The aim of this study was to evaluate the results of conservative and surgical management options for traumatic cerebrospinal fluid (CSF) leakage complicating skull base fractures. The subjects were 81 patients who were treated between 1996 and 2003 for CSF leaks that had persisted for 24 h or longer after head injury. For each case the medical records were reviewed, and the data collected were as follows: demographic features, clinical and radiological findings, management options, complications and outcome scores. Analysis was done with patients grouped according to Glasgow coma scale (GCS) score at admission (8), and findings for three treatment methods (conservative, CSF drainage, surgery) were evaluated. In 32 cases (39.5%), the CSF leakage resolved spontaneously, and the mean hospital stay for these patients was 14+/-11 days. Twenty-four patients (29.6%) were treated by CSF drainage, and seven of these individuals ultimately required surgery to close the leak. Hospital stay was 17+/-7 days. Twenty-five patients (30.9%) underwent surgery as the initial treatment step, and the mean hospital stay for these individuals was 15+/-9 days. The large majority (74.2%) of patients with admission GCS scores 8 resolved spontaneously. The factors that had a critical influence on outcome in this series were level of consciousness on admission and presence of additional intracranial pathology associated with CSF leakage within cases of traumatic CSF fistulae due to skull base fractures. Treatment decisions should be dictated by the severity of neurological decline during the emergency period and the presence/absence of associated intracranial lesions. The timing for surgery and CSF drainage procedures must be decided with great care and with a clear strategy. The authors offer a treatment algorithm.

Study design: Case report. Objective: To report an unusual case of paraplegia. Setting: University Hospital Bursa, Turkey. Case report: A 22-year-old woman presented with paraplegia following a left-sided thoracotomy. Magnetic resonance imaging showed a dorsal epidural mass at the level of T6. The patient underwent an emergency T6/7 laminectomy and removal of a tuft of oxidised regenerated cellulose, which had migrated through the intervertebral foramen causing spinal cord compression. Conclusion: In cases of neurological deficits after surgery at the posterolateral edge of a thoracotomy, the clinician should be aware of the above possibility. Urgent radiological diagnosis and decompressive laminectomy is the treatment of choice.Spinal Cord (2005) 43, 445-447.

Cases of epidural haematoma of nonarterial origin differ from the more common arterial-origin epidural haematomas with respect to lesion location, surgical planning, postoperative complications, and outcome. Epidural haematoma of nonarterial origin should be suspected if preoperative CT shows a haematoma overlying a dural venous sinus or in the posterior fossa and convexity. The sinus-origin group had a high frequency of fractures which crossed the sinuses, and this might be diagnostically and surgically useful in such cases.

The histological subclassification of gliomas is increasingly assisted by the underlying molecular genetics which has major importance in guiding clinical management of the disease. However, the assessment of several molecular events for improving clinical care remains a challenge. Herein, we report on comparative genomic hybridization (CGH) and immunohistochemical (IHC) assessment of EGFR, PTEN, p53, and MIB-1 expression in 13 oligodendrogliomas (10 WHO grade II, 3 WHO grade III), one oligoastrocytoma (WHO grade III) and 23 high-grade astrocytomas (3 WHO grade III, 20 glioblastoma multiforme). The most frequent imbalances in oligodendroglial tumors including the oligoastrocytic case were, in decreasing order of frequency, +7q,-1p, and-4q and in astrocytomas +7q,-10q, +7p,-9p,-10p, +20q, and +20p. Some individual imbalances were associated with increasing numbers of chromosomal changes, that were +7q in both oligodendrogliomas and astrocytomas, and-9p,-10q, +20p, and +20q in astrocytomas. The markers p53 and MIB-1 were significantly higher expressed in astrocytomas than in oligodendrogliomas and expression levels of p53 and EGFR were inversely associated within the astrocytic group. In addition, p53 overexpression correlated positively with +7q and negatively with-1p in the oligodendroglial group whereas EGFR overexpression correlated positively with-1p in the oligodendroglial and positively with +7p and-10p in the astrocytic group. Short overall survival was significantly associated with +7p and-10q in astrocytomas. Collectively, these results contribute to the increasing clinical relevance of assessing tumor biological markers in gliomas.

In this study, we investigated the relationship between genetic alterations such as chromosome 22 aneuploidy and p53 gene deletion, and the pathological types of meningioma of typical and aggressive forms. Thirty-four meningiomas (23 typical and 11 aggressive) were examined by application of fluorescence in situ hybridization (FISH) with chromosome 22 specific alpha satellite probe and a combination of p53 locus specific and chromosome 17 centromere specific alpha satellite probes, to evaluate the chromosome 22 aneuploidy and gain or loss of p53 gene along with chromosome 17. The results showed that, although chromosome 22 aneuploidy was seen in 7 out of 23 typical (30.4%) and 4 out of 11 aggressive meningiomas (36.3%), no p53 deletion was detected in typical meningiomas, and p53 deletion was detected in 3 out of 11 aggressive meningiomas (1 atypical and 2 malignant), which had recurrence. There were no simultaneous occurrences of p53 gene deletions between typical and aggressive meningiomas. The present findings indicate that the loss of chromosome 22 may be involved with tumorogenesis of typical and aggressive meningiomas, while p53 gene deletions may be involved with malignant progression and recurrence in the aggressive meningiomas.