Hyperaemia in rat neocortex produced by acute exposure to methylenedioxymethamphetamine

Cerebral blood flow and glucose utilization were measured in rat neocortex, hippocampus and striatum following methylenedioxymethamphetamine injection (5 mg/kg, i.v.), using the tracers [¹⁴C]iodoantipyrine and [¹⁴C]2-deoxyglucose, respectively. In control rats, blood flow was coupled to glucose metabolism, but in methylenedioxymethamphetamine-treated rats, marked hyperperfusion was measured in frontal and parietal cortex with no change in glucose use. This suggests that methylenedioxymethamphetamine has the potential to disrupt cerebrovascular control.     

Jugular foramen schwannoma in a child treated with complete surgical excision

INTRODUCTION: A rare case of a large jugular foramen tumour presenting as a posterior fossa mass is described. MATERIALS AND METHODS: The patient, a 13-year-old boy presented with symptoms of raised intracranial pressure and on MRI imaging demonstrated the tumour origin within the jugular foramen, with appearances suggestive of schwannoma. He underwent a complete excision as a single-stage procedure thorough a lateral suboccipital craniotomy with minimal morbidity. Histology confirmed the diagnosis of schwannoma (WHO I). Jugular foramen schwannoma is virtually unheard of in the paediatric population. CONCLUSION: The differential diagnosis of a jugular foramen tumour includes tumours of the glomus jugulare, meningiomas, schwannomas, myxomas and chondrosarcomas. The imaging characteristics are important when considering this differential diagnosis.     

Management strategies for recurrent ependymoma in the paediatric population

Introduction  

The management of recurrent ependymoma within the paediatric population remains a therapeutic challenge. The options available are varied and patients may have already received prior radio- or chemotherapy. As yet, no consensus exists regarding their optimal treatment. We review the literature and present our contemporary management strategies for this interesting group of patients.     

Melorheostosis causing lumbar radiculopathy: a case report and a review of the literature

Background contextMelorheostosis is a rare sclerosing bone disorder with a predilection for the appendicular skeleton. Involvement of the spine is infrequent and largely asymptomatic. Surgical treatment for spinal involvement is therefore uncommon with only one reported case of lumbar fusion for painful lumbosacral melorheostosis.PurposeWe report a case of lumbar melorheostosis causing disabling radiculopathy treated with nerve root decompression.ConclusionsMelorheostosis of the lumbar spine causing radicular symptoms has not been reported before. Our message from the management of this particular patient is to consider surgical option in symptomatic individuals.     

11beta-Hydroxysteroid dehydrogenase type 2 protects the neonatal cerebellum from deleterious effects of glucocorticoids

11beta-Hydroxysteroid dehydrogenase type 2 is a glucocorticoid metabolizing enzyme that catalyzes rapid inactivation of corticosterone and cortisol to inert 11-keto derivatives. As 11beta-hydroxysteroid dehydrogenase type 2 is highly expressed in the developing brain, but not in the adult CNS, we hypothesized that it may represent a protective barrier to the deleterious actions of corticosteroids on proliferating cells. To test this hypothesis we have investigated the development and growth of the cerebellum in neonatal C57BL/6 mice and mice lacking 11beta-hydroxysteroid dehydrogenase type 2 (-/-). 11beta-Hydroxysteroid dehydrogenase type 2-/- mice had consistently lower body weight throughout the neonatal period, coupled with a smaller brain size although this was normalized when corrected for body weight. The cerebellar size was smaller in 11beta-hydroxysteroid dehydrogenase type 2-/- mice, due to decreases in size of both the molecular and internal granule layers. When exogenous corticosterone was administered to the pups between postnatal days 4 and 13, 11beta-hydroxysteroid dehydrogenase type 2(-/-) mice were more sensitive, showing further inhibition of cerebellar growth while the wildtype mice were not affected. Upon withdrawal of exogenous steroid, there was a rebound growth spurt so that at day 21 postnatally, the cerebellar size in 11beta-hydroxysteroid dehydrogenase type 2-/- mice was similar to untreated mice of the same genotype. Furthermore, 11beta-hydroxysteroid dehydrogenase type 2-/- mice had a delay in the attainment of neurodevelopmental landmarks such as negative geotaxis and eye opening. We therefore suggest that 11beta-hydroxysteroid dehydrogenase type 2 acts as to protect the developing nervous system from the deleterious consequences of glucocorticoid overexposure.