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Sixty depressed patients were treated first with sleep deprivation (SD) and afterwards with clomipramine or maprotiline. A statistically significant correlation was found between the positive effect of SD and response to clomipramine and the negative effect of SD and response to maprotiline.
In addition to previous investigations another modification of sleep-deprivation (SD) was studied in 28 endogenous depressives: SD during the 1st half of the night. From the day of deprivation - in the self-rating from the 4th day - up to 1 week later a therapeutic effect can be observed. The psychic part of the symptomatology was more reduced than the somatic one. Compared to total and partial SD during the 2nd half of the night, there is, on average, a smaller therapeutic effect which occurs later. The diurnal variation of the depressive symptomatology is less influenced. According to the period without sleep, the circadian course of the heart rate is less and differently modified by SD during the 1st half of the night. Only an existing diurnal variation (before SD) is a predictor of the prompt effect. Implications for the mechanism of the therapeutic SD were discussed. For clinical practice, SD during the 2nd half of the night is the method of choice.
Regional differences in EEG slow wave activity (SWA) during sleep after sleep deprivation (SD) may be a consequence of differential metabolic activation of cortical areas. We investigated the relationship between the regional EEG dynamics and 2-deoxyglucose (DG) uptake after SD in mice. Six hours' SD were combined with natural unilateral whisker stimulation in an enriched environment to selectively activate the barrel cortex and motor areas. As expected, an interhemispheric asymmetry of 2-DG uptake was found in the barrel cortex immediately after SD. To test whether sleep contributes to recovery of the asymmetry, the stimulation was followed by either undisturbed sleep or by an additional SD. The asymmetry vanished after recovery sleep but also after the additional period of wakefulness without stimulation. In addition, relative 2-DG uptake in the primary motor cortex and retrosplenial area was significantly higher immediately after the SD than after the additional sleep or wakefulness, whereas no other region differed between the groups. Whisker stimulation elicited a greater increase in EEG SWA during non rapid eye movement sleep in the stimulated hemisphere than in the control hemisphere; this increase lasted for 10 h. Within a hemisphere, the initial increase in SWA was higher in the frontal than in the parietal derivation. We conclude that the regional SWA differences during sleep are use-dependent and may be related to the regional pattern of metabolism during the previous waking episode. However, the regional metabolic recovery is not dependent on sleep, and is not directly reflected in changes in SWA during sleep.
Total sleep deprivation (TSD) and tricyclic medication are successful treatment modalities for patients with a major depressive disorder. Recent studies have suggested a positive relationship between TSD response and succeeding tricyclic treatment, even on a very specific level, thus supporting the assumption of two distinct biochemical subtypes of depression. The present study tested this hypothesis by treating 10 inpatients with a major depressive disorder first with TSD and succeedingly with clomipramine. Contrary to expectation, a negative relationship between clinical response to the two treatment modalities was found.
Regional brain metabolic activity of six male Sprague-Dawley rats was investigated with 2-[14C]deoxyglucose autoradiography. Regional brain metabolic activity was determined bilaterally for 60 brain structures, using laser densitometry. After 5 days of uninterrupted rapid eye movement sleep deprivation, increased metabolic activity was found in the lateral habenula, the caudal and middle parts of the limbic system, and in the corpus callosum.
The paper presents a brief review of literature data on clinical effects of sleep deprivation (SD), short-term deprivation (up to 40 h), in particular. SD was studied for effects on patients with defected cerebral dopaminergic systems (parkinsonism, dystonic hyperkinesis, persistent lactorrhea-amenorrhea, acromegaly). The control was made using clinical, electrophysiological, psychological, motor and biochemical tests. SD was compared to L-Dopa, parlodel, lisenil action. SD is shown to have therapeutic and differential diagnostic significance in varying pathological conditions of cerebral dopaminergic systems.
