluating the role of evoked potentials (ABR, VEP, P300, motor threshold), and EEG in understanding the pathogenesis of migraine and to detect if there is a functional abnormalities in cortical electrical activity. The study was carried out on 50 patients (30 females and 20 males) and 25 age and sex matched normal controls. The clinical classification of migraine study was based on the criteria of the Headache Classification Committee of the International Headache Society 1988 . Each patient was subjected to the following: full history taking and neurological examinations. A battery of neurophysiological tests including: electroencephalogram (EEG), brain stem auditory evoked potentials (ABR), visual evoked potentials (VEP), event related potentials (P300), and motor threshold were applied for each patient. Mean urinary vanil-mandelic acid (VMA) levels were estimated and used as index of serum levels of catecholamines. Blood samples for serum level of: oestrogen, nitric oxide (NO), and trace elements: : magnesium (Mg), zinc (Zn), copper (Cu), and selenium (Se) were estimated. Control group was subjected to the same batteries of investigations as above. Age of the patients were ranged from 17 to 40 years. Patient group included 30 females (60%) and 20 males (40%) with a female: male ratio of 1.5:1. No correlation was found between the frequency of migraine attacks and the severity of EEG, ABR, VEP, P300 and the motor threshold changes. Thirteen patients (26%) have abnormal EEG records in the form of slowing of background or paroxysmal activity. Regarding to the abnormal EEG records, no statistically significant difference was found between patients during and in-between the attacks or between patients with aura or without aura. There was a significant prolongation of the absolute latency of ABR of both ears in patients compared to controls and significant prolongation of the interpeak latency III-V of the Lt ear in patients compared to controls. A significant prolongation of the latency of VEP both monocular and binocular was found in patients compared to controls, whereas no significant difference was found in respect to the amplitude of VEP. P300 latency was significantly prolonged, while the amplitude was significantly reduced in all patients compared to controls. Significant prolongation of the latency of P300 was found also in patients in-between attacks compared to those during the attacks. No significant difference in the latency or amplitude of P300 was found in relation to presence or absence of aura. Significant decrease in the motor threshold was found in patients compared to controls, also in patients during migraine attacks compared to those in-between the attacks. In 70% of the cases, there was a statistically significant increase in urinary VMA levels compared to control suggesting sympathetic over activity. In thirty female patients with migraine, there was statistically significant decrease in serum estrogen levels (esradiol) in twenty patients. A statistically significant higher serum levels of zinc and copper were seen in patients with migraine compared to control group, while differences in magnesium, nitric oxide, and selenium levels were statistically non significant. In comparing the serum level of these elements, no statistically significant difference could be detected between those during and in-between the attacks. The present study demonstrated a significant increase of the serum level of nitric oxide in patients with migraine with aura compared to those with migraine without aura, whereas no statistically significant difference can be observed between the two patient groups in the serum level of trace magnesium, zinc, copper, and selenium. In conclusion, evoked potentials (ABR, VEP, P300, motor threshold) and EEG studies suggests increased excitability of the nerve cells in patients with migraine, which can be used as nonspecific tools for diagnosis of migraine. Changes in trace elements, nitric oxide, catecholamines, and estrogen indicate the multiple mechanisms that may play role in pathophysiology of migraine. (Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(1): 293-299). Egypt J. Neurol. Psychiat. Neurosurg. Vol. 44 (1) – Jan 2006