The term
dysautonomia refers to a change in autonomic nervous system function that adversely affects health. The changes range from transient, occasional episodes of neurally mediated
hypotension to progressive
neurodegenerative diseases; from disorders in which altered autonomic function plays a primary pathophysiologic role to disorders in which it worsens an independent pathologic state; and from mechanistically straightforward to mysterious and controversial entities. In chronic
autonomic failure (pure autonomic failure,
multiple system atrophy, or autonomic failure in
Parkinson disease),
orthostatic hypotension reflects sympathetic neurocirculatory failure from
sympathetic denervation or deranged reflexive regulation of sympathetic outflows. Chronic
orthostatic intolerance associated with postural
tachycardia can arise from cardiac sympathetic activation after "patchy" autonomic impairment or blood volume depletion or, as highlighted in this discussion, from a primary abnormality that augments delivery of the sympathetic
neurotransmitter norepinephrine to its receptors in the heart. Increased sympathetic nerve traffic to the heart and kidneys seems to occur as
essential hypertension develops. Acute panic can evoke coronary
spasm that is associated with sympathoneural and adrenomedullary excitation. In
congestive heart failure, compensatory cardiac sympathetic activation may chronically worsen myocardial function, which rationalizes treatment with beta-
adrenoceptor blockers. A high frequency of positive results on tilt-table testing has confirmed an association between the
chronic fatigue syndrome and
orthostatic intolerance; however, treatment with the
salt-retaining
steroid fludrocortisone, which is usually beneficial in primary chronic autonomic failure, does not seem to be beneficial in the
chronic fatigue syndrome.
Dysautonomias are an important subject in clinical neurocardiology.