Limits...
A [14C]iodoantipyrine study of inter-regional correlations of neural substrates following central post-stroke pain in rats.

Lu HC, Chang WJ, Kuan YH, Huang AC, Shyu BC - Mol Pain (2015)

Bottom Line: These 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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. nhnsc@hotmail.com.

ABSTRACT

Background: Central 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.

Results: Rats 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.

Conclusions: These 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.

No MeSH data available.


Related in: MedlinePlus

Neural network hypothesis related to the present animal model of CPSP. A. Pathophysiological mechanisms in the MT-ACC pathway and STT are triggered to disinhibit the projection from the lateral thalamus and insula to the medial thalamus, resulting in mechanical and thermal hyperalgesia. B. The mPFC plays an executive function role to interact with the amygdala, which responds to negative emotional information. The mPFC inhibits activation of the amygdala, whereas negative information in the amygdala is conveyed to the mPFC. The mPFC then interprets the emotional information properly. Nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain to induce antinociception.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4358859&req=5

Fig8: Neural network hypothesis related to the present animal model of CPSP. A. Pathophysiological mechanisms in the MT-ACC pathway and STT are triggered to disinhibit the projection from the lateral thalamus and insula to the medial thalamus, resulting in mechanical and thermal hyperalgesia. B. The mPFC plays an executive function role to interact with the amygdala, which responds to negative emotional information. The mPFC inhibits activation of the amygdala, whereas negative information in the amygdala is conveyed to the mPFC. The mPFC then interprets the emotional information properly. Nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain to induce antinociception.

Mentions: A neural correlation hypothesis based on our animal model of CPSP may be proposed that involves changes in various structures, pathways, and circuits (Figure 8). The neural correlation hypothesis of CPSP-induced posits that pain symptoms are associated with spontaneous pain rather an acute pain, which would be different from conventional pain theories. CPSP is likely mediated by multiple pathophysiological mechanisms that involve alterations in various neural substrates. When the VB is damaged in hemorrhagic stroke, pathophysiological mechanisms are triggered in the STT and MT-ACC pathway, in which projections from the lateral thalamus (including the VPM) and insula to the medial thalamus (e.g., the MD) are disinhibited, thus resulting in mechanical and thermal hyperalgesia (Figure 8A) [6-8]. Alternative neural pathways, including the mPFC, amygdala, and PAG, were activated during the pathophysiological changes (Figure 8B). The mPFC, including the PrL and IL, plays a role in executive function and interacts with central or medial nuclei of the amygdala that respond to negative emotion. The mPFC might inhibit activation of the amygdala, whereas negative information from the amygdala is conveyed to the mPFC and mPFC to interpret the emotional information properly. Concurrently, nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain and induce antinociception.Figure 8


A [14C]iodoantipyrine study of inter-regional correlations of neural substrates following central post-stroke pain in rats.

Lu HC, Chang WJ, Kuan YH, Huang AC, Shyu BC - Mol Pain (2015)

Neural network hypothesis related to the present animal model of CPSP. A. Pathophysiological mechanisms in the MT-ACC pathway and STT are triggered to disinhibit the projection from the lateral thalamus and insula to the medial thalamus, resulting in mechanical and thermal hyperalgesia. B. The mPFC plays an executive function role to interact with the amygdala, which responds to negative emotional information. The mPFC inhibits activation of the amygdala, whereas negative information in the amygdala is conveyed to the mPFC. The mPFC then interprets the emotional information properly. Nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain to induce antinociception.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4358859&req=5

Fig8: Neural network hypothesis related to the present animal model of CPSP. A. Pathophysiological mechanisms in the MT-ACC pathway and STT are triggered to disinhibit the projection from the lateral thalamus and insula to the medial thalamus, resulting in mechanical and thermal hyperalgesia. B. The mPFC plays an executive function role to interact with the amygdala, which responds to negative emotional information. The mPFC inhibits activation of the amygdala, whereas negative information in the amygdala is conveyed to the mPFC. The mPFC then interprets the emotional information properly. Nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain to induce antinociception.
Mentions: A neural correlation hypothesis based on our animal model of CPSP may be proposed that involves changes in various structures, pathways, and circuits (Figure 8). The neural correlation hypothesis of CPSP-induced posits that pain symptoms are associated with spontaneous pain rather an acute pain, which would be different from conventional pain theories. CPSP is likely mediated by multiple pathophysiological mechanisms that involve alterations in various neural substrates. When the VB is damaged in hemorrhagic stroke, pathophysiological mechanisms are triggered in the STT and MT-ACC pathway, in which projections from the lateral thalamus (including the VPM) and insula to the medial thalamus (e.g., the MD) are disinhibited, thus resulting in mechanical and thermal hyperalgesia (Figure 8A) [6-8]. Alternative neural pathways, including the mPFC, amygdala, and PAG, were activated during the pathophysiological changes (Figure 8B). The mPFC, including the PrL and IL, plays a role in executive function and interacts with central or medial nuclei of the amygdala that respond to negative emotion. The mPFC might inhibit activation of the amygdala, whereas negative information from the amygdala is conveyed to the mPFC and mPFC to interpret the emotional information properly. Concurrently, nociceptive information from the amygdala is transmitted to the PAG to process acute and chronic pain and induce antinociception.Figure 8

Bottom Line: These 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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. nhnsc@hotmail.com.

ABSTRACT

Background: Central 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.

Results: Rats 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.

Conclusions: These 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.

No MeSH data available.


Related in: MedlinePlus