Cases reported "Sleep Deprivation"

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1/56. A psychodynamic hypothesis on the night eating syndrome.

    The Night eating syndrome (NES) is usually interpreted in organicistic and physiological terms. This paper looks at it dynamically in terms of the psychic dimension of the patient through an examination of the contrasting tensions (emptiness and fullness; saving and destroying the object, etc.) that are the unconscious cause of his NES. A relationship is suggested between nocturnal reawakenings as a form of eating behaviour and the undreamt or avoided dreams used by the patient as a defence against "perception" of the unconscious. ( info)

2/56. Response covariation of escape-maintained aberrant behavior correlated with sleep deprivation.

    We examined the relation between sleep deprivation and changes in level and allocation of aberrant behavior (aggression and self-injury) for a child with moderate mental retardation. First, a series of functional analyses identified that self-injury (SIB) and aggression were maintained by escape from demands (i.e., were members of the same response class). Escape from demand conditions were then held constant over time while natural levels of sleep deprivation occurred. This final analysis demonstrated a correlation between sleep deprivation and increases in escape-maintained aberrant behavior. sleep deprivation seemed to be related to increases in levels of self-injury but did not seem to influence levels of aggression. ( info)

3/56. association between brain size and abstinence from alcohol.

    Brain shrinkage with chronic alcoholism is well acknowledged. We have shown, with quantitative analysis of serial scans, an increase in hippocampal, cerebral, and cerebellar volume after abstinence from alcohol. ( info)

4/56. Can critically timed sleep deprivation be useful in pregnancy and postpartum depressions?

    BACKGROUND: The aim of this study was to test the efficacy of critically timed sleep deprivation in major mood disorders (MMD) occurring during pregnancy and postpartum. methods: Nine women who met DSM-IV criteria for a MMD with onset during pregnancy or within 1 year postpartum underwent a trial of either early-night sleep deprivation (ESD), in which they were sleep deprived in the early part of one night and slept from 03:00-07:00 h, or late-night sleep deprivation (LSD), in which they were deprived of sleep in the latter part of one night and slept from 21:00-01:00 h. Mood was assessed before the night of sleep deprivation, after the night of sleep deprivation, and after a night of recovery sleep (sleep 22:30-06:30 h) by trained clinicians, blind to treatment condition, using standardized scales. RESULTS: More patients responded to LSD (nine of 11 trials: 82%) compared with ESD (two of six trials: 33%) and they responded more after a night of recovery sleep (nine of 11 nights: 82%) than after a night of sleep deprivation (six of 11 nights: 55%). pregnant women were the only responders to ESD and the only nonresponders to LSD. LIMITATIONS: The small and heterogeneous sample size prevents us from making more definitive conclusions based on statistical analyses. CONCLUSIONS: Although the findings are preliminary, the results suggest that with further study, critically timed sleep deprivation interventions may benefit women with pregnancy or postpartum major mood disorders and potentially provide a viable alternative treatment modality for those women who are not candidates for pharmacologic or psychotherapeutic interventions. Such interventions are needed to help prevent the devastating effects of depression during pregnancy and the postpartum period on the mother, infant, her family and society. ( info)

5/56. Therapeutic progress of two sibling cases exhibiting sleep-wake rhythm disorder.

    In this study, two females, siblings who exhibited a non-24 h sleep-wake rhythm (non-24 h) at home were observed. However, they showed a delayed sleep phase syndrome (DSPS) immediately after admission to Kurume University Hospital. melatonin (3 mg) was commenced following chronotherapy and this improved their sleep-wake rhythm. polysomnography (PSG) showed decreased sleep latency and increased sleep stage. In these cases, the involvement of environmental factors was strongly suggested for the sleep-wake rhythm abnormalities as well as familial factors. ( info)

6/56. myocardial infarction during sleep deprivation in a patient with dextrocardia--a case report.

    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. ( info)

7/56. sleep disorders caused by brainstem tumor: case report.

