Abstract
We report the case of a woman presenting with changes on cerebral imaging a year and a half after a bi-thalamic (predominantly left-sided) infarction including lateral and medial thalamic nuclei. Lateral geniculate body and pulvinar were not damaged. Hypoperfusion was observed in left cortical and basal structures. White matter FLAIR hyperintense lesions occurred in the left hemisphere and the occipital region 1 year and half after stroke. Medial and lateral thalamic nuclei are not highly connected to the occipital cortex. Therefore, in addition to Wallerian degeneration after thalamic stroke, we hypothesize that the chronic left temporal hypoperfusion induced by diaschisis can lead to a lateralized chronic hypoxic damage of the occipital fiber tract (optic radiation) that passes through the temporal lobe.
Highlights
Remote hypoperfusion in stroke is frequently considered as a diaschisis induced by deactivation of regions highly connected with the damaged structure [1]
We report the case of delayed unilateral left leukoencephalopathy in chronic hemispheric hypoperfusion after a left medial and lateral thalamic infarct
CASE REPORT We report the case of an 81-year-old woman presenting with changes on cerebral imaging a year and a half after a bi-thalamic infarction including lateral and medial thalamic nuclei
Summary
Remote hypoperfusion in stroke is frequently considered as a diaschisis induced by deactivation of regions highly connected with the damaged structure [1]. We report the case of delayed unilateral left leukoencephalopathy in chronic hemispheric hypoperfusion after a left medial and lateral thalamic infarct. As the leukopathy was restricted in the white matter highly connected to medial and lateral thalamic nuclei (i.e., frontal and temporal lobes), and in the left occipital white matter, a potential toxicity of the chronic remote hypoperfusion is discussed. CASE REPORT We report the case of an 81-year-old woman presenting with changes on cerebral imaging a year and a half after a bi-thalamic (predominantly left-sided) infarction including lateral and medial thalamic nuclei. About 1 year and 8 months later, white matter FLAIR hyperintense lesions and atrophy were observed in the left hemisphere and the occipital region.
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