Abnormal nocturnal melatonin secretion and disordered sleep in abstinent alcoholics.

BACKGROUND: Alcoholic patients show prominent disturbance of sleep as measured by electroencephalogram, with difficulties in the onset and maintenance of sleep. Given the role of melatonin in the regulation of the sleep-wake cycle, this study examined the relationship between nocturnal expression of melatonin and sleep in alcoholics as compared with control subjects. METHODS: Alcoholic patients (n = 11) and comparison control subjects (n = 10) underwent all-night polysomnography and serial blood sampling every 30 min from 10:00 PM to 6:30 AM for measurement of circulating levels of melatonin and cortisol. RESULTS: Coupled with prolonged sleep latency, alcoholics showed lower levels of melatonin during the early part of the night and a delay in the onset of the nocturnal plateau or peak value of melatonin as compared with control subjects. The nocturnal delay of melatonin correlated with prolonged sleep latency. Circulating levels of cortisol were lower during the early part of the night and higher in the late part of night in the alcoholics as compared with the control subjects. CONCLUSIONS: A delay in the nocturnal rise of melatonin may contribute to disordered sleep in chronic alcoholics, with implications for the use of melatonin in the treatment of insomnia in recovering alcoholics.     

Increased nocturnal interleukin-6 excretion in patients with primary insomnia: a pilot study

The aim of the present study was to investigate whether there is a difference in evening/nocturnal interleukin-6 (IL-6) serum excretion in patients with primary insomnia compared to controls. We hypothesized that in insomniac patients, the excretion of evening/nocturnal IL-6 is enhanced, like observed in aged adults and after sleep deprivation in healthy subjects. We studied IL-6 serum concentrations in 11 patients (two males and nine females) with primary insomnia and 11 age and gender-matched healthy controls. Sleep was monitored polysomnographically for three consecutive nights. The measurement of IL-6 (from 19:00 h to 09:00 h) in 2-h intervals were performed prior to and during the last laboratory night. Polysomnographically determined sleep parameters and subjective ratings of sleep demonstrated clear-cut impairments of sleep in the insomniac group. Nocturnal IL-6 secretion was significantly increased (p<.05) in insomniac patients for the whole measurement period (mean area under the curve+/-SD: 27.94+/-14.15 pg/ml x 2h) compared to controls (16.70+/-7.64 pg/ml x 2h). Total IL-6 secretion correlated inversely with subjectively perceived sleep quality and amount of slow wave sleep in the insomniac patients. Amount of Wake Time correlated positively with IL-6 excretion in insomniacs. The results of the present study demonstrate significantly increased nocturnal IL-6 secretion in insomniacs. It might be speculated that chronic primary insomnia with polysomnographically documented sleep impairments activates the production of IL-6 analogous to sleep deprivation studies in healthy subjects. This might also implicate a higher risk for inflammatory and cardiovascular diseases in patients with chronic insomnia.     

Repeated nocturnal sleep latencies in narcoleptic, sleepy and alert subjects.

OBJECTIVES: The purpose of this study was to assess nocturnal sleep latencies among narcoleptics. METHODS: Thirteen narcoleptics and matched sleepy and alert controls participated in this study. Subjects were awakened three times on each of two experimental nights. The latencies to sleep and rapid eye movement sleep were evaluated at the beginning of the night and following each experimental awakening. RESULTS: The alert group (AG) had a significantly longer mean nocturnal sleep latency than the narcoleptic (NG) and sleepy groups (SG). The sleep latencies at 23:00 and 01:10 h were significantly longer than the latencies at 03:10 and 05:10 h. The interaction between group and time of night demonstrated longer latencies at 23:00 and 03:10 h for the AG when compared to the SG and the NG. At 01:10 and 05:10 h all groups had comparable latencies. The number of subjects in the NG who had multiple sleep onset REM periods (SOREMPs) was significantly higher than in either the AG or the SG. CONCLUSIONS: Narcoleptics were found to have a heightened propensity to fall asleep and increased number of SOREMPs during nocturnal sleep opportunities. These characteristics are consistent with the daytime polysomnographic findings known in this patient population.     

