Cerebrovascular disorders are a major cause of morbidity
and death in the United States and Europe [1–10].
Sudden death following acute stroke has been reported,
but is beyond what is expected from a concomitant
coexisting coronary artery disease [11]. Several studies
have demonstrated that cardiac dysfunction may occur
after vascular brain injury without any evidence of primary
heart disease [12–16]. Furthermore, during acute
stroke, autonomic dysfunction, for example, elevated
arterial blood pressure, arrhythmia, and ischemic cardiac
damage, has been reported, which may hinder the prognosis
[17–23]. Autonomic dysfunction after a stroke
involves the cardiovascular, respiratory, sudomotor, and
sexual systems. Although the exact mechanism is not
fully understood, several studies suggest an anatomical
asymmetry between the right and left cerebral hemispheres
in the modulation of autonomic nervous system
activity of the central nervous system (CNS). It is well
known that cerebrovascular diseases, particularly ischemic
stroke, can alter the function of the autonomic system
both acutely and chronically [24–26]. These autonomic
changes can be cardiac, respiratory, sudomotor, or
sexual in nature [27] and can be detected clinically and
electrophysiologically [14]. Some of these changes have
an impact on the morbidity and mortality in patients suffering
a stroke [3,26]. Multiple and different anatomical
regions of the brain have been suggested to be involved,
but the exact pathogenesis and mechanism(s) leading to
these changes is not fully understood [24,28]. In this
review paper, we will discuss the anatomy and physiology
of the autonomic nervous system and the mechanism(s)
suggested to cause autonomic dysfunction after
stroke. We will also review the spectrum of autonomic
dysfunction associated with stroke and the influence of
hemispheric damage location on the occurrence of autonomic
dysregulation.