Effect of tranexamic acid on rebleeding after subarachnoid hemorrhage: a double-blind controlled clinical trial.

In a double-blind controlled clinical trial on 51 patients with subarachnoid hemorrhage, tranexamic acid, 4 gm per day for ten consecutive days, did not favorably affect the outcome. Neither mortality nor rebleeding rates were improved after a follow-up of three months.     

Prostacyclin and vasospasm in subarachnoid hemorrhage from ruptured intracranial aneurysm

Experimental and clinical observations suggest the importance of arachidonate metabolites in the genesis of symptomatic cerebral vasospasm after subarachnoid hemorrhage. Prostacyclin (PG12) has a well demonstrated vasodilator action. The authors monitored CSF prostacyclin concentration in 12 consecutive cases of subarachnoid hemorrhage with the purpose of correlating the prostacyclin concentration trend with the clinical course and the risk for vasospasm. In three cases patients presented with clinical and radiological signs of vasospasm. CSF prostacyclin concentration showed a typical decreasing trend, which amounted to a minor form of protection from vasospastic agents. The nine cases which did not develop vasospasm demonstrated no significant changes in the prostacyclin CSF concentration trend. The authors also presented four cases in which cisternal CSF samples were available. In one case of developing vasospasm, the cisternal prostacyclin concentration was seven times lower than the highest lumbar CSF concentration. In three cases without evidence of vasospasm cisternal CSF demonstrated a balanced biochemical situation and a minor risk of vasospasm.     

Recurrent subarachnoid hemorrhage from ruptured aneurysm

The authors discuss the problem of recurrent haemorrhage in neurosurgical practice on the basis of a material of 36 cases out of a groups of 401 treated surgically for arterial aneurysms in the years 1971--1975. They describe the methods of prevention of recurrent haemorrhage by administration of pharmacological agents, methods of transport to neurosurgical units and selection of time of operation as well as the principles of qualification of patients according to Botterell's scale.     

Magnetic resonance imaging of subarachnoid hemorrhage due to ruptured intracranial aneurysm

We report MRI (magnetic resonance imaging) findings of 31 cases with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysm. Among these cases, 25 were studied within 72 hours after onset of SAH. A resistive type MRI scanner operating at a field of 0.2 Tesla was used in obtaining inversion recovery (IR) and saturation recovery (SR) images. IR 1500/43/400 (T1 weighted image, T1W), SR 1000/60 (SR image) and SR 2000/100 (T2 weighted image, T2W) were chosen for analysis. The SR image was usually adopted and coronal and/or sagittal images were added when there was enough time for examination. Slice thickness was 10 mm and slice interval was 15 mm. The scan was not necessarily aimed at the visualization of aneurysm itself. 1) In the acute phase of SAH, subarachnoid spaces near the ruptured aneurysm were appeared as isointensity areas on T1W and as high intensity areas on SR image. In the subacute phase, they were depicted as high intensity areas on both T1W and SR images, and as high intensity areas on T2W. 2) Intraventricular hemorrhage was visualized as a niveau-like high intensity area, especially, within the posterior horns on the SR images. 3) SR and T2W images were suitable for detection of aneurysm itself. In a resistive-type scanner, small aneurysms were not easily visualized due to the lack of high resolution. However, 29% of aneuysms, which were not giant, could be visualized on MRI. 4) Identification of intracerebral hemorrhage and cerebral ischemia from various causes was easy on both T1W and T2W images.(ABSTRACT TRUNCATED AT 250 WORDS)     

Churg-Strauss syndrome presenting with subarachnoid hemorrhage from ruptured dissecting aneurysm of the intracranial vertebral artery

Churg-Strauss syndrome (CSS) represents a rare systemic vasculitis that is almost invariably accompanied by bronchial asthma and eosinophilia. We report a case of a 36-year-old woman with previously diagnosed CSS presented with subarachnoid hemorrhage (SAH) from dissecting aneurysm in a vertebral artery (VA). Two months before onset of SAH, the patient had presented with numbness on her right lower leg due to peripheral neuropathy. On admission, angiography revealed dissecting aneurysm of the right intracranial VA and stenosis of the basilar artery. Hematological examination revealed an increased percentage of eosinophils. Ruptured dissecting aneurysm of the intracranial VA was diagnosed. Emergent coil embolization of the dissecting aneurysm and occlusion of the parent artery was performed to prevent repeated hemorrhage from the dissecting aneurysm. Then pharmacotherapy with prednisone was initiated for CSS. The patient recovered well and was discharged without any neurological deficit. As far as we know, this is the first reported case of CSS presented with SAH from dissecting aneurysm on posterior circulation.     

