A report in the journal Stroke indicates that a sympathetic nervous system over-activity and predominance is associated with higher rate of infection following acute intracerebral hemorrhage (ICH).
Stroke is a major cause of morbidity and the third leading cause of death in the Western world. Infections occur commonly following stroke and adversely influence outcome. Pulmonary and urinary infections are the most frequent medical complications after stroke and the leading cause of death.
The neuroendocrine and immune mechanisms leading to high occurrence of infections after stroke remain poorly understood. Emerging research suggests that infections early after stroke could be the manifestation of a stroke-induced immunodepression syndrome, which is now recognized as an independent factor associated with increased susceptibility.
This phenomenon has been linked to the enhanced sympathetic nervous system (SNS) activity observed after stroke. Catecholamines, the principal SNS neuromediators are known to drive a shift from T helper (Th)1 to Th2 immune responses, resulting in Th2-related cytokine production predominance.
Th2-related cytokines such as interleukin (IL)-10 exert potent immunosuppressive effects, and previous research has shown that the ‘sympathetic storm’-induced IL-10 release due to acute accidental or iatrogenic brain trauma may cause “brain-mediated” immunodepression and subsequent infections (Woiciechowsky et al., 1998, Nat. Med. 4: 808–813). More recent studies indicate a strong association between high catecholamine levels and poststroke infections in patients with acute ischemic stroke.
In the Stroke study, Marek Sykora and colleagues from the Department of Neurology, University of Heidelberg, Heidelberg, Germany, investigated the role of autonomic shift in increased susceptibility to infection after acute intracerebral hemorrhage (ICH).
The authors report that an autonomic shift toward SNS predominance is independently linked to higher occurrence of infection after ICH.
This, and previous studies indicate that the sympathetic activation may play a central role in the immunodepression associated with central nervous system injury. The authors discuss that the occurrence of bacterial infections after stroke can be prevented by administration of beta-blockers, in animal studies, while in humans, in a recent retrospective study, stroke patients with beta-blocker treatment less often had stroke-related pneumonia.
Thus, according to the authors, the modulation of autonomic nervous system function, alone or in combination with prophylactic antibiotic treatment, may represent an attractive therapeutic option in preventing infective complications after stroke.