Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial

BACKGROUND AND PURPOSE: Magnesium reverses cerebral vasospasm and reduces infarct volume after experimental subarachnoid hemorrhage (SAH) in rats. We aimed to assess whether magnesium reduces the frequency of delayed cerebral ischemia (DCI) in patients with aneurysmal SAH. METHODS: Patients were randomized within 4 days after SAH. Magnesium sulfate therapy consisted of a continuous intravenous dose of 64 mmol/L per day, to be started within 4 days after SAH and continued until 14 days after occlusion of the aneurysm. The primary outcome DCI (defined as the occurrence of a new hypodense lesion on computed tomography compatible with clinical features of DCI) was analyzed according to the "on-treatment" principle. For the secondary outcome measures "poor outcome" (Rankin >3) and "excellent outcome" (Rankin 0), we used the "intention-to-treat" principle. RESULTS: A total of 283 patients were randomized. Magnesium treatment reduced the risk of DCI by 34% (hazard ratio, 0.66; 95% CI, 0.38 to 1.14). After 3 months, the risk reduction for poor outcome was 23% (risk ratio, 0.77; 95% CI, 0.54 to 1.09). At that time, 18 patients in the treatment group and 6 in the placebo group had an excellent outcome (risk ratio, 3.4; 95% CI, 1.3 to 8.9). CONCLUSIONS: This study suggests that magnesium reduces DCI and subsequent poor outcome, but the results are not yet definitive. A next step should be a phase III trial to confirm the beneficial effect of magnesium therapy, with poor outcome as primary outcom

Focus on the management of thunderclap headache: from nosography to treatment

Thunderclap headache (TCH) is an excruciating headache characterized by a very sudden onset. Recognition and accurate diagnosis of TCH are important in order to rule out the various, serious underlying brain disorders that, in a high percentage of cases, are the real cause of the headache. Primary TCH, which may recur intermittently and generally has a spontaneous, benign evolution, can thus be diagnosed only when all other potential underlying causes have been excluded through accurate diagnostic work up. In this review, we focus on the management of TCH, paying particular attention to the diagnostic work up and treatment of the condition

Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage

We studied 28 patients with subarachnoid hemorrhage and normal angiograms. On early CT (within 5 days) in 13 cases, blood was seen mainly or only in the cisterns around the midbrain. This pattern of hemorrhage was found in only 1 of 92 patients with a ruptured aneurysm. None of the unexplained perimesencephalic hemorrhages was associated with intracerebral hematoma or intraventricular hemorrhage. The clinical features also differed from those of aneurysmal hemorrhage; loss of consciousness was rare, and after 3 months, all 13 patients had returned to normal life. The cause of this benign disorder remains elusive, but a venous or capillary source seems likel

Causes of acute deterioration in patients with a ruptured intracranial aneurysm. A prospective study with serial CT scanning

The authors studied the acute neurological deterioration in 150 patients with aneurysmal hemorrhage. These patients were closely observed for a 4-week period or until death or operation. Forty-six patients suffered a total of 62 episodes of deterioration that developed within 5 minutes after aneurysm rupture; 59 of these episodes consisted of severe impairment of consciousness. Computerized tomography (CT) was performed within a few hours of the event. Serial scans were obtained at least weekly after admission. Rebleeding was diagnosed as the cause of 42 episodes (68%), including six patients who died rapidly without a repeat CT scan. The final diagnosis of the cause in other acute episodes was epilepsy (in six), acute onset of ischemia (in three), and ventricular fibrillation (in one). Ten unexplained events occurred in nine patients. Rebleeding could be excluded with confidence in nine of these events, because the residual clots had disappeared or markedly decreased on CT. It is concluded that a purely clinical diagnosis of rebleeding will be incorrect in about every third patient, even if these patients are under close observatio

Rerupture of intracranial aneurysms: a clinicoanatomic study

In a series of 176 prospectively studied patients who survived for at least 24 hours after aneurysmal subarachnoid hemorrhage, 39 had at least one computerized tomography (CT)-proven rebleed within 4 weeks after the first rupture. There were peaks in the incidence of rebleeding at the end of the 2nd and 3rd weeks. Sudden loss of consciousness occurred in 35 patients, preceded in one-third of them by headache. A sudden increase in headache was a symptom of rebleeding in only one patient. Loss of brain-stem reflexes was recorded in 13 patients, respiratory arrest in six, and both symptoms in eight patients. Apnea was temporary in 11 patients. Rebleeding occurred as gross intraventricular hemorrhage in 20 patients, as a space-occupying hematoma in four, as both types of hemorrhage in three, and as a purely subarachnoid hemorrhage in 12. The location of the rebleed could not be inferred from the clinical features. Rebleeding was fatal in 51% of cases (two of 12 patients with a purely subarachnoid hemorrhage, and 18 of the other 27 patients (p less than 0.005)). The risk of rebleeding could not be predicted from the patients' clinical condition on admission or from the amount of subarachnoid blood identified on the initial CT scan. The risk of further rebleeding was significantly increased in survivors of a first rebleed (47%: p less than 0.01). Only seven (18%) of the 39 patients with rebleeding had survived at 3 months after the initial hemorrhag