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Journal of Neurology, Neurosurgery, and Psychiatry 2008;79:743-744; doi:10.1136/jnnp.2008.145797
Copyright © 2008 by the BMJ Publishing Group Ltd.

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EDITORIAL COMMENTARIES

Obstructive sleep apnoea and CMT1A: answers and more questions

Michael E Shy

Correspondence to:
Dr Michael E Shy, Department of Neurology, Wayne State University, 421 East Canfield, Elliman 3217, Detroit MI, 48201, USA; m.shy@wayne.edu

The first 150 words of the full text of this article appear below.

Dziewas and colleagues1 report that patients with Charcot–Marie–Tooth disease type 1A (CMT1A) have an increased prevalence of obstructive sleep apnoea (see page 829). Sleep apnoea can be caused by CNS abnormalities; in these cases there is decreased respiratory effort. In obstructive sleep apnoea, also known as the obstructive sleep apnoea–hypopnoea syndrome (OSAHS), the cause is not from the CNS but from a physical obstruction to breathing. The obstruction can be an anatomical abnormality in the upper airway—for example, enlarged tonsils. Obesity, being male, advanced age and hypertension are all associated with OSAHS. The obstruction site is usually in the collapsible portions of the pharynx: the velopharynx, oropharynx or hypopharynx. Sleeping patients can overcome the obstruction by increasingly forceful inspiration which eventually creates enough inspiratory pressure to re-open the occluded airway. However, this crescendo respiratory pattern disrupts NREM/REM sleep causing daytime sleepiness and fatigue. OSAHS also causes an increased . . . [Full text of this article]


Relevant Article

Increased prevalence of obstructive sleep apnoea in patients with Charcot–Marie–Tooth disease: a case control study
R Dziewas, N Waldmann, M Böntert, H Hor, T Müller, A Okegwo, E B Ringelstein, and P Young
J. Neurol. Neurosurg. Psychiatry 2008 79: 829-831. [Abstract] [Full Text] [PDF]






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