Abstract
W 1. The key finding presented is that cutaneous electrical stimulation delivered over the thoracic spine of subjects with SCI elicits blood pressure elevation and tachycardia, thereby ameliorating symptoms of orthostatic hypotension, which the investigators suggest is the result of direct stimulation of propriospinal and sympathetic preganglionic neurons, or preferential excitation of large diameter afferents. However, an older, related investigation is noteworthy for comparison in this regard: Sampson and colleagues were able to show very similar improvement in SCI subjects' tolerance of orthostatic challenge by applying, in separate trials, cutaneous electrical stimulation over two nonspinal sites, that is, bony prominences and muscle bellies in the lower extremities.
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Their use of the former site as a control allowed them to exclude a muscular pump mechanism for the observed hemodynamic changes, and thereby argue compellingly for an autonomic dysreflexia-based mechanism for the observed responses. We suggest that Phillips and colleagues consider using stimulation over a control site on the anterior chest wall or abdomen in an analogous manner, to bolster their argument that they generated the observed hemodynamic changes by stimulating preganglionic/ganglionic neurons directly, rather than through a more conventional autonomic dysreflexia-based mechanism, as was argued by Sampson and colleagues for their related, albeit distinct, stimulation protocol. 2. With regard to the proposed mechanism, we also suggest further consideration of the contribution of large diameter afferents to the observed responses. Several lines of evidence indicate their frequent involvement in autonomic dysreflexia, in addition to a C-fiber-based mechanism: Burton and collegaues showed hypertension and tachycardia in response to nonpainful cutaneous electrical stimulation in SCI subjects, whereas subcutaneous injection of hypertonic saline produced no such responses.
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Matthews and colleagues showed that autonomic dysreflexia occurs whether or not surface anesthesia is induced before functional electrical stimulation.
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Further, to propose that C-fibers are not involved in mediating the observed response based solely on the absence of an uncontrolled rise in blood pressure may oversimplify the role of C-fibers in the sensory-sympathetic coupling post-SCI, given that these afferent fibers constitute several functionally distinct groups, each with dissimilar responsiveness to numerous innocuous and noxious stimuli.
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Clearly, autonomic dysreflexia may result from a plethora of types of sensory inputs, as the investigators have noted elsewhere,
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and SCI athletes have exploited the “autonomic neuroprosthesis” strategy for many years, for “boosting” their exercise performance by intentionally inducing autonomic dysreflexia.
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We thank Phillips and colleagues for proposing this fascinating approach to an important clinical problem, and look forward to their further work in this area.