Fifteen elderly depressed patients were treated by 36-hour sleep deprivation (SD). The depression was unipolar in 3 cases, bipolar in 3, and secondary in 4. Nine of the 15 patients responded to SD, and 6 had a remission (1 with SD alone and 5 with SD plus an antidepressant drug). Some of the remaining 6 patients might have responded if the treatment had not been interrupted for various reasons. These favorable results in elderly patients were better than anticipated. SD was well tolerated, although in one patient with bipolar depression a manic attack was precipitated. The effectiveness of SD poses interesting theoretic questions.
The relationship between diurnal variation of mood and response to total sleep deprivation (TSD) was investigated in 131 depressed patients. This response was related to (1) the diurnal variation on the day before TSD as assessed by self-ratings of mood, and (2) the propensity to produce diurnal variations (the "diurnality") as assessed by the Hamilton Rating Scale for Depression. Three types of diurnality are distinguished: morning type (the propensity to feel better in the morning), evening type (the propensity to feel better in the evening), and a nondiurnal type. The results show that diurnality does predict the mood response to TSD. The direction of diurnality is decisive: patients who have the propensity to feel better in the evening benefit more from TSD than other patients.
Ten nonobese, healthy elderly adults (M = 73.3 years) were monitored polygraphically during sleep for sleep state changes, breathing, and the development of cardiac arrhythmias. All participated in 2 baseline nights and 1 night of flurazepam 30 mg ingestion; six underwent 1 night of sleep deprivation; four received ethyl alcohol (.6 mg/kg); and four whose apnea worsened significantly with flurazepam 30 mg were pretreated for 3 days with acetazolamide, taking acetazolamide and flurazepam 30 mg on the fourth night. Elderly adults with an Apnea Index (the number of apneas per sleep hour) between 5 and 7 at baseline experienced a worsening of their apnea with each manipulation. Acetazolamide did not protect individuals whose Apnea Index increased after flurazepam ingestion. One person developed premature ventricular contractions in conjunction with an increased Apnea Index after each manipulation.
Responders spent more time in active wakefulness than non-responders. Responders after TSD also spent significantly less time in substage C than non-responders, even before TSD. Parallel to the decrease of substage C, substage B slightly, but not significantly increased in responders after TSD. The Hamilton-scores before TSD correlated significantly with the time spent in substage C. Our system of scoring polygraphically defined waking stages, which combine electrophysiological, behavioral and cognitive aspects of the waking states in a setting comparable a every-day condition, differentiated responders and non-responders to sleep deprivation therapy. Thus it may serve as an useful tool to further elaborate wakefulness within the sleep-wake-cycle with special reference to chronotherapeutic interventions.
The psychostimulant theory of antidepressive sleep deprivation (SD) proposes a contribution of dopamine D3 receptors (DRD3) in the limbic system to the antidepressant effects of SD. Neuroendocrinological studies suggest a positive correlation of clinical response to SD and cortisol secretion. We hypothesized that the clinical response to SD and amount of cortisol secretion upon SD is associated with the 1-1 genotype of the Bal1 polymorphism of DRD3 on exon 1. In this study, aiming at evaluating the feasibility of screening large patient samples, 52 inpatients (19 males/33 females) with unipolar depression and a score of 18 or more on the 21-item Hamilton Depression Rating Scale were treated with 1 night of total SD. We found that 31% of our patients responded to SD. There was no association between response to SD and the genotype of the DRD3 Bal1 polymorphism (p < 0.879). There was also no association between increase in cortisol secretion after SD and DRD3 genotypes (p < 1.000) in a subgroup of patients. Statistical power analysis ruled out a major effect of the DRD3 Bal1 polymorphism on clinical response to SD. These results suggest that the DRD3 Bal1 polymorphism is not a promising lead to be followed up in larger patient samples.
