Axonal injury in the internal capsule correlates with motor impairment after stroke.
Background and Purpose--Magnetic resonance spectroscopy (MRS) in ischemic stroke has shown a correlation between N-acetylaspartate (NAA) loss from the infarcted region and disability. We tested the hypothesis that NAA loss in the descending motor pathways, measured at the level of the posterior limb of the internal capsule, would determine motor deficit after a cortical, subcortical, or striatocapsular stroke. Methods--Eighteen patients with first ischemic stroke causing a motor deficit were examined between 1 month and 5 years after stroke. T2-weighted imaging of the brain and localized proton (voxel, 1.5x2x2 cm3) MRS from the posterior limb of each internal capsule were performed and correlated to a motor deficit score. Results--Mean internal capsule NAA was significantly lower in the patient group as a whole compared with the control group (P<0.001). Reductions in internal capsule NAA on the side of the lesion were seen in cases of cortical stroke in which there was no extension of the stroke into the voxel as well as in cases of striatocapsular stroke involving the voxel region. There was a strong relationship between reduction in capsule NAA and contralateral motor deficit (log curve, r2=0.9, P<0.001). Conclusions--Axonal injury in the descending motor pathways at the level of the internal capsule correlated with motor deficit in patients after stroke. This was the case for strokes directly involving the internal capsule and for strokes in the motor cortex and subcortex in which there was presumed anterograde axonal injury.
Pendlebury
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Centre for Functional MRI of the Brain (FMRIB), John Radcliffe Hospital, and the Department of Clinical Neurology, The Radcliffe Infirmary (S.T.P., M.A.L., P.M.M.), and the MRC Magnetic Resonance Spectroscopy Unit, John Radcliffe Hospital (A.
Blamire
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Lee
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Styles
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Matthews
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PM
D000203:Activities of Daily Living; D000368:Aged; D000369:Aged, 80 and over; D001369:Axons / Q000502:physiology*; D002544:Cerebral Infarction / Q000175:diagnosis / Q000503:physiopathology / Q000534:rehabilitation; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000175:diagnosis / Q000503:physiopathology* / Q000534:rehabilitation; D003342:Corpus Striatum / Q000098:blood supply / Q000166:cytology / Q000502:physiology; D004185:Disability Evaluation; D005260:Female; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009043:Motor Activity; D009044:Motor Cortex / Q000098:blood supply / Q000166:cytology / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology* / Q000648:ultrastructure; D010296:Parietal Lobe / Q000098:blood supply / Q000166:cytology / Q000502:physiology; D011379:Prognosis; D016896:Treatment Outcome; D014855:Wallerian Degeneration / Q000503:physiopathology