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Autonomic neuropathies.

Abstract

There is a spectrum of acute autonomic neuropathies. Acute panautonomic neuropathy (pandysautonomia), characterized by severe widespread sympathetic and parasympathetic failure, is at one extreme. Guillain-Barré syndrome is at the other end of the spectrum, where the brunt of the disorder falls on the somatic nervous system. Pure acute panautonomic neuropathies are relatively rare. The majority of acute autonomic neuropathies have some minor somatic features. Dysautonomia may be restricted to the cholinergic system (acute cholinergic neuropathy), adrenergic system, or other organ systems (eg, motility disorders). Recently, an important gap in the clinical description of idiopathic autonomic neuropathies and their course was filled, with neurologic and autonomic testing end-points. About one in four to one in three patients will improve substantially. Two other manifestations of autonomic neuropathy are the pseudoobstruction and postural tachycardia syndromes. Loss of the baroreceptors and consequent impairment of buffering of blood pressure results in wild swings in blood pressure that are treatable. Correcting anemia improves orthostatic tolerance, if necessary by hemopoietin. Improved evaluation of neural structure, in skin and in the laboratory, has led to better quantitation of autonomic failure and mechanisms of syncope. This understanding has been extended to the frequency domain and to a study of cerebral vasoregulation.

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BibTeXRIS

P A Low. 1994. Autonomic neuropathies.. https://doi.org/10.1097/00019052-199410000-00007

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Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients.

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.

Autonomic Nervous System Diseases↗