Cardiovascular Reflexes and Autonomic Neuropathy

Clinical features of autonomic neuropathy include postural hypotension, sweating abnormalities, disturbance of body temperature regulation, gastric fullness and nausea, intermittent nocturnal diarrhoea, constipation, bladder problems and impotence. In diabetic patients, gustatory sweating and hypoglycaemic unawareness also sometimes occur (Johnson & Spalding, 1974). The onset of symptoms is usually insidious and permanent, but may occasionally be acute and reversible (Young, Asbury, Corbett & Adams, 1975). Autonomic dysfunction can arise from three main causes: first, those where the damage to the autonomic nervous system is isolated, as in primary postural hypotension (Bannister, Sever & Gross, 1977) and familial dysautonomia (Brunt & McKusick, 1970); secondly, those caused by toxic or pharmacological agents which interfere with autonomic reflexes; thirdly, those associated with systemic disease, of which diabetes mellitus is the most common. Other diseases which may cause autonomic dysfunction include amyloidosis, porphyria, tetanus, polyneuritis, tabes dorsalis, parkinsonism, chronic renal failure and alcoholism, and occasionally autonomic neuropathy has been associated with carcinoma of the bronchus or the pancreas (Johnson & Spalding, 1974). Although it is possible to localize lesions within the autonomic nervous system to afferent or efferent sympathetic or parasympathetic pathways (Johnson & Spalding, 1974; Moskowitz, 1977), many of the available tests are complex and invasive and often lack adequate control measurements (Young et al., 1975). Because of the patchy nature of autonomic neuropathy, current interest has centred around the search for bedside tests that are ‘global’, reproducible and non-invasive. This review summarizes the present state of knowledge of simple tests of cardiovascular reflex function in the clinical evaluation of autonomic neuropathy, particularly in diabetic subjects.