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Published on: July 18, 2016
Brain activity changes in a monkey model of central post-stroke pain.
Kazuaki Nagasaka1, Ichiro Takashima2, Keiji Matsuda3
1Human Informatics Research Institute, National Institute of Advanced Industrial Science and Technology, 1-1-1 Umezono, Tsukuba-City, Ibaraki 305-8568, Japan; Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba-City, Ibaraki 305-8577, Japan; Japan Society for Promotion of Science, 5-3-1 Koujimachi, Chiyoda-ku, Tokyo 102-0083, Japan; Institute for Human Movement and Medical Sciences, Niigata University of Health and Welfare, 1398 Shimami, Kita-ku, Niigata-City, Niigata 950-3198, Japan.
Central post-stroke pain (CPSP) involves tactile allodynia. In a macaque model, thalamic lesions caused pain, activating brain areas like the posterior insular cortex. Inactivating these areas reduced allodynia, showing increased cortical activity contributes to CPSP.
Area of Science:
- Neuroscience
- Pain Research
- Stroke Rehabilitation
Background:
- Central post-stroke pain (CPSP) is a debilitating condition often involving tactile allodynia.
- The precise neural mechanisms linking thalamic damage to allodynia remain unclear.
- Previous studies suggest brain plasticity but lack causal evidence.
Purpose of the Study:
- To investigate brain activation changes associated with tactile allodynia in a non-human primate model of CPSP.
- To explore the causal role of specific brain regions in CPSP-induced allodynia.
Main Methods:
- Developed a macaque model of CPSP via thalamic lesions.
- Utilized functional magnetic resonance imaging (fMRI) under anesthesia to assess brain activity.
- Pharmacologically inactivated specific brain regions (posterior insular cortex/secondary somatosensory cortex, anterior cingulate cortex) to observe effects on allodynia.
Main Results:
- Thalamic lesions in macaques induced behavioral signs of tactile allodynia.
- Inactivated sensorimotor cortex showed significant activation in pain-related areas (posterior insular cortex, secondary somatosensory cortex, anterior cingulate cortex, amygdala) upon tactile stimulation.
- Pharmacological inactivation of posterior insular cortex/secondary somatosensory cortex or anterior cingulate cortex reduced tactile allodynia signs.
Conclusions:
- Increased cortical activity in specific pain-related brain areas is causally linked to central post-stroke pain-induced tactile allodynia.
- This study provides crucial insights into the neurobiological underpinnings of CPSP.
- The findings may inform the development of targeted therapies for post-stroke pain.
