Changes in Subjective-Objective Sleep Discrepancy Following Inpatient Cognitive Behavior Therapy for Insomnia.

Discrepancy between objective and subjective sleep parameters is a frequent symptom in persons suffering from insomnia. Since it has an impairing effect on daytime well-being and neglects possible positive objective improvements, it would be useful if it was treated. Apart from hypnotics, cognitive behavior therapy (CBT-I) is the therapy of choice for chronic forms of insomnia. However, there is limited information about whether CBT-I can also improve subjective-objective sleep discrepancy. We investigated a large sample of patients showing chronic forms of insomnia regarding their subjective-objective sleep discrepancy pre and post CBT-I. Objective sleep data were obtained from 3 nights (2 baseline nights and 1 night after therapy) using polysomnography in our sleep laboratory. All 92 patients participated in a 14-day inpatient program with CBT-I including psychoeducation about subjective-objective sleep discrepancy. Repeated measures analyses showed an improvement in subjective-objective sleep discrepancy parameters after CBT-I. Those parameters were also correlated with perceived quality of sleep. We conclude that CBT-I is a useful tool to improve subjective-objective sleep discrepancy in patients showing chronic forms of insomnia.

Ghrelin suppresses secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in women.

CONTEXT: Ghrelin has been shown to suppress secretion of LH and, less regularly, of FSH in male and female animals and human males. However, no such evidence exists for human females. OBJECTIVE: The aim was to study the effect of ghrelin on secretion of LH and FSH in women. DESIGN/PARTICIPANTS/INTERVENTION: Nocturnal (2000-0700 h) secretion profiles of LH and FSH were determined in six healthy women (age, 25.5±2.9 yr) twice, receiving 50 µg ghrelin or placebo at 2200, 2300, 2400, and 0100 h in this single-blind, randomized, crossover study. RESULTS: LH secretion after ghrelin injection as assessed by the area under the curve (4.01±1.37 mIU/min·ml) was significantly (P=0.031) lower than after placebo injection (5.46±1.33 mIU/min·ml). Also, FSH secretion after ghrelin injection (5.54±0.64 mIU/min·ml) was significantly (P=0.038) lower than after placebo injection (5.87±0.56 mIU/min·ml). LH pulses occurred significantly (P=0.007) less frequently after ghrelin injection (2.3±0.5) than after placebo injection (3.8±0.9). Accordingly, the interval between first and second LH pulse after treatment was significantly (P=0.002) longer after ghrelin injection (300±86 min) than after placebo injection (187±60 min). One of the six women exhibited clear FSH pulses, which overall paralleled LH pulses; two FSH and LH pulses occurred after ghrelin injection, but three occurred after placebo in this woman. CONCLUSIONS: This is the first report that ghrelin suppresses the secretion of LH and FSH in women. These findings resemble those in male and female animals and in men.

Ghrelin levels increase after pictures showing food.

The neuropeptide ghrelin is a major signal for food intake in various species including humans. After exogenous ghrelin administration, food intake and body weight increase in rodents. In normal human subjects, ghrelin administration increases self-rated appetite and calorie intake and prompts the imagination of favorite meals. It is unclear so far whether ghrelin levels are affected by external cues such as sight of food. We investigated the influence of pictures showing food compared to neutral pictures on ghrelin levels in young normal male subjects (n = 8). The study consisted of two consecutive sessions with a one-week interval. During each session, blood for later analysis of plasma concentrations of ghrelin was collected between 08:15 and 13:00 every 15 min (between 10:30 and 11:30 every 10 min). Breakfast and lunch was provided at 08:30 and 12:00, respectively. Fifty pictures were presented from 10:30 to 10:45 showing neutral images during the first session and food contents during the second session. As expected, ghrelin levels increased before each meal independent of the picture contents. In addition, ghrelin levels during the 30-min interval following the presentation of pictures with food increased significantly compared to the 30-min interval before this presentation (area under the curve (AUC): 188 % vs. 158 %, P < 0.05). The difference in the increases between the two picture conditions was also significant (P < 0.05). Our findings suggest that sight of food elevates ghrelin levels in healthy volunteers.

