RESUMO
OBJECTIVE: To examine whether the maintenance of elevated magnesium serum concentrations by intravenous administration of magnesium sulfate can reduce the occurrence of cerebral ischemic events after aneurysmal subarachnoid hemorrhage. DESIGN: Prospective, randomized, placebo-controlled study. SETTING: Neurosurgical intensive care unit of a University hospital. INTERVENTIONS: One hundred ten patients were randomized to receive intravenous magnesium sulfate or to serve as controls. Magnesium treatment was started with a bolus of 16 mmol, followed by continuous infusion of 8 mmol/hr. Serum concentrations were measured every 8 hrs, and infusion rates were adjusted to maintain target levels of 2.0-2.5 mmol/L. Intravenous administration was continued for 10 days or until signs of vasospasm had resolved. Thereafter, magnesium was administered orally and tapered over 12 days. MEASUREMENTS AND MAIN RESULTS: Delayed ischemic infarction (primary end point) was assessed by analyzing serial computed tomography scans. Transcranial Doppler sonography and digital subtraction angiography were used to detect vasospasm. Delayed ischemic neurologic deficit was determined by continuous detailed neurologic examinations; clinical outcome after 6 months was assessed using the Glasgow outcome scale. Good outcome was defined as Glasgow outcome scale score 4 and 5.The incidence of delayed ischemic infarction was significantly lower in magnesium-treated patients (22% vs. 51%; p = .002); 34 of 54 magnesium patients and 27 of 53 control patients reached good outcome (p = .209). Delayed ischemic neurologic deficit was nonsignificantly reduced (9 of 54 vs. 15 of 53 patients; p = .149) and transcranial Doppler-detected/angiographic vasospasm was significantly reduced in the magnesium group (36 of 54 vs. 45 of 53 patients; p = .028). Fewer patients with signs of vasospasm had delayed cerebral infarction. CONCLUSION: These data indicate that high-dose intravenous magnesium can reduce cerebral ischemic events after aneurysmal subarachnoid hemorrhage by attenuating vasospasm and increasing the ischemic tolerance during critical hypoperfusion.
Assuntos
Bloqueadores dos Canais de Cálcio/uso terapêutico , Aneurisma Intracraniano/complicações , Sulfato de Magnésio/uso terapêutico , Hemorragia Subaracnóidea/tratamento farmacológico , Vasoespasmo Intracraniano/prevenção & controle , Adulto , Idoso , Bloqueadores dos Canais de Cálcio/administração & dosagem , Feminino , Hospitais Universitários , Humanos , Hipóxia-Isquemia Encefálica/etiologia , Hipóxia-Isquemia Encefálica/prevenção & controle , Infusões Intravenosas , Unidades de Terapia Intensiva , Sulfato de Magnésio/administração & dosagem , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Hemorragia Subaracnóidea/etiologia , Vasoespasmo Intracraniano/etiologiaRESUMO
The Thought Translation Device (TTD) is a brain-computer interface based on the self-regulation of slow cortical potentials (SCPs) and enables completely paralyzed patients to communicate using their brain potentials. Here, an extended version of the TTD is presented that has an auditory and a combined visual and auditory feedback modality added to the standard visual feedback. This feature is necessary for locked-in patients who are no longer able to focus their gaze. In order to test performance of physiological regulation with auditory feedback 54 healthy participants were randomly assigned to visual, auditory or combined visual-auditory feedback of slow cortical potentials. The training consisted of three sessions with 500 trials per session with random assignment of required cortical positivity or negativity in half of the trials. The data show that physiological regulation of SCPs can be learned with auditory and combined auditory and visual feedback although the performance of auditory feedback alone was significantly worse than with visual feedback alone.