Angiocentric glioma transformed into anaplastic ependymoma: Review of the evidence for malignant potential.

Angiocentric glioma (AG) is a low grade glioma, that was first described in 2002. Since this description, 83 patients with AG have been described, including ours. AG typically presents in childhood with medically refractory seizures that are cured with gross surgical resection. Whilst the natural history is that of a benign tumour, there have been reports of recurrence, transformation, and malignant features that suggest that AG is potentially malignant. We add to the literature a case of a 16-year-old girl who presented in May 2011 with a 3-month history of complex partial seizures, with MRI showing a T2-weighted hyperintense lesion in the left insula and inferior frontal lobe. This was confirmed on biopsy as AG and was followed with surveillance imaging. In April 2012, she presented with disease progression and underwent a left temporal lobectomy, with histology showing both AG and grade II astrocytoma. Adjuvant radiotherapy of 50 Gray in 28 fractions was administered. A small area of contrast enhancement appeared in the left parietal lobe in December 2012, which progressed over subsequent months. In June 2013, she underwent a near total excision, with histology showing anaplastic ependymoma. She received six cycles of adjuvant temozolamide. Despite this, the tumour continued to progress, with her seizure control deteriorating, and the development of a right hemiparesis. The patient died in January 2014, aged 19years.

Supratentorial tanycytic ependymoma.

Tanycytic ependymoma is a rare fibrillary variant of ependymoma with a predilection for the spinal cord. We present an unusual supratentorial subcortical tanycytic ependymoma in a 17-year old male presenting with seizures. Only two other cases of subcortical tanycytic ependymoma have been reported.

Expression of the low-affinity neurotrophin receptor, p75(NTR), is upregulated by oligodendroglial progenitors adjacent to the subventricular zone in response to demyelination.

Precursor cells have the capacity to repopulate the demyelinated brain, but the molecular mechanisms that facilitate their recruitment are largely unknown. The low-affinity neurotrophin receptor, p75(NTR), may be one of these regulators; however, its expression profile by oligodendroglia within the multiple sclerosis (MS) brain remains uncertain. We therefore assessed the expression profile of this receptor within 8 MS and 4 control brains. We found no evidence of expression of p75(NTR) by mature oligodendrocytes. Instead, we demonstrated the presence of p75(NTR) on a subgroup of NG2-positive oligodendroglial progenitors in a periventricular plaque in one MS sample. Notably, p75(NTR)-expressing cells were also detected within the subventricular zone (SVZ) of this brain, adjacent to the periventricular plaque. In animals with experimental demyelination we observed similar patterns of p75(NTR) expression, initially confined to precursor cells within the SVZ, followed at later stages in the disease course by its expression amongst a subset of oligodendroglial progenitors within the corpus callosum. These data suggest that a population of precursor cells within the SVZ can be induced to express p75(NTR) and to subsequently assume an oligodendroglial progenitor phenotype in response to demyelination in the adjacent white matter.

Coexistence of aneurysmal subarachnoid haemorrhage and pituitary apoplexy: Case report and review of the literature.

A case of aneurysmal subarachnoid haemorrhage with associated haemorrhagic infarction of a growth hormone secreting pituitary macroadenoma is presented. The subarachnoid haemorrhage was not identifiable on CT, but was apparent on MRI. Angiography revealed a 7mm right posterior communicating aneurysm, a 3mm left A1 segment anterior cerebral aneurysm, and vasospasm. Surgery was performed through a right pterional/subfrontal approach, clipping both aneurysms and debulking the tumour. The left A1 aneurysm was the site of subarachnoid haemorrhage. There was evidence of haemorrhagic infarction of the pituitary tumour. Although rupture of an aneurysm into a pituitary tumour has been previously reported, this is the first case reported of aneurysmal subarachnoid haemorrhage with coexisting pituitary apoplexy where the aneurysm had not bled directly into the pituitary tumour. The literature regarding the association between pituitary tumours and aneurysm is reviewed.