Quantitative volumetric study of brain in chronic striatolenticular stroke
Perforating branches of the middle cerebral artery, namely the striato-lenticular arteries provide the majority of blood supply for the striatum and posterior limb of the internal capsules. Occlusions of these arteries cause a small stroke but have a devastating effect on patients’ functions. Previous studies showed that the anterior two thirds of the internal capsule is occupied by the prefrontal tracts with the posterior one third by connection to/from sensorimotor, temporal and posterior parietal cortices. In this study, we aimed to examine the long-term effect of infarction in the striato-capsular region on cerebral cortex thickness and also its association with stroke volume and different functional tests. We hypothesized that because of extensive connections of striatum and internal capsule with the cerebral cortex, infarction of this area results in an extensive cortical thickness degeneration which could in turn cause low fictional measurement scores. High resolution T1 weighted MRI was obtained from 21 patients with ischemic stroke in the striatum/posterior limb of the internal capsule region. Subjects were carefully selected from a pool of 140 stroke cases recruited for the Northstar Stroke Project. 63 healthy volunteers (30 male), matched for age and gender were also chosen to form the control group from the OASIS database. Patients and normal subjects were right handed except for 3 patients who have the stroke in the left side of the brain. Patients were defined as left-sided stroke and right-sided stroke depending on the side of the stroke in brain. MRI scans were done 6 months to 2 years after the stroke. To measure cortical thickness, we used Freesurfer software. Vertexwise group comparison was carried out using General Linear Models (GLM). With the Significance level set at 0.05. Population maps of stroke lesions showed that the majority of strokes were located in the striatum and posterior internal capsule. Cortical thickness reduction was greater in the ipsilateral hemisphere. Vertex-wise group comparison between leftsided stroke patients and controls group showed significant reduction in the cortical II thickness in the dorsal and medial prefrontal, premotor, posterior parietal, precuneus, and temporal cortex which survived after correction for multiple comparison using false discovery rate at Freesurfer. Similar comparison for rightsided stroke showed a similar pattern of cortical thinning, however the extent of cortical thinning was much less than in that of the left-sided stroke patients but the ROI analysis showed the main effect of side was significant (f (1, 19) =6.909, p=0.017), which showed that the left hemisphere stroke side group had a thicker cortex (mean=2.463, sd= 0.020) on average compare to the right hemisphere stroke side (mean=2.372, sd= 0.028). Primary motor cortex was surprisingly spared in both stroke groups. In addition, volume of the corpus callosum increased significantly in the stroke group. The differences between motor cortex (M1) thickness in left-hemispheric stroke patients versus controls (t=1.24, n=14, p>0.05) and right-hemispheric stroke patients versus controls (t=-0.511, n=7, p>0.05) were not significant. There was a negative correlation between the volume of the stroke lesions and the affected M1 thickness. There was no correlation between the stroke volume and functional tests in patients and also no correlation between the motor cortex thickness and functional tests in patients. Regarding normal subjects, comparison between two sides of the brain showed that the both hemispheres are symmetrical. In addition, correlation between age and cortical thickness showed a negative significant correlation (1-tailed, p<0.0007, manual correction for multiple comparisons) in M1, superior frontal, lingual cortex at both side of the brain and also negative significant correlation in superior temporal cortex and isthmus cingulated cortex on the left side of brain and supramarginal cortex on the right side of brain but there was no significant difference in cortical thickness between males and females. The finding from this study suggests that the size of the lesion can be a predictor of further M1 cortex reduction. The correlation of M1 thickness with stroke volume showed that secondary cortical degeneration may be mainly depends on the size of neuronal loss in strital-capsular stroke. From normal subject study it can be concluded that generally cortical thickness will decrease with ageing but gender does not have an effect on the cortical thickness. III Furthermore, the lack of behavioural correlation with M1 thickness and stroke volume and also the non significant M1 cortex reduction versus control group may suggest that the long-term functional disability after capsular-striatal stroke may not be entirely dependent on primary motor cortex and secondary motor cortex and primary somatosensory cortex could have an important role as well. These results may help to understand why relatively small subcortical infarcts often cause severe disability that is relatively resistant to recovery in the long term.
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