Brain Monitoring in Critically Neurologically Impaired Patients

Abstract

Assessment of neurologic injury and the evolution of severe neurologic injury is limited in comatose or critically ill patients that lack a reliable neurologic examination. For common yet severe pathologies such as the comatose state after cardiac arrest, aneurysmal subarachnoid hemorrhage (aSAH), and severe traumatic brain injury (TBI), critical medical decisions are made on the basis of the neurologic injury. Decisions regarding active intensive care management, need for neurosurgical intervention, and withdrawal of care, depend on a reliable, high-quality assessment of the true state of neurologic injury, and have traditionally relied on limited assessments such as intracranial pressure monitoring and electroencephalogram. However, even within TBI there exists a spectrum of disease that is likely not captured by such limited monitoring and thus a more directed effort towards obtaining a more robust biophysical signature of the individual patient must be undertaken. In this review, multimodal monitoring including the most promising serum markers of neuronal injury, cerebral microdialysis, brain tissue oxygenation, and pressure reactivity index to access brain microenvironment will be discussed with their utility among specific pathologies that may help determine a more complete picture of the neurologic injury state for active intensive care management and long-term outcomes. Goal-directed therapy guided by a multi-modality approach appears to be superior to standard intracranial pressure (ICP) guided therapy and should be explored further across multiple pathologies. Future directions including the application of optogenetics to evaluate brain injury and recovery and even as an adjunct monitoring modality will also be discussed.

Reduced Neuroinflammation and Improved Functional Recovery after Traumatic Brain Injury by Prophylactic Diet Supplementation in Mice

“…Initial treatment for patients with TBI targets the secondary injury to minimize the injury and additional loss of “healthy” brain tissue, to limit the stimulation of pro-inflammatory mechanisms, and to minimize the consequences of these cascades [ 34 , 35 , 36 ]. The limited approach to therapeutic strategies includes continuous monitoring of intracranial pressure, arterial hypotension, hypoxemia, and thromboembolic complications following TBI [ 37 , 38 ]. The impact of nutrition and the effects on the short- and long-term outcomes of mild and severe traumatic brain injuries have been disregarded for a long time [ 39 , 40 ].…”

Neuroprotection of Glibenclamide against Brain Injury after Cardiac Arrest via Modulation of NLRP3 Inflammasome

“…Current clinical treatments include many mechanism-driven therapies, like hypothermia, that aim to improve the survival rate and neurological recovery after CA. We have previously developed multimodal monitoring including neurophysiological signal and CBF recording, to evaluate the hypoxia-induced cerebral damage, and to track brain injury and recovery after CA [4][5][6][7]. Electroencephalography (EEG) is an important method to predict the prognosis of hypoxicischemic brain damage based on its real-time evaluation of neurological function.…”

Effects of clazosentan, cilostazol, and statins on aneurysmal subarachnoid hemorrhage

“…[ 8 , 9 ] In the United States, approximately 30,000 people suffer from aSAH each year, with a mortality rate of nearly 50%. [ 10 , 11 ] Globally, the mortality of aSAH is about 40%, [ 12 ] which seriously threatens human life and health.…”