Brenton Hordacre1, Duncan Austin2, Katlyn E Brown2, Lynton Graetz3, Isabel Pareés4,5, Stefania De Trane6,7,8, Ann-Maree Vallence9,10,11, Simon Koblar3,12, Timothy Kleinig3,12, Michelle N McDonnell13, Richard Greenwood8, Michael C Ridding1, John C Rothwell2. 1. IIMPACT in Health, Allied Health and Human Performance, University of South Australia, Adelaide, South Australia, Australia. 2. UCL Institute of Neurology, London, UK. 3. The University of Adelaide, Adelaide, South Australia, Australia. 4. Hospital Universitario Ramón y Cajal, Madrid, Spain. 5. Hospital Ruber Internacional, Madrid, Spain. 6. Queen Mary University of London, London, UK. 7. The Royal London Hospital, Barts Health NHS Trust, London, UK. 8. National Hospital for Neurology and Neurosurgery, London, UK. 9. Discipline of Psychology, College of Science, Health, Engineering, and Education, Murdoch University, Australia. 10. Centre for Healthy Ageing, Health Futures Institute, Murdoch University, Australia. 11. Centre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, Australia. 12. Royal Adelaide Hospital, Adelaide, South Australia, Australia. 13. The Physio Clinic, Adelaide, South Australia, Australia.
Abstract
BACKGROUND: In preclinical models, behavioral training early after stroke produces larger gains compared with delayed training. The effects are thought to be mediated by increased and widespread reorganization of synaptic connections in the brain. It is viewed as a period of spontaneous biological recovery during which synaptic plasticity is increased. OBJECTIVE: To look for evidence of a similar change in synaptic plasticity in the human brain in the weeks and months after ischemic stroke. METHODS: We used continuous theta burst stimulation (cTBS) to activate synapses repeatedly in the motor cortex. This initiates early stages of synaptic plasticity that temporarily reduces cortical excitability and motor-evoked potential amplitude. Thus, the greater the effect of cTBS on the motor-evoked potential, the greater the inferred level of synaptic plasticity. Data were collected from separate cohorts (Australia and UK). In each cohort, serial measurements were made in the weeks to months following stroke. Data were obtained for the ipsilesional motor cortex in 31 stroke survivors (Australia, 66.6 ± 17.8 years) over 12 months and the contralesional motor cortex in 29 stroke survivors (UK, 68.2 ± 9.8 years) over 6 months. RESULTS: Depression of cortical excitability by cTBS was most prominent shortly after stroke in the contralesional hemisphere and diminished over subsequent sessions (P = .030). cTBS response did not differ across the 12-month follow-up period in the ipsilesional hemisphere (P = .903). CONCLUSIONS: Our results provide the first neurophysiological evidence consistent with a period of enhanced synaptic plasticity in the human brain after stroke. Behavioral training given during this period may be especially effective in supporting poststroke recovery.
BACKGROUND: In preclinical models, behavioral training early after stroke produces larger gains compared with delayed training. The effects are thought to be mediated by increased and widespread reorganization of synaptic connections in the brain. It is viewed as a period of spontaneous biological recovery during which synaptic plasticity is increased. OBJECTIVE: To look for evidence of a similar change in synaptic plasticity in the human brain in the weeks and months after ischemic stroke. METHODS: We used continuous theta burst stimulation (cTBS) to activate synapses repeatedly in the motor cortex. This initiates early stages of synaptic plasticity that temporarily reduces cortical excitability and motor-evoked potential amplitude. Thus, the greater the effect of cTBS on the motor-evoked potential, the greater the inferred level of synaptic plasticity. Data were collected from separate cohorts (Australia and UK). In each cohort, serial measurements were made in the weeks to months following stroke. Data were obtained for the ipsilesional motor cortex in 31 stroke survivors (Australia, 66.6 ± 17.8 years) over 12 months and the contralesional motor cortex in 29 stroke survivors (UK, 68.2 ± 9.8 years) over 6 months. RESULTS:Depression of cortical excitability by cTBS was most prominent shortly after stroke in the contralesional hemisphere and diminished over subsequent sessions (P = .030). cTBS response did not differ across the 12-month follow-up period in the ipsilesional hemisphere (P = .903). CONCLUSIONS: Our results provide the first neurophysiological evidence consistent with a period of enhanced synaptic plasticity in the human brain after stroke. Behavioral training given during this period may be especially effective in supporting poststroke recovery.
Entities:
Keywords:
motor cortex; noninvasive brain stimulation; plasticity; recovery; stroke; transcranial magnetic stimulation
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