Spatiotemporal Remodeling of Neural Excitability Following Ischemic Stroke: Regional Mechanisms From the Infarct Core to Brainstem–Spinal Output Systems: A Structured Narrative Review
- 1Department of Neurology Hunan Provincial Hospital of Integrated Traditional Chinese and Western Medicine (The Affiliated Hospital of Hunan Academy Traditional Chinese Medicine) Changsha 410006 Hunan China
- 2Graduate School Hunan University of Chinese Medicine Changsa 410208 Hunan China hnctcm.edu.cn
Abstract
Changes in neural excitability after ischemic stroke affect lesion growth, recovery of function, and long‐term motor problems. People often think of these changes as just an increase or decrease in neural activity. This view does not explain why excitability changes are different at different stages, brain regions, or mechanisms. It also does not explain why these changes can cause injury, help recovery, or lead to maladaptation. In the acute phase, the main areas involved are the infarct core and the ischemic penumbra. Here, excitability problems include membrane instability, prolonged depolarization, spreading depolarizations (SDs), changes in the fluid environment, and abnormal neurovascular responses. These problems together create harmful excitability that makes the lesion bigger. In the subacute phase, the dominant substrates shift toward the peri‐infarct cortex, ipsilesional primary motor cortex, and bilateral sensorimotor networks. Here, excitability changes are defined by excitatory–inhibitory rebalancing, reduction of excessive tonic inhibition, restoration of cortical responsiveness, and experience‐dependent network reorganization, forming restorative excitability that supports neural plasticity and functional recovery. During the subacute phase, excitatory–inhibitory rebalancing becomes a key synaptic mechanism of recovery, involving glutamatergic transmission, γ‐aminobutyric acid (GABA)ergic tonic and phasic inhibition, synaptic scaling, dendritic remodeling, and activity‐dependent refinement of surviving peri‐infarct circuits. In the chronic phase, in a subset of patients, the dominant substrates further shift toward the brainstem‐spinal output system, where compensatory recruitment of alternative descending pathways may contribute to abnormal synergies, spasticity, and low‐resolution motor control, representing maladaptive hyperexcitability. We therefore argue that poststroke excitability should not be interpreted within a static high‐/low‐excitability dichotomy but defined by when it occurs, where it is expressed, and at which mechanistic level it predominates.
Related
- Axonal transcriptome remodeling during PGE2 induced sensitization identifies Tnfrsf12a/FN14 as a regulator of sensory neuron excitability
- Characterizing bilateral M1 excitability changes after learning a novel spatiotemporal coordination pattern
- Bottom‐Up Engineering of a Human Neuromuscular System for Modeling Activity‐Induced Remodeling, Metabolic Stress, and Endothelial‐Modulated Excitability
- Progressive Actomyosin Remodeling Defining a Structured Podocyte Injury Response in Nephrotic Syndrome
- Three-dimensional animation compression optimization based on structured processing and adaptive spatiotemporal segmentation algorithm
BibTeX
@article{li2026spatiotemporal,
title = {{Spatiotemporal Remodeling of Neural Excitability Following Ischemic Stroke: Regional Mechanisms From the Infarct Core to Brainstem–Spinal Output Systems: A Structured Narrative Review}},
author = {Lu Li and Hongmei Shi and Shanshan Zeng and Lin Huang and Miaomiao Yang and Xiongxing Sun and Dahua Wu and Le Xie},
journal = {Neural Plasticity},
year = {2026},
month = oct,
doi = {10.1155/np/3095088},
url = {https://doi.org/10.1155/np/3095088},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Spatiotemporal Remodeling of Neural Excitability Following Ischemic Stroke: Regional Mechanisms From the Infarct Core to Brainstem–Spinal Output Systems: A Structured Narrative Review
AU - Lu Li
AU - Hongmei Shi
AU - Shanshan Zeng
AU - Lin Huang
AU - Miaomiao Yang
AU - Xiongxing Sun
AU - Dahua Wu
AU - Le Xie
PY - 2026
DA - 2026/10/29
JO - Neural Plasticity
DO - 10.1155/np/3095088
UR - https://doi.org/10.1155/np/3095088
AB - Changes in neural excitability after ischemic stroke affect lesion growth, recovery of function, and long‐term motor problems. People often think of these changes as just an increase or decrease in neural activity. This view does not explain why excitability changes are different at different stages, brain regions, or mechanisms. It also does not explain why these changes can cause injury, help recovery, or lead to maladaptation. In the acute phase, the main areas involved are the infarct core and the ischemic penumbra. Here, excitability problems include membrane instability, prolonged depolarization, spreading depolarizations (SDs), changes in the fluid environment, and abnormal neurovascular responses. These problems together create harmful excitability that makes the lesion bigger. In the subacute phase, the dominant substrates shift toward the peri‐infarct cortex, ipsilesional primary motor cortex, and bilateral sensorimotor networks. Here, excitability changes are defined by excitatory–inhibitory rebalancing, reduction of excessive tonic inhibition, restoration of cortical responsiveness, and experience‐dependent network reorganization, forming restorative excitability that supports neural plasticity and functional recovery. During the subacute phase, excitatory–inhibitory rebalancing becomes a key synaptic mechanism of recovery, involving glutamatergic transmission, γ‐aminobutyric acid (GABA)ergic tonic and phasic inhibition, synaptic scaling, dendritic remodeling, and activity‐dependent refinement of surviving peri‐infarct circuits. In the chronic phase, in a subset of patients, the dominant substrates further shift toward the brainstem‐spinal output system, where compensatory recruitment of alternative descending pathways may contribute to abnormal synergies, spasticity, and low‐resolution motor control, representing maladaptive hyperexcitability. We therefore argue that poststroke excitability should not be interpreted within a static high‐/low‐excitability dichotomy but defined by when it occurs, where it is expressed, and at which mechanistic level it predominates.
SN - 2090-5904
SN - 1687-5443
ER -