Striatocapsular Infarct and Aphasia

BACKGROUND: Determining the mechanism for aphasia following a subcortical infarct involving the striatum and internal capsule has been controversial. The aim of this study was to determine the underlying mechanism, which might clarify the relationship between the severity of aphasia and the cortical hypoperfusion in a striatocapsular infarct. METHODS: We included 33 patients with striatocapsular infarcts in the dominant hemisphere on precontrast CT/MRI. A MR angiography (MRA) was done in all patients. Contrast enhanced MRI and/or triphasic perfusion CT (TPCT) were performed in 26 patients to identify slow collateral blood flows. The regional cerebral blood flow was evaluated in 14 out of 33 patients by perfusion SPECT. The index of aphasia severity was the aphasia quotient, measured by the Korean version-Western Aphasia Battery. RESULTS: Twenty-five of 33 patients (75.7%) showed aphasia with different degrees of severity. The four aphasic subgroups were mild (n=9), mild-to-moderate (n=8), moderate-to-severe (n=3), and severe (n=3) groups. Six patients with moderate-to-severe or severe degree of aphasia showed larger infarcts, occlusions of the middle cerebral artery (MCA) stem or internal carotid artery (ICA) on MRA, and abnormal delayed cortical vascular enhancements on MRI and/or TPCT. The severity of aphasia correlated strongly with the degree of perisylvian cortical hypoperfusion on SPECT. Focal perisylvian cortical atrophy on follow-up MRI was found in two patients with greater than moderate-to-severe aphasia. CONCLUSIONS: Aphasia of greater than moderate-to-severe degree following a striato-capsular infarct may be explained by selective neuronal loss of the perisylvian cortex due to the occlusion of the MCA stem or ICA and insufficient collateral blood flow. (J Korean Neurol Assoc 19(1):10~18, 2001

Thalamic syndrome and cortical hypoperfusion on technetium-99m HM-PAO brain SPECT

The six patients included in this study had painful dysesthesia, resulting from vascular lesions in or near the thalamus, confirmed by computerized tomography(CT) brain scan. Using hexamethyl propyleneamine oxime(HM-PAO) single photon emission computed tomography(SPECT) brain scanning, regional cerebral perfusion(rCP) was demonstrated. In contrast to three patients with lesions near the thalamus who showed symmetrical cortical radioactivity, the other three patients with thalamic lesions revealed decreased rCP in the ipsilateral cerebral cortex on HM-PAO brain SPECT. We thought that the loss of afferent activating stimuli from the thalamus led to decreased cortical neuronal activity and the following hypoperfusion. In patients with thalamic syndrome resulting from thalamic lesions, the role of the remote effect of the thalamic damage and consequent cortical deregulation in the development of thalamic pain and/or neuropsychological symptoms cannot be excluded completely.