Frontoethmoidal encephalomeningocele is a herniation of brain and meninges through a congenital bone defect in the skull at the junction of the frontal and ethmoidal bones. From 1992 to 1996, 120 cases of frontoethmoidal encephalomeningocele were seen in our institutes, and the morphology of the skull defects was studied. The patients underwent thorough physical examinations and radiographic investigations including spiral three-dimensional computed tomography scan. Together with intraoperative findings, we found more types of the defects than previously reported. Our findings were categorized into the following types: type I, a single external opening between frontal, nasal, ethmoidal, and orbital bones; type IA, opening is limited between two bones of the area; type IB, opening is extended transversely or cephalad to involve adjacent structures; type II, multiple external openings in the region; type IIA, all of the openings are limited types; type IIB, one or more of the openings is/are extended type(s) that involve adjacent structures. There are 14 subtypes in these two types: 3 in type IA, 6 in type IB, 3 in type IIA, and 2 in type IIB. This classification is helpful in understanding the herniation pathway and in keeping informative records.

The aim of the study was to assess the relationship between the rate of clinical tumour growth and various histological features, including Ki67 labelling index, in skull base chordoma. Cases of skull base chordoma from 19 patients (six female, 13 male; age range 8-63 years) were reviewed and the diagnosis confirmed based on histological and immunohistochemical features. In each biopsy cellularity, pleomorphism, mitotic activity, apoptotic bodies, necrosis and inflammatory cell infiltrate were graded and Ki67 labelling index (LI) calculated as a measure of proliferation. Tumour doubling time was assessed by quantitative analysis of tumour volumes in post-operative magnetic resonance images and correlated with age, sex, histological parameters and Ki67 LI. It was shown that increasing patient age, the presence of mitotic figures or a Ki67 LI in excess of 6% were associated with faster growing tumours.

Three patients are reported on who presented with communicating hydrocephalus due to presumed tuberculous meningitis. Subsequent clinical deterioration despite antituberculous chemotherapy prompted reassessment with FDG-PET scanning and meningeal biopsy in one case and repeat CSF cytology with special staining in the second. The third patient died and postmortem confirmed a diagnosis of primary diVuse leptomeningeal gliomatosis. In the first two patients, MRI of the entire neuraxis showed no evidence of a primary intraparenchymal tumour. These cases emphasise the need for repeated reassessment in patients with culture negative lymphocytic meningitis. In addition, this is the first report of FDG-PET scanning in leptomeningeal gliomatosis. (J Neurol Neurosurg Psychiatry 2001;70:120-122) Keywords: leptomeningeal; gliomatosis; tuberculous meningitisThe presenting features of tuberculous meningitis (TBM) consist of subacute headache, drowsiness, confusion, and meningism. Cerebrospinal fluid examination typically shows a raised protein concentration, a depressed glucose concentration, and a pleocytosis, initially polymorphs then lymphocytes. Failure to respond to treatment should prompt a search for fungal infections or malignancy.Primary diVuse leptomeningeal gliomatosis (PDLG) is a rare condition whereby a glioma arises from heterotopic cell nests in the leptomeninges and produces a clinical picture similar to chronic infectious meningitis. This disease should not be confused with the much more often occurring secondary meningeal gliomatosis, due to primary CNS tumours, particularly medulloblastoma and glioblastoma, spreading along CSF pathways.Cases of PDLG are usually only diagnosed at postmortem when a full microscopic examination of the CNS can be carried out to exclude a small primary tumour. We describe three cases of primary diVuse leptomeningeal gliomatosis, presenting as TBM, two of which were diagnosed in life and the third at postmortem. Case 1A 34 year old Greek woman was referred for further investigation of possible TBM, not responding to therapy. She presented with a progressive 2 month history of headaches, diplopia, and unsteadiness, rendering her bedbound. Neurological examination disclosed bilateral papilloedema, sixth nerve palsies, and neck stiVness. She was afebrile. Brain CT showed communicating hydrocephalus. Examination of CSF disclosed a raised opening pressure of 70 cm CSF, a lymphocyte pleocytosis (17/mm 3 ), an increased CSF protein concentration (0.69 g/dl), and a low CSF/ plasma glucose ratio (20%). A Mantoux test and seven CSF examinations including microscopy, culture, and PCR analysis were negative for mycobacteria. Cytology for malignant cells was also consistently negative. She was started on quadruple antituberculous therapy and dexamathasone. One month later, she went blind despite insertion of a ventriculoperitoneal shunt. Soon after, she became febrile with swinging temperatures of up to 38°C and developed increasing weakness of her legs due to a steroid myopathy. T...