Sleep-wake behavior and responses of interleukin-6-deficient mice to sleep deprivation

Interleukin (IL)-1 and tumor necrosis factor (TNF) are involved in the regulation of non-rapid eye movements sleep (NREMS). Accumulating evidence suggests IL-6 modulates sleep under some pathophysiologic conditions. We used mice lacking a functional IL-6 gene to investigate further a potential role for IL-6 in the regulation of sleep. IL-6 knockout mice (B6.129S6-Il6tm1Kopf; n=10) and C57BL/6J mice (n=10) were purchased from the Jackson Laboratory (Bar Harbor, ME). Twenty-four-hour baseline recordings were obtained from mice in the absence of any experimental manipulation. Mice were then subjected to 6-h sleep deprivation beginning at light onset. Recordings were obtained during the deprivation period and for 18 h thereafter. During baseline conditions there were no differences between mouse strains with respect to the duration, timing or intensity of NREMS. However, across the 24-h recording period IL-6 knockout mice spent approximately 30% more time in rapid eye movements sleep (REMS) than did C57BL/6J mice. Relative to C57BL/6J mice, core body temperatures of IL-6 knockout mice were higher during the light period of the light:dark cycle. Both strains responded to sleep deprivation by spending more time in NREMS and REMS. Although the total increase in the amount of NREMS after sleep deprivation was the same in both strains, IL-6 knockout mice took 6h longer to accumulate this additional sleep. Under the conditions of this study, IL-6 does not appear necessary for the full manifestation of NREMS, although this cytokine may influence the dynamics of responses to sleep deprivation. That mice lacking IL-6 spend more time in REMS suggests that interactions between IL-6 and REMS regulatory mechanisms may differ from those of IL-1 and/or TNF.     

Changes in subjective sleepiness, subjective fatigue and nocturnal sleep after anaesthesia with propofol

The purpose of this study was to clarify the changes in psycho-physiological functions after anaesthesia with propofol (PF). The subjects were seven healthy male volunteers and the duration of the anaesthesia was 1 h (14:00-15:00 h). The plasma concentration of PF immediately decreased after the anaesthesia. The subjective sleepiness and VAS (visual liner analogue scale) scores (i.e. effort to do something) increased significantly at 20 min after the anaesthesia. However, these changes were improved at 80 min after the anaesthesia. The sleep latency at the nocturnal sleep 8 h after the anaesthesia was prolonged significantly, but the other parameters including the distributions of stage 3 + 4 and the rapid eye movement 'REM' stage were not changed.     

Differential effects of scopolamine on nocturnal cortisol secretion, sleep architecture, and REM latency in normal volunteers: relation to sleep and cortisol abnormalities in depression

Scopolamine (SCOP) (3.0 mu/kg and 6.0 micrograms/kg) and saline were administered intramuscularly at 11:00 PM to eight normal male volunteers in a randomized design, and the effects on the sleep electroencephalogram (EEG) and nocturnal cortisol secretion (via blood sampling every 15 min) were evaluated. Compared to saline, SCOP produced a significant dose-related delay in rapid eye movement (REM) latency. In contrast, neither dose of SCOP significantly affected nocturnal plasma cortisol concentrations. These results suggest that the central cholinergic system that regulates the onset of REM sleep is more sensitive to dysregulation than the cholinergic system that controls the degree of nocturnal cortisol secretion. If central cholinergic overactivity is responsible for both the REM sleep latency and cortisol abnormalities in depressed patients, then our findings with SCOP might help explain why the incidences of these abnormalities are different.     

