Objective: To determine the frepuency and severity of cognitive impairments associated with aneurysmal subarachnoid hemorrhage. Methods: A series of 37 patients with aneurysmal subarachnoid hemorrhage were examined by means of a battery of cognitive tests before surgical treatment. Results: In 70.3% of the patients, one or more cognitive functions were impaired. Compared with normative data, 2.7% of patients showed impairment on arithmetic, digit symbal and picture complement respectively, 5.4% on digit span, 48.6% on Visual Reproduction , 27%(food) and 18.9% (ordinary tools) on verbal fluency test, 18.9%(part A) and 21.6% (part B) on trail-making test,?18.9% on MMSE (mini mental state examination). Conclusion: The patients have impressive cognitive deficits after aneurysmal subarachnoid hemorrhage. SAH patients were especially impaired in functions that are related to short-term memory, concentration capacity, and frontocortical functions.

The single colonel composition of pituitary adenomas of human attests to the molecular basis of pituitary tumorigenesis. This review offers a specific overview of the involvement of alternation of tumor oncogenes and tumor suppressor genes (TSGs) in the pathogenesis of human pituitary adenomas. Mutations of gsp and H ras oncogenes genes and amplification of PKC have been identified in pituitary adenomas. Especially the mutation of gsp has been detected in 40% human GH secreting pituitary adenomas. The role of TSGs(tumor suppressor genes) including MEN 1, p53, Rb and p16 in pituitary adenoma formation and progression has yet be observed. Providing evidence proves that activation of oncogenes and inactivation of tumor suppressor genes seem to be at least one mechanism by which human pituitary adenomas origin and progress.

Owing to the specific distribution and pathology of intracranial giant aneurysm, the parent artery must frequently be interdicted. In order to avoid cerebral ischemia, many neurosurgeons create effective techniques of extracranial intracranial artery bypass(EIAB) for the treatment of intracranial giant aneurysm. In this review, the author summarized advances in the application of EIAB for the treatment of intracranial giant aneurysm.

Acute brain injury is usually complicated by systemic inflammatory response syndrome (SIRS) which is initiated by cytokines and inflammatory mediators and induces a series of adverse physiological changes, culminating in the development of multiple organ failure. SIRS plays a pivotal role on the function of brain and extra cerebral organs, exacerbates the brain edema, and increases the septic rate. The diagnostic criteria and pathological courses of SIRS, and its relationship with acute brain injury and sepsis are briefly reviewed.

Objective:To determine the changes of intramucosal pH(pHi) after severe craniocerebral injuries and the correlation to bleeding from stress ulceration. Methods:Nineteen cases of severe head trauma patients were enrolled, their pHi were determined at different time point with tonometry. The pH of gastric juice and plasma gastrin concentrations were monitored for 7 days. Results:Five cases(bleeding group) developed stress ulcer bleeding. On admission, the pHi were not significantly different in the non bleeding group, but the differences between two groups at 12 hours, 24 hours, the 3rd day, the 5th day, the 7th day after admission were significant, pHi in the bleeding group was statistically lower than non bleeding group. The pH values of gastric juice and the plasma gastrin concentrations were not different significantly between two groups during each therapeutic periods. Conclusion:Bleeding group had significantly lower pHi than non bleeding group during the therapeutic periods. pHi was predictive for bleeding from stress ulceration after severe craniocerebral injury.

The metabolic response to traumatic brain injury includes hypermetabolism, hypercatabolism, hyperglycemia, acute phase response and immunosuppression, which are mediated mainly by hypothalamus pituitary adrenal axis and cytokines. Sufficient nutritional support and appropriate metabolic intervention are believed clinically to play an important role on the mitigation of secondary brain damage, reduction of septic rate and improvement of patient′s outcomes.

