Stroke-associated infection is a leading cause of death in patients with stroke.Recent research indicated that stroke-induced immunodepression increases the susceptibility to infection.The immune system shows a biphasic change after stroke.Tne resident cells (mainly microglia) in the central nervous system are activated following stroke and produce pro-inflammatory cytokines and chemokines,which are involved in ischemic injury.Subsequent systemic immunodepression can result in increases susceptibility to infection,but it also facilitate neurogenesis.The ovcractivity of the sympathetic nervous system is the key to the development of immune suppression.The strategies for controlling stroke-associated infection include sympathetic antagonists,immunomodulators and prophylactic antibiotic therapy.

Cerebral amyloid angiopathy (CAA) is characterized by leptomeningeal and β-amyloid deposition in arteriole wall in cortex, and it is one of the common cerebral vascular diseases in the elderly. It is correlated with Alzheimer's disease, intracerebral hemorrhage, cerebral infarction and leukoencephalopathy. CAA is divided into hereditary and sporadic types, and the latter is most common. This article reviews the advances in research on the pathophysiological mechanisms of sporadic CAA, particularly the production of β-amyloid protein and clearance mechanism in brain tissue.

BACKGROUND:Treatment after intracerebral hemorrhage can effectively suppress immune function. The immune suppression after ischemic stroke has been studied in detail.
OBJECTIVE:To construct an immunosuppressed rat model after cerebral hemorrhage, and assess its stability.
METHODS:Sixty Wistar rats were randomly divided into control group, sham group, and cerebral hemorrhage group, with 20 rats in each group. Rat models of acute cerebral hemorrhage were established by 50μL arterial blood injection in the rat basal ganglia. Rats in the sham group were injected with 50μL of saline, and the operation was identical to cerebral hemorrhage model. Rats in the control group received no treatment. At 24, 48, 72 and 96 hours after model establishment, leukocytes, lymphocytes, and lymphocyte percentage were analyzed by blood analyzer. Enzyme linked immunosorbent assay was used to determine the levels of serum proinflammatory cytokine interleukin-6 and anti-inflammatory cytokine transforming growth factorβin rats. Dissected rat spleen tissue was subjected to histological and histopathological detection. RT-PCR and western blotting were utilized to measure changes in transforming growth factorβ, interleukin-6 gene and protein expression in the spleen.
RESULTS AND CONCLUSION:(1) Compared with the sham group and control group, leukocyte number was significantly higher, but lymphocyte percentage gradual y reduced in the cerebral hemorrhage group at 24, 48, 72 and 96 hours (P<0.05). (2) Compared with the sham group and control group, interleukin-6 levels in the blood and spleen were higher at 24 hours, peaked at 72 hours, and decreased at 96 hours in the cerebral hemorrhage group (P<0.05). (3) Compared with the sham group and control group, transforming growth factorβexpression was lower at 24 hours, gradual y increased at 72 hours, and higher at 96 hours in the rat blood and spleen of the cerebral hemorrhage group (P<0.05). (4) These findings indicate that immune function excitement first appeared after cerebral hemorrhage, and immune suppression appeared at 96 hours, indicating successful model establishment and good stability.

Objective To discuss the opportunity of hemilateral craniotomy in treatment of a large area combined middle cerebral artery (MCA) infarction.Methods Thirty-two patients with a large area combined MCA infarction were performed by hemilateral craniotomy.Initial clinical presentation was evaluated by the Glasgow coma scale(GCS).All survivors were assessed three months after surgical decompression according to Barthel index(BI).The effects of pre-hemia decompressive surgery(before any signs of cerebral hernia,based on clinical status and CT or DWI findings)versus post-hernia surgery (after signs of hernia) on mortality,functional outcome.Results In 18 patients with pre-hernia decompressive surgery,3 patients (16.7%)were dead and average BI was (66.94±7.75)scores.The mortality was 57.1%(8/14)and average BI was (38.43±9.82)scores of post-hernia surgery with 3 cases severe aphasia.Conclusion Hemilateral craniotamy is performed before occurrence of cerebral hernia may decrease the mortality and improve outcome in these patients.

BACKGROUND:Clinical studies have demonstrated that systemic mild hypothermia could significantly reduce the disability and mortality rate of patients with severe traumatic brain injury. In recent years, the researches about the treatment of spinal cord injury by mild hypothermia have been successively carried out. OBJECTIVE:To investigate the effects of mild hypothermia on nerve regeneration microenvironment after spinal cord injury and explore the possible underlying mechanism of nerve regeneration and functional recovery after spinal cord injury in rats. METHODS:Twenty out of sixty-seven rats were randomly selected as the sham group, and other rats were used to establish spinal cord injury models in T9 segment using modified Alen's method. Three rats were excluded for failure in spinal cord injury induction and four rats for death during modeling. The rest 40 rats were randomly and evenly divided into the spinal cord injury and mild hypothermia groups (n=20 rats/group). The rats in the sham and spinal cord injury groups were placed in the operating table with normal temperature, making their rectal temperature at 37.0±0.5℃ for 72 hours. The rats in the mild hypothermia group were placed on ice blanket machine, making their rectal temperature at 34.0±0.5℃ for 72 hours, then the temperature was naturaly rewarmed. RESULTS AND CONCLUSION:Compared with spinal cord injury group, the apoptosis index and the level of aquaporin 4/9 mRNA and protein expression in spinal cord injury tissue were al decreased, somatosensory evoked potential latency and amplitude were recovered, and the motor functional scores were increased in the mild hypothermia group. These results indicate that mild hypothermia play its protective effect on spinal cord injury through attenuating apoptosis of neural cels and decreasing aquaporin 4/9 mRNA and protein expression levels.