Objective measurement of sleepiness in summer vacation long-distance drivers

The study investigated whether sleepiness at the wheel is a problem in non-commercial drivers going on summer vacation. All drivers, who stopped at a rest area on a large European freway while one of the interviewers was available, were systematically approached and asked to respond to a questionnaire. All subjects who had driven at least 400 km (240 miles), whose age was between 20 and 46 years of age, and who agreed to participate were asked to undergo a longer investigation that included a short sleep/wake diary describing overall sleep habits during the year, a sleep/wake log covering the days just prior to departure, an analog visual scale indicating sleepiness at time of interview, and a polygraphically monitored two nap sleep test (TNST). A control group was recruited that consisted of subjects of the same age range, normal sleep habits, and normal nocturnal sleep time before administration of the TNST. One hundred and four drivers (2 women) participated between 08:00 and 20:00 h. The total group was subdivided into 6 subgroups based upon the time of day of their investigation (08:00–10:00 h, 10:01–12:00 h, etc.). The control group included 50 men with 50–55% of control subjects, relative to the total number of index-cases, in each subgroup. Eighty-eight percent (n =92) of studied drivers had experienced acute sleep deprivation within one day prior to departure due to the planned long driving. The TNST demonstrated that, overall, drivers had a significantly shorter sleep latency in nap 1 and nap 2 than controls, had a significantly longer sleep duration in nap 1 and nap 2, and there was a significant correlation between the sleep debt prior to departure and the sleep stage reached during the TNST. It is concluded that the TNST is a test which allows the objective study of sleepiness in drivers without the burden of the multiple sleep latency test. Many drivers are excessively sleepy when making long summer vacation journeys.     

Diurnal variations of interleukin-6 plasma levels are confounded by blood drawing procedures

Recent findings suggest that inflammatory cytokines are involved in sleep regulation. In part, this idea is based on studies showing that systemic levels of interleukin-6 (IL-6) are affected by sleep and sleep deprivation. However, intravenous (IV) catheters used for repetitive blood sampling were reported to increase local IL-6 production, which might confound sleep-dependent or circadian changes in the plasma concentrations of this cytokine. To further examine the effects of blood drawing procedures on IL-6 plasma levels, 12 healthy young male subjects participated in a 24-h cross-over study protocol involving sleep and sleep deprivation. Blood was collected half-hourly through an IV line and one additional sample was taken by a simple needle stick from the contralateral arm in parallel to the last sample from the catheter. Difficulties in blood sampling, the plasma levels of IL-6, cortisol and subjective sleepiness were quantified. In samples from the IV line there was a linear increase in IL-6 levels in both conditions, whereas the amount of IL-6 detected in the needle stick sample at the end did not differ from baseline. IL-6 levels were significantly higher in samples rated as difficult and those difficulties were more frequent during sleep compared to nocturnal wakefulness. IL-6 levels did not correlate to variations in sleepiness or cortisol levels. We conclude that variations in IL-6 plasma levels measured in samples from an IV catheter are caused, at least in part, by changes in local cytokine production rather than by physiological changes in circulating IL-6 levels.     

The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults

Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders. Few studies have examined how sleep deprivation acutely affects inflammatory markers, which was the aim of the current study. Nineteen healthy men and women aged 28.05+/-8.56 (mean+/-SD) were totally sleep deprived for 40 h under constant routine conditions. Pro-inflammatory markers: intracellular adhesion molecule-1 (ICAM-1), E-selectin, vascular adhesion molecule-1 (VCAM-1), c-reactive protein (CRP), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta), and the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1ra) were assayed in plasma. Daytime levels during baseline (hours 1-15 of scheduled wakefulness) were compared to daytime levels during sleep deprivation (hours 25-39 of scheduled wakefulness), thus controlling for circadian phase within an individual. Repeated measures ANOVA with planned comparisons showed that 40 h of total sleep deprivation induced a significant increase in E-selectin, ICAM-1, IL-1beta, and IL-1ra, a significant decrease in CRP and IL-6, and no significant change in VCAM-1. Alterations in circulating levels of pro- and anti-inflammatory cytokines and cell adhesion molecules during sleep deprivation were consistent with both increased and decreased inflammation. These findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.     

Sleep loss activates cellular markers of inflammation: Sex differences

Sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. Given sex differences in the prevalence of inflammatory disorders with stronger associations in females, this study was undertaken to test the effects of sleep loss on cellular mechanisms that contribute to proinflammatory cytokine activity. In 26 healthy adults (11 females; 15 males), monocyte intracellular proinflammatory cytokine production was repeatedly assessed at 08:00, 12:00, 16:00, 20:00, and 23:00 h during a baseline period and after partial sleep deprivation (awake from 23:00 to 3.00 h). In the morning after a night of sleep loss, monocyte production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) differentially changed between the two sexes. Whereas both females and males showed a marked increase in the lipopolysaccharide (LPS) — stimulated production of IL-6 and TNF-α in the morning immediately after PSD, production of these cytokines during the early- and late evening was increased in the females as compared to decreases in the males. Sleep loss induces a functional alteration of monocyte proinflammatory cytokine responses with females showing greater cellular immune activation as compared to changes in males. These results have implications for understanding the role of sleep disturbance in the differential risk profile for inflammatory disorders between the sexes.     

