Cases reported "Sleep Disorders"

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1/7. sleep and dream suppression following a lateral medullary infarct: a first-person account.

    consciousness can be studied only if subjective experience is documented and quantified, yet first-person accounts of the effects of brain injury on conscious experience are as rare as they are potentially useful. This report documents the alterations in waking, sleeping, and dreaming caused by a lateral medullary infarct. Total insomnia and the initial suppression of dreaming was followed by the gradual recovery of both functions. A visual hallucinosis during waking that was associated with the initial period of sleep and dream suppression is described in detail. Since the changes in sleep and their recovery are comparable to results of animal experiments, it can be concluded that damage to the medullary brain stem causes extreme but short-lived alterations in conscious state and that substantial recovery occurs even though the damage to the brain stem endures.
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2/7. Status dissociatus--a perspective on states of being.

    During the course of routine clinical study, it has become apparent that the all-or-none concept of state determination (wakefulness, nonrapid eye movement sleep, rapid eye movement sleep) does not always exist, and that ambiguous, multiple, or rapid oscillation of state-determining variables appear in a wide variety of experimental and clinical situations. Six cases of extreme state dissociation are presented, with a review of the human and animal clinical and experimental literature. This multiple component concept of state determination must be kept in mind when pharmacologic or lesion studies are employed to suppress one or another state. Such manipulation may suppress some of the commonly used markers for that state (i.e., polygraphic) without affecting other variables of that state. The existence of mixed states will be a challenge to the development of automated computerized polysomnogram scoring.
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3/7. melatonin stabilises sleep onset time in a blind man without entrainment of cortisol or temperature rhythms.

    The pineal hormone melatonin (N-acetyl-5-methoxytryptamine) is normally secreted at night: in animals it serves to transmit information about light-dark cycles to body physiology Suitable timed administration will alleviate 'jet-lag' severity ratings in humans, the major effect being to improve sleep. It has been suggested that this may be mediated by melatonin re-entraining the endogenous circadian oscillator. We have examined this possibility by feeding melatonin to a blind individual (HK) with a free-running temperature rhythm and a pronounced 35-day cycle in his ability to fall asleep at 'normal' times. Our results show a clear stabilizing effect of melatonin on sleep onset time with elimination of day time sleep, but no entrainment of rectal temperature or urinary cortisol rhythms. Thus melatonin may act on the timing mechanism of sleep onset, rather than as a entrainer of all circadian rhythms. It may well help shiftworkers to sleep at inappropriate phases of their circadian oscillators.
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4/7. Abnormal central monoamine metabolism in humans with "true hypersomnia" and "sub-wakefulness".

    A case of kleine-levin syndrome with true hypersomnia and a case of sub-wakefulness are described. In both patients lumbar cerebrospinal fluid homovanillic acid, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylethylene glycol levels have been assayed during episodes of hypersomnia and normal sleep-waking cycles. Besides an increased 5-hydroxytryptamine turnover, mainly an increased dopamine turnover has been detected in both kinds of hypersomnia, and this finding was more remarkable in the case with sub-wakefulness. The probable role of dopamine in abnormalities in the sleep-waking cycle is discussed on the basis of results in experimental animal hypersomnias.
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5/7. Clival chordoma associated with pathological laughter. Case report.

    The case of a 40-year-old man with a clival chordoma who presented with symptoms of pathological laughter and left sixth cranial nerve paresis is reported. Laughing and talking during sleep were noted on polygraphic and videotape recordings of nocturnal sleep. Selective disorganization of sleep was observed, with laughing facial expressions and a lack of muscular atonia. The tumor developed in the prepontine cistern, compressing the pontomesencephalic structures backward and involving the upper clivus and the left cavernous sinus. No recurrence of laughter attacks were noted after total removal of the tumor. The sleep patterns observed were similar to those of experimental animals with lesions of the peri-alpha locus ceruleus. The importance of uncontrolled laughter as a sign of a ventral brain-stem mass is emphasized.
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6/7. sleep abnormalities in patients with brain stem lesions.

    Seven patients with "locked-in" syndrome were studied by prolonged polygraphic recordings. Severe alterations in the sleep pattern were observed in five patients who had bilateral extensive pontine lesions resulting in tetraplegia, facial and pseudobulbar paralysis, and absence of conjugate horizontal gaze. Rapid eye movement (REM) sleep was entirely absent while non-rapid eye movement (NREM) sleep was absent, reduced, or altered. The remaining two patients, both of whom had relative sparing of horizontal gaze and apparently either no or minimal pontine tegmental involvement, showed both REM and NREM sleep with only a minimal alteration in the sleep pattern. The study suggests that, in human beings as in animals, pontine structures near the midline are essential for control of sleep states.
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7/7. Monozygotic twins with Alzheimer's disease treated with melatonin: Case report.

    Monozygotic twins with Alzheimer's disease of 8 years duration were studied. The onset of the disease differed by about 6 months between twins and was characterized by a primary impairment of memory function. Clinical evaluation at the time of diagnosis indicated a similar cognitive and neuroimaging alteration in both patients, as well as a similar neuropsychologic impairment. A possible genetic origin of the disease was suggested by a similar disease suffered by the mother. patients were initially treated with vitamin e (800 I.U./day). Starting at approximately the same time (about 3 years ago), they received 50 mg/day thioridazine because of the behavioral and sleep disorder. One of the patients was treated with melatonin (6 mg orally) at bed time daily for 36 months. Evolution of the disease in the melatonin-treated patient indicated a milder impairment of memory function, with substantial improvement of sleep quality and reduction of sundowning. This led to discontinuance (after 3 months) of thioridazine treatment. Present clinical evaluation indicated a difference in functional stage of the disease between the twins (Functional Assessment Tool For Alzheimer's disease, FAST), with a score of 5 in the twin who received melatonin and of 7b in the twin who did not receive it. Since experimental data on melatonin in animals indicated its antioxidant, antiapoptotic, and beta-amyloid-decreasing activity, the hypothesis that melatonin has a beneficial effect in Alzheimer's disease patients should be considered.
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