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PURPOSE: Sleepiness and sleep deprivation are associated with injury, but few case-control studies have addressed them. We sought to add to the body of analytic observational studies. METHODS: Case-control and case-crossover study of 2517 injured patients interviewed in person in 3 emergency departments and matched by age, sex, rural versus urban, day of week, and hour of day with 1856 controls. Sleep constructs were measured by the following: (1) self-perceived sleepiness at injury or matched control time using 3 adjectives (tired, sleepy, drowsy); (2) usual sleep quality and quantity, and differences in those in the past 7 days; and (3) hours of sleep in the 24 hours before injury and the 24 hours before that. RESULTS: Better sleep quality in the past 7 days was associated with a lower risk of injury (odds ratio (OR) 0.88, 95% confidence interval (CI) 0.80 to 0.97). Self-reported sleepiness just before injury compared with control time was associated with a lower risk of injury, with ORs of 0.82 per unit on a 0-to-12 scale (95% CI 0.78 to 0.86) in case-control analysis and 0.76 (0.73 to 0.80) in case-crossover analysis. In case-crossover analysis, additional sleep in the 24 hours before injury compared with the 24 hours before that was associated with an increased risk of injury (OR 1.06 per hour, 95% CI 1.03 to 1.09), but this effect disappeared when we controlled for activity, location, and recent alcohol consumption. CONCLUSIONS: Better recent sleep quality was associated with a lower risk of injury, but surprisingly, feeling sleepy was also.
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In choice serial reaction time (RT), Response-to-next-Stimulus Interval (RSI) was varied from 0 to 600 msec in 40-msec steps. In three experiments, RT fell and errors rose as RSI was increased to 480 msec; they remained unchanged thereafter. The effect of RSI on RT was not linear, was reduced by 6- as compared with 4- or 3-choice responding, and was unaffected by sleep deprivation, despite loss of sleep reducing RT overall. The effect of penultimate RSI on RT was similar to that current RSI, but smaller. Two explanations of RSI--response-generated kinaesthetic feedback blocking a "central processor" and a preparatory interval as in warned simple RT--are rejected. Instead, the idea of "relative refractory state" is revived but now, because of the RSI/error finding, biased more towards responding than stimulus reception and encoding. In all three experiments the influence of RSI on RT was reduced with practice. If practice encourages automatic rather than controlled processing (Shiffrin & Schneider, 1977), the prediction is that the former will show less refractoriness.
We studied the importance of genetic predisposition in the development of stress-induced hypertension in the spontaneously hypertensive rat (SHR), Wistar-Kyoto (WKY) rat, and borderline hypertensive rat (BHR; first-generation offspring of SHR and WKY). Rats were submitted to seven 72-hour sessions of rapid eye movement sleep deprivation (REM-sd) every other week during 13 weeks. Tail arterial pressure was determined throughout the experiment. At the end of the study, mean arterial pressure (direct measurement), sympathetic activity (acute blockade with propranolol and phentolamine), and ventricular weight were determined. Results showed that REM-sd induced sustained hypertension only in rats with a partial predisposition to developing hypertension (BHRs). Values of tail arterial pressure at the end of the study were BHR REM-sd, 175 +/- 1.6 mm Hg and control BHR, 155.9 +/- 0.9 mm Hg, p less than 0.05; SHR REM-sd, 219 +/- 2.6 mm Hg and control SHR, 211.9 +/- 3.4 mm Hg, NS; WKY REM-sd, 123.9 +/- 2 mm Hg and control WKY, 125.4 +/- 2.2 mm Hg, NS. Stressed groups showed higher reduction of mean arterial pressure than their controls when submitted to sympathetic blockade (SHR REM-sd, -75.7 +/- 13.2 mm Hg and control SHR, -60 +/- 4.5 mm Hg, p less than 0.05; BHR REM-sd, -38.4 +/- 3.6 mm Hg and control BHR, -24.3 +/- 2.1 mm Hg, NS; WKY REM-sd, -34.4 +/- 2.5 mm Hg and control WKY, -25.6 +/- 3.3 mm Hg, NS). REM-sd increased ventricular weight in all strains. These increments showed no correlation with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
The primary purpose of this article is to determine whether sleep deprivation (SD) of 24 h or longer has been demonstrated to be an effective procedure for eliciting epileptiform and/or seizure patterns in the EEG in epilepsy patients as compared with those of nonepileptics. The relevant literature is reviewed, first chronologically and then critically. Methodological problems are discussed. Although no absolutely definitive study has been done, the preponderance of evidence supports the conclusion that SD is effective in activating the EEGs of epileptics. Recommendations concerning the application of SD are offered.