Efficacy of mechanisms of neuroplasticity after a stroke

Author:

Cabral Danylo F.1,Fried Peter2,Koch Sebastian3,Rice Jordyn1,Rundek Tatjana34,Pascual-Leone Alvaro567,Sacco Ralph34,Wright Clinton B.8,Gomes-Osman Joyce134

Affiliation:

1. Department of Physical Therapy, University of Miami, Coral Gables, FL, USA

2. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA

3. Department of Neurology, University of Miami, Miami, USA

4. Evelyn McKnight Brain Institute, University of Miami, Miami, USA

5. Department of Neurology, Harvard Medical School, Boston MA, USA

6. Hinda and Arthur Marcus Institute for Aging Research and Deanna and Sidney Wolk Center for Memory Health, Hebrew SeniorLife, Rosindale, MA, USA

7. Guttmann Brain Health Institute, Barcelona, Spain

8. National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA

Abstract

Background: The sequelae of stoke, including the loss and recovery of function, are strongly linked to the mechanisms of neuroplasticity. Rehabilitation and non-invasive brain stimulation (NIBS) paradigms have shown promise in modulating corticomotor neuroplasticity to promote functional recovery in individuals post-stroke. However, an important limitation to these approaches is that while stroke recovery depends on the mechanisms of neuroplasticity, those mechanisms may themselves be altered by a stroke. Objective: Compare Transcranial Magnetic Stimulation (TMS)-based assessments of efficacy of mechanism of neuroplasticity between individuals post-stroke and age-matched controls. Methods: Thirty-two participants (16 post-stroke, 16 control) underwent an assessment of mechanisms of neuroplasticity, measured by the change in amplitude of motor evoked potentials elicited by single-pulse TMS 10–20 minutes following intermittent theta-burst stimulation (iTBS), and dual-task effect (DTE) reflecting cognitive-motor interference (CMI). In stroke participants, we further collected: time since stroke, stroke type, location, and Stroke Impact Scale 16 (SIS-16). Results: Although there was no between-group difference in the efficacy of TMS-iTBS neuroplasticity mechanism (p = 0.61, η2 = 0.01), the stroke group did not exhibit the expected facilitation to TMS-iTBS (p = 0.60, η2 = 0.04) that was shown in the control group (p = 0.016, η2 = 0.18). Sub-cohort analysis showed a trend toward a difference between those in the late-stage post-stroke and the control group (p = 0.07, η2 = 0.12). Within the post-stroke group, we found significant relationships between TMS-iTBS neuroplasticity and time since stroke onset, physical function (SIS-16), and CMI (all rs > |0.53| and p-values < 0.05). Conclusions: In this proof-of-principle study, our findings suggested altered mechanisms of neuroplasticity in post-stroke patients which were dependent on time since stroke and related to motor function. TMS-iTBS neuroplasticity assessment and its relationship with clinical functional measures suggest that TMS may be a useful tool to study post-stroke recovery. Due to insufficient statistical power and high variability of the data, generalization of the findings will require replication of the results in a larger, better-characterized cohort.

Publisher

IOS Press

Subject

Neurology (clinical),Developmental Neuroscience,Neurology

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