Axonal injury in the internal capsule correlates with motor impairment after stroke

Citation
St. Pendlebury et al., Axonal injury in the internal capsule correlates with motor impairment after stroke, STROKE, 30(5), 1999, pp. 956-962
Citations number
36
Categorie Soggetti
Neurology,"Cardiovascular & Hematology Research
Journal title
STROKE
ISSN journal
00392499 → ACNP
Volume
30
Issue
5
Year of publication
1999
Pages
956 - 962
Database
ISI
SICI code
0039-2499(199905)30:5<956:AIITIC>2.0.ZU;2-D
Abstract
Background and Purpose-Magnetic resonance spectroscopy (MRS) in ischemic st roke 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, su bcortical, or striatocapsular stroke. Methods-Eighteen patients with first ischemic stroke causing a motor defici t were examined between 1 month and 5 years after stroke. T2-weighted imagi ng of the brain and localized proton (voxel, 1.5X2X2 cm(3)) MRS from the po sterior limb of each internal capsule were performed and correlated to a mo tor deficit score. Results-Mean internal capsule NAA was significantly lower in the patient gr oup as a whole compared with the control group (P<0.001). Reductions in int ernal 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 wa s a strong relationship between reduction in capsule NAA and contralateral motor deficit (log curve, r(2)=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 then was presumed a nterograde axonal injury.