PubMed HealthSearch

PubMed · 8690959

Understanding central post-stroke pain.

Abstract

Almost a century ago, two French neurologists described an unusual pain syndrome following stroke. This so-called "thalamic" pain of Dejerine-Roussy exists today, affecting approximately 30,000 survivors of stroke in the United States (US) alone. Lesions involving the neospinothalamocortical tract are thought to cause thalamic pain, but the exact pathogenesis is unclear. Pharmacotherapeutic and surgical approaches offer pain relief in selected patients. Although definitive relief of central post-stroke pain (CPSP) may not be achievable for all at this time, intelligent and informed examination of the full range of options offers every sufferer a real potential for relief and mastery of pain. It is hoped that information provided herein will foster "intelligent caring" and facilitate informed decision making by consumers and caregivers alike.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Segatore. 1996. Understanding central post-stroke pain.. https://doi.org/10.1097/01376517-199602000-00006

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Substance P is expressed in hippocampal principal neurons during status epilepticus and plays a critical role in the maintenance of status epilepticus.

Substance P (SP), a member of the tachykinin family, is widely distributed in the central nervous system and is involved in a variety of physiological processes including cardiovascular function, inflammatory responses, and nociception. We show here that intrahippocampal administration of SP triggers self-sustaining status epilepticus (SSSE) in response to stimulation of the perforant path for periods too brief to have any effect in control rats, and this SSSE generates a pattern of acute hippocampal damage resembling that known to occur in human epilepsy. The SP receptor (SPR) antagonists, spantide II and RP-67,580, block both the initiation of SSSE and SSSE-induced hippocampal damage and terminate established anticonvulsant-resistant SSSE. SSSE results in a rapid and dramatic increase in the expression of preprotachykinin A (a precursor of SP) mRNA and SP in principal neurons in CA3, CA1, and the dentate gyrus as well as in hippocampal mossy fibers. SP also increases glutamate release from hippocampal slices. Enhanced expression of SP during SSSE may modulate hippocampal excitability and contribute to the maintenance of SSSE. Thus, SPR antagonists may constitute a novel category of drugs in antiepileptic therapy.

Analgesics