Abstract
Cortical and subcortical plastic reorganization occurs in the course of motor recovery after stroke. It is largely accepted that plasticity of ipsilesional motor cortex primarily contributes to recovery of motor function, while the contributions of contralesional motor cortex are not completely understood. As a result of damages to motor cortex and its descending pathways and subsequent unmasking of inhibition, there is evidence of upregulation of reticulospinal tract (RST) excitability in the contralesional side. Both animal studies and human studies with stroke survivors suggest and support the role of RST hyperexcitability in post-stroke spasticity. Findings from animal studies demonstrate the compensatory role of RST hyperexcitability in recovery of motor function. In contrast, RST hyperexcitability appears to be related more to abnormal motor synergy and disordered motor control in stroke survivors. It does not contribute to recovery of normal motor function. Recent animal studies highlight laterality dominance of corticoreticular projections. In particular, there exists upregulation of ipsilateral corticoreticular projections from contralesional premotor cortex (PM) and supplementary motor area (SMA) to medial reticular nuclei. We revisit and revise the previous theoretical framework and propose a unifying account. This account highlights the importance of ipsilateral PM/SMA-cortico-reticulospinal tract hyperexcitability from the contralesional motor cortex as a result of disinhibition after stroke. This account provides a pathophysiological basis for post-stroke spasticity and related movement impairments, such as abnormal motor synergy and disordered motor control. However, further research is needed to examine this pathway in stroke survivors to better understand its potential roles, especially in muscle strength and motor recovery. This account could provide a pathophysiological target for developing neuromodulatory interventions to manage spasticity and thus possibly to facilitate motor recovery.
Highlights
Stroke is a leading cause of adult disability [1]
We found that acoustic startle reflex (ASR) responses were within normal limits in stroke survivors without spasticity (Flaccid or Recovered)
Following focal cortical lesions in monkeys, there are reports of upregulation of contralateral supplementary motor area (SMA)/premotor cortex (PM)-corticoreticular projections [100,101,102]. Taken these findings into consideration, we propose a unifying account in understanding the role of reticulospinal tract (RST) hyperexcitability in post-stroke spasticity, abnormal synergy, and disordered motor control
Summary
Stroke is a leading cause of adult disability [1]. According to the centers for disease control and prevention (CDC), ∼800,000 people have a stroke every year in the United States, resulting in a total of 7 million stroke survivors. Spasticity and its related abnormal joint postures often interact with weakness and loss of dexterity, resulting in disordered motor control and functional limitations, such as inability to grasp, reach, walk, and transfer. These motor impairments result in difficulties in mobility and activities of daily living, and limit their vocational and social participation in more than half of stroke survivors at age 65 and over [1]. As a consequence of damages to iM1 and its descending pathways, both animal studies and human imaging studies suggest that there is increased excitability in the brainstem reticular system and its descending reticulospinal tract (RST) [25,26,27] Both animal and human studies support the maladaptive role of RS hyperexcitability in spasticity. A unifying account is proposed to better understand the brainstem roles and to consolidate controversial findings for spasticity and disordered motor control
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