OBJECTIVE: Cerebral vasospasm (CVS) induced by subarachnoid hemorrhage (SAH) is a difficulty in neurosciences. Because the pathogenesis of CVS remains a matter of discussion, clinical prevention and treatment are currently not sufficient. With the application of advanced experimental technology in recent years, great breakthroughs have been achieved in domestic and foreign studies on potassium channels. Definite mechanism in the region plays a significant role in instruction for clinical prevention and treatment. In this paper, researches related to potassium channels in cerebral vascular vessels after SAH are reviewed.DATA SOURCES: Related articles published between January 1991 and December 2005 were searched by the computer in Medline database with the key words of "potassium channels, subarachnoid hemorrhage, cerebral vasospasm" and the language was limited to English. Meanwhile, relevant articles were also searched in CNKI and Wanfang database with the same key words in Ghinese.STUDY SELECTION: All articles were selected firstly, and literatures related to potassium channel on physiology and pathogenesis of SAH-induced CVS were selected. Researches on biochemistry and gene etc were excluded.DATA EXTRACTION: A total of 45 English articles were collected, among which, 17 met the inclusion criteria. Of 2 Chinese articles collected,one study was in accordance with the inclusion criteria. Eighteen literatures on the pathological and physiological mechanism of CVS after SAH were looked for the full text.DATA SYNTHESIS: Researches showed that remarkable changes occurred in potassium channels in CVS after SAH, while potassium channel modulators had significant interventional effect on CVS in animal experiment by promoting or blocking the ion movements.CONCLUSION: Potassium channels plays an important role in the pathogenesis of SAH-indueed CVS. Some therapeutic intervention may be provided based on the studies of potassium channels in CVS.

OBJECTIVE: Aneurysmal subarachnoid hemorrhage is mainly due to intracranial aneurysm rupture. Modern techniques enable most survivors to make a good functional recovery Nevertheless,it has been suggested that such patients suffer from a persistent disturbance of cognitive function,which affects their life quality. Therefore,cognitive assessment following aneurysmal subarachnoid hemorrhage has been gradually drawing increasing attention in recent years.DATA SOURCES: Related literature was searched through the computer in PUBMED with key terms of "aneurysmal subarachnoid hemorrhage" and"cognitive deficit" and the language was limited to English. Meanwhile literature between 2001 an.d 2004 was also searched with key terms of"subarachnoid hemorrhage" and "cognitive function" in the Chinese or English language,respectively.STUDY SELECTION: Literature with cognitive assessment as its main index determined by standardized measurement was enrolled in this study.DATA EXTRACTION: A total of 101 related articles were collected,including 15 ones closely related to the present study,while those with cognitive assessment as part of their content and cognitive function determined with new methods were excluded.DATA SYNTHESIS: Cognitive assessment was analyzed in respect of its content,measurement,results and risk factors. Effect of aneurysmal subarachnoid hemorrhage itself and its complications,as well as therapeutic methods on the onset and development of cognitive disturbance were also explored.CONCLUSION: Patients with aneurysmal subarachnoid hemorrhage suffer from cognitive impairment,which also results from operation,anesthesia and drugs.

Subarachnoid hemorrhage ( SAH) especially aneurismal SAH is a deadly cerebrovascular disorder with very high mortality and morbidity rates, but there is still no effective treatment in clinical practice.In recent years, more and more studies have suggested that early brain injury ( EBI) may be the main factor for poor prognosis of SAH.The pathogenesis of EBI after SAH includes a series of complicated pathophysiological changes.This paper reviews the related progress of EBI after SAH from the aspects of acute cerebral ischemia, the disruption of blood brain barrier, apoptosis, autophagy, oxidative stress, inflammation, and so on.

Cerebral ischemia and reperfusion can cause delayed neuronal death in rodents,such as Mongolian gerbils and stroke-prone spontaneously hypertensive rats(SHRSP),which are used as an experimental stroke model.The protective effects of antioxidant nutrients such as vitamin E,green tea extract,ginkgo biloba extract,resveratrol,niacin and isoflavones in cerebral ischemia and reperfusion brain injury were reviewed.