Sharon A. Hietter

Cassette EEG sleep recordings in Gilles de la Tourette syndrome

Tourette syndrome (TS) patients often complain of sleep problems, and questionnaire studies indicate that sleep disturbance is frequent. Decreased slow wave sleep and increased awakenings have been reported in laboratory polysomnography in TS patients, and a serotoninergic disorder of arousal has been postulated. We recorded outpatient sleep in 20 patients newly diagnosed with TS utilizing a 4-channel cassette EEG system. The newly-diagnosed patients were predominantly male, and ranged in age from 10 to 36 years. Some had taken psychotropic medications in the past, but none had been treated systematically for TS. Seven patients had chronic tics only, 8 had tics and attention deficit-hyperactivity, and 5 had tics plus obsessions and compulsions. None had other medical, neurologic, or psychiatric disorders. All were nocturnal sleepers, and were recorded in their usual sleeping environments and routines. TS patients had reduced sleep, decreased sleep efficiency, increased awakenings, and decreased slow wave sleep. Tic patients had increased nocturnal awakenings and movements, particularly those who had tics during sleep. Sleep fragmentation and loss of slow wave sleep was most marked in TS patients with attention deficit-hyperactivity. Sleep latency was increased, REM sleep reduced, and REM sleep latency decreased in TS patients with obsessions and compulsions. These findings accord with previous reports of sleep disturbance in TS, and suggest that these disturbances may vary with TS symptoms. Chronic tics may persist in sleep and cause awakenings, TS with attention deficit may be associated with a disorder of arousal and alertness, and obsessions and compulsions may be manifestations of a biochemical disturbance involving paradoxical sleep.

Auditory Evoked Potentials in Gilles de la Tourette Syndrome

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.

Auditory event related potentials in violent and nonviolent prisoners.

SummaryThe neurophysiologic substrates of violence and aggression have been extensively studied. Although the EEG is often normal in violent persons any abnormalities are generally nonspecific in nature. Evoked potentials have been infrequently used to study such behavior disorders. Long latency auditory event-related potentials (AEPs) were studied in prison inmates incarcerated for unmotivated violent crimes or violence during the commission of other crimes, and in prisoners jailed for non-violent offenses. Habitually violent inmates were compared with an equal number of non-violent prisoners and neurologically and audiologically intact controls. AEPs were recorded to an “oddball” paradigm from vertex and left and right temporal electrodes. None of the prisoners had latencies more than 3 standard deviations beyond the normal group mean. N1 and P2 components were longer in latency and lower in amplitude in prisoners than in controls, but this was not statistically significant. Violent and non-violent individuals did not differ in these measures. P3 was significantly prolonged in latency in violent inmates, but not in those who had committed a violent act. All components were longer in latency on the right in violent prisoners, while amplitudes were lower but not significantly so. This asymmetry was not present in non-violent prisoners or control subjects. Caution is needed in identifying differences between criminals and the general population, and in seeking markers of violent behavior. These findings may indicate cerebral dysfunction in some perpetrators of antisocial behavior, however, and suggest that evidence of non-dominant cerebral hemisphere dysfunction, possibly subtle and chronic, may be found in some habitually violent individuals.

EEG and Evoked Potentials in Episodic-Dyscontrol Syndrome

The neurophysiologic correlates of explosive rage and violence are uncertain and controversial. We recorded 17-channel electroencephalograms (EEGs), brainstem auditory-evoked potentials (BAEPs), and long-latency auditory-event-related potentials (AEPs) in 23 patients with impulsive, aggressive and violent behavior satisfying criteria for episodic-dyscontrol syndrome. Most patients also satisfied criteria for intermittent explosive disorder, although some had had conduct disorders in childhood or had previously used psychoactive substances. Sixteen of 23 patients had normal EEGs, while 7 had diffuse or focal slowing not ascribable to drowsiness or the effects of medication. They differed significantly from 20 age-matched patients with headaches, of whom 1 had an abnormal EEG (chi 2 = 4.68, p < 0.05), and from 24 depressed patients, all of whose EEGs were normal (chi 2 = 4.83, p < 0.05). Patients and normal control subjects did not differ in BAEP latencies. N100 and P160 AEP amplitudes were lower in episodic-dyscontrol patients than in control, but the difference was not significant. These findings suggest that non-specific cerebral dysfunction and EEG changes may be associated with disordered impulse or behavior control. Episodic dyscontrol may be associated with other evidence of minimal brain dysfunction.

