ArticleMolecular pain2015
A [14C]iodoantipyrine study of inter-regional correlations of neural substrates following central post-stroke pain in rats.
Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Role of Sensory Pathway Injury in Central Post-Stroke Pain: A Narrative Review of Its Pathogenetic Mechanism.Journal of pain research · 2023Review
- The effect and mechanism of exercise for post-stroke pain.Frontiers in molecular neuroscience · 2022Review
- Behavioral Assessment of Sensory, Motor, Emotion, and Cognition in Rodent Models of Intracerebral Hemorrhage.Frontiers in neurology · 2021Review
- Secondary Pathology of the Thalamus after Focal Cortical Stroke in Rats is not Associated with Thermal or Mechanical Hypersensitivity and is Not Alleviated by Intra-Thalamic Post-Stroke Delivery of Recombinant CDNF or MANF.Cell transplantation · 2019Article
- Botulinum Toxin for Central Neuropathic Pain.Toxins · 2018Review
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCentral pain syndrome is characterized by a combination of abnormal pain sensations, and pain medications often provide little or no relief. Accumulating animal and clinical studies have shown that impairments of the spinothalamic tract (STT) and thalamocingulate pathway causes somatosensory dysfunction in central post-stroke pain (CPSP), but the involvement of other neuronal circuitries in CPSP has not yet been systematically examined. The aim of the present study was to evaluate changes in brain activity and neuronal circuitry using [(14)C]iodoantipyrine (IAP) in an animal model of CPSP.
resultsRats were subjected to lateral thalamic hemorrhage to investigate the characteristics of CPSP. Thermal and mechanical hyperalgesia developed in rats that were subjected to thalamic hemorrhagic lesion. The medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), striatum, thalamus, hypothalamus, and amygdala were more active in the CPSP group compared with rats that were not subjected to lateral thalamic hemorrhage. The inter-regional correlation analysis showed that regional cerebral blood flow in the mPFC was highly correlated with the amygdala in the right brain, and the right brain showed complex connections among subregions of the ACC. Rats with CPSP exhibited strong activation of the thalamocingulate and mPFC-amygdala pathways.
conclusionsThese results corroborate previous findings that the STT and thalamocingulate pathway are involved in the pathophysiological mechanisms of CPSP symptoms. The mPFC, amygdala, and periaqueductal gray emerged as having important correlations in pain processing in CPSP. The present data provide a basis for a neural correlation hypothesis of CPSP, with implications for CPSP treatment.
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