Neurophysiologic monitoring in the neuroscience intensive care unit.
Neurologically critically ill patients, more often than others, are unable to communicate and, for a crucial period of time, have the vital functions of their brains hidden in the "black box" of the cranial vault behind a curtain of ambiguity and immobility. Customarily--and naively--we have relied upon beside clinical observations to pierce these barriers. Recent insights lead us to conclude that these "neurochecks" no longer suffice. This article has surveyed four major monitoring systems relied upon by neurointensivists to evaluate the pathophysiology of their patients. Of these, ICPM has the longest clinical track record. It provides a quantitative measure of the brain's capacity to withstand ICP and helps us monitor interventions to reduce it. To utilize this information intelligently requires an understanding of the principles of ICC, CPP, ICP wave morphology, and the hardware available. NICU-CEEG is a more recent introduction but, in principle, it transfers from the laboratory and operating suite to the ICU bedside, established correlations among electrophysiology, CBF, and CM. Digital EEG has allowed us to overcome significant logistical barriers and made NICU-CEEG a practical ICU tool. Early but impressive data suggest that NICU-CEEG has a significant clinical impact in patients with ACI, uncontrolled seizures, or coma. It also has revealed that NICU patients have a surprisingly high incidence of NCS, which may adversely affect their outcome. TCD has contributed greatly to diagnosis and management of SAH vasospasm. It also can be applied with benefit to patients with increased ICP, and has promising value in patients with ACI. It may prove beneficial in monitoring unstable cerebral embolization. Several bedside methods for monitoring CBF are available, but they require refinement to become true monitoring systems. These methods have revealed clinically important insights in patients with head trauma, SAH vasospasm, and ACI. Methods for directly monitoring CM and CMRo2 are improving our understanding of the brain's responses to injury, and becoming increasingly relevant to bedside management. SjvO2 can detect cerebral ischemia caused by overzealous hyperventilation and accelerated ICP. ICO holds promise as a noninvasive transcranial method for assessing Scvo2. We soon may see a scalp array of such detectors, similar to an EEG "montage," that allows us to assess multiregional Scvo2. To be useful, a clinical method should raise questions for further investigation. If the neurophysiologic monitoring systems described here provide us with some answers and lead us to ask useful new questions, they will prove their benefit to our patients.
D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D002533:Cerebral Angiography; D002560:Cerebrovascular Circulation; D003128:Coma / Q000209:etiology / Q000503:physiopathology; D003422:Critical Care; D004453:Echoencephalography; D004569:Electroencephalography; D004827:Epilepsy / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007427:Intracranial Pressure; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000503:physiopathology; D008875:Middle Aged; D010092:Oximetry; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D014057:Tomography, X-Ray Computed; D017585:Ultrasonography, Doppler, Transcranial