Systemic immune parameters and sleep after ultra-low dose administration of IL-2 in healthy men

A somnogenic function is suspected for various cytokines. Foregoing experiments in humans indicated a selective increase in the production of interleukin-2 (IL-2) during sleep as compared with nocturnal wakefulness. Here, we examined whether conversely, IL-2 exerts a promoting influence on sleep. Also, the effects of IL-2 administered at ultra-low doses on systemic immune and endocrine parameters were assessed. Eighteen healthy men participated in three night sessions, receiving subcutaneously at 19:00 h either placebo or recombinant human IL-2 at doses of 1000 and 10,000 IU/kg bw. Polysomnographical recordings were obtained between 23:00 and 07:00 h. Blood was collected repeatedly to determine (i) white blood cell (WBC) counts including the enumeration of monocytes, natural killer (NK) cells, and lymphocyte subsets, (ii) serum concentrations of IL-2, soluble IL-2 receptor (sIL-2r), IL-4, IL-6, and interferon-gamma (IFN-gamma), and (iii) concentrations of adrenocorticotropin (ACTH), cortisol, thyreotropin (TSH), and growth hormone (GH). Changes after 1000 IU/kg bw IL-2 generally remained non-significant. However, distinct effects occurred after 10,000 IU/kg bw IL-2, inducing serum IL-2 concentrations selectively activating the high affinity IL-2 receptor. At this dose, IL-2 reduced the number of circulating lymphocytes (including all major subtypes) and NK cells, while counts of monocytes and neutrophils were increased. IL-4 release was stimulated and IFN-gamma concentration reduced after IL-2. Also, IL-2 increased the TSH concentration. There were no hints at a sleep promoting effect of IL-2. Immune changes suggest that nocturnal IL-2 administration induces a shift towards Th2 mediated defense.     

Diurnal and sleep-wake dependent variations of soluble TNF- and IL-2 receptors in healthy volunteers

There is very little published information on the diurnal variation of cytokines and their receptors, in healthy individuals during normal sleep-wake patterns or during sustained wakefulness. The aim of the current investigation was to characterize concentrations of soluble tumor necrosis factor receptors (sTNF-Rs) and interleukin-2 receptor (sIL-2R) during normal sleep and wakefulness, as well as during a 24 h vigil. Plasma levels of the sTNF-R p55, sTNF-R p75, and sIL-2R did not differ significantly between nocturnal sleep and nocturnal wakefulness. Rhythmic analysis (2-h intervals) revealed significant diurnal variations for both sTNF-R p55 and sTNF-R p75, but not levels of sIL-2R. Diurnal variations of both sTNF-Rs were characterized by a single cosine curve with an average peak near 06:00 h in the morning. This peak occurred well before that of cortisol, and fluctuated inversely with the diurnal rhythm of temperature. These diurnal variations in sTNF-Rs levels are consistent with the hypothesis that the TNF system plays a role in normal diurnal temperature regulation.     

Oculomotor impairment after 1 night of total sleep deprivation: a dissociation between measures of speed and accuracy.

OBJECTIVES: The present study examined the effects of 40 h of sleep deprivation and of time-of-day on saccadic and smooth pursuit oculomotor performance. METHODS: Nine normal subjects slept for 3 consecutive nights in the laboratory (one adaptation, one baseline, one recovery). Baseline and recovery were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every 2 h. Oculomotor performance assessed at the following hours: 10:00, 12:00, 14:00, 16:00, 18:00, 20:00, 22:00, of both the days preceding and following the sleep deprivation night, as well as at 24:00, 02:00, 04:00, 06:00 and 08:00 h during the deprivation period. RESULTS: Saccade latency increased and peak velocity decreased significantly during the post-deprivation day; saccadic accuracy was unaffected. As regards smooth pursuit performance, phase (a measure of accuracy) was not affected by sleep loss, while velocity gain significantly decreased during the day that followed the sleep deprivation night. Significant time-of-day effects on the considered oculomotor variables except saccadic accuracy were also found, indicating an overall performance impairment during the night. CONCLUSIONS: It is concluded that 40 h of sleep deprivation significantly impaired diurnal performance in pursuit and saccadic tasks. This performance worsening is limited to the measures of speed, while accuracy is not affected by sleep loss. A significant operational relevance of these results is suggested, since saccadic velocity has recently been found to be negatively correlated with simulator vehicle crash rates.     

