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BackgroundMeasures of impulsivity and aggression help to indicate risk of future violence or rule‐breaking. Both clinician‐rated risk assessment and self‐report measures have been used but hardly ever compared in their ability to predict inpatient incidents.AimsTo compare the self‐report on the Barratt Impulsiveness Scale (BIS‐11) and Buss‐Perry Aggression Questionnaire (BPAQ) with the clinician‐rated HKT‐30, a Dutch adaptation of the Historical Clinical Risk Management‐20, for their capacity to predict inpatient incidents.MethodsAll men newly admitted to a forensic psychiatric hospital were invited to participate in this study unless in intensive care. Tests of correlation were run between the BIS‐11 and BPAQ scale scores and the HKT‐30. Each was then tested separately for capacity to predict the number of aggressive and nonaggressive incidents while resident. Finally, scores of all rating scales were entered together into a negative binomial regression to compare their relative strengths in predicting later incidents.ResultsPatient and staff baseline impulsivity and aggression ratings correlated moderately well. All measures performed well in univariate analyses of relationship between baseline measures and later incidents. In final models, which included both patient and staff baseline ratings, the HKT‐30 generally outperformed the self‐report measures in the prediction of aggressive and nonaggressive incidents in both the first year and total length of stay.Implications for clinical practiceOur findings suggest that some reliance may be placed on patient ratings of their own propensity for impulsive and/or violent acts, but, when used, they should remain combined with clinician‐rated risk assessment for the time being. Future research should explore their utility in dialogue about treatment, and also the relative strength of staff response to each.

To investigate the impact of regular physical exercise on sleep, we assessed sleep-wake behaviour in male C57BL/6N mice with and without long-term access (i.e. 4 weeks) to a running wheel. We studied sleep-wake behaviour during undisturbed conditions as well as after social stress. The exercising mice ran approximately 4 km/day, which affected their physical constitution, their spontaneous sleep-wake pattern and their endocrine and sleep responses to stress. When compared with the control mice, exercising animals had more muscle substance, less body fat and heavier adrenal glands. At baseline, exercising mice showed fewer, but longer-lasting, sleep episodes (indicating improved sleep consolidation) and less rapid-eye-movement sleep. In both control and exercising mice, mild social stress (elicited by a 15-min social conflict) evoked elevated plasma levels of adrenocorticotrophic hormone and corticosterone, an increase in non-rapid-eye-movement sleep, an enhancement of low-frequency activity in the electroencephalogram within non-rapid-eye-movement sleep (indicating increased sleep intensity) and a decrease in wakefulness. However, as compared with the control animals, exercising mice responded to social stress with higher corticosterone levels, but not adrenocorticotrophic hormone levels, suggesting an increased sensitivity of their adrenal glands to adrenocorticotrophic hormone. Moreover, in control mice, social stress increased rapid-eye-movement sleep in parallel to non-rapid-eye-movement sleep, whereas this stressor selectively decreased rapid-eye-movement sleep in exercising animals. Corticosterone is known to decrease rapid-eye-movement sleep. Therefore, changes in the regulation of the hypothalamic-pituitary-adrenocortical axis as a result of the long-term exercise may contribute to the observed differences in spontaneous and social stress-affected sleep. In conclusion, regular exercise appears to increase sleep quality and reverses the effects of mild social stress on rapid-eye-movement sleep.

Brainstem serotonergic neurotransmission is implicated in sleep regulation. However, the role of serotonin (5-HT) in forebrain regions in sleep-wake mechanisms is still unclear. Here, we have investigated, using a combined in vivo microdialysis/electroencephalogram method, the relationship between hippocampal 5-HT levels and sleep-wake behaviour in the rat. A clear-cut relationship was found between hippocampal 5-HT levels and vigilance state. The highest levels of 5-HT were observed during wakefulness, whereas a progressive decrease of 5-HT going from nonrapid eye movement sleep to rapid eye movement sleep was found. Sleep deprivation (SD) causes a transient enhancement of mood in depressed patients. Given the putative role of 5-HT in the aetiology of depression and the therapeutical efficacy of selective serotonin reuptake inhibitors in this illness, we also studied hippocampal 5-HT during 4 h of SD and during the subsequent recovery period. During the whole SD period, 5-HT levels were elevated substantially when compared to 5-HT levels during basal wakefulness. However, no changes in 5-HT levels and the relationship between hippocampal 5-HT and vigilance state were found during the subsequent recovery period. As SD is a potentially stressful experience and glucocorticoids are involved in the regulation of serotonergic neurotransmission and sleep, we investigated the effects of SD on free corticosterone levels. SD caused a marked rise in free corticosterone levels. However, the effects of SD on 5-HT seem not to be mediated by this hormone, because adrenalectomy did not affect the rise in hippocampal 5-HT during SD. We hypothesize that the elevated hippocampal 5-HT levels during SD may participate in the transient mood enhancing properties of forced wakefulness observed in depressed patients.