Analysis of phospholipase C gene in patients with subarachnoid hemorrhage due to ruptured intracranial saccular aneurysm.

This study is designed to determine whether patients with aneurysmal subarachnoid hemorrhage have mutations in the phospholipase C-delta 1 (PLC-delta 1) gene, which was identified as a gene responsible for hypertension in spontaneously hypertensive rats. Seventy-two cases (31 male and 41 female) with intracranial saccular aneurysms were analyzed. The mean age was 60.1 +/- 11.5 years (mean +/- SD) (range 24-85 years). There were 35 patients (48.6%) with hypertension, 5 (6.9%) with diabetes mellitus, 12 (16.7%) with hyperlipidemia, 8 (11.1%) with ischemic heart disease, and 25 (34.7%) who were active smokers. The location of aneurysm was distributed as follows: 33 (33%) were at anterior cerebral artery, 23 (23%) were at middle cerebral artery, 28 (28%) were at internal carotid artery, and 16 (16%) were at vertebro-basilar artery. Six patients (8.3%) had a family history of intracranial aneurysms. There were 20 patients (27.8%) with multiple aneurysms, and 8 patients (11.1%) with a large or giant aneurysm. The four regions of PLC-delta 1 gene (bases 1099-1271, 1254-1401, 1343-1481, and 1882-2023) where genetic mutations were found in spontaneously hypertensive rats, were screened by PCR-SSCP analysis and their nucleotide sequences of all patients were determined. However, no mutations were detected in all patients. These results suggest that mutations of PLC-delta 1 gene previously implicated in hypertensive factor in rats may not be the case with human patients and therefore may be poorly related with aneurysmal subarachnoid hemorrhage.     

Analysis of phospholipase C gene in patients with subarachnoid hemorrhage due to ruptured intracranial saccular aneurysm

Abstract

This study is designed to determine whether patients with aneurysmal subarachnoid hemorrhage have mutations in the phospholipase C-dl (PLC-51) gene, which was identified as a gene responsible for hypertension in spontaneously hypertensive rats. Seventy-two cases (31 male and 4 1 female) with intracranial saccular aneurysms were analyzed. The mean age was 60.1 ± 11.5 years (mean± SD) (range 24-85 years). There were 35 patients (48.6%) with hypertension, 5 (6.9%) with diabetes mellitus, 72 (16.7%) with hyperlipidemia, 8 (11.1%) with ischemic heart disease, and 25 (34.7%) who were active smokers. The location of aneurysm was distributed as follows: 33 (33%) were at anterior cerebral artery, 23 (23%) were at middle cerebral artery, 28 (28%) were at internal carotid artery, and 16 (16%) were at vertebro-basilar artery. Six patients (8.3%) had a family history of intracranial aneurysms. There were 20 patients (27.8%) with multiple aneurysms, and 8 patients (11.1 %) with a large or giant aneurysm. The four regions of PLC-51 gene (bases 1099-1271, 1254-1401, 1343-1481, and 1882-2023) where genetic mutations were found in spontaneously hypertensive rats, were screened by PCR-SSCP analysis and their nucleotide sequences of all patients were determined. However, no mutations were detected in all patients. These results suggest that mutations ofPLC-d 1 gene previously implicated in hypertensive factor in rats may not be the case with human patients and therefore may be poorly related with aneurysmal subarachnoid hemorrhage. [Neurol Res 1999; 21: 368-372]     

Evaluation of pituitary and thyroid hormones in patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm

