Many headache patients complain of poor sleep, and sleep disturbance has been shown to play a role in chronic pain. We recorded nocturnal sleep with a 4-channel cassette EEG monitoring device in 10 common migraine patients, 10 individuals with muscle contraction (tension) headache, and 10 chronic tension-vascular headache sufferers. Migraine patients had essentially normal sleep, although rapid eye movement (REM) sleep and REM latency were increased. Patients with tension headache had reduced sleep time and sleep efficiency, decreased sleep latency but frequent awakenings, increased nocturnal movements, and marked reduction in slow wave sleep, without change in REM sleep or latency. Mixed-element headaches with both tension and vascular features were associated with reduced sleep, increased awakening, diminished slow wave sleep, and REM sleep that was decreased in amount and reduced in latency. The findings suggest that patients with intermittent migraine may have minimal sleep disturbance, while chronic headache may be worsened by chronically poor sleep. Muscle contraction headache may be associated with frequent awakenings and decreased slow wave sleep similar to the sleep changes of fibrositis, while chronic tension-vascular headache may have a depressive substrate. Four-channel sleep recording may miss contributory sleep apnea, but nonetheless cassette EEG may facilitate outpatient evaluation of refractory headaches.
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.
The Contingent Negative Variation (CNV) may measure arousal and attention, and is affected by various dopaminergic disorders. We recorded CNVs in 12 patients fulfilling diagnostic criteria of Gilles de la Tourette Syndrome (TS). Ten of 12 patients were male, 10 had attention deficit disorder (ADD), and 3 also had obsessions and compulsions (OCD). Medication had been stopped or TS treatment not yet started. TS patients had higher CNV amplitude and more frequent postimperative negative variation than controls. CNV2 was enhanced in all TS patients, while CNV1 was attenuated in TS patients with ADD or OCD. This suggests that CNV may be increased in TS, mostly because of CNV2 and perhaps due to dopaminergic excess. CNV2, considered to reflect adrenergic arousal mechanisms, may be effected by neurobehavioral concomitants of TS. Neurophysiological categorization of TS patients may be possible and valuable.
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.
Sudden unexpected death associated with epilepsy (SUDEP) is an important clinical problem. Peri-ictal autonomic dysfunction is thought to play a role in SUDEP and few means exist for clinical identification of patients at risk. Sympathetic function was assessed by measuring sympathetic skin responses (SSR) elicited in the hand by auditory or tactile stimulation or by inspiration. Parasympathetic function was assessed by recording the R-R interval (RRI) and determining its variability in subsequent heartbeats. Fifty epilepsy patients had significantly greater SSR amplitudes and latencies than controls. The RRI was shorter in patients than in controls and the mean successive difference (MSD) was less, but significance was not reached. Twenty patients at possible risk for SUDEP (male, generalized seizures, intermittent medication noncompliance, drug and alcohol abuse, traumatic or structural aetiology) differed significantly from controls in SSR and RRI. Epilepsy patients may differ in autonomic function from the general population, and these differences may be relevant to SUDEP. The SSR and the RRI may be a simple means of assessing autonomic function in epilepsy outpatients.
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