Auditory Evoked Potentials in Anxiety Disorder

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.

Electroencephalography in childhood conduct and behavior disorders.

The pathophysiology of behavior disorders in children is controversial. In particular, the relationship of episodic behavior disturbance to epilepsy and chronic behavior problems to subclinical neurologic disorder has been debated. It has been suggested that EEG may assist in this sometimes difficult determination. We report on routine screening EEGs in children hospitalized over an 18-month period for behavior problems. Eighty-six children were admitted for conduct disorder, attention deficit hyperactivity disorder, or both. Seventy-eight tracings (91%) were normal or showed normal variant patterns. Eight records (9%) were abnormal, showing background slowing or paroxysmal discharges not associated with behavioral manifestations. None of these neurologically normal, nonretarded patients had epilepsy or other known cerebral disorder. This suggests that routine EEG screening may be of limited value in childhood behavior problems without clinical evidence of neurologic disorder.

Computerized EEG Frequency Analysis in Gilles de la Tourette Syndrome

EEG abnormality has been reported in Gilles de la Tourette Syndrome but not confirmed in later studies. We carried out computerized EEG frequency analysis in 30 patients with the disorder, using Nicolet Pathfinder II frequency analysis software, versions 1.2 and 3.1 EEG was recorded from 01-A1+A2, 02-A1+A2, Fz-A1+A2, F7-C3, F8-C4, T5-01, and T6-02 in Tourette Syndrome patients and controls. Controls were taking no medications, and drug therapy for Tourette Syndrome had been stopped or not yet initiated in the patient group. Modal alpha frequency (MAF), maximal alpha frequency (MxAF), and spectral edge frequency (SEF) was measured in occipital and frontal derivations in 24 patients and controls. Left frontal (MOLF) and right frontal (MORF) mobility was calculated in F7-C3 and F8-C4 in 21 patients and controls. No significant differences were found between Tourette Syndrome patients and controls by two-tailed t-test. These findings are in accord with recent evidence of little or no EEG abnormality in Tourette Syndrome patients as compared to normals.

Auditory Evoked Potentials in Narcolepsy and Sleep Terrors

Dysfunction of brainstem reticular activating centers has been suggested in some sleep disorders, including narcolepsy and sleep terrors. Previous studies have suggested normal brainstem auditory evoked potentials (BAEPs) in narcolepsy and enhancement of long-latency auditory event-related potentials (ERPs) in sleep deprivation and conditions of pathological somnolence. Sleep terrors have not to date been studied neurophysiologically. We recorded early latency BAEPs and long-latency auditory ERPs in 8 patients with narcolepsy and 5 individuals with sleep terrors, and compared them to 10 normal controls. Narcolepsy patients and controls did not differ significantly in absolute or interpeak latency of BAEPs. Sleep terror patients had significant prolongation relative to controls of III-V and I-V interpeak latencies. The N1, N2, and P3 AEP components were prolonged in latency in narcoleptic patients as compared to controls, while sleep terror patients did not differ from controls. No significant differences in amplitude were found. These findings suggest that a disturbance of integration of brainstem centers subserving wakefulness and sleep may play a role in the disordered arousal of sleep terrors, but suggest no specific abnormality in brainstem function in narcolepsy. The AEP changes in narcolepsy may be a manifestation of pathological sleepiness.

Auditory evoked potentials in vertebrobasilar transient ischemic attacks

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.

Effects of carbamazepine and valproate on long-latency auditory event-related potentials

Abstract Seizure patients on anticonvulsant monotherapy were studied with long-latency auditory event-related potentials (ERPs). Twenty non-epileptic controls were compared with 10 patients taking carbamazepine (CBZ) and 13 patients taking valproate (VPA). Patients taking CBZ had significantly longer N1 and NII latencies than controls or patients on VPA. These findings suggest that CBZ and VPA may have differential effects on the hippocampal and limbic structures, which are thought to generate ERPs and may be related to the effects of antiepileptic drugs and behavior. No significant differences were noted between controls or patient groups in latency of the PII or PIII components.