Abstract
Purpose: Ongoing post-stroke structural degeneration and neuronal loss preceding neuropsychological symptoms such as cognitive decline and depression are poorly understood. Various substructures of the limbic system have been linked to cognitive impairment. In this longitudinal study, we investigated the post-stroke macro- and micro-structural integrity of the limbic system using structural and diffusion tensor magnetic resonance imaging.Materials and Methods: Nineteen ischemic stroke patients (11 men, 8 women, average age 53.4 ± 12.3, range 18–75 years), with lesions remote from the limbic system, were serially imaged three times over 1 year. Structural and diffusion-tensor images (DTI) were obtained on a 3.0 T MRI system. The cortical thickness, subcortical volume, mean diffusivity (MD), and fractional anisotropy (FA) were measured in eight different regions of the limbic system. The National Institutes of Health Stroke Scale (NIHSS) was used for clinical assessment. A mixed model for multiple factors was used for statistical analysis, and p-values <0.05 was considered significant.Results: All patients demonstrated improved NIHSS values over time. The ipsilesional subcortical volumes of the thalamus, hippocampus, and amygdala significantly decreased (p < 0.05) and MD significantly increased (p < 0.05). The ipsilesional cortical thickness of the entorhinal and perirhinal cortices was significantly smaller than the contralesional hemisphere at 12 months (p < 0.05). The cortical thickness of the cingulate gyrus at 12 months was significantly decreased at the caudal and isthmus regions as compared to the 1 month assessment (p < 0.05). The cingulum fibers had elevated MD at the ipsilesional caudal-anterior and posterior regions compared to the corresponding contralesional regions.Conclusion: Despite the decreasing NIHSS scores, we found ongoing unilateral neuronal loss/secondary degeneration in the limbic system, irrespective of the lesion location. These results suggest a possible anatomical basis for post stroke psychiatric complications.
Highlights
Stroke research and clinical management have been predominantly focused on the acute phase of injury and little is known about the rates of ongoing chronic degeneration
The lesions were identified as middle cerebral artery infarct (n = 10), posterior cerebral artery infarcts (n = 5), anterior cerebral artery infarct (n = 2), and pontine infarct (n = 2)
Hippocampus, amygdala, entorhinal, and perirhinal cortices to be most vulnerable to degeneration
Summary
Stroke research and clinical management have been predominantly focused on the acute phase of injury and little is known about the rates of ongoing chronic degeneration. Chronic thalamic neuronal loss remote from the lesion was noted in an animal study [9] Later research validated this evidence, and further found that neuroinflammation was not limited to the lesion area, but globally impacted the ipsilesional hemisphere [10]. Another longitudinal primate study demonstrated ipsilesional hemispheric atrophy and secondary neuronal degeneration in the lentiform nucleus [11]. Several cross-sectional studies and a handful of longitudinal studies suggested an association between post-stroke tissue loss in the limbic system and cognitive impairment [14,15,16,17,18,19,20,21,22] These studies reported only two or three substructures of the limbic system and in some cases the primary lesions were within the limbic system
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