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These studies suggest that stroke can lead to permanent neurological deficits, including motor, cognitive, and psychological impairments, with factors such as age, white matter damage, and cerebral glucose metabolism influencing outcomes.
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Stroke is a leading cause of disability and cognitive deficits worldwide, primarily resulting from the occlusion of cerebral vessels, leading to ischemic strokes. These strokes cause brain infarcts, cerebral tissue death, and focal neuronal damage, with the severity of neurological deficits depending on various factors such as the time since occurrence, severity of ischemia, and location of infarcts.
Research indicates that age significantly influences the severity and persistence of neurological deficits post-stroke. In aged mice, stroke results in more severe long-term sensorimotor and cognitive deficits compared to younger mice. This is linked to more dramatic and sustained reductions in cerebral blood flow (CBF) and greater brain infarct size and neuronal tissue loss. Additionally, aged mice show significant and long-lasting deterioration of white matter, which is crucial for favorable neurological outcomes.
The mechanisms underlying neuronal injuries in ischemic stroke include excitotoxicity, oxidative stress, inflammation, and apoptosis. These processes contribute to the extent of brain damage and the resulting neurological deficits. Genetic factors also play a role, with certain genetic variations influencing early neurological instability and long-term outcomes.
Stroke-induced damage is not limited to focal tissue but also affects white matter tracts and neural interactions across widespread brain networks. This network disruption contributes significantly to neurological deficits and their persistence. The loss of myelin basic protein (MBP) in white matter is particularly associated with poor neurological outcomes.
Cognitive impairment is a common consequence of stroke, particularly in older adults. This impairment affects quality of life and requires ongoing support, impacting both patients and caregivers. Effective management strategies, including preventive measures targeting modifiable risk factors, are crucial for addressing post-stroke cognitive impairment.
The potential for recovery and rehabilitation after stroke is influenced by several factors, including the functional status of brain tissue outside the infarct. Measurement of cerebral glucose metabolism (CMRglu) in non-infarcted brain regions can predict rehabilitative capacity, with higher CMRglu associated with better outcomes. Rehabilitation efforts are increasingly focusing on targeting specific neural network patterns to enhance recovery.
Permanent neurological deficits after stroke are influenced by a complex interplay of factors, including age, white matter damage, genetic variations, and the extent of neuronal injury. Understanding these factors is crucial for developing effective management and rehabilitation strategies to improve outcomes for stroke survivors.
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