Abstract: The autonomic nervous system comprises a vast and tightly integrated network that regulates well-known functions like blood pressure (BP), heart rate, respiration and sleep. It also extends to such important functions as endocrine regulation, appetite and diurnal rhythms. This richness is exemplified in the presentations of this forum, that extends from brain, spinal cord to peripheral nerve. I will briefly exemplify how we can track autonomic failure, focusing on sudomotor and adrenergic evaluation and finally, how we can harness known autonomic physiology to enhance treatment of orthostatic hypotension. Sudomotor failure can be due to lesions of the brain, spinal cord, autonomic ganglia or peripheral nerve. The pattern of anhidrosis on the thermoregulatory sweat test (TST) can provide insights to the site of the lesion. The postganglionic axon can be evaluated using the quantitative sudomotor axon reflex test (QSART). Combining the 2 tests can define the site (preganglionic vs postganglionic) of the lesion. Baroreflex failure is responsible for orthostatic hypotension (OH) and a fixed heart rate. It is possible to separately evaluate the vagal and adrenergic components of the baroreflex in the clinical autonomic laboratory. The vagal component of the baroreflex is evaluated by relating heart period to BP change. The adrenergic component can be quantitated by evaluating BP recovery indices. Finally, by enhancing ganglionic neurotransmission, it has been possible to define strategies to alleviate or reduce OH without aggravating supine hypertension. This has been achieved by the use of a cholinesterase inhibitor that increases the safety factor of ganglionic neurotransmission.
Publication Year: 2007
Publication Date: 2007-08-02
Language: en
Type: article
Indexed In: ['crossref']
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