Remodeling of Neuronal Circuits After Reach Training in Chronic Capsular Stroke

What protocols were created out of this research? Send your doctor after them.  I assume the pellet reaching task will need to be changed for humans.
http://nnr.sagepub.com/content/30/10/941?etoc

1. Jongwook Cho1
2. Dae-Hyuk Kwon, PhD1
3. Ra Gyung Kim1
4. Hanlim Song1
5. Pedro Rosa-Neto, MD, PhD2
6. Min-Cheol Lee, MD, PhD3
7. Hyoung-Ihl Kim, MD, PhD1,4⇑

1. ¹Gwangju Institute of Science and Technology, Gwangju, Republic of Korea
2. ²Douglas Mental Health University Institute, Montréal, Canada
3. ³Chonnam National University Medical School, Gwangju, Republic of Korea
4. ⁴Presbyterian Medical Center, Jeonju, Republic of Korea

1. Hyoung-Ihl Kim, MD, PhD, Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, 261 Cheomdan-gwagiro, Gwangju, 500-712, South Korea. Email: hyoungihl@gist.ac.kr

Abstract

Background. Subcortical capsular stroke has a poor prognosis, and it is not yet fully understood how and under what circumstances reach training contributes to motor recovery.  

Objective. This study was performed to investigate changes in neuronal circuits and motor recovery in a chronic capsular stroke model in the presence or absence of reach training.  

Method. We generated photothrombotic capsular lesions in 42 Sprague-Dawley rats and evaluated motor recovery with or without daily training in a single-pellet reaching task (SPRT). We used 2-deoxy-2-[18F]-fluoro-D-glucose-microPET (positron emission tomography) to assess remodeling of neuronal circuits.  

Results. SPRT training was selectively beneficial only for the group with incomplete capsular destruction (P < .05), suggesting the relevance of plasticity in the remaining capsular fibers for motor recovery. Groups that did not receive SPRT training showed no motor recovery at all. The microPET analysis demonstrated that motor recovery was correlated with a reduction in cortical diaschisis in ipsilesional motor and sensory cortices and in the contralesional sensory cortex (Pearson’s correlation, P < .05). We also observed training-dependent subcortical activation in the contralesional red nucleus, the internal capsule, and the ventral hippocampus (P < .0025; false discovery rate q < 0.05). The groups without reach training did not show the same degree of reduction in diaschisis or activation of the red nucleus.  

Conclusions. Our results suggest that motor recovery and remodeling of neuronal circuits after capsular stroke depend on the magnitude of the capsular lesion and on the presence or absence of reach training. Task-specific training is strongly indicated only when there is incomplete destruction of the capsular fibers.