Intracranial hypertension remains the key biomarker of severe traumatic brain injury for neurosurgery doctors. The monitoring of intracranial pressure (ICP) provides the technical support of precision and effective treatment strategy. In this article, the authors analyze the methodology, timing, function and development trend of ICP monitoring. The developing process of ICP monitoring contains the efforts of exploring a safe and precise technique to reflect the pressure in an injured brain. The modern ICP monitoring technology provides sufficient information flow for the management of craniocerebral trauma. Neurosurgeons could follow the information in the value and trends of ICP monitoring and implement it into decision making throughout the whole process of patient management. With the advanced data collecting and analyzing system the clinician can look into the waveform and parameter generalized by ICP value, and can interpret to the pathophysiological profiling in brain. ICP monitoring could exert efficacy not only in reflecting the mechanism of brain injury but also in the directing the clinical practice.

To evaluate the protective effect of MgSO_4 during cerebral ischemia reperfusion,twentyfour SD rats were divided randomly into control group (n=7),ischemic reperfusion group (n=9)and MgSO_4 treatment group (n=8)with Pnlsinelli and Brierley's animal ischemic reperfusion model. Compared with the control and ischemic reperfusion group,cerebral tissue contents of water and malondialdehyde reduced markedly (P

Progressive brain injury after traumatic brain injury,including intracranial hemorrhage,cerebral ischemia and edema,is an important factor affecting the prognosis of patients with traumatic brain injury.On basis of reviewing literatures,the research progress on incidence,mechanism,methods for early diagnosis,treatment and prognosis of progressive brain injury after traumatic brain injury was reviewed.

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective To determine the effect of hypothermia on gene transcription and protein expression of calpain after traumatic brain injury (TBI). Methods Twenty-seven rats were randomly divided into three groups, ie, normal control group, normothermia TBI group and hypothermia TBI group. All rats with TBI were suffered from a lateral fluid percussion injury (FPI) at the right parietal lobe. Hy-pothermia intervention [rectal temperature for (32 ± 0.5) ℃] was performed for four hours immediately after TBI in hypothermia TBI group. Fluorescence PCR and Western blot were utilized to semi-quantify gene transcription and protein expression of ealpain and immunofluorescence used to observe protein dis-tribution of Calpain. Results Compared with normothermia TBi group and normal control group, hypo-thermia TBI group showed increased calpain gene transcription at 12 and 24 hours respectively after FPI (P <0.05). However, the increase of ealpain protein expression in hypothermia TBI group was inhibited more significantly by hypothermia at 6,12,24 and 72 hours after TBI, compared with normothermia TBI group (P < 0.05). Conclusion Neuroproteetion of hypothermia after TBI may somewhat be related to the decrease of calpain protein expression after its gene transcription.

Objecfive To explore pathological mechanism and treatment of central hyponatrem-ia. Methods Synchronous assay was made to detect changes of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),endogenous digitalis-like substance(EDLS),antideuretic hormone (ADH),Na+ concentrations in blood and urine as well as osmotic pressure of plasma and urine in 68 pa-tients with traumatic brain injury(TBI). Results Of all,there were 27 patients with hyponatremia,mostly in patients with severe or critical TBI.There found syndrome of inappropriate secretion of antidi-uretic hormone(SIADH)in 7 patients and cerebral salt wasting syndrome(CSWS)in 20. Conclu-sions The central hyponatremia in patients with TBI may be related to the increased secretion of EDLS and ADH.The decrease of ANP and BNP in blood has no direct effect on Na+ concentration in blood.In-travenous injection of extrinsic thyrotropin releasing hormone(TRH)may inhibit dilutional hyponatremia resulted from increased secretion of ADH in TBI patients.

Objective To investigate the therapeutic effect of NSR siRNA on nerve regeneration following spinal cord hemi-transsection injury in rats. Methods Rats with T8 spinal cord hemi-trans-section were didded into 3 groups, ie, siRNA group, NS group and control group. SiRNA or NS was in-jected into lateral cerebral ventricle just after spinal cord injury. The therapeutic effect of NgR siRNA was evaluated by using BBB locomotor rating scale, retrograde horseradish peroxidase(HRP)tracing and HE staining. Results BBB locomotor rating scale showed that the recovery of the locomotor function of siRNA group seemed to be better than that of the other two groups from the 4th week, but there was no statistical difference. Retrograde HRP tracing showed a large number of positive cells in the anterior horn of spinal cord, with statistical difference compared with NS group and control group(P<0. 05). Eight weeks after spinal injury, HE staining showed disorderly distribution of the fibres in NS group and control group but serial fibres in the injury region in siRNA group. Conclusion NSR siRNA may promote the nerve regeneration following spinal cord injury.

Objective To investigate the changes of circulating endothelial progenitor cells (EPCs) in patients with acute cerebral infarction or chronic cerebral ischemia and discuss the related clinical significance.Methods Circulating EPCs were isolated using staining markers of CD34,CD133,and kinase insert domain receptor (KDR).Peripheral venous blood was collected from patients with acute cerebral infarction within 24 hours of onset (infarction group,n =30),with chronic cerebral ischemia (ischemia group,n =20),and without cerebral ischemia (control group,n =10) to quantify circulating level of EPCs using flow cytometry and measure parameters of systolic pressure,glycosylated hemoglobin (HbAlc),total cholesterol (TC),and triglyceride (TG),and low density lipoprotein-cholesterol (LDL-C),and high density lipoprotein-cholesterol (HDL-C).Results CD34-,CD34/CD133-,and CD34/KDR-positive cells counted (14.2 ± 8.1)‰,(7.1 ± 4.1)‰ and (5.0 ± 3.7)‰ in infarction group,(28.5 ± 9.9)‰,(15.2 ± 3.7)‰ and (6.8 ± 2.0)‰ in ischemia group,and (44.8 ± 9.5) ‰,(22.1 ± 6.6) ‰ and (16.7 ± 6.9) ‰ in control group.Taken together,circulating level of EPCs lowered substantially in infarction and ischemia groups compared to control group (P ＜ 0.05) and a far lower level was observed in infarction group (P ＜ 0.05).Circulating level of EPCs in infarction group was in a moderate negative correlation with systolic pressure,TC,TG,and LDL-C (P ＜ 0.05).Conclusions Decreased circulating level of EPCs may be a risk factor to the development of cerebral ischemia in acute cerebral infarction patients.Therefore,level of EPCs is vital for prediction,prevention and treatment of acute cerebral infarction.

Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.