BACKGROUND AND PURPOSE: Cerebral venous flow obstruction (CVFO) is a fatal complication of traumatic brain injury. To compare the outcomes of patients with CVFO secondary to traumatic-brain-injury-induced transsinus fracture who were diagnosed early versus those diagnosed late in the therapeutic course. METHODS: In total, 403 patients with transsinus fracture were reviewed retrospectively. The patients were divided into an early-diagnosis group (n=338) and a delayed-diagnosis group (n=65). The patients submitted to 2D time-of-flight magnetic resonance venography (2D-TOF MRV) and/or CT venography (CTV), depending upon the findings of intracranial pressure monitoring, in order to identify potentially complicated CVFO. These examinations took place within 3 days of the onset of malignant intracranial hypertension symptoms in the early-diagnosis group, and after an average of 7 days in the delayed-diagnosis group. Once diagnosed, patients received intravenous thrombolytic therapy with low-dose urokinase. Patients with massive transsinus epidural hematoma, depressed fracture, or cerebral hernia were treated surgically to relieve the compression and repair any damage to the venous sinuses. RESULTS: Cerebral venous flow obstruction was much more severe in the delayed-diagnosis group than in the early-diagnosis group (p<0.001), and hence patients in the former group were given a higher dose of urokinase (p<0.001) for thrombolytic therapy. They were also significantly more likely to need surgery (48.1% vs. 20.6%, p=0.003) and had a higher mortality rate (37.0% vs. 4.1%, p<0.001). However, patients in both groups experienced a similarly favorable prognosis, not only with regard to functional outcome but also with respect to neuroradiological improvement, as evaluated by 2D-TOF MRV/CTV at the final follow-up (p=0.218). CONCLUSIONS: Delayed diagnosis can result in increased risk of surgery and death in the acute phase. Thrombolytic therapy with low-dose urokinase resulted in promising improvements in both functional and neuroradiological outcomes in all of the patients in this study, regardless of the time to diagnosis.
Brain Injuries* ; Delayed Diagnosis ; Early Diagnosis* ; Encephalocele ; Follow-Up Studies ; Hematoma ; Humans ; Intracranial Hypertension ; Intracranial Pressure ; Magnetics ; Magnets ; Phlebography ; Prognosis ; Retrospective Studies ; Thrombolytic Therapy ; Urokinase-Type Plasminogen Activator

OBJECTIVETo investigate the effect of microwave radiation on synaptic structure, characteristic of synaptosome, the contents and release of neurotransmitters in hippocampus in Wistar rats.

METHODSWistar rats were exposed to microwave radiation with average power density of 30 mW/cm(2). Electron telescope was used to study the change of the synaptic structure at 6 h after radiation and to identify synaptosome. Flow cytometry and electron spin resonance were used to study the change of the concentration of Ca(2+) in synapse and the fluidity of membrane proteins of synaptosome. High performance liquid chromatography (HPLC) and spectrophotometer were used to study the changes of contents and release of amino acids and acetylcholine in hippocampus.

RESULTSMicrowave radiation of 30 mW/cm(2) caused deposits of synapse vesicle, elongation of active zone, the increase of thickness of postsynaptic density (PSD) and curvature, and perforation of synapse. The concentration of Ca(2+) in synapse (P<0.01) and tc of membrane proteins (P<0.01) of synaptosome increased contents of glutamic acid and glycine (P<0.01) and release of GABA increased the increase of contents and release of acetylcholine, and activity of acetyl cholinesterase (P<0.01) increased.

CONCLUSIONMicrowave radiation can induce the injure of synaptic structure and function of hippocampus, and then induce the disorder of the ability of learning and memory in rats.

Animals ; Hippocampus ; metabolism ; pathology ; radiation effects ; Male ; Microwaves ; adverse effects ; Rats ; Rats, Wistar ; Synapses ; metabolism ; pathology ; radiation effects ; Synaptosomes ; metabolism ; radiation effects

Objective To investigate the clinical benefits of emergent burr hole drainage in combination with decompressive craniotomy for patients with traumatic intracerebral haematoma-induced cerebral hernia. Methods A total of 291 patients with brain hernia caused by acute traumatic epidural and/or subdural hematoma were chosen in our study; 143 of them were treated with decompressive craniotomy alone (ordinary decompression group, admitted to our hospital from January 2003 to December 2006) and 148 of them were treated with emergent burr hole drainage in combination with decompressive craniotomy (emergent surgical intervention group,admitted to our hospital from January 2007 to June 2011).Clinical parameters,including Glasgow Outcome Scale (GOS) scores,incidence of massive cerebral infarction,pupil retraction rate,and Glasgow Coma Scale (GCS) scores,were evaluated retrospectively analyzed. Results Patients in ordinary decompression group had higher GOS scores than those in emergent surgical intervention group (Z=-4.012,P=0.000); mean rank indicated that the treatment efficacy in the emergent surgical intervention group was better than that in the other group.Patients in ordinary decompression group had significantly reduced incidence of massive cerebral infarction (45/148) as compared with patients in ordinary decompression group (70/143,P=0.000).Much more patients (124/148) enjoyed increment of GCS scores in the emergent surgical intervention group as compared with those in the ordinary decompression group (65/143,P=0.000). Conclusion Emergent burr hole drainage followed by decompressive craniotomy is an effective method in saving patients with brain hernia caused by acute traumatic intracerebral haematoma, which can notably resolve intracranial hypertension as soon as possible and give longer time for surgery,therefore,it can improve the prognosis.