ObjectiveThe technique of short segment pedicle screw fixation (SSPSF) has been widely used for stabilization in thoracolumbar burst fractures (TLBFs), but some studies reported high rate of kyphosis recurrence or hardware failure. This study was to evaluate the results of SSPSF including fractured level and to find the risk factors concerned with the kyphosis recurrence in TLBFs.MethodsThis study included 42 patients, including 25 males and 17 females, who underwent SSPSF for stabilization of TLBFs between January 2003 and December 2010. For radiologic assessments, Cobb angle (CA), vertebral wedge angle (VWA), vertebral body compression ratio (VBCR), and difference between VWA and Cobb angle (DbVC) were measured. The relationships between kyphosis recurrence and radiologic parameters or demographic features were investigated. Frankel classification and low back outcome score (LBOS) were used for assessment of clinical outcomes.ResultsThe mean follow-up period was 38.6 months. CA, VWA, and VBCR were improved after SSPSF, and these parameters were well maintained at the final follow-up with minimal degree of correction loss. Kyphosis recurrence showed a significant increase in patients with Denis burst type A, load-sharing classification (LSC) score >6 or DbVC >6 (p<0.05). There were no patients who worsened to clinical outcome, and there was no significant correlation between kyphosis recurrence and clinical outcome in this series.ConclusionSSPSF including the fractured vertebra is an effective surgical method for restoration and maintenance of vertebral column stability in TLBFs. However, kyphosis recurrence was significantly associated with Denis burst type A fracture, LSC score >6, or DbVC >6.
Stereotactic brain biopsy was used to establish diagnoses of conditions in patients with AIDS. Two hundred fifty stereotactic biopsies and one open resection were performed for 243 patients. Pathologically abnormal tissue was obtained in 246 (98%) of the procedures, and 16 patients (6%) had >1 diagnosis. Diagnoses included lymphoma in 82 (33%), progressive multifocal leukoencephalopathy in 73 (30%), and tumors not ordinarily associated with AIDS in 7 (3%). In one-third of the cases, the tissue diagnosis differed from the predicted diagnosis. Four of the first 32 patients (12%) developed intracranial bleeding hours after surgery, which was fatal in 3 (9%). Subsequently, all patients were treated with a coagulopathy protocol that included preoperative and postoperative administration of coagulation factors, and there were no further instances of delayed bleeding in the 218 subsequent patients. Among those later patients, there were 7 complications (3%), leading to 4 deaths (2%), a complication rate that compares favorably with that among patients without AIDS.
Recent molecular studies indicate two different genetic pathways leading to the development of glioblastoma; final progression of astrocytoma and de novo formation. To define the mutual relationships of cytogenetic changes in the pathogenesis of glioblastoma, molecular histopathologic alterations of p53 and epidermal growth factor receptor (EGFR) were evaluated by single stranded conformational polymorphion, reverse transcriptase-polymerase chain reaction and immunohistochemical stains in 15 primary and 21 secondary glioblastomas. Mutations in p53 gene and positive immunoreactivity to p53 protein (DO1) were more prevalent in secondary glioblastomas than in primary glioblastomas. A correlation between p53 mutations and p53 immunopositivities in glioblastomas was observed in 83.3% of the cases. All cases with positive p53 immunoreactivities showed p53 mutations; however, 13.9% of glioblastomas with p53 immuno-positivities lacked the relevant mutations. EGFR amplifications were detected in 73.3% of primary glioblastomas and 9.5% of secondary glioblastomas (p<0.001). The concurrence of p53 mutation and EGFR amplification was revealed in only 2 out of 15 primary glioblastomas and none among the secondary glioblastomas. Immunoreactivities for EGFR were noted in 66.7% of primary glioblastomas and in 9.5% of secondary glioblastomas (p<0.001). A correlation between EGFR amplification and EGFR immunopositivity in glioblastomas was observed in 91.7% of the cases. These data indicate that EGFR amplification and p53 mutations are two independent genetic events in the development of glioblastomas.
Amenorrhea is rarely presented as a manifestation of endocrinological disturbances in patients of chronic hydrocephalus. We describe two cases of secondary amenorrhea caused by hydrocephalus due to aqueductal stenosis. Two female patients of age 30 and 20 yr presented with amenorrhea and increasing headache. Magnetic resonance images revealed marked, noncommunicating hydrocephalus without any tumorous lesion. In one patient, emergent extraventricular drainage was necessary because of progressive neurological deterioration. Each patient underwent surgical intervention for the hydrocephalus-ventriculoperitoneal shunt and endoscopic third ventriculostomy. Both resumed normal menstruation continuing so far with further normal menstrual bleeding. These two cases and others reported in the literature indicated that the surgical intervention for hydrocephalus resolves amenorrhea in all the cases of amenorrhea due to hydrocephalus. The suspected role of the surgery is the correction of increased intracranial pressure, which is an important pathogenetic factor in the development of amenorrhea.
Following kainate (KA)-induced epilepsy, rat hippocampal neurons strongly express immediate early gene (IEG) products, i.e., c-FOS and c-JUN, and neural stress protein, HSP72. Prolonged expression of c-JUN and c-FOS 48 hr after cerebral ischemia has been underwent delayed neuronal death. However, it is not yet clear whether IEGs actually assume the essential roles in the cell death process or simply as a by-product due to external stimuli because of the prolonged expression of c-FOS, more than one week, on intact CA2 neurons of the hippocampus in a KA-induced epilepsy model. This study investigated the relationships between prolonged expression of c-JUN and hippocampal neuronal apoptosis in a KA-induced epilepsy model. Epileptic seizure was induced in rats by a single microinjection of KA (1 microgram/microL) into the left amygdala. Characteristic seizures and hippocampal neuronal injury were developed. The expression of c-JUN was evaluated by immunohistochemistry, and neuronal apoptosis by in situ end labeling. The seizures were associated with c-JUN expression in the hippocampal neurons, of which the level showed a positive correlation with that of apoptosis. Losses of hippocampal neurons, especially in the CA3 region, were partly caused by apoptotic cell death via a c-JUN-mediated signaling pathway. This is thought to be an important component in the pathogenesis of hippocampal neuronal injury via KA-induced epilepsy.
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