Raised intracranial pressure and seizures in the neurological intensive care unit

Abstract

BackgroundThe relationship between changes in intracranial pressure and incidence of subclinical seizures in patients requiring neurological intensive care is not fully understood. The aim of this study was to investigate if acute increases in intracranial pressure were accompanied by subclinical seizures.MethodsWe prospectively studied 17 intensive care patients (11 male, aged 3–66 yr) who were selected from 85 patients requiring intracranial pressure measurement. Patients were selected to have a 30 min, 16-channel electroencephalogram (EEG) recorded when intracranial pressure remained increased despite preliminary treatments.ResultsDiagnoses included head injury, intracranial haemorrhage, subarachnoid haemorrhage and sagittal sinus thrombosis. All patients had at least one acute episode of intracranial pressure increase. Pressures ranged from 90 to 440 mm H2O. Encephalopathic features (delta/theta rhythms and burst suppression) were noted on all EEGs. No seizure activity was recorded.ConclusionsWe conclude from this pilot study that seizures are an uncommon cause of acute raised intracranial pressure. To determine whether raised intracranial pressure causes seizures, long-term monitoring in a large cohort of intensive care patients would be necessary, studying patients with similar diagnoses and ages. The relationship between changes in intracranial pressure and incidence of subclinical seizures in patients requiring neurological intensive care is not fully understood. The aim of this study was to investigate if acute increases in intracranial pressure were accompanied by subclinical seizures. We prospectively studied 17 intensive care patients (11 male, aged 3–66 yr) who were selected from 85 patients requiring intracranial pressure measurement. Patients were selected to have a 30 min, 16-channel electroencephalogram (EEG) recorded when intracranial pressure remained increased despite preliminary treatments. Diagnoses included head injury, intracranial haemorrhage, subarachnoid haemorrhage and sagittal sinus thrombosis. All patients had at least one acute episode of intracranial pressure increase. Pressures ranged from 90 to 440 mm H2O. Encephalopathic features (delta/theta rhythms and burst suppression) were noted on all EEGs. No seizure activity was recorded. We conclude from this pilot study that seizures are an uncommon cause of acute raised intracranial pressure. To determine whether raised intracranial pressure causes seizures, long-term monitoring in a large cohort of intensive care patients would be necessary, studying patients with similar diagnoses and ages.