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Erschienen in: Current Neurology and Neuroscience Reports 11/2016

01.11.2016 | Demyelinating Disorders (DN Bourdette and M Cameron, Section Editors)

Hypothalamic Dysfunction and Multiple Sclerosis: Implications for Fatigue and Weight Dysregulation

verfasst von: Kevin G. Burfeind, Vijayshree Yadav, Daniel L. Marks

Erschienen in: Current Neurology and Neuroscience Reports | Ausgabe 11/2016

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Abstract

Signs and symptoms of multiple sclerosis are usually attributed to demyelinating lesions in the spinal cord or cerebral cortex. The hypothalamus is a region that is often overlooked yet controls many important homeostatic functions, including those that are perturbed in multiple sclerosis. In this review we discuss how hypothalamic dysfunction may contribute to signs and symptoms in people with multiple sclerosis. While dysfunction of the hypothalamic-pituitary-adrenal axis is common in multiple sclerosis, the effects and mechanisms of this dysfunction are not well understood. We discuss three hypothalamic mechanisms of fatigue in multiple sclerosis: (1) general hypothalamic-pituitary-adrenal axis hyperactivity, (2) disordered orexin neurotransmission, (3) abnormal cortisol secretion. We then review potential mechanisms of weight dysregulation caused by hypothalamic dysfunction. Lastly, we propose future studies and therapeutics to better understand and treat hypothalamic dysfunction in multiple sclerosis. Hypothalamic dysfunction appears to be common in multiple sclerosis, yet current studies are underpowered and contradictory. Future studies should contain larger sample sizes and standardize hormone and neuropeptide measurements.
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Metadaten
Titel
Hypothalamic Dysfunction and Multiple Sclerosis: Implications for Fatigue and Weight Dysregulation
verfasst von
Kevin G. Burfeind
Vijayshree Yadav
Daniel L. Marks
Publikationsdatum
01.11.2016
Verlag
Springer US
Erschienen in
Current Neurology and Neuroscience Reports / Ausgabe 11/2016
Print ISSN: 1528-4042
Elektronische ISSN: 1534-6293
DOI
https://doi.org/10.1007/s11910-016-0700-3

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