No abstract

Obstructive sleep apnea syndrome (OSAS) provokes oxidative stress and ischemia, which affects the central nervous system. The degeneration of neurons in the brainstem due to periodic hypoxia can be evaluated by vestibular and audiologic tests. The objective of this study is to determine brainstem damage in severe OSAS patients with the help of vestibular evoked myogenic potential (VEMP) responses. Prospective, randomize, double-blind. Research-training hospital. We compared cervical vestibular evoked myogenic potential (cVEMP) responses between severe OSAS patients and a control group. 54 patients were included and divided into the OSAS group, with severe OSAS (apnea-hypopnea index, AHI >70), and a control group with snoring without OSAS (AHI <5). Both groups underwent cVEMP. Bilateral recordings with simultaneous binaural logon stimulations were used during VEMP recordings. The existing p1n1 and n2p2 responses, p1, n1, n2, and p2 latencies and amplitudes, and p1n1 and n2p2 intervals were measured. Statistically significant differences were revealed between patients and controls for the response rate of the p1n1, n2p2 and p1n1, n2p2 amplitudes. There were no significant differences between the two groups with respect to the latencies of p1, n1, n2 and p2, or the p1n1 and n2p2 intervals. The VEMP response rate was lower in severe OSAS patients, and all amplitudes were shorter than in healthy subjects. VEMP recordings in severe OSAS subjects demonstrates abnormalities in brainstem pathways. It appears that brainstem damage in severe OSAS can be detected by cVEMP recordings.

Vestibular-evoked myogenic potentials (VEMP), short-latency electromyographic responses elicited by acoustic stimuli, evaluate the function of vestibulocollic reflex and may give information about brainstem function. The aim of the present study is to evaluate the potential contribution of VEMP to the diagnosis of multiple sclerosis (MS). Fifty patients with MS and 30 healthy control subjects were included in this study. The frequency of VEMP p1-n1 and n2-p2 waves; mean p1, n1, n2, and p2 latency; and mean p1-n1 and n2-p2 amplitude were determined. The relation between clinical and imaging findings and VEMP parameters was evaluated. The p1-n1 and n2-p2 waves were more frequently absent in MS than in control subjects [p1-n1 wave absent: MS, 25 (25 %) ears; control, 6 (10 %) ears; P ≤ 0.02] [n2-p2 wave absent: MS, 44 (44 %) ears; control, 7 (12 %) ears; P ≤ 0.001]. The mean p1-n1 amplitude was lower in MS than in control subjects (MS, 19.1 ± 7.2 μV; control, 23.3 ± 7.4 μV; P ≤ 0.002). A total of 24/50 (48 %) MS patients had VEMP abnormalities (absent responses and/or prolonged latencies). VEMP abnormalities were more frequent in patients with than without vestibular symptoms (P ≤ 0.02) and with brainstem functional system score (FSS) ≥ 1 than FSS = 0 (P ≤ 0.02). In patients with MS, absence of p1-n1 wave was more frequent in patients with than without vestibular symptoms [absence of p1-n1 wave: vestibular symptoms, 9 (45 %) ears; no vestibular symptoms, 16 (20 %) ears; P ≤ 0.03] and patients with Expanded Disability Status Scale (EDSS) score ≥ 5.5 [absence of p1-n1 wave: EDSS ≥ 5.5, 7 (70 %) ears; EDSS <5.5, 18 (20 %) ears; P ≤ 0.001]. Abnormal VEMP may be noted in MS patients, especially those with vestibular symptoms and greater disability. The VEMP test may complement other studies for diagnosis and follow-up of patients with MS.

Our findings suggested that CPAP therapy provides more homogenous conduction through atria in patients with OSA. This effect may translate into decreased risk for AF associated with OSA.