A double dissociation of memory impairments in major depression.

Sleep benefits the consolidation of both declarative and nondeclarative memories, however the question if these two memory systems profit from sleep in more or less similar ways is still under debate. Studying the on-line and off-line consolidation of declarative and nondeclarative memory tasks in depressed patients and healthy controls, we here present a clear double dissociation between memory systems and consolidation phases, suggesting radically different ways how sleep benefits memory consolidation. 37 medicated inpatients with an acute episode of major depression and 31 healthy controls were assessed using a nondeclarative (sequential finger tapping) memory task before and after a night with polysomnography, 27 of the depressed and 22 of the control subjects additionally performed a declarative (paired associates) task. Although depressed patients and control subjects did not differ in practice-dependent learning of the nondeclarative motor task in the wake state, healthy subjects showed overnight improvements in tapping performance of 11.4%, while the patients' performance decreased overnight by 11.5%. This pattern was reversed for the declarative task: While patients learned 33.5% less word pairs than controls in the wake state, overnight changes did not differ between the two groups. These results suggest a double dissociation of memory consolidation processes in major depression: Off-line memory consolidation in major depression is impaired for nondeclarative, but not declarative tasks. The same tasks in the wake state show a reversed pattern, with performance in declarative but not nondeclarative tasks being impaired in major depression.

Ghrelin in mental health, sleep, memory.

Ghrelin acts as a neuropeptide. It participates in sleep-wake regulation. After systemic ghrelin treatment nonREM sleep is promoted in male humans and mice. This effect is influenced by gender, time of administration and depression. Ghrelin does not modulate sleep in healthy women and during the early morning in male subjects. In depressed women REM sleep is diminished after ghrelin. In elderly men and depressed men sleep promotion by ghrelin was preserved. In rats after central ghrelin feeding and wakefulness increased. The nocturnal secretion pattern of cortisol, GH, LH, FSH and hypothalamo-pituitary-thyroid hormones are influenced by ghrelin. Furthermore ghrelin appears to be related to memory and to be involved in the pathophysiology of CNS disorders, particularly depression.

Effects of ghrelin on psychopathology, sleep and secretion of cortisol and growth hormone in patients with major depression.

Ghrelin showed antidepressant-like effects in mice. Furthermore, ghrelin influences sleep and the activity of hypothalamic-pituitary-adrenal (HPA) and somatotropic axis in healthy humans as indicated by increased cortisol and growth hormone (GH) plasma levels. Both sleep and the activity of these endocrine axes are disturbed in depression. We therefore studied the impact of ghrelin on psychopathology, sleep and secretion of cortisol and GH in patients with major depression. Depressive symptoms as assessed by a validated self rating scale ('Befindlichkeits-Skala', [mental state scale]), secretion profiles of cortisol and GH and sleep-EEGs were determined in 14 unmedicated patients with major depression (7 women) twice, receiving 50 µg ghrelin or placebo at 22:00, 23:00, 00:00, and 01:00 hours. Overall, depressive symptoms did not change significantly after ghrelin administration (placebo: 37 ± 8; ghrelin: 33 ± 10, p = 0.178). However, there was an improvement at trend level in men (placebo: 36 ± 9 to ghrelin: 30 ± 9, p = 0.093) but not in women. In men, ghrelin was associated with less time awake (placebo: 149.0 ± 11.1; ghrelin: 88.0 ± 12.2 min, p = 0.029) and more non-REM sleep (placebo: 263.2 ± 24.1; ghrelin: 304.9 ± 14.1 min, p = 0.027), in women with less REM sleep (placebo: 108.6 ± 15.7; ghrelin: 74.1 ± 13.8 min, p = 0.031) and longer REM latency (placebo: 49.9 ± 6.5; ghrelin: 85.6 ± 14.1 min, p = 0.019). In both sexes, ghrelin caused strong transient increases of GH and cortisol. In conclusion, our study may provide some initial indication that ghrelin can exert antidepressant effects in patients with major depression. Ghrelin strongly affected sleep and secretion of GH and cortisol in a partly different way as previously reported in healthy subjects.

