Huynh William, Kwai Natalie, Arnold Ria, Krishnan Arun V, Lin Cindy S-Y, Vucic Steve, Kiernan Matthew C
Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia
Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia.
Diabetes. 2017 Jun;66(6):1661-1670. doi: 10.2337/db16-0961. Epub 2017 Mar 21.
Diabetes may impair the capacity for neuroplasticity such that patients experience a slower and poorer recovery after stroke. The current study investigated changes in cortical function in stroke patients with diabetes to determine how this comorbidity may affect poststroke cortical plasticity and thereby functional recovery. From a cohort of 57 participants, threshold-tracking transcranial magnetic stimulation was used to assess cortical function over the ipsilateral and contralesional hemispheres in 7 patients with diabetes after an acute stroke compared with 12 stroke patients without diabetes. Cortical function was also assessed in 8 patients with diabetes without stroke and 30 normal control subjects. After acute stroke, short-interval intracortical inhibition (SICI) was reduced over both motor cortices in stroke patients without diabetes compared with normal control patients, while in stroke patients with diabetes, SICI was only reduced over the contralesional but not the ipsilesional cortex compared with control patients with diabetes. In addition, SICI was significantly reduced in the control patients with diabetes compared with normal control patients. These results have demonstrated the absence of ipsilesional cortical excitability change after diabetic strokes, suggesting impaired capacity for neuroplasticity over this hemisphere as a consequence of a "double-hit" phenomenon because of preexisting alterations in cortical function in nonstroke patients with diabetes. The reliance on reorganization over the contralesional cortex after stroke will likely exert influence on poststroke recovery in patients with diabetes.
糖尿病可能会损害神经可塑性，导致患者中风后恢复较慢且较差。本研究调查了糖尿病中风患者的皮质功能变化，以确定这种合并症如何影响中风后皮质可塑性，进而影响功能恢复。在57名参与者中，对7名急性中风后患有糖尿病的患者以及12名无糖尿病的中风患者，使用阈值跟踪经颅磁刺激来评估同侧和对侧半球的皮质功能。还对8名无中风的糖尿病患者和30名正常对照者进行了皮质功能评估。急性中风后，与正常对照患者相比，无糖尿病的中风患者双侧运动皮质的短间隔皮质内抑制（SICI）均降低，而与糖尿病对照患者相比，患有糖尿病的中风患者仅对侧皮质而非同侧皮质的SICI降低。此外，与正常对照患者相比，糖尿病对照患者的SICI显著降低。这些结果表明，糖尿病中风后同侧皮质兴奋性没有变化，这表明由于糖尿病非中风患者皮质功能的先前改变导致的“双重打击”现象，该半球的神经可塑性能力受损。中风后对侧皮质重组的依赖可能会影响糖尿病患者的中风后恢复。
