Brain Ischemia ; Cerebral Infarction ; Humans ; Subarachnoid Hemorrhage ; Vasospasm, Intracranial/etiology*

Vasospasm is an important cause of morbidity and/or mortality with a subarachnoid haemorrhage (SAH). The roles of lipid peroxidation in a vasospasm caused by a SAH remain to be investigated. The effect of an intracisternal administration of alphatochopherol on a cerebral vasospasm was investigated in an experimental model. The authors assessed whether the administration of alphatochopherol reduced the vasospasm. By means of an intracisternal blood injection model, a SAH was induced in 30 rats, which were randomly divided into three groups, as follows: group I (G1), without a SAH and drug, group II (G2), a SAH alone, group III (G3), a SAH and alphatochopherol. Following the withdrawal of cerebrospinal fluid (CSF), a fresh unheparinized arterial blood was injected into the cisterna magna to induce a SAH. In G3, 20 U (0.4ml) alphatochopherol was intracisternally injected forty-five hours after induction of the SAH. All rats were sacrificed 72 hours after the induction. The basilar artery, with surrounding tissue, was removed from the cranium. The cross-sectional diameter of the lumen and vessel wall of the rat basilar artery was assessed from a planimetric analysis, and changes compared with G1 and G2. The reduction in the luminal cross-sectional diameter of the vessels exposed to subarachnoid blood was found to be 29.01 % (p=0.001). The group treated with alphatochopherol had a 9% reduction (p=0.004). The role of lipid peroxidation on a vasospasm caused by SAH is well known to be critical. Data from the present study indicated that antioxidant therapy, with topical alphatochopherol, may be promising on a vasospasm caused by a SAH.
Animals ; Antioxidants/*administration & dosage ; Injections, Intraventricular ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage/*complications ; Vasospasm, Intracranial/*etiology/*physiopathology ; alpha-Tocopherol/*administration & dosage

OBJECTIVETo observe the improvement of acupuncture in cerebral vasospasm (CVS) after embolization of ruptured aneurysms.

METHODSSixty cases were randomly divided into two groups, an acupuncture-medication group and a conventional treatment group, 30 cases in each one. The cases of CVS in conventional treatment group were treated with Nimodipine. In acupuncture-medication group, on the basis of the treatment as conventional treatment group, Baihui (GV 20) and Fengchi (GB 20) were selected as the main acupoints in the treatment of CVS. The treatment lasted for 3 weeks. Hunt-Hess scale for the standard assessment was adopted to determine the severity of disease before and after treatment and compare the efficacy between two groups. The transcranial Doppler (TCD) was conducted on the 1st, 4th, 7th, 10th, 14th and 21st days successively after operation, and the average flow velocity of 3 pairs of vessels (ACA, MCA, and PCA) was recorded. CT perfusion (CTP) was taken to test cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) on the 1st, 7th, 14th and 21st days successively.

RESULTSThe improvement of Hunt-Hess scale in acupuncture-medication group was superior to that in conventional treatment group (P < 0.05). The analysis of variance (ANOVA) was adopted in the comparison of ACA, MCA, PCA, CBF, CBV and MTT between two groups. The results showed that the therapy in either group achieved the effect on CVS (all P < 0.05). But, the improvements in the above mentioned indices in acupuncture-medication group were superior to those in conventional treatment group (all P < 0.05).

CONCLUSIONAcupuncture at Baihui (GV 20) and Fengchi (GB 20) down-regulates the peak values or upregulates the valley values. It releases the peak of CVS effectively, improves the clinical prognosis significantly and is the effective therapy for CVS after subarachnoid hemorrhage.

Acupuncture Therapy ; Adult ; Aged ; Aneurysm, Ruptured ; complications ; surgery ; therapy ; Balloon Occlusion ; Female ; Humans ; Male ; Middle Aged ; Treatment Outcome ; Vasospasm, Intracranial ; etiology ; therapy

OBJECTIVETo assess the value of (1)H-magnetic resonance spectroscopy ((1)H-MRS) in evaluating cerebral vasospasm resulting from subarachnoid hemorrhage (SAH).

METHODSSix dogs were subjected to autologous non-heparinized blood injection via cisternal puncture twice at one-day interval to establish models of SAH, and another 6 received injections with normal saline in an identical manner. (1)H-MRS scan was performed on the 3rd, 7th and 14th days after the injections to measure the changes of N-acetylaspartate (NAA), creatine (Cr) and choline (Cho). After the (1)H-MRS scan, all the dogs underwent brain digital subtraction angiography (DSA) for determining the basilar artery diameter.

RESULTSDSA results on day 3 presented development of obvious vasospasm of the basilar artery, which was most evident on day 7 and recovered obviously on day 14. (1)H-MRS results demonstrated obvious changes of NAA, Cho and Cr on days 3 and 7 in SAH model group, and NAA declined to the lowest level on day 3 followed by gradual ascending till reaching the normal level on day 14. Cho decreased slightly on day 3, then increased and reached the peak level on day 7 and then decreased. Cr rose steadily from day 3 to 14, but since day 7, the rise slowed down obviously and Cr maintain a level not significantly different from that on day 14 (P>0.05). The functional results of (1)H-MRS were consistent with the DSA results.

