1997/10/01 by Michael A. Persinger, M. A. Persinger, Oksana Peredery +5
Medicine · #Botulinum Toxin and Related Neurological Disorders #Neurological disorders and treatments #Pain Mechanisms and Treatments
paper · doi:10.2466/pms.1997.85.2.387
crossref issued 1997/10/01 · crossref published 1997/10/01 · crossref published-online 1997/10/01 · crossref published-print 1997/10/01 · openalex publication_date 1997/10/01 · crossref created 2011/08/31 · openalex created_date 2025/10/10 · crossref deposited 2026/05/01 · crossref indexed 2026/07/29 · openalex updated_date 2026/07/29
Flinch (pain) thresholds for electric current delivered to the feet were correlated with the amount of necrosis within the diencephalon and telencephalon for rats in which seizures had been induced by lithium and pilocarpine about two months before the testing. The shared variance of the quantitative damage within the claustrum, the anterior part of the paraventricular nucleus of thalamus, (central) mediodorsal thalamus, and lateral amygdala (ventromedial part) explained 81% of the variance in the nociceptive (flinch) thresholds. A primary role of the claustrum within the neuropathways that mediate the response to the interoceptive and "painful" characteristics of stimuli is indicated. The concept of primary pathways versus "emergent" pathways subsequent to excitotoxic damage within the neuromatrix is discussed.