Off-line memory consolidation impairments in multiple sclerosis patients receiving high-dose corticosteroid treatment mirror consolidation impairments in depression.

BACKGROUND: Sleep supports the consolidation of procedural memory, however patients with major depression show impaired motor memory performance after a night of sleep. It was hypothesized that this impairment is related to hypothalamic-pituitary-adrenal (HPA) axis dysfunction. We tested if high-dose administration of corticosteroids impairs off-line motor memory consolidation in patients with multiple sclerosis (MS). METHODS: Nine patients with MS receiving high-dose corticosteroid therapy (methylprednisolone) and nine MS patients receiving alternative therapy (mitoxantrone) were assessed using a sequential finger tapping task before and after a night with polysomnography. In addition, nine patients with major depression (MD) receiving antidepressants and nine healthy controls were assessed. RESULTS: Although the four groups did not differ in practice-dependent learning, healthy subjects and MS patients receiving mitoxantrone showed markedly overnight-improvements in tapping performance of 17% and 24% while MS patients receiving high-dose corticosteroid therapy and depressed patients showed -9% and -10% overnight decrease. MS patients with and without corticosteroid therapy did not differ in their amount of REM sleep, nor did MD patients and healthy controls. In addition, we did not find any correlation between REM sleep and memory consolidation. CONCLUSION: Our results show that a strong intervention into the HPA system like in MS high-dose corticosteroid therapy impairs off-line motor memory consolidation comparable to the impairments seen in depressed patients. We propose therefore that depression-related changes in plasma corticosteroid levels rather than in sleep per se underlie off-line memory consolidation impairments in MD.

Impaired off-line memory consolidation in depression.

Sleep is critically involved in the consolidation of procedural memory. In major depression (MD) and during antidepressant pharmacotherapy, changes in sleep EEG are well documented. Here, we test if off-line motor memory consolidation is impaired in MD. 50 medicated patients with an acute episode of MD, 50 normal controls and 12 patients with a remitted episode of MD were assessed using a sequential finger tapping task before and after a night of sleep. Although depressed patients and control subjects did not differ in practice-dependent learning, healthy subjects showed markedly overnight improvements in tapping performance of 18% while patients failed to show any improvement. This pattern became even more striking when the subjects were divided by an age threshold of 30years: In the 30+yrs group the healthy subjects showed 16% overnight increase in motor performance, whereas the patients showed -10% overnight decrease. In contrast, patients and controls in the

Sleep and active renin levels--interaction with age, gender, growth hormone and cortisol.

AIMS: In young normal male subjects, plasma renin activity (PRA) shows large oscillations with a distinct association to the cyclic occurrence of rapid eye movement (REM) and non-REM (NREM) periods. Until now the sleep-related course of active renin levels is unknown. Furthermore, there are no data on the effects of age and gender on nocturnal renin and the interaction between these variables, sleep, growth hormone (GH) and cortisol. METHODS: We investigated simultaneously sleep EEG (23:00-07:00 h) and the plasma concentrations (23:00-07:00 h) of active renin (in 10-min intervals) and of GH and cortisol (in 20-min intervals) in 47 healthy volunteers (24 women and 23 men) aged 19-69 years. RESULTS: In the total sample, significant positive correlations were found between renin concentrations and NREM sleep and the sleep efficiency index, whereas a significant negative correlation exists to wakefulness. Renin shows also a positive correlation to GH levels which is restricted to the younger subjects (<40 years) during NREM sleep. No association exists between renin and cortisol. The averaged nocturnal mean renin levels were significantly lower in female than in male subjects, and in subjects older than 40 years than in younger subjects. Oscillations of active renin levels were found with increases during NREM periods and decreases during REM periods. CONCLUSIONS: In all, nocturnal averaged renin levels are lower in women than in men, decrease during ageing and correlate positively with GH, whereas the interaction between renin and sleep is independent from age and gender.

