The pathophysiology of migraine and its associated perceptual symptoms remains controversial. We recorded long-latency auditory event related potentials (AEPs) in 30 unmedicated patients with common migraine, and compared them to 20 controls. 1,000 and 3,000 Hz tones were presented in an 80:20 ratio at 75 dB SL. 200 responses were recorded and replicated from Cz-A1 + A2, with filter band-pass of 1-100 Hz, analysis time of 1,000 ms., and interstimulus interval of 1.1 second. N100, P200, and N200 ERP components did not differ in latency or amplitude between migraine patients and controls. P300 was longer in latency among those with common migraine, and P300 amplitude was significantly reduced (P greater than 0.05). These findings suggest that migraine may have a central mechanism, and that migraineurs may have a difference in task involvement or perception which may influence their clinical course and response to therapy.
The interictal EEG is often normal in epilepsy patients, particularly with partial seizures of extratemporal origin. Quantitative techniques of EEG analysis may increase the yield of diagnostic abnormality in such patients. Thirty patients with partial seizures of frontal or temporal origin had EEG recorded from left frontal (F7-C3), right frontal (F8-C4), left posterior (T5-O1), and right posterior (T6-O2) derivations. Four-second epochs were used to compute power in the delta (0.25-4.0 Hz), theta (4.25-8.0 Hz), alpha (8.25-13 Hz), and beta (13.25-30 Hz) bands. The ratio of high (8.25-30 Hz) to low (0.25-8 Hz) power on the left and the right was measured, as was the ratio between the left and the right hemisphere total power. The mean frequency deviation in the alpha band between the left and the right hemispheres was also measured, and spectral mobility was determined in the right and the left frontal regions. These values were also calculated in normal subjects and tension headache patients with normal EEGs. Seizure patients with abnormal interictal EEGs had decreased ratios of high to low power, greater asymmetry of total power and alpha frequency, and reduced spectral mobility on the side of their EEG foci. Epileptics with normal interictal EEGs had lower ratios of high to low power, greater alpha frequency asymmetry, and lower spectral mobility than did headache patients or normal controls. Power and frequency measurements, and determination of spectral measures such as mobility, can be done with commercially available digital EEG equipment. They may demonstrate otherwise obscure asymmetries in the interictal EEG and thereby aid in epilepsy diagnosis and classification.
The pathophysiology of anxiety has received much recent attention. EEG findings in anxiety are nonspecific, and some changes in psychophysiological measures have been reported. We recorded short-latency brainstem auditory evoked potentials (BAEPs) and long-latency auditory event-related potentials (AEPs) in 12 patients with generalized anxiety disorder. All 12 patients had BAEP latencies within clinical norms, but I-V interpeak latencies were significantly longer in patients with anxiety than controls. N1, N2, P2, and P3 AEP components were within normal limits; N1 and P2 were reduced in amplitude in anxiety patients, but differences from controls were not significant. The BAEP findings may suggest altered brain-stem function in anxiety, which has been implied by biochemical studies of anxiety and depression. AEP differences may be related to difficulties in concentration and attention direction reported by anxious patients.
Gilles de la Tourette syndrome (TS) has been increasingly studied neurophysiologically as well as clinically. Obsessive-compulsive disorder (OCD) and attention deficit disorder (ADD) have been recognized to be part of the continuum of TS. We recorded brainstem auditory evoked potentials (BAEPs) and long-latency auditory event-related potentials (ERPs) in 20 patients with TS, 10 of whom had ADD and 6 OCD. TS patients with and without OCD and ADD did not differ in BAEP latencies, and no differences were found from normal controls. AEP latencies did not differ between TS patients and controls. TS patients with ADD had longer N100 and N200 latencies than TS patients without ADD, and TS patients with OCD had shorter N200 and P300 latencies. These findings suggest that TS is neurophysiologically heterogenous, and that TS patients with OCD or ADD may differ from those without.
