A previously undescribed variant of the confluence of sinuses.

An 8-year-old female with a history of chronic headaches and uncertain papilloedema was found to have a variant of the posterior intracranial dural venous sinuses on magnetic resonance imaging assessment of the brain. Magnetic resonance venography included in the imaging revealed a circular formation of the confluence of sinuses and absent right-sided transverse sinus. The confluence of sinuses is a highly variable structure; however, to the authors' knowledge, a circular confluence of sinuses variant has not been reported in the literature.

Ectopic arachnoid granulation involving a rare intracranial venous sinus variant.

Arachnoid granulations are hypertrophied arachnoid villi, which extend from the subarachnoid space into the venous system and aid in the passive filtration and reabsorption of cerebrospinal fluid. These macroscopic structures have been described in various locations, with the transverse and sigmoid sinuses seen as normal variants on imaging. Here we present the occurrence of an enlarged arachnoid granulation at the foramen rotundum where a variant intracranial venous sinus was identified during routine dissection. Variations, such as the one described herein, should be recognised by those who operate or interpret images of the skull base.

Cell cycle times of short-term cultures of brain cancers as predictors of survival.

Tumour cytokinetics estimated in vivo as potential doubling times (T(pot) values) have been found to range in a variety of human cancers from 2 days to several weeks and are often related to clinical outcome. We have previously developed a method to estimate culture cycle times of short-term cultures of surgical material for several tumour types and found, surprisingly, that their range was similar to that reported for T(pot) values. As T(pot) is recognised as important prognostic variable in cancer, we wished to determine whether culture cycle times had clinical significance. Brain tumour material obtained at surgery from 70 patients with glioblastoma, medulloblastoma, astrocytoma, oligodendroglioma and metastatic melanoma was cultured for 7 days on 96-well plates, coated with agarose to prevent proliferation of fibroblasts. Culture cycle times were estimated from relative (3)H-thymidine incorporation in the presence and absence of cell division. Patients were divided into two groups on the basis of culture cycle times of < or =10 days and >10 days and patient survival was compared. For patients with brain cancers of all types, median survival for the < or =10-day and >10-day groups were 5.1 and 12.5 months, respectively (P=0.0009). For 42 patients with glioblastoma, the corresponding values were 6.5 and 9.0 months, respectively (P=0.03). Lower grade gliomas had longer median culture cycle times (16 days) than those of medulloblastomas (9.9 days), glioblastomas (9.8 days) or melanomas (6.7 days). We conclude that culture cycle times determined using short-term cultures of surgical material from brain tumours correlate with patient survival. Tumour cells thus appear to preserve important cytokinetic characteristics when transferred to culture.

Mouse spinal cord compression injury is reduced by either activation of the adenosine A2A receptor on bone marrow-derived cells or deletion of the A2A receptor on non-bone marrow-derived cells.

Activation of the adenosine A(2A) receptor (A(2A)R) at the time of reperfusion has been shown to reduce ischemia-reperfusion injury in peripheral tissues and spinal cord. In this study we show that treating mice with the A(2A)R agonist, 4-{3-[6-amino-9-(5-cyclopropylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-piperidine-1-carboxylic acid methyl ester for four days beginning before or just after the onset of reperfusion after compression-induced spinal cord injury rapidly (within 1 day) and persistently (>42 days) reduces locomotor dysfunction and spinal cord demyelination. Protection is abolished in knockout/wild type bone marrow chimera mice selectively lacking the A(2A)R only on bone marrow-derived cells but retaining receptors on other tissues including blood vessels. Paradoxically, reduced spinal cord injury is also noted in A(2A)R -/- mice, and in wild type/knockout bone marrow chimera mice selectively lacking the A(2A)R on non-bone marrow-derived cells, or in mice treated with the A(2A) antagonist, 4-(2-[7-amino-2-[2-furyl][1,2,4]triazolo[2,3-a][1,3,5]triazin-5-yl-amino]ethyl)phenol. The greatest protection is seen in knockout/wild type bone marrow chimera mice treated with 4-{3-[6-amino-9-(5-cyclopropylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-piperidine-1-carboxylic acid methyl ester, i.e. by activating the A(2A)R in mice expressing the receptor only in bone marrow-derived cells. The data suggest that inflammatory bone marrow-derived cells are the primary targets of A(2A) agonist-mediated protection. We conclude that A(2A) agonists or other interventions that inhibit inflammation during and after spinal cord ischemia may be effective in reducing spinal cord injury in patients, but excessive or prolonged stimulation of the A(2A)R may be counterproductive. It may be possible to devise strategies to produce optimal spinal cord protection by exploiting temporal differences in A(2A)R-mediated responses.

Endovascular management of unruptured intracranial aneurysms.

Endovascular coil embolisation is increasingly used to treat unruptured intracranial aneurysms (UIA). Endovascular coil embolisation of UIA is associated with a 5-10% risk of morbidity and nearly zero mortality from the procedure. Complete or near complete occlusion is usually achieved in >90% of cases, and endovascular therapy seems to reduce the risk of future rupture significantly. Specific selection criteria for endovascular embolisation and novel approaches to endovascular treatment of aneurysms are discussed. Endovascular therapy appears to be a safe and effective treatment for selected UIA. Treatment failure rates will probably decrease with greater experience and advances in techniques and devices. Further study with long term follow up, however, is still necessary to characterise the efficacy, durability, and cost efficiency of endovascular treatment of UIA.

Collagen sponge repair of small cerebrospinal fluid leaks obviates tissue grafts and cerebrospinal fluid diversion after pituitary surgery.

OBJECTIVE: Repair of a cerebrospinal fluid (CSF) leak created at the time of transsphenoidal surgery typically involves placement of a fat, fascial, or muscle graft and sellar floor reconstruction. In this report, a simplified repair for small, "weeping" CSF leaks using collagen sponge is described. METHODS: All patients underwent an endonasal transsphenoidal procedure using the operating microscope. At the completion of tumor removal, if a small CSF leak was noted but no obvious large arachnoidal defect was present, a piece of collagen sponge was fashioned to cover the exposed diaphragma sellae. Titanium mesh was then wedged into the intrasellar, extradural space and a larger piece of collagen was placed over the reconstructed sellar floor. Nasal packing was removed within 24 hours. RESULTS: During an 18-month period, 62 consecutive transsphenoidal procedures were performed for tumor removal. Of 20 patients with a small CSF leak (18 pituitary adenomas, 1 Rathke's cleft cyst, and 1 chordoma), all had successful repair with collagen sponge. At follow-up examinations at 1 to 18 months, no patient had required a lumbar drain or had developed meningitis. One other patient had a large intraoperative arachnoidal defect that was unsuccessfully repaired with the collagen sponge technique; in this patient, a second operation was required with a fat graft, sellar floor reconstruction, and lumbar drainage. CONCLUSION: A simplified repair of small CSF leaks after transsphenoidal surgery using a two-layered collagen sponge technique with sellar floor reinforcement is thought to be safe and effective and obviates the need for tissue grafts, fibrin glue, or lumbar drain placement.