Ghrelin increases slow wave sleep and stage 2 sleep and decreases stage 1 sleep and REM sleep in elderly men but does not affect sleep in elderly women.

Ghrelin increases non-REM sleep and decreases REM sleep in young men but does not affect sleep in young women. In both sexes, ghrelin stimulates the activity of the somatotropic and the hypothalamic-pituitary-adrenal (HPA) axis, as indicated by increased growth hormone (GH) and cortisol plasma levels. These two endocrine axes are crucially involved in sleep regulation. As various endocrine effects are age-dependent, aim was to study ghrelin's effect on sleep and secretion of GH and cortisol in elderly humans. Sleep-EEGs (2300-0700 h) and secretion profiles of GH and cortisol (2000-0700 h) were determined in 10 elderly men (64.0+/-2.2 years) and 10 elderly, postmenopausal women (63.0+/-2.9 years) twice, receiving 50 microg ghrelin or placebo at 2200, 2300, 0000, and 0100 h, in this single-blind, randomized, cross-over study. In men, ghrelin compared to placebo was associated with significantly more stage 2 sleep (placebo: 183.3+/-6.1; ghrelin: 221.0+/-12.2 min), slow wave sleep (placebo: 33.4+/-5.1; ghrelin: 44.3+/-7.7 min) and non-REM sleep (placebo: 272.6+/-12.8; ghrelin: 318.2+/-11.0 min). Stage 1 sleep (placebo: 56.9+/-8.7; ghrelin: 50.9+/-7.6 min) and REM sleep (placebo: 71.9+/-9.1; ghrelin: 52.5+/-5.9 min) were significantly reduced. Furthermore, delta power in men was significantly higher and alpha power and beta power were significantly lower after ghrelin than after placebo injection during the first half of night. In women, no effects on sleep were observed. In both sexes, ghrelin caused comparable increases and secretion patterns of GH and cortisol. In conclusion, ghrelin affects sleep in elderly men but not women resembling findings in young subjects.

Ghrelin plasma levels are not altered in major depression.

BACKGROUND: In patients with major depression, the function of most endocrine axes is altered compared to healthy subjects. The orexigenic hormone ghrelin, which shows higher plasma levels in females than males, interacts with several of these endocrine axes. In addition, ghrelin levels in depressed patients decrease with psychopathological improvement. Therefore, we hypothesized that ghrelin levels in patients with major depression would be higher than in healthy subjects. METHODS: Nocturnal (20:00-07:00 h) secretion patterns of ghrelin in 20 patients with major depression [11 females, age 39.4 +/- 10.2 years (mean +/- standard deviation); 9 males, age 38.3 +/- 10.4 years] with a total score on the Hamilton Depression Rating Scale, 21-item version, of 24.8 +/- 5.2 and 20 healthy subjects [11 females, age 38.7 +/- 10.8 years; 9 males, age 39.1 +/- 11.2 years] were determined following an adaptation night. RESULTS: Ghrelin plasma levels of depressed patients and matched healthy subjects did not differ at any point in time when stratified for sex. Accordingly, the area under the curve was comparable: depressed females, 423.3 +/- 103.4; healthy females, 398.0 +/- 94.6; depressed males, 266.3 +/- 56.9, and healthy males, 228.4 +/- 41.3. CONCLUSION: This is the first comparison of ghrelin secretion patterns in patients with major depression and healthy controls. Surprisingly, no relevant differences were ascertained between the two groups.

The glutamatergic system and its relation to the clinical effect of therapeutic-sleep deprivation in depression - an MR spectroscopy study.