The effect of stimulants on nocturnal motor activity and sleep quality in adults with ADHD: an open-label case-control study.

OBJECTIVE: Sleep disturbances are common in adults with attention-deficit/hyperactivity disorder (ADHD). In a case-control study, adult ADHD was associated with increased nocturnal motor activity and reduced self-perceived quality of sleep. METHOD: Eight adults with DSM-IV-diagnosed ADHD (combined type, N = 7; inattentive type, N = 1) were treated with stimulants in open-label form at 8:00 a.m., 12:00 noon, and 4:00 p.m. The mean daily dose was 51 mg of methylphenidate (range, 30-90 mg) in 7 subjects and 30 mg of dextroamphetamine in 1 subject. Actimeters were used to assess nocturnal motor activity during 6 consecutive nights both at baseline and after 3 weeks of treatment. The data were compared with those of 8 matched normal controls. RESULTS: ADHD patients slept worse and showed significantly higher nocturnal motor activity at baseline compared with controls. No baseline differences between patients and controls were found in sleep latency, number of awakenings, and total time in bed. Changes from baseline to week 3 within the ADHD patients indicated improvement of sleep quality (p = .05) and reduction of Activity Level (p = .10) and Movement Index (p = .07) scores. When within-group changes were compared between ADHD subjects and controls, treatment with stimulants tended to be associated with a reduction of Activity Level (p < .01) and Movement Index (p = .04) scores and improved sleep quality (p = .02) in ADHD patients. Sleep latency, number of awakenings, and total time in bed were unaffected in within-group and between-group analyses. CONCLUSION: The results should be interpreted cautiously given the open-label design and small sample size. Further study is warranted into the influence of stimulants on sleep in larger samples of ADHD patients by using controlled designs, multiple dose levels, and polysomnographic measures.     

Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol

Numerous studies have evaluated the sleep homeostasis of rats after short- or long-periods of sleep deprivation, but none has assessed the effects of prolonged sleep restriction on the rat's sleep pattern. The purpose of the present study, therefore, was to evaluate the sleep homeostasis of rats under a protocol of chronic sleep restriction. Male Wistar rats were implanted with electrodes for EEG and EMG recordings. Using the single platform method, the animals were submitted to 18 h of sleep restriction, beginning at 16:00 h (lights on at 07:00 h), followed by a 6 h sleep window (from 10:00 h to 16:00 h) for 21 days. Immediately after this period, rats were allowed to sleep freely for 4 days (recovery period). The sleep–wake cycle was recorded throughout the entire experiment and the results showed that during the 6 h sleep window there was an increase on the percentage of sleep time, reflected by augmented time in high amplitude slow wave sleep and in paradoxical sleep, when compared to baseline sleep, whereas bouts of awakening longer than 1.5 min were greatly reduced, with the animals exhibiting a monophasic-type sleep pattern. During the deprivation period, paradoxical sleep was abolished. High amplitude slow wave sleep was also greatly affected by the protocol. Nonetheless, one day of recovery was sufficient to restore the normal sleep pattern. These findings indicate that this protocol was capable to induce many changes in the rat's sleep patterns, suggesting that during the 6 h sleep window there is a sleep adaptive homeostatic process.     

The effects of caerulein on nocturnal, sleep

1. Caerulein, a decapeptide chemically related to cholecystokinin octapeptide, was examined polysoninographically for its effect on nocturnal sleep in healthy volunteers.

2. The subjects were 6 males (20–24 years of age). Either a placebo (saline) or caerulein 0.6 μg/kg was administered intramuscularly to volunteers at 23:00.

