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We retrospectively analysed the incidence, clinical presentation, endocrinological and radiological findings, medical and surgical management of pituitary apoplexy in our department (single-centre study), having a large experience in pituitary surgery. Among 1540 pituitary lesions, 24 patients presented with pituitary apoplexy. Their charts were retrospectively reviewed. The symptoms included headache (92%), nausea and vomiting (54%), visual deficit (50%), oculomotor paresis (54%) and/or an altered mental state (42%). Skull X-rays ( n = 14) demonstrated an enlarged sella turcica in all cases; CT-scan and/or MRI always revealed a sellar and suprasellar expanding lesion. Panhypopituitarism was present on admission in 70% of the patients. Urgent therapeutic management included high-dose cortisone treatment in all but one patients and CSF drainage in three. Three patients were treated conservatively. Nine patients were operated on rapidly, within hours or a few days because of severe visual deficit and/or altered level of consciousness. Nineteen patients were operated by the trans-sphenoidal approach; one of them required a second operation by craniotomy. There were two deaths related to the illness and one to an ill-defined reason at 4 months. Among the other patients 95% made a good recovery. All but two patients required a substitutive treatment with adrenal (83%), thyroid (68%), gonadal (42%) and/or growth (16%) hormones. The preoperative visual deficits recovered in all but one patients (92%) whereas the oculomotor pareses improved in all but two patients (85%). In conclusion, pituitary tumour apoplexy is a rare event, complicating in our series 1.6% of 1540 pituitary adenomas. Even in severe cases, complete recovery is possible if the diagnosis is rapidly obtained and adequate management is initiated in time. Surgical results after trans-sphenoidal approach are in the majority of cases very satisfactory.

This study evaluates the usefulness of PET for the preoperative evaluation of brain gliomas and methods of quantification of PET results. Fifty-four patients with brain gliomas were studied by PET with 18F-fluorodeoxyglucose (FDG) (n = 45) and/or 11C-methionine (MET) (n = 41) before any treatment. Results of visual analysis, calculation of glucose consumption and five tumor-to-normal brain ratios for both tracers were correlated with two histologic grading systems and with follow-up. Visual analysis (for FDG) and tumor-to-mean cortical uptake (T/MCU) ratio proved to be the best tools for the evaluation of PET results. Methionine was proven to be better than FDG at delineating low-grade gliomas. Tumor-to-mean cortical uptake ratios for FDG and MET were clearly correlated (r = 0.78), leading to the equation T/MCU(FDG) = 0.4 x T/MCU(MET). We showed a good correlation between FDG PET and histologic grading. MET uptake could not differentiate between low-grade and anaplastic astrocytomas but was significantly increased in glioblastomas. Low-grade oligodendrogliomas exhibited high uptake of FDG and MET, probably depending more on oligodendroglial cellular differentiation than on proliferative potential. Uptake was decreased in anaplastic oligodendrogliomas, probably due to dedifferentiation. Care must be taken with peculiar histologic subgroups, i.e., juvenile pilocytic astrocytomas and oligodendrogliomas, because of a discrepancy between high PET metabolism and low proliferative potential (good prognosis). Both tracers proved useful for the prediction of survival prognosis. Methionine proved slightly superior to FDG for predicting the histologic grade and prognosis of gliomas, despite the impossibility of differentiation between Grades II and III astrocytomas with MET. This superiority of MET could be explained by patient sampling (low number of Grade III gliomas submitted to examination with both tracers). The combination of both tracers improved the overall results compared to each tracer alone. Both tracers are useful for the prediction of the histologic grade and prognosis. The apparent superiority of MET over FDG could be due to the small number of Grade III gliomas studied with both tracers.

