Automated MRI-based volumetry of basal ganglia and thalamus at the chronic phase of cortical stroke

Abstract

Purpose We aimed at assessing the potential of automated MR morphometry to assess individual basal ganglia and thalamus volumetric changes at the chronic phase after cortical stroke. Methods Ninety-six patients (mean age: 65 ± 18 years, male 55) with cortical stroke at the chronic phase were retrospectively included. Patients were scanned at 1.5 T or 3 T using a T1-MPRAGE sequence. Resulting 3D images were processed with the MorphoBox prototype software to automatically segment basal ganglia and thalamus structures, and to obtain Z scores considering the confounding effects of age and sex. Stroke volume was estimated by manual delineation on T2-SE imaging. Z scores were compared between ipsi- and contralateral stroke side and according to the vascular territory. Potential relationship between Z scores and stroke volume was assessed using the Spearman correlation coefficient. Results Basal ganglia and thalamus volume Z scores were lower ipsilaterally to MCA territory stroke (p values < 0.034) while they were not different between ipsi- and contralateral stroke sides in non-MCA territory stroke (p values > 0.37). In MCA territory stroke, ipsilateral caudate nucleus (rho = − 0.34, p = 0.007), putamen (rho = − 0.50, p < 0.001), pallidum (rho = − 0.44, p < 0.001), and thalamus (rho = − 0.48, p < 0.001) volume Z scores negatively correlated with the cortical stroke volume. This relation was not influenced by cardiovascular risk factors or time since stroke. Conclusion Automated MR morphometry demonstrated atrophy of ipsilateral basal ganglia and thalamus at the chronic phase after cortical stroke in the MCA territory. The atrophy was related to stroke volume. These results confirm the potential role for automated MRI morphometry to assess remote changes after stroke.

Neuroinflammation as a Key Driver of Secondary Neurodegeneration Following Stroke?

“…Particularly, a magnetic resonance imaging (MRI) study demonstrated evidence of SND in the thalamus of patients three months after an ischaemic insult [ 29 ], whereas another study noted thalamic degeneration on MRI within the first few weeks post-stroke, with one patient demonstrating degeneration in the ventral nuclei as early as eight days following an ischaemic stroke [ 25 ]. In line with this, a recent neuroimaging study reported atrophy of the caudate nucleus, putamen, pallidum and thalamus following middle cerebral artery (MCA) stroke in patients more than three weeks post-stroke [ 30 ]. Interestingly, the authors demonstrated that localization of the infarct significantly influenced the secondary changes seen in the basal ganglia and thalamus, as atrophy of these structures was not seen following anterior cerebral artery or posterior cerebral artery stroke [ 30 ].…”

“…This phenomenon, termed secondary neurodegeneration (SND), involves the progressive death of neurons in distal regions of the brain that are anatomically connected to the site of infarction, but which were not initially affected by the reduction in cerebral blood flow brought on by the initial stroke [ 28 ]. SND has consistently been observed in both clinical neuroimaging studies [ 25 , 29 , 30 ] and in experimental studies at the cellular level [ 31 , 32 , 33 ]. Various sites appear to be affected by SND, dependent on their connectivity with the infract site, as well as other cortical structures undergoing degeneration.…”

Smaller spared subcortical nuclei are associated with worse post-stroke sensorimotor outcomes in 28 cohorts worldwide

“…This finding is in line with previous work showing that direct damage to the putamen relates to post-stroke gait impairment, 44 upper limb impairment 45 and spasticity, 46 all deficits which overlap with the behavioural measures used here. In addition, secondary atrophy of the putamen has been reported after cortical stroke and is associated with infarct volume 47 and post-stroke cognitive deficits. 48 The relationship between chronic sensorimotor behavioural deficits and atrophy of the ipsilesional putamen after stroke, however, has not previously been reported.…”

Smaller spared subcortical nuclei are associated with worse post-stroke sensorimotor outcomes in 28 cohorts worldwide

“…Direct damage to the putamen has been related to post-stroke gait impairment (Alexander et al ., 2009), upper limb impairment (Lee et al ., 2015), and spasticity (Cheung et al ., 2016), deficits which overlap with the behavioral measures used here. Secondary atrophy of the putamen has been reported after cortical stroke and associated with infarct volume (Baudat et al ., 2020) and post-stroke cognitive deficits (Lopes et al ., 2012). The relationship between chronic sensorimotor behavioral deficits and the volume of the non-lesioned ipsilesional putamen after stroke, however, has not been reported.…”