It is well known that the central nervous system (CNS) influences the pituitary hormone secretions and that diseases of CNS are frequently associated with an altered endocrine function. The aim of this study has been the evaluation of the serum concentrations of the pituitary and thyroid hormones in a series of patients with subarachnoid hemorrhage due to a ruptured cerebral aneurysm. Thirty-five patients (23 females and 12 males), aged 51.9 +/- 13.3 years on the mean were admitted. They were evaluated to assess the clinical severity of the subarachnoid hemorrhage by Hunt & Hess scale: nine patients were in the grade I, 14 in the grade II, and 12 in the grade III. Blood samples were obtained between 8:00 and 9:00 a.m. and serum hormones were measured by commercial kits (IRMA or MEIA methods). Cortisol serum levels (normal range (NR) = 5 to 18 micro g/dL) were increased in all the patients (mean +/- standard deviation = 31.4 +/- 12.4 micro g/dL). Mean prolactin levels (NR < 20 ng/mL) were 18.6 +/- 17.1 ng/mL and five patients (14.2%) had levels higher than normal. FSH and LH levels were normal according to age and sex: men: FSH = 4 +/- 2.9 mUI/mL (NR = 1 to 10.5 mUI/mL); LH = 6.1 +/- 6.3 mUI/mL (NR = 2 to 12 mUI/mL); premenopausa women: FSH = 2.5 +/- 1.5 mUI/mL (NR = 2.4 to 9.3 mUI/mL); LH 3.9 +/- 5.1 mUI/mL (NR =2 to 15 mUI/mL); post- menopausal women: FSH = 48.3 +/- 18.5 mUI/mL (NR =31 to 134 mUI/mL); LH = 29 +/- 13.8 mUI/mL (NR =16 to 64 mUI/mL). Mean TSH levels were 3.9 +/- 5.2 micro UI/mL (NR =0.5 to 4.7 micro UI/mL) and five patients (14.2%) had levels higher than normal. Mean triiodothyronine levels (T3) were 66.4 +/- 18.7 ng/dL (NR = 45 to 137 ng/dL) and five patients (14.2%) had levels lower than normal (33.8 +/- 9 ng/dL). Mean thyroxine levels (T4) (NR= 4.5 to 12.5 micro g/dL) were 7.4 +/- 1.7 micro g/dL and two patients (5.6%) had levels lower than normal. Thyroglobulin and microsomal antibodies were not detectable. CONCLUSIONS: In the first 24 hours following ictus, the hormonal changes may be due to the stress produced by the intracranial bleeding; thyroid hormone alterations suggest that patients with subarachnoid hemorrhage might have an euthyroid sick syndrome.     

颅内动脉瘤致蛛网膜下腔出血合并慢性脑积水治疗体会

自发性的蛛网膜下腔出血(subarachnoid hemorrhage,SAH)80%为颅内动脉瘤破裂所引起[1].本病死亡率与致残率均较高,其预后影响因素主要为脑积水的出现、再出血、血管痉挛和继发性缺血的发生等.慢性脑积水是较为常见的并发症,可导致患者明显的神经功能损害,加速病情进展.由于此时脑积水的发病机制复杂,临床表现多样,早期的发现和治疗十分困难,而导致患者预后不良[1,2].     

Spontaneous disappearance of an intracranial aneurysm after subarachnoid hemorrhage.

Spontaneous disappearance of an intracranial aneurysm after subarachnoid hemorrhage is an uncommon event and usually associated with severe cerebral vasospasm, giant aneurysms or the use of antifibrinolytics. We present a young woman who suffered a grade 5 subarachnoid hemorrhage with severe vasospasm caused by a small anterior communicating artery aneurysm. The patient underwent a slow recovery and two years later requested surgery. Angiography demonstrated complete disappearance of the aneurysm. The neurosurgeon should be aware that spontaneous thrombosis of cerebral aneurysms can occur and ensure that angiography is repeated when surgery is significantly delayed.     

Clipping versus coiling for ruptured intracranial aneurysms after the international subarachnoid aneurysm trial. United Kingdom experience

The International Subarachnoid Aneurysm Trial (ISAT) was designed as the first multi-central international prospective randomized trial aiming to compare the safety and efficacy of the 2 available treatments for ruptured intracranial aneurysms; endovascular coiling and surgical clipping. The initial results were published in the Lancet (2002), and it showed clearly a superiority of coiling over clipping in the treatment of ruptured intracranial aneurysms; 22.7% of coiled patients were dependent or dead compared with 30.6% in the surgical group with absolute risk reduction of 6.9%. The results of the ISAT drew huge attention from both scientific authorities and lay media. Despite criticisms, the study has made a significant impact on the treatment of aneurysmal subarachnoid hemorrhage, especially in the United Kingdom and Europe. Since their initial results, the ISAT group has published further papers and updates covering more interesting results regarding the risks of rebleeding, repeat procedures, epilepsy, and the cost effectiveness of both treatments.     