Rapid improvement of depressive symptoms occurs after the administration of the NMDA antagonist ketamine. Ketamine administration is accompanied by an increase in GLX (sum-peak of glutamate, glutamine (GLN) and GABA) and GLN in the brain, as measured by magnetic-resonance (MR) spectroscopy. In healthy subjects, we observed an increase in GLX and GLN levels after total sleep deprivation (TSD), which has a rapid antidepressant effects. We examined, if an increase in GLX or GLN is related to the therapeutic effect of TSD. We examined 13 patients with major depression by means of proton MR spectroscopy (field strength: 1.5T) before and after 24h of TSD. Two anatomical areas (dorsolateral prefrontal cortex (DLPC) and parieto-occipital cortex (POC)) were studied. In the DLPC TSD did not change GLX or its elements, whereas the total creatine and choline signal increased marginally. No change could be observed in the POC. For further exploration we took gender and the presence of vegetative characteristics of melancholic depression into account, i.e. the presence of early morning awakening, appetite and weight loss was taken into account, to define vegetative melancholia (VM). TSD led to an increase in GLX and GLN in the DLPC only of male patients. In patients with VM an increase in GLN occurred in this area. The low field strength limits the accuracy for GLX and GLN estimates. Despite the exploratory nature of the study, it nevertheless supports earlier data on the importance of glutamatergic neurotransmission and furthermore of gender and/or vegetative features in depression.

Ghrelin alone or co-administered with GHRH or CRH increases non-REM sleep and decreases REM sleep in young males.

Ghrelin activates the somatotropic and the hypothalamic-pituitary-adrenal axes, being crucially involved in sleep regulation. Simplified, growth hormone releasing hormone (GHRH) increases slow-wave sleep and REM sleep in males, whilst corticotropin-releasing hormone (CRH) increases wakefulness and decreases REM sleep. Ghrelin's role in sleep regulation and particularly its interactions with GHRH and CRH are not entirely clear. We aimed to elucidate the interactions between ghrelin, GHRH and CRH in sleep regulation and the secretion of cortisol and GH. Nocturnal GH and cortisol secretion and polysomnographies were determined in 10 healthy males (25.7+/-3.0 years) four times, receiving placebo (A), ghrelin (B), ghrelin and GHRH (C), or ghrelin and CRH (D) at 22:00, 23:00, 00:00, and 01:00h, in this single-blind, randomized, cross-over study. Non-REM sleep was significantly (p<0.05) increased in all verum conditions (mean+/-SEM: B: 355.3+/-7.4; C: 365.4+/-8.1; D: 371.4+/-3.9min) compared to placebo (336.3+/-6.8min). REM sleep was decreased (B: 84.3+/-4.2 [p<0.1]; C: 74.2+/-7.0 [p<0.05]; D: 80.4+/-2.7min [p<0.05]) compared to placebo (100.9+/-8.3). CRH+ghrelin decreased the time spent awake and enhanced the sleep efficiency; furthermore, the REM latency was decreased compared to the other treatment conditions. CRH enhanced the ghrelin-induced cortisol secretion but had no relevant effect on GH secretion. In turn, GHRH enhanced the ghrelin-induced GH secretion but had no effect on cortisol secretion. In conclusion, ghrelin exhibited distinct sleep effects, which tended to be enhanced by both GHRH and CRH. CRH had sleep-improving and REM permissive effects when co-administered with ghrelin, being in contrast to the effect of CRH alone in previous studies.

Ghrelin enhances the nocturnal secretion of cortisol and growth hormone in young females without influencing sleep.

Ghrelin was shown to increase slow wave sleep (SWS) and the secretion of growth hormone (GH) and cortisol in young males. In terms of sleep, such information for females, however, is lacking. Therefore, polysomnographies were recorded (23:00-07:00 h) and nocturnal (20:00-07:00 h) secretion profiles of GH and cortisol were determined in 10 healthy females (24.9+/-2.4 years, body mass index: 21.2+/-1.1) twice, receiving four boluses of 50 microg ghrelin or placebo at 22:00, 23:00, 00:00, and 01:00 h, in this single-blind, randomized, cross-over study. No significant differences of conventionally or quantitatively analyzed sleep were observed between ghrelin and placebo condition. First administration of ghrelin caused a marked mean increase of GH by 53.3 to 64.4+/-14.2 ng/ml (placebo: 5.9+/-1.5 ng/ml) and cortisol by 54.2 to 96.4+/-15.3 ng/ml (placebo: 27.5+/-4.7 ng/ml). The following ghrelin injections were associated with smaller increases of GH and cortisol. In the ghrelin condition, GH plasma levels remained significantly (P<0.05) higher from 22:20 to 02:00 h and cortisol plasma levels from 22:20 to 02:20 h. In contrast to findings in young men, ghrelin did not affect sleep in young women, indicating a sexual dimorphism. In accordance with the findings in young men, ghrelin stimulated secretion of GH and cortisol.

