Transient total sleep loss in cerebral Whipple's disease: a longitudinal study
Autor: | Freimut D. Juengling, Horst Gann, Mathias Berger, Martin Schumacher, Klaus Lieb, Ulrich Voderholzer, Martin Reincke, Axel von Herbay, Dieter Riemann, Seiji Nishino, Magdolna Hornyak, Emmanuel Mignot |
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Rok vydání: | 2002 |
Předmět: |
Adult
Male medicine.medical_specialty Hydrocortisone Polysomnography Cognitive Neuroscience Hypothalamus Thyrotropin Fixation Ocular Neuropsychological Tests Melatonin Behavioral Neuroscience Cerebrospinal fluid Fluorodeoxyglucose F18 Sleep Disorders Circadian Rhythm Internal medicine medicine Insomnia Humans Whipple's disease Circadian rhythm Fatal familial insomnia Orexins Neuropeptides Intracellular Signaling Peptides and Proteins Brain Electroencephalography General Medicine medicine.disease Circadian Rhythm Orexin Endocrinology Sleep Deprivation Brainstem Radiopharmaceuticals medicine.symptom Carrier Proteins Psychology Whipple Disease Follow-Up Studies Tomography Emission-Computed medicine.drug |
Zdroj: | Journal of Sleep Research. 11:321-329 |
ISSN: | 1365-2869 0962-1105 |
DOI: | 10.1046/j.1365-2869.2002.00311.x |
Popis: | SUMMARY 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. |
Databáze: | OpenAIRE |
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