A 22-year-old female was seen in the emergency within one hour of acute onset of right sided headache followed by weakness of the left side of body. On neurological examination, she was mildly drowsy, had forced right gaze deviation, dysarthria, left hemiplegia and left hemisensory loss. Computed tomography (CT) scan revealed early ischemic changes in the right middle cerebral artery (MCA) territory. The CT angiography done showed evidence of dissection of the supraclinoid segment of the right internal carotid artery with reduced flow distally into the MCA, which was confirmed by a conventional angiogram. In view of the intracranial carotid dissection, the patient was not treated with intravenous tissue plasminogen activator. Magnetic resonance imaging (MRI) of the brain done on the next day revealed evidence of acute ischemic lesions in the right MCA and anterior cerebral artery territory on diffusion-weighted imaging (DWI), with normal brainstem. [Figure 1] A repeat MRI performed 13 days after ictus showed hyperintense signal on DWI in the right cerebral peduncle which was hypointense on apparent diffusion coefficient (ADC) map suggestive of Wallerian-like degeneration. [Figure 2] The signal changes were less conspicuous on T2-weighted images. She had antigravity strength in the left leg but remained weak in her left arm at one month.

The patient is a previously healthy 19-month-old child who became symptomatic in October 1998 with right hand weakness and cessation of new words with progression of right sided weakness and decreased sensation over the next month. The computed tomography (CT) and magnetic resonance imaging (MRI) scans demonstrated a large, deep, left frontal periventricular enhancing mass with several cystic areas. A left frontoparietal craniotomy was performed and the tumour was grossly resected. The pathological diagnosis was AT/RT. Grossly, the tumour was composed of firm, pink-tan hemorrhagic tissue. Sections showed a densely cellular, infiltrating neoplasm with areas of necrosis (some calcified), fascicular and focal sheets of collagen, and a variable, often prominent reticulin network. There was no endothelial proliferation. Light microscopy with hematoxylin and eosin stain (Figure 1) revealed a varied tumour appearance predominantly composed of larger tumour cells, with randomly dispersed nests of small undifferentiated cells close to the interface of tumour and normal brain tissue. The larger cells had several growth patterns: some were loosely arranged bi- or multi-polar cells forming cords and acinar structures against a faintly basophilic mucinous background, some were elongated cells arranged in coarse follicles or other compact bundles, while others were arranged in sheets or nests with prominent, sometimes glassy eosinophilic and cytoplasmic inclusions and eccentric nuclei (rhabdoid cells). Larger cells had nuclei with vesicular chromatin and prominent nucleoli, and smaller cells had hyperchromatic nuclei. Mitoses were focally numerous with some atypical in form, and cytoplasmic glycogen was inconspicuous. Immunohistochemical studies revealed widespread staining for epithelial membrane antigen (EMA), vimentin (Figure 2), glial fibrillary acid protein (GFAP), groups of cells with membranous patterns of staining for CD99, regional staining for neuron-specific enolase (NSE), scattered staining for transthyretin, and rare staining for actin, cytokeratin, and synaptophysin. The tumour was positive for chromosome 22 monosomy. Electron microscopy showed polygonal cells arranged in ill-defined acini that formed inconspicuous, sometimes entwined short microvillus processes. Variable numbers of intermediate filaments were identified and some cells showed a rudimentary basal lamina. Desmosomes were not seen, and there was no evidence of neural differentiation.

Uremia is a syndrome of clinical and metabolic abnormalities, which develops in parallel with the deterioration of renal function. Uremic encephalopathy is one of many manifestations of acute or chronic renal failure. It is usually applied to patients with cortical involvement, such as confusion, seizure, tremor, myoclonus, or asterixis. Some cases of acute extrapyramidal movement disorders associated with bilateral basal ganglia lesions, especially parkinsonism have been reported in uremic patients. Here, we report a diabetic uremic patient who developed acute chorea associated with bilateral basal ganglia lesions.

Pineal gland tumors in adults account for about 0.4 to 1 % of all intracranial tumors. A wide variety of tumors can occur in the pineal gland. The most common are the pineal parenchymal tumors (pineocytomas, pineoblastomas, and pineal parenchymal tumors of intermediate differentiation), germ cell tumors, and glial tumors. Uncommonly in the pineal gland one may encounter a metastatic tumor, a meningioma or a melanoma.

We here report a case of primary pineal gland melanoma with prolonged survival of 56 weeks after radiotherapy alone. To our knowledge, this is the first reported case of prolonged survival after radiotherapy alone, without surgical intervention or chemotherapy. Contrary to previous reports, our case demonstrates that a pineal melanoma with leptomeningeal dissemination can still yield a better survival with radiation treatment only.

Jaw claudication (JC) results from ischemia of the masticatory muscles, typically caused by temporal arteritis and other arteriopathies affecting the external carotid artery (ECA).

We documented a case of JC resulting from cardioembolic occlusion of the ECA and searched both English and French literature on the Medline database (1966-October 2006) to identify previous reports. We combined the keywords “jaw claudication” with either “cardiogenic embolism”, “cardiac embolism”, “cardioembolism”, “etiology”, “cause”, or “carotid occlusion”.