Ghrelin suppresses secretion of luteinizing hormone in humans.

CONTEXT: Ghrelin affects the hypothalamic-pituitary-gonadal axis in various nonhuman mammalians, predominantly by suppressing secretion of LH. However, for humans, no such evidence exists. OBJECTIVE: Our objective was to study the effect of ghrelin on secretion of LH and testosterone in humans. DESIGN, PARTICIPANTS, AND INTERVENTION: Nocturnal (2000-0700 h) secretion profiles of LH and testosterone were determined in 10 healthy males (25.7 +/- 3.0 yr) twice, receiving 50 microg ghrelin or placebo at 2200, 2300, 2400, and 0100 h, in this single-blind, randomized, cross-over study. RESULTS: Ghrelin was associated with significantly (P < 0.05) lower mean plasma levels of both LH (2340-0200 h) and testosterone (0040-0300 h) than placebo. LH peak levels of the pulse after first administration of ghrelin/placebo were significantly (P = 0.014) smaller in the ghrelin (2.98 +/- 1.34 mIU/ml) than in the placebo condition (4.37 +/- 1.09 mIU/ml). In addition, the interval between this and the preceding peak was significantly (P = 0.010) longer in the ghrelin (255.8 +/- 79.1 min) than in the placebo condition (190.8 +/- 51.0 min). Significantly (P = 0.005) more LH pulses occurred with placebo (3.2 +/- 0.75) than ghrelin (2.6 +/- 0.7) subsequent to ghrelin/placebo administration. CONCLUSIONS: Ghrelin caused both a delay and suppression of the amplitude of LH pulses. These findings are in accordance with those in nonhuman mammalians.

Duloxetine increases stage 3 sleep and suppresses rapid eye movement (REM) sleep in patients with major depression.

Sleep studies in patients with major depression receiving the new selective norepinephrine and serotonin reuptake inhibitor (SNRI) duloxetine are lacking. Therefore, polysomnography in 10 patients with major depression (7 males, 39.9+/-7.6 years, HAMD-21 score: 23.6+/-5.6) was recorded twice, before and after 7-14 days of treatment with duloxetine. Stage 3 sleep significantly (P<0.01) increased from 21.0+/-10.7 to 37.4+/-20.1 min. Rapid eye movement (REM) latency significantly (P<0.005) increased from 58.5+/-31.1 to 193.6+/-72.6 min. REM sleep significantly (P<0.005) decreased from 94.8+/-34.5 to 51.5+/-42.5 min. These results partly differ from those in healthy subjects receiving duloxetine.

Persistent generalized anxiety after brief exposure to the dopamine antagonist metoclopramide.

The authors describe a 31-year-old woman who developed persistent generalized anxiety after brief exposure to the dopamine antagonist metoclopramide. Independently of that, she had experienced a panic attack followed by dystonias, shortly after a single dose of that drug, 17 years before. Both temporal association and recurrence of anxiety symptoms after re-challenge with metoclopramide suggest a causal relationship. The case might provide an initial piece of evidence that dopaminergic neurotransmission can be involved in the pathogenesis of generalized anxiety disorder.

Ghrelin administered in the early morning increases secretion of cortisol and growth hormone without affecting sleep.

