Original ArticleHyperviscosity as a possible cause of positive acoustic evoked potential findings in patients with sleep apnea: A dual electrophysiological and hemorheological study
Introduction
Obstructive sleep apnea (OSA) syndrome is often associated with substantial vascular morbidity and mortality, but why that is the case remains controversial.
A recent study concluded that OSA significantly increases the risk of stroke and death from any cause [1]. In this study, risk association was independent of major factors for stroke such as hypertension, suggesting that additional pathogenetic mechanisms may play a contributory role. OSA induced hyperviscosity [2], [3] leading to altered cerebral blood flow and hypercoagulability could be one of these possible mechanisms. Based on our prior observation [4] of an association among OSA, hyperviscosity and changes in normal patterns of brain stem auditory evoked potentials (BAEPs) in OSA patients with hyperviscosity, we sought to study BAEPs changes in OSA patients with and without hyperviscosity in an effort to more carefully document specific BAEPs changes that are reliably associated with hyperviscosity in OSA patients. BAEP is an inexpensive, reproducible method used in a variety of clinical settings.
A small number of studies have investigated BAEP functions in OSA patients, but these studies were plagued by small sample sizes, lack of control groups and inconsistent findings across laboratories [5], [6], [7], [8], [9]. While several studies have reported symmetric wave prolongations in OSA patients of varying severities, a few studies reported normal BAEP functions in OSA [10], [11], [12].
In at least one study of severe OSA patients, BAEP abnormalities have been linked with lesions localized to the middle brain stem regions, and BAEP abnormalities increased with the duration of the disease [13].
Interestingly, although OSA is often characterized by altered hemorheological state, the lack or presence of hyperviscosity was not considered in these previous BAEP studies. In this study we studied a large sample of OSA patients with hyperviscosity of varying severity and compared them with control patients without hyperviscosity. We also studied BAEP functions before and after CPAP therapy. This experimental design allowed us to definitively test the effect of hyperviscosity on BAEP functions in OSA patients.
Section snippets
Patients
We recruited a convenience sample of 800 newly diagnosed patients with OSA to carry out hemorheological and BAEP studies both at baseline and after CPAP therapy. Those patients with abnormal rheology and/or BAEP evaluation at six months had an additional hemorheological and BAEP study following hemodilution.
Out of 800 consecutive male patients (aged between 30–55 years) newly diagnosed with OSA (apnea/hypopnea index > 5/h) by a polysomnographic study, 763 were candidates for CPAP therapy
Results
Forty-six percent (N = 282) of the patients evidenced hyperviscosity and 53% (N = 328) had normal rheological findings. Evoked potential changes appeared only in the hyperviscosity positive subgroup. Of these, 84% (N = 239) evidenced BAEP changes with 24% (N = 57) demonstrating sensorineuronal and 76% (N = 182) demonstrating brain stem type abnormalities. Abolition of all waves including wave I was evident in the sensorineuronal cases. This pattern indicates cochlear lesion. In all cases abnormalities
Discussion
The present study was designed to explore the potential relationship between hyperviscosity and abnormal BAEP findings in OSA. Although not all OSA patients with hyperviscosity had abnormal BAEP findings, the fact that BAEP changes were restricted to the hyperviscosity positive OSA subgroup supported our hypothesis. Reversibility of brain stem type BAEP changes with the normalization of the viscosity – following effective CPAP or hemodilution therapy – provided further evidence for this
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Comparison tests for plasma viscosity measurements
2012, International Communications in Heat and Mass TransferCitation Excerpt :Hyperviscosity syndrome described as elevated plasma viscosity manifests in a large number of diseases such as cardiovascular diseases [1,2], acute stroke and transient ischemic attack [3,4], dementia [5], diabetic microcirculatory diseases [6], peripheral arterial disease [7,8], rheumatoid arthritis [9], systemic lupus erythematosus [10], paraproteinemia [11], leukemia [12], sickle cell disease [13], retinal vein occlusion [14], sudden hearing loss [15], sleep apnea [16], mental disorders [17], Raynaud's syndrome [18], and preeclampsia [19].
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