Abstract

Substance P and swallowing after stroke

Author(s): David G Smithard

Swallowing is essential for independent living. The swallowing center is based within the brain stem, generating a patterned swallow which is modified both by peripheral feedback and cortical input. The striatum and thalamus are intimately involved in swallowing initiation and control. Substance P, a neuropeptide, appears to play a pivitol role in swallowing. Centrally, it acts as a neuromodulator within the striatal–nigral pathway, but distally it may act as a neurotransmitter within the plexus of nerves in the pharyngeal epithelium in response to nocioceptive stimuli. Inhibition of substance P, centrally, with direct antagonists or dopamine antagonists, interrupt the swallow. Peripherally, agents that deplete nerve endings of substance P also delay the swallow. It is proposed that the difficulties in swallowing, and any subsequent aspiration, after stroke may be related to reduced levels of substance P, which may be ameliorated by angiotensin-converting enzyme inhibitors, dopamine agonists and capsaicin, all of which increase substance P levels.