CONCLUSION(1)H-MRS can be used to monitor the development of cerebral vasospasm resulting from SAH as a good evaluation method for functional imaging.

Animals ; Aspartic Acid ; analogs & derivatives ; metabolism ; Choline ; metabolism ; Creatine ; metabolism ; Dogs ; Female ; Magnetic Resonance Spectroscopy ; methods ; Male ; Protons ; Subarachnoid Hemorrhage ; complications ; Time Factors ; Vasospasm, Intracranial ; diagnosis ; etiology ; metabolism

OBJECTIVETo investigate the relationship between cerebral vasospasm and occurrence of delayed ischemic neurological deficit (DIND).

METHODSThe clinical records and radiographic images of 118 patients with subarachnoid hemorrhage admitted during last 5 years were reviewed. The incidence,degree and localization of cerebral vasospasm were evaluated, and morbidity of related DIND was analyzed. Patients with cerebral vasospasm were divided into three groups: Group MCA (middle cerebral artery), Group ACA (anterior cerebral artery) and Group ICA (intracranial carotid artery) according to the location of cerebral vasospasm. The consistency of DIND and image of cerebral infarction were examined.

RESULTThere was a weak correlation between cerebral vasospasm and incidence of DIND (r=0.22; P=0.016). The incidence of DIND was increased with severity of cerebral vasospasm (U=2.589, P<0.05). The group MCA had a significantly higher incidence of DIND than that of ACA and ICA groups (68.0% compared with 36.7% and 25.0%, respectively, chi(2)=8.195, P=0.004), the difference between later two groups was not statistically significant (chi(2)=0.646, P=0.421).

CONCLUSIONCerebral vasospasm may be an important factor leading to DIND occurrence; the severity and location of cerebral vasospasm is related to the incidence of DIND.

Adult ; Aged ; Aneurysm, Ruptured ; complications ; Carotid Artery, Internal ; Female ; Humans ; Intracranial Aneurysm ; complications ; Ischemic Attack, Transient ; etiology ; Male ; Middle Aged ; Rupture, Spontaneous ; Subarachnoid Hemorrhage ; complications ; Time Factors ; Vasospasm, Intracranial ; etiology

OBJECTIVETo study whether endothelial nitric oxide synthase gene (eNOS) polymorphisms is implicated in the development of cerebral vasospasm following subarachnoid hemorrhage.

METHODSThree groups of patients with subarachnoid hemorrhage were selected to test this hypothesis, including 98 patients with cerebral vasospasm following aneurysmal subarachnoid hemorrhage (ASAH), 96 with cerebral vasospasm following traumatic subarachnoid hemorrhage (TSAH), and 195 patients without cerebral vasospasm following aneurysmal or traumatic subarachnoid hemorrhage. The parents of 194 patients and 100 control subjects were also examined for transmission disequilibrium test according to a family-based study design to test the associations.

RESULTSWe examined four eNOS gene polymorphisms, and two of these polymorphisms, the T to C substitution in the promoter at position -786 and the a-deletion/b-insertion in intron 4, were found to associate with cerebral vasospasm in subarachnoid hemorrhage in the case-control comparisons. For the former polymorphism, the risk of cerebral vasospasm was higher in C allele homozygotes than in the other two genotypes (odds ratio: 2.8, 95% CI: 1.4 to 5.6); for the latter polymorphism, the a-deletion carriers were exposed to a increased risk (odds ratio: 2.3, 95% CI: 1.3 to 4.0) in comparison with the noncarriers. The two polymorphisms were analyzed together as haplotypes in a family-based study using the transmission disequilibrium test. The C/a-deletion haplotype was transmitted from the heterozygous parents to cases of cerebral vasospasm in subarachnoid hemorrhage with a significantly higher frequency than expected (P=0.005).

CONCLUSIONThe findings of the case-control and family-based studies clearly demonstrate that DNA sequence differences in eNOS gene influence the risk of cerebral vasospasm in subarachnoid hemorrhage.

Adolescent ; Adult ; Case-Control Studies ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Nitric Oxide Synthase Type III ; genetics ; Polymorphism, Genetic ; Risk Factors ; Subarachnoid Hemorrhage ; complications ; enzymology ; genetics ; Vasospasm, Intracranial ; enzymology ; etiology ; Young Adult

OBJECTIVETo investigate the effects and possible mechanisms of puerarin on the vascular active factors correlated to cerebral vasospasm (CVS) after aneurysm subarachnoid hemorrhage (aSAH).

METHODSFifty-four patients with aSAH were randomly assigned to the puerarin group (30 cases) and the control group (24 cases) by lot. On the basis of routine treatment, the patients in the puerarin group were intravenously dripped with 0.5 g puerarin by adding in 250 mL glucose injection once daily. The injection was given starting from the 3rd day of the disease course, for 14 successive days. The plasma levels of nitric oxide (NO), endothelin-1 (ET-1), thromboxane B, (TXB2), 6-Keto-prostaglandin F1alpha (6-K-PGF1alpha) were compared between the two groups pre- and post-therapy. The incidence of cerebral vasospasm (CVS) was observed using transcranial Doppler (TCD). The Glasgow outcome scale (GOS) were compared at discharge between the two groups.

