A Review of Exercise-Induced Neuroplasticity in Ischemic Stroke: Pathology and Mechanisms
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A Review of Exercise-Induced Neuroplasticity in Ischemic Stroke: Pathology and Mechanisms Ying Xing 1 & Yulong Bai 1 Received: 24 May 2020 / Accepted: 8 July 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract After ischemic stroke, survivors experience motor dysfunction and deterioration of memory and cognition. These symptoms are associated with the disruption of normal neuronal function, i.e., the secretion of neurotrophic factors, interhemispheric connections, and synaptic activity, and hence the disruption of the normal neural circuit. Exercise is considered an effective and feasible rehabilitation strategy for improving cognitive and motor recovery following ischemic stroke through the facilitation of neuroplasticity. In this review, our aim was to discuss the mechanisms by which exercise-induced neuroplasticity improves motor function and cognitive ability after ischemic stroke. The associated mechanisms include increases in neurotrophins, improvements in synaptic structure and function, the enhancement of interhemispheric connections, the promotion of neural regeneration, the acceleration of neural function reorganization, and the facilitation of compensation beyond the infarcted tissue. We also discuss some common exercise strategies and a novel exercise therapy, robot-assisted movement, which might be widely applied in the clinic to help stroke patients in the future. Keywords Ischemic stroke . Exercise . Neuroplasticity . Neurotrophins . Regeneration . AMPA receptors
Introduction Stroke is a cerebrovascular disease characterized by high morbidity, mortality, and disability. The occurrence rate of acute first-ever ischemic stroke is higher than that of acute first-ever hemorrhagic stroke in terms of the Global Burden of Disease (GBD) 2015 study [1]. In 5-year post-stroke survivors, twothirds showed good functional outcome in neurologic deficit and disability, 20% underwent a second stroke, 22.5% showed dementia symptoms, 29.6% showed depression, and approximately 15% were institutionalized [2]. The symptoms after ischemic stroke are associated with the disruption of normal neuronal function, i.e., interhemispheric connections and synaptic activity, due to neuronal death in the ischemic core and hence the disruption of the normal neural circuit [3–5]. The recovery processes induced by various therapies often involve spared axonal sprouts that contribute to
* Yulong Bai [email protected] 1
Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing’an District, Shanghai 200040, China
establishing new circuits by innervating denervated target regions [6–8]. That is, functional recovery after ischemic stroke is related to neuroplasticity. Neuroplasticity is defined as structural and functional changes in the brain that enable adaptation to learning, memory, the environment, and rehabilitation following brain damage. It is a dynamic process involving alterations in the number of brain nuclei and structures, numero
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