    Few studies concerning sleep disorders in brainstem lesions or tumors have been published. We report the case of a girl who was operated on for a brainstem tumor at the age of 4 years. In postsurgery, she had hemiparesis of the left side, swallowing difficulties, and severe apneas requiring a tracheotomy with nocturnal ventilation. The child's health improved progressively. Two sleep recordings were performed at 7 and 9 years without nocturnal ventilation. These recordings showed sleep disorders with a decrease in total sleep time and rapid eye movement (REM) sleep. Several central apneas were observed. The apneas were more frequent during REM sleep in the first recording and were associated with desaturation and microarousals. ( info)

8/56. Insomnia associated with thalamic involvement in E200K Creutzfeldt-Jakob disease.

    BACKGROUND: Insomnia with predominant thalamic involvement and minor cortical and cerebellar pathologic changes is not characteristic of familial Creutzfeldt-Jakob disease (CJD) but is a hallmark of fatal familial insomnia. OBJECTIVE: To report a 53-year-old woman with intractable insomnia as her initial symptom of disease. methods: The authors characterized clinical, pathologic, and molecular features of the disease using EEG, polysomnography, neurohistology, Western blotting, protein sequencing, and prion protein (PrP) gene (PRNP) analysis. RESULTS: The patient developed dysgraphia, dysarthria, bulimia, myoclonus, memory loss, visual hallucinations, and opisthotonos, as well as pyramidal, extrapyramidal, and cerebellar signs. Polysomnographic studies showed an absence of stages 3 and 4, and REM. She died 8 months after onset. On neuropathologic examination, there was major thalamic involvement characterized by neuronal loss, spongiform changes, and prominent gliosis. The inferior olivary nuclei exhibited chromatolysis, neuronal loss, and gliosis. Spongiform changes were mild in the neocortex and not evident in the cerebellum. PrP immunopositivity was present in these areas as well as in the thalamus. PRNP analysis showed the haplotype E200K-129M. Western blot analysis showed the presence of proteinase K (PK)-resistant PrP (PrP(sc)) with the nonglycosylated isoform of approximately 21 kd, corresponding in size to that of type 1 PrP(sc). N-terminal protein sequencing demonstrated PK cleavage sites at glycine (G) 82 and G78, as previously reported in CJD with the E200K-129 M haplotype. CONCLUSIONS: Insomnia may be a prominent early symptom in cases of CJD linked to the E200K-129M haplotype in which the thalamus is severely affected. ( info)

9/56. Relationship between amount of sleep and daytime sleepiness in three cases.

    The effect of sleep amount on daytime sleepiness was investigated, and the appropriate amount of sleep for each subject was evaluated. Three children were longitudinally evaluated for three conditions: control, sleep extension, and sleep reduction. A sleep latency test was conducted five times for each condition at 2-h intervals from 10.00 hours. The results showed that the effects of sleep loss increased sleepiness at 10.00 hours and 18.00 hours, and there were positive correlations between sleep amount and sleep latency for each subject (r = 0.590-0.903). Whether or not the amount of sleep for each subject was sufficient was evaluated from the relationship between the two measures. ( info)

10/56. Transient total sleep loss in cerebral Whipple's disease: a longitudinal study.

    A case with transient, almost complete sleep loss caused by cerebral manifestation of Whipple's disease (WD) is presented. Cerebral WD is rare and in most cases occurs after gastrointestinal infection. In our case, a progressive and finally almost complete sleep loss was the initial and predominant symptom. Polysomnographic studies in several consecutive nights and over 24 h showed a total abolition of the sleep-wake cycle with nocturnal sleep duration of less than 15 min. Endocrine tests revealed hypothalamic dysfunction with flattening of circadian rhythmicity of cortisol, TSH, growth hormone and melatonin. cerebrospinal fluid (CSF) hypocretin was reduced. [18F]deoxyglucose positron emission tomography (FDG-PET) revealed hypermetabolic areas in cortical and subcortical areas including the brainstem, which might explain sleep pathology and vertical gaze palsy. In the course of treatment with antibiotics and additional carbamazepine for 1 year, insomnia slowly and gradually improved. Endocrine investigations at 1-year follow-up showed persistent flattening of circadian rhythmicity. The FDG-PET indicated normalized metabolism in distinct regions of the brain stem which paralleled restoration of sleep length. The extent of sleep disruption in this case of organic insomnia was similar to cases of familial fatal insomnia, but was at least partially reversible with treatment. ( info)
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