Tranexamic acid in subarachnoid hemorrhage. A double-blind study

The effects of intravenous tranexamic acid were compared with placebo in 64 patients with subarachnoid hemorrhage. A double-blind procedure was used. One gram of tranexamic acid was given intravenously every 4 hours up to the time of operation on an intracranial arterial aneurysm or for up to 21 days after the first bleeding if operative treatment was not feasible. There were no differences in re-bleeds, morbidity or mortality between the tranexamic and placebo-treated groups. No thromboembolic complications were noted in either group. Our results do not support the use of tranexamic acid in subarachnoid hemorrhage in daily doses of 6 g.     

Lipids metabolism of the patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm, in comparison with other cerebrovascular diseases

Lipids metabolism has been extensively studied in the large number of patients with hypertensive cerebral hemorrhage or cerebral infarction, however, the patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm were customarily excluded from the study. Total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride and atherogenic index were determined in 40 cases, who had undergone surgical treatment for ruptured intracranial aneurysm in various locations, and the results were compared with the data obtained from 20 operative cases with hypertensive cerebral hemorrhage, 40 cases with non-operative cases with hypertensive cerebral hemorrhage, 60 cases with cerebral infarction and 20 cases of cerebral lesions other than cerebrovascular disease (non-CVA). Serum levels of LDL-cholesterol and atherogenic index were significantly correlated with the preoperative grading of subarachnoid hemorrhage when compared with non-CVA (p less than 0.05). Total cholesterol, LDL-cholesterol and atherogenic index were well correlated with operative morbidity and active daily life (ADL) in the follow-up study of the patients with intracranial aneurysm, where the higher value of cholesterol indicated the poorer risk of the patients. In our present study, none of the data was found significant, when compared with non-CVA, in the other groups of cerebrovascular diseases except for the HDL-cholesterol, which was found significantly in low level in the group of cerebral infarction (p less than 0.001). Triglyceride was found elevated in the group of hypertensive hemorrhage indicating negative correlation to the severity, and rather similar pattern was seen in the subarachnoid hemorrhage, however, the data were not conclusive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fibrinolytic activity in blood and cerebrospinal fluid in subarachnoid hemorrhage from ruptured intracranial saccular aneurysm before and during EACA treatment

10 patients suffering from intracranial aneurysm causing subarachnoid hemorrhage (SAH) have been treated during the acute pre-and postoperatory phase with omega-aminocaproic acid. The blood and the cerebrospinal fluid of the treated patients have been analyzed in order to study fibrin(ogen) degradation products (FDP) and fibrinolytic activity (FA). The results so obtained show only an alteration of local fibrinolytic processes either inside or around the aneurysmatic clot: there were no alterations of the systemic FA. Furthermore, monitoring of FDP and FA was a very useful tool in those patients who took advantage of the treatment with omega-aminocaproic acid which protected them from rebleeding.     

Subarachnoid hemorrhage from ruptured intracranial aneurysm and surgical procedures as a cause of neuropsychological disorders

The results of preoperative and postoperative examinations in 30 patients operated on for ruptured intracranial aneurysm are reported. The examinations included neuropsychological, neurological and EEG assessment. The agreements and divergencies in the assessment of the condition of the patients by these methods were analysed suggesting the necessity of consideration of psychological disturbances as a consequence of the disease in the general evaluation of the therapeutic results in such cases.     

Rebleeding during transport of patients with a ruptured intracranial aneurysm.

Although many reports have described the rebleeding risk of the ruptured aneurysm in already hospitalized patients, there are only a few reports that have addressed the incidence of rebleeding in these patients before hospitalization. To improve the prognosis of patients with a ruptured intracranial aneurysm, it seems very important to know the incidence of rebleeding before hospitalization. We focused on changes in the computed tomographic (CT) scans and neurological findings at the primary hospital and our institution in 366 patients with ruptured aneurysms who were transferred on the day of the initial hemorrhage, and studied the rebleeding rates in these patients. In 73 (19.9%), we confirmed that rebleeding from the ruptured aneurysm had occurred during transport. The incidence of rebleeding in the prehospitalized patients with a ruptured aneurysm is supposed to by very high. Appropriate medical countermeasures for prevention of rebleeding in prehospitalized patients are crucial to decrease the overall mortality and morbidity rate of intracranial aneurysm.