Increased sympathetic nervous system activity and reduced parasympathetic activity poststroke contribute to cardiac arrhythmias and higher infection rates.
Poststroke autonomic dysfunction is a key contributor to non-neurogenic mortality, including cardiac arrhythmias and infections, highlighting the need to understand the chronic systemic effects of stroke.
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Stroke is the fourth leading cause of death in the United States and the second most common cause of death worldwide; stroke is also the leading cause of long-term disability worldwide. It is clear that the consequences of cerebral ischemia reach beyond the brain into the periphery, and a significant number of stroke related deaths are the result of conditions that develop poststroke in the periphery. The two leading causes of non-neurogenic death poststroke are cardiac abnormalities and infections. Changes in autonomic nervous system function that favor increased sympathetic nervous system activity and reduced parasympathetic nervous system activity appear to be causative factors in both conditions. Here, we review the evidence that sympathetic nervous system activity increases and parasympathetic nervous system activity declines poststroke. We discuss effects of autonomic dysfunction on cardiac arrhythmias and heart rate variability. Finally, we discuss the evidence supporting a role for autonomic dysfunction in the increased incidence of infection poststroke. Although the death rate from stroke is declining in the United States, the incidence of stroke is not. With more patients surviving the initial ischemic event it is important that we broaden our understanding of the chronic effects of stroke on the human condition.
Dorrance et al. (Wed,) reported a other. Increased sympathetic nervous system activity and reduced parasympathetic activity poststroke contribute to cardiac arrhythmias and higher infection rates.
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