Biomedical subjects
Publications and source records attributed to S E Southmayd.
A patient with dextrocardia who suffered his first myocardial infarction after approximately 26 hours of a diagnostic sleep deprivation protocol is described. The infarction started about 3 hours after a significant improvement in mood, which persisted during and after infarction. Total sleep deprivation may be an acute risk factor for myocardial infarction.
BACKGROUND: Clinical depression is associated with abnormalities of the hypothalamic-pituitary-thyroid axis. Changes in thyroid function during sleep deprivation may be related to its antidepressant effects. METHODS: Levels of thyroid-stimulating hormone, tri-iodothyronine, tri-iodothyronine uptake, thyroxine, and free thyroxine were measured before, during, and after a 48-hour sleep deprivation in nine treatment-resistant depressed patients. Clinical state was assessed every 4 hours. A retrospective study of 26 similar patients was added for cross-validation. RESULTS: Significant increases in thyroid-stimulating hormone and tri-iodothyronine during sleep deprivation were not correlated with clinical improvement. Sleep deprivation responders had lower tri-iodothyronine uptake levels than nonresponders in both the prospective (p <.02) and the retrospective (p <.03) samples. CONCLUSIONS: The lower tri-iodothyronine uptake values in responders may identify a subgroup of depressed patients who respond to sleep deprivation by virtue of some abnormality of the hypothalamic-pituitary-thyroid axis that is temporarily corrected by sleep deprivation.
A 53-year-old woman with major depression was studied throughout 7 trials of therapeutic sleep deprivation (SD). Under conditions where the patients was either medication-free or receiving antidepressant therapy, improvement with SD was followed by full relapse on returning to sleep. Four SD sessions conducted while the patient was receiving thyroxine each resulted in remission, sustained for several days. These results suggest that the beneficial effects of SD may be mediated by thyroid hormones, or associated activity in the hypothalamic-pituitary-adrenal axis.
The well documented observation of a characteristic sleep disturbance in depression has been accorded a good deal of significance. Several current hypotheses regarding the etiology of depression, are based on these findings. However, a review of the descriptive studies shows that care has not generally been taken either to restrict or objectively measure daytime sleep. Evidence is presented suggesting that daytime sleep may occur in depressed patients more frequently than commonly thought and that, in normal subjects, daytime napping can result in nocturnal sleep changes similar to those seen in depressed patients. A model is proposed in which the nocturnal sleep disturbance in depression reflects the occurrence, during the daytime, of frank slow wave sleep or periods of large amplitude, slow wave EEG activity as a consequence of a dampening of the circadian rhythm of sleep propensity.
The pattern of relapse following therapeutic response to 40-hr sleep deprivation (SD) was examined in nine depressed patients. On the night ending SD patients were awakened from polygraphically recorded sleep on one or more occasions, in order to assess the clinical state. All subjects were found to demonstrate a precipitous and full relapse over this night, the timing of the relapse varying considerably between individuals. No association was found between deterioration in the clinical state and characteristics of preceding sleep. These results are consistent with the notion that, in predisposed individuals, some process associated with sleep has a depressogenic effect. However, they necessitate revision of theories of SD and depression that emphasize the infrastructure of sleep.
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Four cases are described in which observation of the response to forty hour sleep deprivation was used in resolving the differential diagnosis between depression and dementia. In each case it was possible to conduct psychometric assessment of cognitive ability during the period of improvement of the clinical state. The utility of this approach and some of the difficulties associated with its use are discussed.
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Six drug-free depressed patients, each of whom acted as their own control, were studied for eleven consecutive days during which they were twice deprived of sleep for either 36 or 40 hours. The sequence of events was baseline (3 days), SD, recovery (3 days), SD, recovery (3 days). Blind ratings of clinical state were made on the basis of four-hourly interviews (standardized for each case), which were videotaped; sleep was monitored by conventional electrophysiological methods. Sleep deprivation had a beneficial, but transient, effect on four of the six patients studied. Changes in sleep were unrelated to changes in clinical state.
Systematic variation in aspects of the sleep-wakefulness cycle of a depressed woman showed that recovery occurred reliably after 19 to 20 hours sustained wakefulness, unrelated to diurnal rhythm. Depression returned during as little as 15 minutes sleep. The effect of sleep deprivation was a specific response, probably unrelated to REM sleep.
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