Proceedings of The Physiological Society
University of Cambridge (2008) Proc Physiol Soc 11, PC108
Effects of essential hypertension on short latency human somatosensory evoked potentials
L. Edwards1, C. Ring1, D. McIntyre1, U. Martin2, J. B. Winer3
1. School of Sport & Exercise Sciences, University of Birmingham, Birmingham, United Kingdom. 2. School of Medicine, University of Birmingham, Birmingham, United Kingdom. 3. Neurology, University Hospital Birmingham, Birmingham, United Kingdom.
Reduced sensitivity to peripheral nerve stimulation in hypertension may be explained by subclinical axonal neuropathy of sensory afferents (Edwards et al. 2008). The current study aimed to further explore this phenomenon by investigating whether the ascending somatosensory pathway is affected by hypertension. Following ethical approval and in accordance with the Declaration of Helsinki, we examined the peripheral median nerve N9, spinal N13 and cortical N20 short latency somatosensory evoked potentials (sSEPs) in 14 patients with unmedicated essential hypertension (9 men, 40 ± 6 years; mean ± sd) and 22 normotensive volunteers (10 men, 37 ± 6 years). The sSEPs were elicited by 100 μs electrocutaneous stimulation of the median nerve at the wrist for 2000 trials (Mauguiere et al. 1999). A series of 2 Group (hypertensive, normotensive) ANCOVAs were performed on sSEP amplitudes and latencies, with age and arm length as covariates. N9 amplitudes were significantly reduced (P<.01) in hypertensives (3.60 ± 1.26 μV) compared to normotensives (5.71 ± 2.24 μV). In contrast, N20 amplitudes were not different between hypertensives (4.38 ± 2.35 μV) and normotensives (3.87 ± 2.20 μV). Furthermore, none of the sSEP latencies differed between groups: N9 (hypertensives: 10.21 ± 0.78 ms, normotensives: 10.36 ± 0.76 ms), N13 (hypertensives: 13.33 ± 0.99 ms, normotensives: 13.57 ± 0.98 ms) and N20 (hypertensives: 19.23 ± 1.26 ms, normotensives: 19.35 ± 0.95 ms). In addition, a 2 Group (hypertensive, normotensive) ANCOVA, with age as a covariate, performed on the sensory median nerve conduction velocity, revealed no differences between hypertensives (61.46 ± 3.77 m/s) and normotensives (61.27 ± 3.63 m/s). Two hierarchical regression analyses were conducted to determine the association between N9 amplitude and 24-hour ambulatory systolic and diastolic blood pressures while accounting for confounding by age and stimulation-to-recording distance. N9 amplitudes were inversely associated with systolic (P<.01) and diastolic (P<.05) blood pressure. As the amplitude of a sensory action potential reflects the number of large diameter myelinated fibres synchronously depolarised in the vicinity of the active recording electrode (Buchthal & Rosenfalck, 1966), a reduction may indicate axonal loss (Gilliatt, 1978). As N9 amplitudes, generated by peripheral sensory nerve fibres at the brachial plexus, were 37% smaller in hypertensives than normotensives these data suggest that hypertension affects the peripheral nervous system by reducing the number of active sensory nerve fibres without affecting myelination. However, hypertension does not seem to affect the afferent somatosensory pathway within the central nervous system. In sum, hypertension may represent a risk factor for peripheral neuropathy of the sensory nerves.
Where applicable, experiments conform with Society ethical requirements