Electrophysiological diagnosis of possible brain-stem lesions in patients with severe obstructive sleep apnoea syndrome

Citation
J. Schlegel et Pp. Urban, Electrophysiological diagnosis of possible brain-stem lesions in patients with severe obstructive sleep apnoea syndrome, DEUT MED WO, 124(20), 1999, pp. 613-617
Citations number
32
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Volume
124
Issue
20
Year of publication
1999
Pages
613 - 617
Database
ISI
SICI code
Abstract
Background and objective: The pathophysiological basis of obstructive sleep apnoea syndrome (OSAS) is a loss of tone of the oropharyngeal muscles duri ng sleep, leading to partial and/or total collapse of the oropharyngeal mus cle tube. The norma I inspiration-synchronous activation (ISA) of the tongu e muscles is diminished or lost in patients with OSAS. Observations of OSAS in patients with ischaemic pontomedullary lesions, syringobulbia (syringom yelia), olivo-ponto-cerebellar atrophy or disseminated encephalopathy have indicated that it is due to impairment of ISA, In this study systematic ele ctrophysiological studies (EPS) were undertaken in patients with severe OSA S, as demonstrated by polysomnography, to determine whether, in addition to the central abnormality of oropharyngeal muscular tone, one can demonstrat e an increased incidence of sublinical, functional disorder in the brain st em as well as any pointers to a central localization of abnormalities in OS AS. Patients and methods: 19 patients with severe OSAS were examined for the pr esence of subclinical brain-stem lesions by means of acoustic evoked potent ials, blinking reflex, masseter reflex, masseter silent period, electronyst agmogram together with vestibular testing and magnetic evoked potentials of the tongue musculature. Results: Findings were unremarkable in 15 of the 19 patients. EPS gave repr oducible evidence of functional left pontine (blink reflex) brain-stem lesi ons in two of the patients and of bilateral pontomesencephalic (masseter re flex) brain-stem lesions in the other two. Conclusion: In the absence of systematic abnormalities our findings speak a gainst relevant brain-stem lesions being the cause and/or consequence of OS AS.