Outcomes of tumour related epilepsy in a specialised epilepsy surgery unit.

INTRODUCTION: Seizures are an important cause of morbidity in patients with low grade gliomas with approximately 40% of cases drug resistant. The pathogenesis is quite complex and poorly understood. The treatment aims vary between almost purely epilepsy considerations and those that are primarily oncologic. AIM: To determine whether patients who present with seizures and are found to have a low grade glioma have better outcomes when managed through a specialized epilepsy unit compared to the general neurosurgical service. METHODS: A review of the prospectively collected database was performed over a 10 year period to identify 48 adult patients who present with a seizure and were subsequently found to have a low grade glioma. These patients were analysed with respect to management through the specialized epilepsy service or the general neurosurgical service. The primary outcome was Engel classification between the two groups. Secondary outcomes included recurrence, postoperative deficits, delay to surgery, histology, grade and extent of resection. OUTCOMES: The patients managed through the epilepsy service had significantly higher rate of favourable Engel outcomes (I and II) compared to the general neurosurgery service (OR: 13.2, 95% CI: 1.239-140.679; P = 0.033). The epilepsy surgery group patients had a significantly higher delay to surgery (P < 0.001). The patients in the epilepsy service had a significantly higher resection ratio compared to the general neurosurgery service (73% vs 127%, P = 0.014). Rates of recurrence were not different between the two groups. CONCLUSION: Patients with tumour related epilepsy who undergo an intensive presurgical evaluation may obtain better seizure related outcomes.

MR and positron emission tomography with fludeoxyglucose F 18 in gliomatosis cerebri.

A 16-year-old girl presented with a unilateral third nerve palsy and predominant gray matter involvement on MR and positron emission tomography with fludeoxyglucose F 18. These findings were manifestations of gliomatosis cerebri. The antemortem diagnosis was made by partial temporal lobectomy.

The surgical management of contralateral anterior circulation intracranial aneurysms.

This study reviews the surgical management of contralateral anterior circulation aneurysms in patients with bilateral intracranial aneurysms repaired following a unilateral craniotomy. Between 1993 and 1999, 27 patients had 88 intracranial aneurysms repaired. Eleven patients presented following subarachnoid haemorrhage. Excluding midline aneurysms, 31 anterior circulation aneurysms were contralateral to the craniotomy and all were repaired at the same time that ipsilateral or midline aneurysms were repaired. Morbidity included one death and one case of loss of unilateral vision directly attributable to surgery and two cases of cerebral infarction due to vasospasm. No new neurological deficit or mortality could be directly attributed to the repair of a contralateral aneurysm. The repair of all accessible aneurysms, including those contralateral to the craniotomy, during one session avoids the risk of haemorrhage from incidental or unrecognised ruptured aneurysms (particularly during the aggressive treatment of vasospasm), avoids a second craniotomy, decreases overall hospitalisation and can improve visualisation of carotid-ophthalmic aneurysms.

Injury patterns in patients who "talk and die".

Despite advances in the quality of and access to cerebral imaging, patients with mild head injuries still deteriorate and die in neurotrauma units. The term "talk and die" was first used by Reilly et al. to describe a subset of patients with head injuries who died following what was initially thought to be only a mild traumatic brain injury. A retrospective review of a database from a major Australian trauma center was performed to identify 25 patients who met the "talk and die" criteria between January 2000 and December 2009. The medical records of these patients and their imaging studies were analyzed to identify potentially preventable factors and injury patterns in this group of patients. The factors analyzed included age, modality of injury, therapeutic narcotic usage, seizures, and hyponatremia. Two groups of patients are described herein based on intracranial pathology, with statistically significant differences in age, mechanism, and coagulopathy identified.

Rosette-forming glioneuronal tumour of the lateral ventricle in a patient with neurofibromatosis 1.

We report a 33-year-old man with neurofibromatosis type 1 (NF-1) with a rosette-forming glioneuronal tumour (RGNT) in the lateral ventricle. The patient had been treated with radiotherapy and chemotherapy for a typical juvenile pilocytic astrocytoma of the hypothalamus seven years prior. MRI revealed a contrast-enhancing mass in the anterior horn of the left lateral ventricle. Histological examination demonstrated two distinct regions characterised by a rosette-forming neurocytic component and an astrocytic predominant component. Immunohistochemical studies showed glial fibrillary acidic protein and S-100 positivity in the astrocytic component and neuron-specific enolase was positive in the neurocytic cells. Although RGNT has been reported at other sites within the central nervous system, this report documents a previously undescribed lateral ventricular location of a rare RGNT in an asymptomatic patient with NF-1.

Late onset Rasmussen's encephalitis with triple pathology.

Rasmussen's encephalitis is a devastating illness characterized by intractable focal seizures due to chronic localised encephalitis. We report on a rare variant of delayed onset Rasmussen's encephalitis with triple pathology. A 27-year-old male, who was initially diagnosed with seizures when he was 16 years old, presented with focal seizures that became refractory to multiple anticonvulsants. Multiple investigations, including subdural electrode monitoring, revealed foci of onset in the right frontotemporal region. The patient underwent right front-temporal lobectomy. Post-operatively, the seizures became more severe and he developed new epilepsia partialis continua. Treatment with intravenous immunoglobulin was unsuccessful. He subsequently underwent a right hemispherectomy that rendered him seizure free. The three pathologies identified were old ischemic changes, type II cortical dysplasia and stage II Rasmussen's encephalitis.