Fatal familial insomnia: Sleep, neuroendocrine and vegetative alterations
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Repeating patterns of sleep restriction and recovery: Do we get used to it?
2016, Brain, Behavior, and ImmunityFatal familial insomnia and the role of the thalamus in sleep regulation
2011, Handbook of Clinical NeurologyCitation Excerpt :Autonomic features can be seen to have a state-dependent modulation, sympathetic activity decreasing whenever short periods of SWS appear on the EEG. They are attended by increased plasma levels of catecholamines, such as norepinephrine and epinephrine, and are associated with endocrine changes with hypercortisolemia in the presence of normal or even low levels of adrenocorticotropic hormone (Portaluppi et al., 1994a; Montagna et al., 1995). Abnormal plasma levels of catecholamines and sympathetic activation are associated with loss of their circadian rhythmicity (Avoni et al., 1991) with, in particular, disruption of somatotropin secretion (Portaluppi et al., 1995).
Sleep, Breathing, and Neurologic Disorders
2009, Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects: Third EditionSleep and Psychoneuroimmunology
2009, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Mice devoid of the prion protein gene have alterations in circadian rhythms and sleep.38,39 Human fatal familial insomnia is characterized by profound alterations in sleep secondary to prion-induced degeneration of the thalamus.40 “Sleeping sickness,” perhaps the most notorious of infection-induced alterations in sleep, is caused by the protozoan Trypanosoma brucei.
Sleep, Breathing, and Neurologic Disorders
2009, Sleep Disorders Medicine