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BackgroundIn patients with urinary bladder cancer, brain metastases are quite rare and occur in only 1–7% of these patients. Of the urinary bladder cancers, large cell neuroendocrine carcinoma (LCNEC) is extremely rare; only 16 cases have been reported to date. In this report, a case of brain metastasis from LCNEC of the urinary bladder is described.Case DescriptionA 74-year-old man was admitted with confusion and left-sided hemiparesis. Head magnetic resonance imaging demonstrated a ring-enhancing lesion in the right frontal lobe. Whole body computed tomography revealed a suspicious lesion in the urinary bladder. These findings were considered consistent with metastatic brain tumor. Craniotomy and tumor removal were performed. After craniotomy, the patient underwent cystoscopy and the bladder mass was biopsied. Histological and immunohistochemical examination of both the brain tumor and bladder mass revealed LCNEC. According to these findings, the patient was diagnosed with a brain metastasis from LCNEC of the urinary bladder.ConclusionTo our knowledge, this is the first report of a patient with a brain metastasis from LCNEC of the urinary bladder.

Patients with non-traumatic, non-aneurysmal, and non-perimesencephalic subarachnoid hemorrhage (SAH) tend to have clots circumscribed along the cortical convexity, a condition referred to as acute cortical SAH. Cerebral venous thrombosis (CVT) is a potential cause of cortical SAH. The study tried to establish the diagnosis and management of cortical SAH caused by CVT. Retrospective review of 145 patients with non-traumatic SAH identified 15 patients with no ruptured aneurysm. Clinical features were investigated with a specific focus on patients with SAH caused by CVT. Eight of the 15 patients had perimesencephalic SAH, and 7 had cortical SAH. SAH caused by CVT was diagnosed in 4 of the 7 patients with cortical SAH. The cortical SAH involved the unilateral convexity or sylvian cistern and spared the basal cistern on computed tomography in all 4 patients. CVT occurred in the transverse sinus and cortical vein (1 patient), insular vein (1 patient), and cortical vein (2 patients). Identification of thrombosed veins or sinuses was established directly by T 2 *-weighted and diffusion-weighted magnetic resonance (MR) imaging in the acute stage and diffusion-weighted and T 1 -weighted MR imaging in the subacute stage. All patients had cortical swelling without findings of venous hemorrhagic infarction on T 2 *-weighted MR imaging. None of the 4 patients received active treatment, and all had favorable outcomes. CVT in patients with non-traumatic cortical SAH should be first excluded as a potential hemorrhagic cause by MR imaging for thrombosed veins or sinuses before initiating antifibrinolytic therapy.

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