These findings extend previous observations that suggested a diagnostic and localizing utility of diffusion-weighted imaging in CJD.
Background and Purpose-Correlation of MRI findings with atherosclerotic vascular lesions has rarely been attempted in patients with cerebellar infarction. The aim of this study was to correlate the MRI lesions with the vascular lesions seen on conventional cerebral angiography in cerebellar infarction. Methods-The subjects included 31 patients with cerebellar infarcts who underwent both MRI and conventional cerebral angiography. We analyzed the risk factors, clinical findings, imaging study, and angiography results. We attempted to correlate MRI lesions with the vascular lesions shown in the angiograms. Results-The vascular lesions seen on angiograms were subdivided into 3 groups: large-artery disease (nϭ22), in situ branch artery disease (nϭ6), and no angiographic disease with hypertension (nϭ3). The proximal segment (V1) lesions of vertebral artery were the most common angiographic features in patients with large-artery disease in which stroke most commonly involved the posterior inferior cerebellar artery (PICA) cerebellum. The V1 lesions with coexistent occlusive lesions of the intracranial vertebral and basilar arteries were correlated with cerebellar infarcts, which had no predilection for certain cerebellar territory. The intracranial occlusive disease without V1 lesion was usually correlated with small cerebellar lesions in PICA and superior cerebellar artery (SCA) cerebellum. The subclavian artery or brachiocephalic trunk lesion was associated with small cerebellar infarcts. The in situ branch artery disease was correlated with the PICA cerebellum lesions, which were territorial or nonterritorial infarct. No angiographic disease with hypertension was associated with small-sized cerebellar infarcts within the SCA, anterior inferior cerebellar artery, or SCA cerebellum. Conclusions-Our study indicates that the topographic heterogeneity of cerebellar infarcts are correlated with diverse angiographic findings. The result that large-artery disease, in which nonterritorial infarcts are more common than territorial infarcts, is more prevalent than in situ branch artery disease or small-artery disease, suggest that even a small cerebellar infarct can be a clue to the presence of large-artery disease.
Background and Purpose-MRI has superior capabilities for the detection of cerebral infarcts compared with CT. CT was used to locate infarcts in most previous studies of atherothrombotic middle cerebral artery (MCA) territory infarcts. Thus, there was a possibility of missing concomitant small infarcts. More accurate identification of topographic lesions in MCA territory with MRI may help to establish the pathogenesis of stroke. The present study determines topographic patterns, distribution of vascular lesions, and probable mechanisms. Methods-Forty-two patients with MCA territory infarcts on routine MRI and no major cause of cardioembolism were studied with conventional angiography or MR angiography. Results-The topographic patterns seen on MRI were subdivided into 4 groups: cortical border-zone infarcts (nϭ6), pial territory infarcts without insular infarct (nϭ3), pial territory infarcts with insular infarct (nϭ14), and large subcortical infarcts (nϭ19). Of 6 patients with cortical border-zone infarcts, 4 had concomitant small cortical or subcortical multiple lesions. Angiography showed intrinsic MCA disease in 4 patients. Of 3 patients with pial territory infarcts without insular infarct, 2 also had small multiple centrum ovale lesions. All had intrinsic MCA disease. Pial territory infarcts with partial or whole insular lesions were present in 10 and 4 patients, respectively. Five patients had additional multiple cortical or subcortical lesions. Ten patients had intrinsic MCA disease. Of the 19 patients with large subcortical infarcts, 12 had centrum ovale infarcts, and 4 had both basal ganglia and centrum ovale lesions. Ten had concomitant small cortical or subcortical lesions. Six patients had intrinsic MCA disease. Conclusions-Similar vascular lesions induce different topographic patterns in MCA territory infarction, which are related to individual vascular variability, degree of primary and secondary collateralization, and pathogenesis of infarcts. Our study indicates that concomitant small cortical or subcortical lesions are also commonly associated findings in diverse patterns of MCA territory infarction, which can mostly be explained by probable embolic mechanism. Key Words: angiography, magnetic resonance Ⅲ cerebral embolism Ⅲ magnetic resonance imaging Ⅲ middle cerebral artery M ost middle cerebral artery (MCA) territory infarcts have been attributed to embolism from the heart or internal carotid artery (ICA), poor perfusion due to ICA occlusion, intrinsic MCA occlusive disease, or intrinsic disease in the lenticulostriate penetrating vessels.Previous studies 1,2 indicated racial differences in atherothrombotic occlusive diseases of the anterior cerebral circulation. Specifically, extracranial atherosclerosis is more common in whites, whereas intracranial atherosclerosis is more frequent in blacks, Chinese, and Japanese. However, how the common intracranial atherosclerotic vascular lesions are associated with topographic patterns of infarcts has not been studied sufficiently.MRI of the brain has supe...
INTRODUCTIONMultifocal inflammatory leukoencephalopathy (MIL) is a rare syndrome associated with 5-fluorouracil (5-FU) and levamisole chemotherapy (1-6). The radiographic and clinical features of this syndrome often pose difficulties in distinguishing it from other diseases, especially multiple brain metastases. We herein describe a patient with MIL related to oral tegafur (derivative of 5-FU) and levamisole therapy using thallium-201 ( 201 Tl) single photon emission computed tomography single photon emission computed tomography (SPECT) and proton magnetic resonance spectroscopy (MRS) as adjunctive noninvasive tools in the diagnosis of this reversible syndrome. CASE REPORTA 45-yr-old man was admitted to our department with a gradual onset of right hemiparesis, left facial and arm paresthesias, and hiccups. Five months before admission, he had underwent primary resection of adenocarcinoma of the rectum. Two months after the operation, he received adjuvant chemotherapy with tegafur ([1-(2-tetrahydrofuryl)-5-FU], 600 mg/day orally) and levamisole (100 mg/day orally for three days, each week) for moderately differentiated stage II adenocarcinoma. One month before admission, he developed paresthesia in the left face and arm, and complained of intermittent hiccups. One week later, he experienced progressive weakness of right extremities and gait disturbance. On admission, he was alert with intact cognitive function. Neurologic examination showed decreased left facial and arm sensation, mild right hemiparesis, moderately increased deep tendon reflexes, and clumsiness of right side on gait. He was afebrile throughout the illness.Brain MRI revealed multiple, ring-or nodular-enhancing white matter lesions, scattered throughout the cerebral hemispheres and two separate non-enhancing brainstem lesions involving the left middle cerebellar peduncle and dorsolateral medulla oblongata (Fig. 1). Cerebrospinal fluid (CSF) examination showed a normal opening pressure, pleocytosis (22 cells/ L, 90% of lymphocytes), normal glucose, and increased protein; cultures for bacterial, fungal, and acid-fast bacilli, and cytologic findings were negative; ELISA test for parasites and PCR test for viruses were all negative. Other general laboratory tests revealed no abnormalities.On the fourth day of admission, proton MRS (Simens Vison Plus 1.5T, PRESS 2D with single voxel) was performed, which revealed high choline (Cho) and lactate with relative preservatioan of N-acetylaspartate (NAA) (Fig. 2). On the 10th day, brain 201 Tl SPECT showed no abnormal uptake. A stereotactic brain biopsy targeting the ring-enhancing lesion in the left frontal area was done on the 14th day.Histopathology revealed demyelinating lesions in white matter with relative axonal sparing; perivascular lymphocytic cuffing, macrophage infiltration, and scattered hyperplastic astrocytes were noted.With discontinuation of tegafur and levamisole, he began to receive corticosteroid therapy. Two weeks after discharge, his neurologic condition improved markedly, as evidenced by...
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