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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

Key brain regions that showed significant differences in pixel counts between the CPSP and sham groups. The results were obtained by differential subtraction between the CPSP and sham groups. The signals in the cortex, thalamus, hypothalamus, and amygdala in the CPSP group were significantly higher than in the sham group, and the signal in the ventral basal nucleus in the CPSP group was significantly lower than in the sham group.
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Fig3: Key brain regions that showed significant differences in pixel counts between the CPSP and sham groups. The results were obtained by differential subtraction between the CPSP and sham groups. The signals in the cortex, thalamus, hypothalamus, and amygdala in the CPSP group were significantly higher than in the sham group, and the signal in the ventral basal nucleus in the CPSP group was significantly lower than in the sham group.

Mentions: To examine the brain areas that are involved in CPSP symptoms and their signal intensity, Statistical Parametric Mapping (SPM) was used. Whole-brain images were composed of a sequence of images in a coronal section that were normalized and analyzed by SPM. The differences between the sham and CPSP groups were indexed by subtracting the sham group from the CPSP group. Pixel counts were significantly different (p < 0.05) and are presented in pseudo color in Figure 3. Compared with the sham group, the CPSP group showed significant alterations in the pixel count ratio, reflecting [14C]IAP expression in some major brain regions, including the cortex, striatum, thalamus, hypothalamus, and amygdala.Figure 3


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)

Key brain regions that showed significant differences in pixel counts between the CPSP and sham groups. The results were obtained by differential subtraction between the CPSP and sham groups. The signals in the cortex, thalamus, hypothalamus, and amygdala in the CPSP group were significantly higher than in the sham group, and the signal in the ventral basal nucleus in the CPSP group was significantly lower than in the sham group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig3: Key brain regions that showed significant differences in pixel counts between the CPSP and sham groups. The results were obtained by differential subtraction between the CPSP and sham groups. The signals in the cortex, thalamus, hypothalamus, and amygdala in the CPSP group were significantly higher than in the sham group, and the signal in the ventral basal nucleus in the CPSP group was significantly lower than in the sham group.
Mentions: To examine the brain areas that are involved in CPSP symptoms and their signal intensity, Statistical Parametric Mapping (SPM) was used. Whole-brain images were composed of a sequence of images in a coronal section that were normalized and analyzed by SPM. The differences between the sham and CPSP groups were indexed by subtracting the sham group from the CPSP group. Pixel counts were significantly different (p < 0.05) and are presented in pseudo color in Figure 3. Compared with the sham group, the CPSP group showed significant alterations in the pixel count ratio, reflecting [14C]IAP expression in some major brain regions, including the cortex, striatum, thalamus, hypothalamus, and amygdala.Figure 3

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