A 67-year-old female with a history of hypertension and cerebral infarction presented with subarachnoid hemorrhage (SAH) (Hunt and Kosnik grade 4). Brain computed tomography (CT) revealed a clot dominantly on the right (Fisher's classification Group 4). Cerebral angiography showed funnelshaped widenings at the origins of the bilateral posterior communicating arteries. The maximum diameter of the widening was greater than 3 mm, so this widening was called an enlarged infundibular widening. Angiography showed a small bulge protruding posterolaterally from the wall of the right enlarged infundibular widening, and the right posterior communicating artery arose from the apex of the enlarged infundibular widening. Based on the findings of the brain CT and cerebral angiography, the diagnosis was SAH due to rupture of the right enlarged infundibular widening. Approximately 12 hours after the onset, the clot was evacuated through the right pterional approach. Bleeding from the small bulge of the right enlarged infundibular widening occurred intraoperatively, so a right-angled ring clip was applied parallel to the right internal carotid artery to obliterate the rupture point. Postoperatively, she was discharged without neurological deficit, and follow-up CT showed no other new infarction. We recommend clipping rather than wrapping or coating for similar cases of ruptured enlarged infundibular widening.
A 47-year-old male receiving anticoagulant therapy for thrombophlebitis in the left leg for several years presented with mild left hemiparesis and ipsilateral hypesthesia. The cause of the thrombophlebitis was still unknown. Magnetic resonance (MR) imaging showed subacute thrombosis of both the superior sagittal sinus (SSS) and a cortical vein in the right cerebral hemisphere. Fluid attenuation inversion recovery axial MR imaging demonstrated these lesions more obviously than conventional T2-weighted axial MR imaging. Right carotid angiography showed a partial SSS filling defect and occlusion of the cortical vein with collateral circulation. Coagulation studies revealed decreases in both protein C activity and antigen levels with normal levels of blood coagulation factors II, VII, IX, and X and protein S activity and antigen. The patient's mother had normal levels of both protein C activity and antigen, but his father had decreased levels. The diagnosis was SSS and cerebral cortical venous thrombosis caused by congenital protein C deficiency. The patient was treated conservatively, and his clinical course was uneventful. His neurological dysfunctions recovered within approximately 3 weeks after the onset. Ten months later, right carotid angiography showed recanalization of the SSS and partial filling of the cortical vein. Anticoagulant therapy has been continued, and no cerebral venous thrombosis has recurred during the 1.5 years after the onset.
An 80-year-old male with a history of hypertension presented with chronic subdural hematoma manifesting as progressive consciousness disturbance and left hemiparesis. T 1 -weighted and fluid attenuation inversion recovery (FLAIR) magnetic resonance imaging showed a fresh hematoma in the right subdural space with a midline shift of 15 mm. FLAIR and diffusion-weighted imaging showed a hyperintense area in the right paraventricular white matter compressed by the hematoma. Apparent diffusion coefficients (ADCs) corresponding to the hyperintense area in the central area of the affected cerebral hemisphere on FLAIR images were measured before and one month after the operation. The motion probing gradient was applied in the right-left direction to the body axis. Since the central area in the cerebrum includes nerve fibers perpendicular to the direction of the gradient, the measured ADC appeared to be anisotropic. Preoperative ADC in the right paraventricular white matter was anisotropic and greater than in age-matched normal subjects, so the edema was identified as the vasogenic type. The edema in the right paraventricular white matter resolved promptly with improvement of the midline shift and normalization of the ADC.
A 61-year-old female with a past history of gastric cancer presented with altered mental status, a few seizures, and low-grade fever. Lumbar puncture revealed elevated cerebrospinal fluid (CSF) pressure, lymphocytic pleocytosis, elevated protein level, remarkably decreased glucose level, and presence of cryptococcal antigen. Cryptococcus neoformans was identified by India ink staining and culture of CSF. The patient was given antifungal agents intravenously and intrathecally. CSF findings improved and C. neoformans could not be detected in CSF one month after the onset. Cerebral sulcal hyperintensity was identified in the bilateral frontal and parietal lobes on fluid-attenuated inversion recovery (FLAIR) magnetic resonance (MR) imaging one month after the onset, but no leptomeningeal enhancement was detected in the affected sulci on T 1 -weighted MR imaging. The sulcal hyperintensity on FLAIR imaging developed in the bilateral temporal and occipital lobes 2 months after the onset. CSF findings obtained by lumbar puncture were within the normal range except for pressure. However, neurological deterioration and reconfirmation of C. neoformans in CSF indicated recurrent cryptococcal inflammation. The sulcal hyperintensity on FLAIR imaging may indicate a high CSF protein concentration in the subarachnoid space. Such cerebral sulcal hyperintensity is an unusual MR imaging finding of cryptococcal meningoencephalitis, and may be an early sign of procrastinating process or recurrent inflammation even if the findings of CSF obtained by lumbar puncture are normal.
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