2026-06-05 生理学研究所
◆研究では、5頭のサルに片側脊髄損傷を作製し、把握運動能力と機能的MRI（fMRI）による脳活動・脳領域間結合性を継続的に評価した。その結果、良好な回復を示した個体では、損傷後2～5週間に非麻痺手への刺激に対する両側感覚運動野の応答が一時的に増強し、その後減弱する動的変化が観察された。この変化は運動前野や補足運動野を含む広範な運動ネットワークの再編を伴っていた。一方、回復不良例では強い脳応答が持続し、運動機能低下と関連していた。研究チームは、初期の応答増強は神経回路の「脱抑制」を反映し、その後適切に収束することが運動回復に重要であると考察している。
◆本成果は、脊髄損傷後の脳の適応メカニズム理解を深めるとともに、リハビリテーション戦略の改善につながる可能性を示した。
＜関連情報＞
- https://www.nips.ac.jp/nips_research/2026/06/–_1.html
- https://www.nature.com/articles/s41598-026-54528-7
霊長類における脊髄損傷後の回復期における、非麻痺側の手への刺激に対する感覚運動皮質の反応性の向上と運動ネットワークの構築 Enhanced sensorimotor cortex responsiveness to nonplegic hand stimulation and motor network assembly during recovery after spinal cord injury in primates
Takamichi Tohyama,Reona Yamaguchi,Naokazu Goda,Tetsuya Yamamoto,Norihiro Sadato,Tadashi Isa & Masaki Fukunaga
Scientific Reports Published:27 May 2026
DOI:https://doi.org/10.1038/s41598-026-54528-7 Unedited version
Abstract
Previous studies have reported changes in cortical responses to stimulation of the plegic or nonplegic hand after unilateral neuronal injury. We aimed to investigate the relationship between these responsiveness changes in central sensorimotor systems and functional recovery. Five macaque monkeys underwent lower cervical cord subhemisection surgery. Their hand movements were observed, and longitudinal functional MRI (fMRI) was performed under anaesthesia to assess responses to tactile stimulation of each hand and resting-state connectivity. Eigenvector centrality was computed from resting-state fMRI data to examine network assembly. Following severe paralysis of the ipsilesional hand, four monkeys showed recovery of grasping movements, with an average success rate improving until 16 weeks post-injury. Bilateral sensorimotor hand areas exhibited increased responses to contralesional (nonplegic hand) stimulation 2–5 weeks post-injury, which declined over time. These changes correlated with the centrality of the bilateral premotor cortices and supplementary motor areas. An inverse correlation was observed between responses in the ipsilesional sensorimotor cortex and success rates. These findings suggest that cortical responsiveness enhancement may be caused by post-injury disinhibitory mechanisms involving motor network assembly. Our results indicate that disinhibitory mechanisms can drive large-scale sensorimotor reorganisation, and disinhibition reduction leads to long-term recovery after spinal cord injury in primates.