Seizure patients often complain of sleepiness or disturbed sleep. Although susceptible of medication effect, the multiple sleep latency test (MSLT) may quantify daytime sleepiness and help to establish whether qualitative sleep disturbance accompanies epilepsy. In order to measure daytime sleepiness in epilepsy patients, 30 patients with newly diagnosed or presently untreated complex partial seizures had MSLT after an overnight sleep EEG that showed no sleep deprivation or nocturnal seizures. Four 20-minute naps were undertaken at 09:00, 11:00, 13:00, and 15:00, and sleep latency was recorded along with 8 channels of EEG. Twenty of 30 seizure patients reported subjective sleepiness. Eight patients had average sleep latencies less than 8 minutes, and 3 had latencies less than 5 minutes. No sleep onset REM or respiratory disturbance was noted. Twenty-five patients had EEG abnormalities but none had ictal seizures. Right temporal epileptiform activity correlated with sleepiness. MSLT may quantify sleepiness in epilepsy patients, which is common but may be subjective or psychophysiological. Some patients with partial seizures have persistent daytime sleepiness independent of medication, possibly related to residual medication effects or non-specific effect of their epileptogenic foci.
Spindles are a ubiquitous phenomenon in sleep, but their physiology and the effects of neurologic disorder on their frequency and amplitude are incompletely understood. We compared the incidence of three commonly defined spindle types (14-15 Hz, 12-13 Hz, and 10 Hz) and the frequency and amplitude of spindles during Stage II sleep in 50 patients with complex partial, partial and secondarily generalized, and primary generalized seizures, with and without interictal behavioral symptoms. All patients had 12-13 Hz and 14-15 Hz spindles of symmetric character in C3-A1 and C4-A2 derivations during prolonged sleep-deprived EEG recordings, which were normal except for partial or generalized epileptiform activity. Seventy-one per cent of complex partial seizure patients had 10 Hz spindles, and they occurred in 50% of the other two groups, predominating among those with interictal behavioral symptoms in all groups. Spindle frequency was significantly less in patients with generalized epilepsy than with partial seizures, and patients with complex partial seizures and partial seizures with secondary generalization differed significantly in spindle frequency. Spindle frequency was significantly lower with polypharmacy than with monotherapy. Patients whose regimens included phenobarbital had significantly lower spindle frequencies and spindle frequencies differed significantly between phenytoin and carbamazepine. Differences in spindle frequency may be due to residual medication effects, underlying encephalopathy or physiological differences between partial and generalized epilepsy.
Brainstem auditory evoked potentials (BAEPs) are affected by stroke or migraine in the vertebrobasilar arterial system. Some studies have reported BAEP changes in vertebrobasilar transient ischemic attacks (TIAs), but others have shown no alterations. We recorded BAEPs in 35 patients with TIAs in the vertebrobasilar system who did not have a stroke, other neurologic disease or significant hearing loss. Thirty patients were recorded after resolution of symptoms, while five individuals still had some resolving signs or symptoms. TIA patients as a group had longer interpeak latencies, but I-III, III-V, and I-V latencies were not significantly longer than in controls. Wave V was significantly longer in latency and lower in amplitude in TIA patients, however. The patients whose TIAs had resolved at absolute and interpeak latencies were within normal limits, but three of five had interpeak latencies at or above three standard deviations beyond the normal mean in the still symptomatic group. One of these was later tested and found to be within normal limits. BAEPs after subsidence of symptoms may add little to the evaluation of vertebrobasilar ischemia, but further AEP analysis may show more definitive differences of diagnostic use. The occasional BAEP abnormality during the resolving transient ischemia supports the recently suggested continuum between ischemia and infarction in the vertebrobasilar territory.
Nightmares have long attracted neurologic and psychiatric attention, yet little is known of their pathophysiology. We recorded 17-channel electroencephalograms (EEGs), brainstem auditory evoked potentials (BAEPs), long-latency auditory event-related potentials (AEPs), and overnight cassette sleep EEGs (AEEGs) in 10 individuals with recurrent nightmares. They were all nocturnal sleepers, took no medications, do not abuse alcohol or drugs, and had no known medical or psychiatric illnesses. Five patients were being evaluated for other complaints, 3 reported disturbed nocturnal sleep and daytime sleepiness, and 2 sought attention chiefly for nightmares. All 10 patients had normal EEGs and BAEPs. BAEP latencies did not differ significantly from control subjects. Latencies and amplitudes of AEPs were not significantly different in nightmare sufferers and controls, but the former had higher amplitude N100, P160, and N200. Those patients with sleep complaints had on overnight AEEG, less sleep, decreased slow-wave sleep, and more awakenings than those without sleep complaints, but nightmares did not occur during the AEEG recordings.
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