RESULTSCompared with the control group, the plasma levels of NO, ET-1, and 6-K-PGF1alpha increased in the puerarin group (P < 0. 05), the TXB2 level decreased (P < 0.05), the incidence of CVS decreased (P < 0.05), the mean MCA velocity increased (P < 0.05), and the GOS at discharge increased (P < 0.05).

CONCLUSIONSPuerarin is an effective agent for the prophylaxis and treatment of the CVS in patients after aSAH. Moreover, it can improve the prognosis. The mechanism might be correlated with improving the levels of the vascular active factors, i.e., increasing the plasma levels of NO and PGl2, decreasing TXA, in plasma, increasing the cerebral blood flow, and improving cerebral perfusion.

6-Ketoprostaglandin F1 alpha ; blood ; Adult ; Aged ; Endothelin-1 ; blood ; Female ; Humans ; Isoflavones ; therapeutic use ; Male ; Middle Aged ; Nitric Oxide ; blood ; Prognosis ; Subarachnoid Hemorrhage ; blood ; complications ; drug therapy ; Thromboxane B2 ; blood ; Vasospasm, Intracranial ; blood ; drug therapy ; etiology

Fluoxetine, an anti-depressant drug, has recently been shown to provide neuroprotection in central nervous system injury, but its roles in subarachnoid hemorrhage (SAH) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates early brain injury (EBI) after SAH. We demonstrated that intraperitoneal injection of fluoxetine (10 mg/kg per day) significantly attenuated brain edema and blood-brain barrier (BBB) disruption, microglial activation, and neuronal apoptosis in EBI after experimental SAH, as evidenced by the reduction of brain water content and Evans blue dye extravasation, prevention of disruption of the tight junction proteins zonula occludens-1, claudin-5, and occludin, a decrease of cells staining positive for Iba-1, ED-1, and TUNEL and a decline in IL-1β, IL-6, TNF-α, MDA, 3-nitrotyrosine, and 8-OHDG levels. Moreover, fluoxetine significantly improved the neurological deficits of EBI and long-term sensorimotor behavioral deficits following SAH in a rat model. These results indicated that fluoxetine has a neuroprotective effect after experimental SAH.
Animals ; Apoptosis ; drug effects ; Blood-Brain Barrier ; drug effects ; Brain Edema ; drug therapy ; etiology ; Cytokines ; genetics ; metabolism ; Disease Models, Animal ; Fluoxetine ; pharmacology ; therapeutic use ; In Situ Nick-End Labeling ; Male ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Pain Measurement ; Psychomotor Performance ; drug effects ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; complications ; drug therapy ; pathology ; Time Factors ; Vasospasm, Intracranial ; drug therapy ; etiology

OBJECTIVETo discuss the mechanism of cerebral vessel spasm caused by concussion and the effect of Nimodipine on concussion.

METHODSA total of 224 patients who were treated from March 1995 to October 1999 were divided into two groups randomly, ie, Nimodipine group (113 cases) and control group (111 cases). Middle cerebral artery (MCA), basilar artery (BA) and the average peak forward velocity of cerebral blood flow were observed by color three-dimensional transcranial Doppler (3D-TCD) within 24 hours after admission and at the end of 3-6 days of treatment. Cerebral blood flow changes, characteristics and treatment effect were analyzed and determined by clinical main symptom disappearance rate.

RESULTSIn concussion, cerebral blood flow was divided into 3 phases: cerebral blood flow low infusion dilation phase, cerebral blood vessel spasm phase and cerebral blood flow recovery phase. In the Nimodipine group, clinical main symptom disappearance rate was higher than that in the control group in the cerebral spasm and recovery phases with a significant difference (P < 0.01).

CONCLUSIONSCerebral vessel spasm, hypoxia and ischemia lesion are the main pathological changes. Whether cerebral dysfunction is reversible or not is mainly determined by spasm time of cerebral blood vessel. Nimodipine has a good effect on releasing spasm and diminishing the cerebral blood flow velocity. It not only improves curative effect on concussion, but also reduces and prevents concussion sequelae. Hence, concussion patients who have cerebral spasm confirmed by 3D-TCD should be given Nimodipine routinely and early.

Adolescent ; Adult ; Aged ; Blood Flow Velocity ; Brain Concussion ; complications ; diagnostic imaging ; Cerebral Arteries ; diagnostic imaging ; drug effects ; Cerebrovascular Circulation ; drug effects ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Humans ; Infusions, Intravenous ; Injury Severity Score ; Male ; Mannitol ; administration & dosage ; Middle Aged ; Nimodipine ; administration & dosage ; Reference Values ; Treatment Outcome ; Ultrasonography, Doppler, Transcranial ; Vasospasm, Intracranial ; drug therapy ; etiology ; physiopathology