Ghrelin and growth hormone (GH) releasing hormone (GHRH) both stimulate GH secretion and slow wave sleep (SWS), whereas ghrelin increases, and GHRH decreases cortisol in males. However, GHRH's effect on sleep and cortisol was abolished, on GH mitigated, when administered in the early morning, possibly due to counteracting corticotropin releasing hormone (CRH). Aim of this study was to investigate ghrelin's influence on sleep, GH and cortisol when administered in the early morning. Nocturnal (2000-1000 h) GH and cortisol patterns and polysomnography (2300-1000 h) were determined in 12 healthy males (25.3+/-3.2 yr) twice, receiving 50 microg ghrelin or placebo at 0400, 0500, 0600, and 0700 h, in this single-blind, randomized, cross-over study. The first ghrelin bolus caused the strongest (38.7+/-6.5 ng/ml, placebo: 0.4+/-1.1 ng/ml), second and third smaller, the fourth no GH peak. GH levels remained significantly (p<0.05) higher from 0420-0740 h in the ghrelin condition. Comparably, the first ghrelin bolus caused the strongest cortisol response (156.0+/-12.6 ng/ml; placebo: 78.0+/-10.5 ng/ml). Cortisol was significantly higher from 0440 to 0540 and at 0720 h and decreased thereafter to significantly lower levels (0820-0840 h). Sleep variables did not differ in both conditions. In contrast to GHRH, ghrelin's stimulatory effects were apparently not counteracted (GH), and enhanced (cortisol), respectively, by high CRH in the second half of night.

Sleep onset REM periods in obsessive compulsive disorder.

Sleep studies in patients with obsessive compulsive disorder (OCD) are sparse and results inconsistent. Moreover, in 3 out of 4 published studies up to 50% of patients suffered from secondary major depression. In this study, 10 inpatients with a DSM-IV diagnosis of OCD without comorbid major depression (Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score >15; Hamilton Depression Rating Scale (HAMD)-21 total score <17) and 10 healthy matched controls were included. Polysomnography of patients (7 males, 3 females, 34.5+/-12.7 years, Y-BOCS: 27.8+/-4.6, HAMD-21: 13.3+/-1.9) and controls (7 males, 3 females, 34.4+/-12.8 years) was recorded, following an adaptation night. Sleep variables did not significantly differ in both groups except that stage 4 sleep was reduced in patients. Three of the patients with OCD, however, exhibited sleep onset REM periods (SOREMPs), i.e. rapid-eye-movement (REM) latencies <10 min. Obsessive compulsive symptoms were significantly (P<0.05) more severe in these patients (Y-BOCS: 32+/-2.0) compared to those without SOREMPs (Y-BOCS 26+/-4.2). This is, to our knowledge, the first report of sleep onset REM periods in OCD.

Increased nocturnal secretion of ACTH and cortisol in obsessive compulsive disorder.

Information on the function of the hypothalamic-pituitary-adrenal (HPA) axis, the main mammalian system of stress response, in obsessive compulsive disorder (OCD) is inconsistent. In this study, nine inpatients with a DSM-IV diagnosis of OCD without comorbid major depression (Yale-Brown Obsessive Compulsive Scale [Y-BOCS] score >15; HAMD-21 total score 16) and nine healthy matched controls were included. Blood of patients (seven males; 31.8 +/- 9.3 years, Y-BOCS: 27.3 +/- 4.3, HAMD-21: 13.3 +/-1.9) and controls (seven males, 31.6 +/- 9.1 years) was drawn every 20 min between 23:00 and 7:00 h during sleep using a long catheter for later ACTH and cortisol analysis. Secretion patterns of cortisol and ACTH were similar in both groups, in OCD, however, at a higher level. Area under the curve plasma concentrations of both ACTH (p<0.05) and cortisol (p<0.005) were significantly greater in patients with OCD (ACTH: 674.3 +/- 57.4; cortisol: 2148.4 +/-271.7) than in controls (ACTH: 460.2 +/- 61.0; cortisol: 1191.2 +/- 124.1). In conclusion, our findings suggest that the activity of the HPA axis in patients with OCD is increased compared to healthy controls.