Article

Idiopathic orthostatic hypotension

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Abstract

NORMAL persons have adaptive mechanisms that help to maintain a constant cerebral blood flow. Changes from the recumbent to the upright position may cause pooling of fluid in the lower extremities, which leads to decreases in venous return and in cardiac output. This results in increased action in sympathetic output, which leads to increases in heart rate, in peripheral resistance, in plasma norepinephrine content, in urinary catecholamine concentration, and to venous constriction. Adequate cerebral circulation is maintained by a rise in the diastolic arterial pressure as a consequence of the sympathetic action and a dilatation of the cerebral blood vessels.

Postural hypotension may result from the use of hypotensive drugs, blood volume depletion from blood loss or sodium depletion, and conditions associated with low blood volume such as Addison’s disease. Neurologic diseases including diabetic peripheral neuropathy, tabes dorsalis, multiple sclerosis, syringomyelia, and cerebral arteriosclerosis, have been associated with postural hypotension.

In some cases of postural hypotension there is no recognized disease. Idiopathic orthostatic hypotension was clearly described by Bradbury and Eggleston1 in 1925. The pathognomonic feature is the orthostatic hypotension. Other evidences of autonomic dysfunction are anhidrosis, impotence, and sphincter and especially bladder dysfunction. In a few patients there are, in addition to the autonomic dysfunction, evidences of motor disturbance with a parkinsonian-like syndrome, general muscle weakness, ataxia, increased tendon reflexes, positive Babinski responses, fasciculation, and ptosis.2–4 This report concerns a patient with such impairment.

Report of a case

A 51-year-old Caucasian housewife was first examined at the Cleveland Clinic . . .


 

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