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Developmental Remodelling of the Motor Cortex in Hemiparetic Children With Perinatal Stroke
Kayla Baker1, Helen L Carlson2, Ephrem Zewdie2
1Calgary Pediatric Stroke Program, Alberta Children's Hospital, Calgary, Alberta, Canada; Alberta Children's Hospital Research Institute (ACHRI), Calgary, Alberta, Canada; Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada; Department of Neurosciences, University of Calgary, Calgary, Alberta, Canada.
Insights
Perinatal stroke can alter brain organization, shifting motor cortex activity in both hemispheres. These brain changes, particularly in arterial ischemic stroke, may not directly correlate with motor function recovery.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Pediatric Neurology
Background:
- Perinatal stroke, a leading cause of lifelong motor impairment, presents with distinct subtypes: periventricular venous infarcts (PVI) and arterial ischemic strokes (AIS).
- Both PVI and AIS disrupt motor system development and primary motor cortex (M1) plasticity, often resulting in retained ipsilateral corticospinal fibers from the non-affected motor cortex (M1').
Purpose of the Study:
- To investigate functional brain organization in children with perinatal stroke using task-based fMRI.
- To compare motor cortex activity patterns between PVI and AIS subtypes and age-matched controls.
- To explore the relationship between motor cortex displacement and clinical motor function.
Main Methods:
- Task-based functional magnetic resonance imaging (fMRI) was employed to assess motor cortex activity during paretic and unaffected hand movements.
- Peak activation coordinates in the primary motor cortex (M1), secondary motor cortex (M1'), and supplementary motor area were analyzed.
- Comparisons were made between 14 PVI patients, 13 AIS patients, and 22 healthy controls, with correlations to clinical motor assessments.
Main Results:
- Arterial ischemic stroke (AIS) showed the most significant M1 displacement in the lesioned hemisphere compared to controls, while periventricular venous infarcts (PVI) locations were similar to controls.
- Both PVI and AIS exhibited displaced M1' activations from the typical 'hand knob' region.
- Displacement extent of M1 and M1' showed a correlation (r = 0.50, P = 0.025) but was not significantly associated with clinical motor function.
- Supplementary motor area activity during paretic hand tapping was displaced in AIS patients compared to controls (P = 0.003).
Conclusions:
- Motor network components can be reorganized in both hemispheres following perinatal stroke, especially in AIS and cases with ipsilateral motor control.
- The modest correlation between brain reorganization and clinical function suggests that current models of developmental plasticity may be insufficient.
- Further research into complex plasticity models is needed to guide individualized neuromodulatory therapies for children with perinatal stroke.
Background:
Perinatal stroke often leads to lifelong motor impairment. Two common subtypes differ in timing, location, and mechanism of injury: periventricular venous infarcts (PVI) are fetal white matter lesions while most arterial ischemic strokes (AIS) are cortical injuries acquired near term birth. Both alter motor system development and primary motor cortex (M1) plasticity, often with retained ipsilateral corticospinal fibers from the non-lesioned motor cortex (M1').
Methods:
Task-based functional magnetic resonance imaging was used to define patterns of motor cortex activity during paretic and unaffected hand movement. Peak coordinates of M1, M1', and the supplementary motor area in the lesioned and intact hemispheres were compared to age-matched controls. Correlations between displacements and clinical motor function were explored.
Results:
Forty-nine participants included 14 PVI (12.59 ± 3.7 years), 13 AIS (14.91 ± 3.9 years), and 22 controls (13.91 ± 3.4 years). AIS displayed the greatest M1 displacement from controls in the lesioned hemisphere while PVI locations approximated controls. Peak M1' activations were displaced from the canonical hand knob in both PVI and AIS. Extent of M1 and M1' displacement were correlated (r = 0.50, P = 0.025) but were not associated with motor function. Supplementary motor area activity elicited by paretic tapping was displaced in AIS compared to controls (P = 0.003).
Conclusion:
Motor network components may be displaced in both hemispheres after perinatal stroke, particularly in AIS and those with ipsilateral control of the affected limb. Modest correlations with clinical function may support that more complex models of developmental plasticity are needed to inform targets for individualized neuromodulatory therapies in children with perinatal stroke.
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