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The treatment of depression in senile patients with dementia is difficult with the drugs used formerly. The effects of a new anxiolytic drug, tandospirone, were investigated on depression symptoms in nine senile patients with dementia using Hamilton Depression Rating Scale (HAM-D) items. Tandospirone improved the symptoms, especially the depressive mood, agitation and anxiety, although a slight gastrointestinal symptom was found in one patient. The findings in the present study may suggest that tandospirone is a useful and comparatively safe drug for depression symptoms in senile patients with dementia. Copyright © 2002 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to identify the acute effects of ethanol on the relationship between sleep and heart rate variability (HRV) during sleep. Methods: Ten healthy male university students were enrolled in this study. An alcoholic beverage was given to each subject at a dosage of 0 (control), 0.5 (low dose: LD), or 1.0 g (high dose: HD) of pure ethanol/kg of body weight. All experiments were performed at 3-week intervals. On the day of the experiment, a Holter electrocardiogram was attached to the subject for a 24-hour period, and the subject was instructed to drink the above-described dosage of alcoholic beverage 100 minutes before going to bed; polysomnography was then performed for 8 hours. Power spectral analysis of the HRV was performed using the maximum entropy method, and the low- (LF: 0.04 to 0.15 Hz) and high-frequency (HF: 0.15 to 0.4 Hz) components along with LF/HF ratio were calculated. Results: As alcohol consumption increased, the heart rate increased and the spectral power of HRV measured at each frequency range decreased. Higher doses of ethanol also increased the LF/HF ratio compared with the measured ratio of the control group. Conclusions: Acute ethanol intake inhibits parasympathetic nerve activity and results in predominance of sympathetic nerve activity during sleep, in a dosage-dependent manner. The results of this study suggest that ethanol interferes with the restorative functions of sleep. [ABSTRACT FROM AUTHOR]

In spite of the accumulation of knowledge regarding the neuropharmacological action of benzodiazepines (Bz), the physiological process by which their sedative/hypnotic effects are induced remains poorly understood. We conducted a single-blind, crossover trial to evaluate the role of the thermoregulatory process in sleepiness and impaired psychomotor performance induced by a standard Bz, diazepam (DZP). Each of the eight healthy young male volunteers (mean age, 19.75 years; range, 18-23 years) was given a single oral dose of either 5 or 10mg of DZP or placebo 12 h after his average sleep onset time. Changes in plasma DZP concentration, proximal body temperature (p-BT), distal body temperature (d-BT), subjective sleepiness measured by the Visual Analog Scale and Stanford Sleepiness Scale, and psychomotor performance measured by Choice Reaction Time were monitored under a modified constant routine condition in which various factors affecting thermoregulation, alertness, and psychomotor performances were strictly controlled. Orally administered DZP induced a significant transient decrease in p-BT and psychomotor performance as well as an increase in d-BT and subjective sleepiness. Distal--p-BT gradient (DPG; difference between d-BT and p-BT), which is an indicator of blood flow in distal skin regions, showed a strong positive correlation with the plasma DZP concentration, indicating that DZP in clinical doses promotes heat loss in a dose-dependent manner. The DPG also correlated positively with the magnitude of subjective sleepiness and impaired psychomotor performance. These findings indicate that the sedative/hypnotic effects of Bz could be due, at least in part, to changes in thermoregulation, especially in the process of heat loss, in humans. [ABSTRACT FROM AUTHOR]

The process of heat loss has been shown to be a key pathway regulating sleepiness in humans. The influence of physical exercise with its attending heat production on subjective sleepiness and performance levels during total sleep deprivation (SD) was assessed in eight healthy young volunteers (mean age 21.1 years). Each subject participated in a SD cross-over study in which sleepiness and performance levels were tested under exercise and non-exercise conditions. The exercise entailed 15 min walking/h (3.0 Kcal/kg per h caloric consumption). Physical exercise significantly alleviated subjective sleepiness depending on the magnitude of the core body temperature elevation. This indicates that suppressing heat loss could prevent progression of subjective sleepiness during the nighttime. We found a strong positive correlation between increased sleepiness and decreased performance levels in each of the two experimental sessions. However, ANCOVA revealed a significant difference in the slope of the regression lines representing two sessions, indicating less subjective sleepiness with physical exercise despite the same decrease in performance. The present findings alert us to the possibility that increased physical activity during extended wakefulness could increase the dissociation between subjective evaluation of sleepiness and actual brain function, resulting in increased risk of human error. [Copyright &y& Elsevier]

Abstract Six healthy male volunteers (average age = 22.5 years) received orally melatonin (MLT; 3 mg or 9 mg) or placebo at 0930 hours in a randomized, single-blind, cross-over study. Both doses of exogenously administered melatonin (ex-MLT) induced transient, significant suppression of core body temperature (BT) compared to the placebo condition. There was no significant difference in the degree of BT suppression among the two MLT conditions in spite of significantly higher levels of serum MLT with the close of 9 mg, suggesting that there may be a threshold level of ex-MLT inducing the hypothermic action. Daytime administered ex-MLT also induced a significant sleep-inducing effect only in the 9 mg condition, while 3 mg ex-MLT failed to produce statistical significance. These findings suggest that the sleep-inducing action of ex-MLT occurs only at relatively high doses, and this action is probably not due to its BT lowering action. The present study led us to assume that ex-MLT produce its therapeutic effect for circadian rhythm sleep disorders through induction of circadian phase-shifting preceded by an acute, transient hypothermic action rather than light entrainment after setting sleep time by induction of sleep propensity. [ABSTRACT FROM AUTHOR]

We report on a schizophrenic patient, in whom drug-induced tardive dystonia and parkinsonism as well as depressive symptoms and panic attacks improved remarkably following electroconvulsive therapy. The present finding suggests that the electroconvulsive therapy reduced tardive dystonia possibly by enhancing the dopaminergic function in the brain. [ABSTRACT FROM AUTHOR]

Investigates the prevalence of sleep-related respiratory disorders in schizophrenic patients in Japan. Occurrence of snoring among patients; Administration of sedative drugs; Application of ambulatory pulse-oximetric device.

Determines the occurrence of cortical activity characterizing rapid eye movement (REM) sleep. Use of N300 appearing in response to sound stimulus; Appearance of muscle atonia characterizing REM sleep; Reduction of N300 amplitude.

Examines the effects of sensory stimuli on spontaneous K-complex. Components of K-complex; Origin of K-complexes; Inducers of K-complex.

Reports a case on onset of myopathy in adult patient with peculiar sleep-related disorder. Effect of tracheostomy on respiration; Atrophy of sternocleidomastoid muscle cells; Performance of sleep recordings using respirators.

Examines the behavior of event related potential (ERP) components in the drowsy state. Frequency stimulus generated in the drowsy state; Emphasis on negative component (N300); Resemblance between N300 and vertex sharp wave.

Panic attacks meeting the diagnostic criteria for panic disorder (DSM-III-R) were found in nine (20%) of 45 patients suffering chronic schizophrenia for more than 5 years. The scores of the Hamilton Depression Rating Scale and the Simpson Angus Scale were significantly higher in the group of patients with panic attacks. They also tended to be taking neuroleptics in larger doses than in the other group. The present report suggests that long-term treatment with neuroleptics is closely related to the manifestation of panic attacks in chronic schizophrenia. It also suggests that when panic attacks are seen frequently in patients taking high doses of neuroleptics, dose reduction of neuroleptics should be considered. [ABSTRACT FROM AUTHOR]