Hyperpolarization-activated cation (HCN) channels are believed to be involved in the generation of cardiac pacemaker depolarizations as well as in the control of neuronal excitability and plasticity. The contributions of the four individual HCN channel isoforms (HCN1–4) to these diverse functions are not known. Here we show that HCN2-deficient mice exhibit spontaneous absence seizures. The thalamocortical relay neurons of these mice displayed a near complete loss of the HCN current, resulting in a pronounced hyperpolarizing shift of the resting membrane potential, an altered response to depolarizing inputs and an increased susceptibility for oscillations. HCN2-null mice also displayed cardiac sinus dysrhythmia, a reduction of the sinoatrial HCN current and a shift of the maximum diastolic potential to hyperpolarized values. Mice with cardiomyocyte- specific deletion of HCN2 displayed the same dysrhythmia as mice lacking HCN2 globally, indicating that the dysrhythmia is indeed caused by sinoatrial dysfunction. Our results define the physiological role of the HCN2 subunit as a major determinant of membrane resting potential that is required for regular cardiac and neuronal rhythmicity.

Insomnia, which can be defined as a discrepancy between the need for sleep and the perceived quantity and/or quality of sleep, constitutes a major medical problem. The most frequently prescribed sleeping pills are agonistic modulators of GABA(A) receptors. To examine the changes in sleep that can be induced by a stimulation of GABA(A) receptor function, this article reviews the hypnotic properties of the different classes of agonistic modulators of GABA(A) receptors-barbiturates, benzodiazepines, zolpidem, zopiclone, and neuro(active) steroids-and of selective GABA(A) agonists assessed in various mammalian species, including noninsomniac subjects. Although quantitative differences clearly exist, the agonistic modulators appear to have many actions in common. They are very effective in inducing and maintaining sleep, but, with the possible exception of the neurosteroids, inhibit the dream- associated rapid eye movement (REM) stage of sleep. With regard to the signals in the electroencephalogram during non-REM sleep, all these drugs promote the occurence of spindles, which are characteristic for shallow sleep, and, with the exception of barbiturates, have been shown to depress slow waves, which usually identify deep sleep. Upon chronic usage, all these drugs may produce tolerance and dependence. This occurs to the greatest extent with the barbiturates, and to the least extent with the newer hypnotics zolpidem and zopiclone. The small number of studies on the GABA analogues and the selective GABA(A) agonists muscimol and 4,5,6,7- tetrahydroisoxazolo-pyridin-3-ol (THIP) indicate that these compounds have little effect on sleep initiation, but may increase sleep maintenance and promote deep sleep, without disrupting REM sleep. The hypnotic properties of these GABA(A) agonists seem to differ considerably from those of agonistic modulators, and may have beneficial effects in the treatment of disturbances in maintaining sleep and of nonrefreshing sleep.

The sleep profiles induced by agonists and agonistic modulators of γ-aminobutyric acidA (GABAA) receptors differ markedly. With regard to GABAA agonists, the effects may be due to the fact that these agents are poor substrates for uptake and are therefore likely to activate GABAA receptors tonically. To investigate this possibility, we assessed the sleep effects of two doses (2 and 10 mg kg−1) of the GABA re-uptake inhibitor tiagabine, administered intraperitoneally at light onset in 8 rats. Electroencephalogram (EEG) and electromyogram were recorded during the first 8 h after the injection. Compared with vehicle, tiagabine had minimal effects on the temporal pattern of non-rapid eye movement sleep (non-REMS) and on the total time spent therein. However, tiagabine dose-dependently elevated EEG activity during non-REMs, most prominently in the lower frequencies (1–8 Hz) and least pronounced in the frequencies between 11 and 16 Hz. During the first 2 h after the injection, 10 mg kg−1 tiagabine elicited repetitive episodes of hypersynchronous EEG waves during wakefulness and slightly suppressed REMS. Except for these effects, tiagabine hardly influenced the time spent in and EEG activity during wakefulness and REMS. The effects of tiagabine on state-specific EEG activity were qualitatively very similar to those elicited by GABAA agonists. These findings support the hypothesis that the influence of GABAA agonists on EEG signals may be caused by tonic stimulation of GABAA receptors. British Journal of Pharmacology (1998) 123, 1471–1477; doi:10.1038/sj.bjp.0701769

During 3 baseline nights (2 for adaptation) and during 3 days of a sleep-wake reversal, electrophysiological characteristics of sleep and rectal temperature were recorded in 8 morning-type (M-type) and 8 evening-type (E-type) subjects, living in a quiet sleep laboratory. Outcomes of visual sleep scoring revealed the following general tendencies for day-sleep as compared to night-sleep: shorter sleep latencies, shorter REM (rapid eye movement sleep) latencies, advance of the time of maximum REM duration, increased duration of slow wave sleep, more intermittent wakefulness, and decreased subjective sleep quality. Furthermore, for the M-types consistently shorter sleep latencies and--for day-sleep--longer REM latencies were observed than those for the E-types. With regard to the parabolic time course of REM duration, M-types appeared to be relatively phase advanced, in particular for their day-sleep. In addition, subjective sleep quality was consistently higher for the M-types, with the exception of the first day-sleep. The temporal distributions of EEG delta (0.5-3.5 Hz) energy over the first four NREM/REM cycles of day-sleep all deviated from a monotonically decreasing trend. Compared to night-sleep the M-types showed a relative increase of delta energy for Cycle 2, whereas for the E-types a relative increase for Cycles 3 and 4 was observed. An analysis of delta energy, employing a pattern-recognition technique independently from visual sleep scoring, revealed an overall faster rate of accumulation for the M-types. Following sleep onset, rectal temperature showed a decrement, which was larger for the M-types. Moreover, rectal temperature and delta energy were negatively related, as indicated by a negative mean intra-individual correlation. These results are discussed in relation to the characteristic sleep-wake behavior of M-types and E-types.