3. Polysomnograms were then recorded from 23:00 till 06:30.

4. Little variation in sleep period time, total sleep time, sleep efficiency index, sleep latency, or REM sleep latency in the drug night were found as compared to the control night values.

5. The percentage of REM stage sleep increased significantly (P < 0.01) on the drug administered night, whereas the change in the percentages of each of the other stages was not significant.

6. The REM density of the vertical eye movements tended to increase on the drug night, but the density of the horizontal eye movements showed no change.

7. There were no changes in the spontaneous GSRs in either vola or dorsum manus.

8. As caerulein shows alpha-1 adrenergic receptor blocker activity, it is suggested that caerulein may increase REM sleep by affecting the central noradrenergic neurons.     

Growth hormone and cortisol secretion in relation to sleep and wakefulness.

The study investigated secretory patterns of growth hormone (GH) and cortisol in relation to sleep and wakefulness. Plasma hormone levels were monitored in 10 young men during baseline waking and sleeping, during 40 hours of wakefulness, and during sleep following deprivation. The normal nocturnal GH surge disappeared with sleep deprivation, and was intensified following sleep deprivation. Mean GH levels were higher during slow wave sleep (SWS) compared with other sleep stages. During sleep after deprivation, GH secretion was prolonged, and second GH peaks occurred in three subjects which were not associated with SWS. Average 24-hour cortisol levels were not altered by sleep deprivation or sleep following deprivation, but the nocturnal cortisol rise occurred approximately one hour earlier with sleep deprivation and one hour later with resumed sleep, compared to baseline. This effect on the timing of the rise is consistent with an initial inhibitory influence of sleep on cortisol secretion. The results demonstrate that: the nocturnal growth hormone surge is largely sleep-dependent; temporal associations between GH and SWS are not reliable after sleep deprivation; although the cortisol rhythm is not sleep-dependent, the timing of the cortisol rise may be influenced by sudden changes in the sleep-wake schedule.     

Effects of sleep and sleep loss on immunity and cytokines

Sleep is hypothesized to be a restorative process that is important for the proper functioning of the immune system. Severity of disordered sleep in depressed- and alcoholic subjects correlates with declines in natural- and cellular immunity and is associated with alterations in the complex cytokine network. Sleep loss has a role in mediating these immune changes as experimentally induced partial night sleep deprivation replicates the kind of sleep loss found in clinical samples and induces a pattern of immune alterations similar to that found in depressed- and alcoholic patients. Despite evidence that sleep and sleep loss have effects on immune processes and nocturnal secretion of cytokines, the clinical significance of these immune changes is not known. Moreover, in view of basic evidence of a reciprocal interaction between sleep and cytokines, further research is needed to understand whether alterations in cytokines contribute to disordered sleep in patient populations.     

Outpatient sleep recording during antiepileptic drug monotherapy

The effects of sleep and sleep deprivation on epilepsy are well known, but the effects of seizures and antiepileptic drugs (AEDs) on sleep have been less well studied. We recorded nocturnal sleep in 17 patients receiving antiepileptic monotherapy with ambulatory cassette EEG devices. Twelve patients had complex partial seizures and five had tonic-clonic convulsions. Two patients' seizures were largely nocturnal, and no seizures occurred during sleep recording. Five patients each were taking phenytoin (PHT), carbamazepine (CBZ), and valproate (VPA), and two were taking clonazepam (CZP), all with therapeutic serum levels and no toxic symptoms. Total sleep time was reduced, wakefulness increased, and sleep latency prolonged in partial seizures as compared with generalized epilepsy. REM sleep was reduced and its latency decreased in partial seizure patients. Both groups had decreased slow wave sleep; that of partial seizure patients was decreased more markedly. PHT increased sleep latency and decreased sleep time, and CBZ increased awakening and diminished slow wave and REM sleep. Patients taking VPA had slight reduction in slow wave sleep; those taking CPZ had decreased sleep and REM latencies. Epilepsy may affect nocturnal sleep, and the effects of partial and generalized seizure disorders may be different. AEDs may also have differential effects on nighttime sleep. These may prove important in the long-term management of epileptic patients.     

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.