Abstract OBJECTIVE To evaluate the clinical, endocrinological, and radiological presentation of nine cases of surgically verified intrasellar arachnoid cysts and to discuss the physiopathological mechanisms of formation of these cysts. METHODS Among 1540 patients presenting with pituitary lesions, nine presented with an intrasellar arachnoid cyst. Their charts were retrospectively reviewed. RESULTS Presenting symptoms included headache (n = 2), visual symptoms (n = 3), menstrual irregularities (n = 2), rapid weight gain (n = 1), vertigo (n = 1), and/or confusion (n = 1). Two cysts were discovered incidentally. T1-weighted magnetic resonance imaging scans showed an intrasellar cystic lesion in all cases, with a huge suprasellar extension in six cases. The cyst was of the same intensity as the cerebrospinal fluid (CSF) in only two patients. A transsphenoidal approach allowed the transdural aspiration of fluid and injection of a water-soluble contrast agent under mild pressure. In three patients, the contrast infiltrated along the pituitary stalk toward the subarachnoid spaces; in the other patients, it remained in the intrasellar compartment. Cyst membranes were removed as completely as possible with fenestration toward the subarachnoid spaces in communicating cysts. In spite of tight packing of the sella and sphenoid sinus, CSF fistulae requiring reoperation developed in two patients. CONCLUSION The clinical picture of an intrasellar arachnoid cyst resembles that of a nonfunctional pituitary adenoma. Magnetic resonance imaging scans typically show a cystic intrasellar lesion with suprasellar extension, containing isointense or, more often, hyperintense fluid on T1-weighted sequences. In spite of the risk of CSF fistulae, the preferred surgical approach is transsphenoidal. A physiopathological mechanism is proposed according to anatomic variations of the sellar diaphragma allowing penetration of subarachnoid spaces into the sellar compartment and their enlargement by a ball-valve mechanism.

A consecutive series of 28 \"operated\" juxtafacet cysts is reported. We emphasize the clinical and radiological aspects leading to diagnosis. We also discuss the results of the surgical treatment. Medical information and radiological studies involving 28 patients were analyzed. Each patient has been operated on by decompressive laminectomy and resection of the cyst. The diagnosis was always confirmed by a pathological examination. The cyst most frequently occurred at the L4-L5 level (n = 18), and seldom at the L5-S1 (n - 6) or L3-L4 (n - 4) levels. The differential diagnosis from other pathological causes responsible for a radicular compression could not be done by physical examination. Spine X-rays or myelogram were nonspecific. Computed Tomography or CT-myelography could help in the diagnosis but MR imaging was the most sensitive. In our series, the respective sensitivities of these techniques are 56, 42 and 77%. The preoperative diagnosis was correct in 18 patients (64%). The cyst was sometimes adherent to the underlying dura, then significantly increasing the risk of dural tear and spinal fluid leak, especially when located at L3-L4 level. Surgical ablation lead to a complete recovery or an important improvement in 26 patients. The diagnosis of the juxtafacet cyst of the lumbar spine is better achieved by MRI. Surgery is the gold standard treatment, safe and long-term effective. When a total cyst removal with an internal facetectomy are performed, recurrence is exceptional.

We retrospectively analyzed 32 cases of primary central nervous system lymphoma (PCNSL). Five cases were diagnosed in the period 1987–1994, for 27 cases in the period 1995–2002. There were 17 men and 15 women whose median age was 69 years. Three patients were immunodeficient. The commonest symptoms were focal deficit (16 patients) and cognitive/behaviour disturbances (14 patients). Radiologically, a total of 47 contrast-enhancing lesions were observed in 32 patients; 18 patients had deep-seated lesions. All but two patients underwent histological diagnosis following craniotomy (11 patients) and/or stereotaxic biopsy (22 patients); diagnosis was obtained on CSF cytology in one patient with a third ventricle tumour. In the last patient, the diagnosis was based on the finding of marked tumour shrinkage under corticotherapy, despite two negative histological examinations. Treatment included surgical resection (10 patients), chemotherapy (25 patients) and/or radiotherapy (12 patients). According to the therapeutic recommendations of the GELA (Groupe d’Etude des Lymphomes de l’Adulte), 19 patients received at least two courses of high-dose methotrexate; intrathecal chemotherapy was used in 20 patients with methotrexate and/or cytosine arabinoside. Radiation therapy consisted of whole brain irradiation followed by a boost on tumour site. Nine patients received a combined treatment of chemotherapy and radiotherapy. Twelve patients showed rapid progression to death. At the time of last contact, 28/32 patients (88%) had died, all from PCNSL disease or from complications due to its treatment. The median survival time was 13.9 months. We conclude that PCNSL is an increasingly frequent tumour. The diagnosis is obtained by stereotactic biopsy in the majority of cases. The prognosis appears dismal despite an intensive multidisciplinary therapeutic approach.