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Carotid intima-media thickness (IMT) is a surrogate marker for evaluating atherosclerotic vascular diseases. The phosphodiesterase inhibitor cilostazol attenuates the increase in carotid IMT in diabetes patients. We studied whether cilostazol can reduce the progression of carotid IMT in symptomatic ischemic stroke patients. From our prospective registry of acute ischemic stroke patients who were admitted during a 4.5-year period, follow-up carotid ultrasound was performed in a random sample of survivors. Patients were divided into two groups: the cilostazol group, who continued cilostazol treatment during the follow-up period; and the control group, who were prescribed antiplatelets other than cilostazol. Analysis of covariance and propensity score-matched analysis were used to evaluate the difference between groups. Among a total of 1,049 cases in our registry, 208 patients were utilized to construct two comparable sets by propensity score analysis, including 101 who received cilostazol and 107 who took antiplatelet medication without cilostazol. Both maximum and mean carotid IMT values were significantly reduced in the cilostazol group but increased in the control group (maximum left –0.048 ± 0.186 vs. 0.022 ± 0.163 mm, p = 0.001; maximum right –0.037 ± 0.173 vs. 0.050 ± 0.200 mm, p = 0.001; mean left –0.052 ± 0.102 vs. 0.023 ± 0.112 mm, p

Hemichorea-hemiballism (HCHB) was infrequently related to cortical lesions such as tumor or infarction. Although functional derangement of the basal ganglia (BG) or the thalamus (Th) was suggested, pathomechanism of HCHB secondary to cortical lesions remains uncertain. We recruited the patients with HCHB secondary to cerebrovascular diseases, excluding other causes such as hyperglycemia. All the patients were studied with brain magnetic resonance imaging/angiography (MRI/MRA) and single-photon emission computed tomography (SPECT). Those with only cortical abnormalities in neuroimaging studies were sorted out as the cases of cortical HCHB. Statistical parametric mapping (SPM) analysis of SPECT was performed to investigate the pathomechanism of cortical HCHB. Ten patients (three males and seven females) were included in our study. Six patients had acute BG lesions with SPECT abnormalities, and one had old BG lesions with abnormal SPECT. Three patients were classified as cortical HCHB with lesions only in the frontal and parietal cortices in MRI and SPECT. SPM analysis revealed additional hypoperfusion in frontal areas, leaving BG and Th free of any perfusion abnormalities. Although cortical HCHB was strictly defined by MRI and SPECT, cortical HCHB was not uncommon (30 %). Further analysis showed intertwined networks among the frontal and parietal lobes for cortical HCHB. Cortical dysfunction is important in the pathogenesis of cortical HCHB even without significant involvement of BG and Th.