Long-Term Brain Atrophy after Focal Ischemic Stroke: A Longitudinal Study Applying Deformation-Based Morphometry

Introduction: Cerebral ischemia leading to brain infarction results in an area of focal damage. Results from clinical, electrophysiological and neuroimaging studies clearly suggest remote effects ipsi- and contralaterally which are believed to play a role in the dynamic mechanisms of cerebral reorganization and functional recovery. Remote structural alterations have also been detected in terms of, e.g., ventricular enlargement, accelerated global atrophy after large ischemic stroke, cerebellar diaschisis and with recent quantitative MRI studies. This pilot MR study addresses volume alterations after focal cerebral ischemia with a focus on perilesional and also remote ipsi- and contralateral changes in brain volume and cortical thickness. Methods: 14 patients suffering from acute ischemia in the middle cerebral artery territory with small lacunar infarctions were included in the study. 3D T₁-weighted MRI scans (Siemens Symphony, 1.5 Tesla) were obtained in the acute stage and at 6 and 12 months follow-up. In addition to neuroimaging, all patients were neurologically assessed and scored on three outcome measures (NIHSS, Rankin Scale and Barthel Index). Image analysis was carried out with the Brain Image Analysis tool (BRIAN, MPI Leipzig) with subvoxel accuracy using linear and non-linear registration methods and subsequent visualization of changes. Results: Direct perilesional but no remote ipsilateral changes were seen in 8 patients with microvascular hemispheric lesions. Contralesional volume changes in a distinct, presumably homologous area, were detected only in a patient suffering from a larger ischemia. Neurological deficits improved in all patients, the majority reported only minor handicaps in daily activities. Conclusion: The present study shows that small infarcts are associated with brain volume changes mainly in the vicinity of the infarct. The detection of remote volume changes seems to be associated with the size of the lesion. These remote effects are particularly pronounced in the ipsilateral hemisphere, but can also be detected contralateral to the lesion. The lack of callosal changes suggests a mechanism which is not bound to fiber degeneration. Although neurological impairment was found to improve in all patients, it may be helpful to further elucidate the mechanisms behind this remote cortical atrophy. The understanding of these processes may help to further improve outcome and to prevent long-term sequelae after stroke.