Treatment of Patients with Neurogenic Orthostatic Hypotension

Neurogenic orthostatic hypotension (OH) is caused by disorders of the autonomic nervous system, and these disorders are classified as either primary (mainly multiple system atrophy, pure autonomic failure, and autonomic failure associated with Parkinson’s disease) or secondary (central nervous system diseases, peripheral neuropathies and systemic diseases). The effects of OH are often debilitating, in many cases confining the patient to bed. Moreover, longitudinal studies have shown that OH increases the risk of stroke, myocardial ischaemia and mortality.Treatment of patients with OH is aimed at reducing the postural symptoms. Nonpharmacological measures represent the first step in therapy, of which fluid repletion and physical counter manoeuvres have proven very effective.The pharmacological management of patients with OH can be problematic, and the possibility of developing supine hypertension and subsequent congestive heart failure should be kept in mind, especially in those patients with a pre-existing cardiovascular risk, such as diabetes mellitus or ischaemic heart disease.Randomised and controlled studies for the treatment of OH are still scarce and limited to a few agents and groups of patients. The drugs currently used are fludrocortisone, midodrine and dihydroergotamine. Fludrocortisone expands the extravascular body fluid volume and improves α-adrenergic sensitivity. Midodrine is a peripheral, selective α1-adrenergic agonist that causes arterial and venous vasoconstriction. Dihydroergotamine is an α1-adrenergic agonist with a selective venous vasoconstriction effect. In anaemic patients, erythropoietin has proven beneficial; postprandial hypotension responds to octreotide, which also improves orthostatic tolerance and does not cause supine hypertension.This review will discuss the therapeutic strategies for treating patients with symptomatic neurogenic OH.