Potential role of continuous magnesium infusion to prevent vasospasm and consequent ischaemic deficit correlated to subarachnoid haemorrhage

BACKGROUND: The incidence and treatment of vasospasm remains a crucial problem of clinical practice. Various drugs have failed to demonstrate a significant effect in reducing the incidence of the delayed ischemic deficit (DID) subsequent to subarachnoid hemorrhage (SAH). Magnesium sulfate (MgSO ₄) has been studied as a neuroprotective agent and in the prophylaxis of vasospasm since its use has become routine in the treatment of epilepsy in the course of pre-eclampsia. STUDY OBJECTIVES: To evaluate the effect of continuous MgSO₄ infusion and Nimodipine against Nimodipine alone in the incidence of vasospasm, the cerebral blood flow velocity and the GOS at 3 and 6 months following onset in patients with SAH. PATIENTS AND METHODS: Seventeen patients who had undergone craniotomy following SAH were recruited for analysis. The patients were randomized into two groups, to receive either Nimodipine alone (the N group) or Nimodipine and MgSO₄ continuous infusion until serum levels (in mg/g; the Mg group) doubled physiological concentrations. Patients were followed up for 15 days post SAH and assessed by laboratory assays, Doppler transcranial sonography (TCD), computerized axial tomography (CAT) and single-photon emission computed tomography (SPECT). These findings were recorded together with Glasgow Outcome Scale (GOS) assessment at 3 and 6 months. RESULTS: The incidence of vasospasm (cerebral artery flow velocity >120 cm/s) reached 47 percent and sub-critical vasospasm (flow velocity >80 <120 cm/s) 71 percent with no statistically significant difference between the two groups. Significant (P < 0.05) differences were found for vasospasm incidence (25% in the Mg group vs 80% in the N group) and recorded mean velocity (V_MCA 79cm/s +11 SD in the Mg group vs 92 cm/s +14 SD in the N group) among patients with Fisher grade II. DISCUSSION: No effect of MgSO₄ in reducing blood velocity was recorded at TCD. TCD does not appear to be an appropriate instrument for the analysis of flow velocity in distal cerebral vessels which play an important part in the development of DID. Thus, although a neuroprotective effect of MgSO₄ may not be excluded, further studies are needed in patients with SAH.