a-bedside-single-burr-hole-approach-to-multimodality-monitoring

A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury

Intracranial pressure (ICP) monitoring is a cornerstone of the intensive care management of patients with severe acute brain injuries, including traumatic ...

University of Cincinnati

We conducted a survey of providers to assess for practice patterns in diagnosing and treating new-onset refractory status epilepticus (NORSE). NORSE is the occurrence of prolonged seizures that are not responsive to initial therapies in otherwise healthy individuals without obvious cause on initial presentation. This entity is thought to have multiple etiologies, including autoimmune.

Survey of the diagnostic and therapeutic approach to new-onset refractory status epilepticus.

Subarachnoid hemorrhage (SAH) is a devastating form of stroke. Approximately one in four patients develop progressive neurological deterioration and silent infarction referred to as delayed cerebral ischemia (DCI). DCI is a complex, multifactorial secondary brain injury pattern and its pathogenesis is not fully understood. We aimed to study the relationship between cerebral blood flow (CBF) and neuronal activity at both the cortex and in scalp using electroencephalography (EEG) in poor-grade SAH patients undergoing multimodality intracranial neuromonitoring. Twenty patients were included, of whom half had DCI median 4.7 days (interquartile range (IQR): 4.0-5.6) from SAH bleed. The rate of decline in regional cerebral blood flow (rCBF) was significant in both those with and without DCI and occurred between days 4 and 7 post-SAH. The scalp EEG alpha-delta ratio declined early in those with DCI. In the group without DCI, CBF and cortical EEG alpha-delta ratio were correlated (r = 0.53; p <  0.01) and in the group without DCI, inverse neurovascular coupling was observed at CPP <  80 mmHg. We found preliminary evidence that as patients enter the period of highest risk for the development of DCI, the absence of neurovascular coupling may act as a possible pathomechanism in the development of ischemia following SAH.

Intracortical electrophysiological correlates of blood flow after severe SAH: A multimodality monitoring study.

Coagulopathy and platelet dysfunction commonly develop after traumatic brain injury (TBI). Thromboelastography (TEG) and platelet function assays (PFAs) are often performed at the time of admission; however, their roles in assessing post-TBI coagulopathy have not been investigated. We hypothesized that compared to blunt TBI, penetrating TBI would (1) demonstrate greater coagulopathy by TEG, (2) be associated with abnormal PFA results, and (3) require more blood product transfusions.

Relationship of Coagulopathy and Platelet Dysfunction to Transfusion Needs After Traumatic Brain Injury.

Benign meningiomas uncommonly lead to significant cerebral edema, with only a few cases previously reported in the medical literature. The present study describes the case of a 49-year-old female who had a meningioma resection. She subsequently developed malignant cerebral edema and had episodes that were initially concerning for seizure activity. However, transient blood flow changes concerning for intracranial pressure (ICP) crises, were demonstrated on electroencephalogram (EEG) as well as noninvasive cerebral blood flow monitoring. The present case highlights the importance of close monitoring in patients with post meningioma resection cerebral edema because of the possibility of ICP crises.

Blood Flow and Continuous EEG Changes during Symptomatic Plateau Waves.

Restoring the circulation is the primary goal in emergency treatment of cerebral ischemia. However, better understanding of how the brain responds to energy depletion could help predict the time available for resuscitation until irreversible damage and advance development of interventions that prolong this span. Experimentally, injury to central neurons begins only with anoxic depolarization. This potentially reversible, spreading wave typically starts 2 to 5 minutes after the onset of severe ischemia, marking the onset of a toxic intraneuronal change that eventually results in irreversible injury.

Terminal spreading depolarization and electrical silence in death of human cerebral cortex.

Elevated intracranial pressure (ICP) following brain injury contributes to poor outcomes for patients, primarily by reducing the caliber of cerebral vasculature, and thereby reducing cerebral blood flow. Careful monitoring of ICP is critical in these patients in order to determine prognosis, implement treatment when ICP becomes elevated, and to judge responsiveness to treatment. Currently, the gold standard for monitoring is invasive pressure transducers, usually an intraventricular monitor, which presents significant risk of infection and hemorrhage. These risks made discovering non-invasive methods for monitoring ICP and cerebral perfusion a priority for researchers. Herein we sought to review recent publications on novel minimally invasive multi-modality monitoring techniques that provide surrogate data on ICP, cerebral oxygenation, metabolism and blood flow. While limitations in various forms preclude them from supplanting the use of invasive monitors, these modalities represent useful screening tools within our armamentarium that may be invaluable when the risks of invasive monitoring outweigh the associated benefits.

Novel minimally invasive multi-modality monitoring modalities in neurocritical care.

Commentary: Detecting Cortical Spreading Depolarization with Full Band Scalp Electroencephalography: An Illusion?

We aimed to provide a systematic description of our 2-year experience using a standardized bedside, single burr hole approach to intracranial multimodality monitoring (MMM) in patients with severe traumatic brain injury (sTBI), focusing on safety and probe reliability.

Safety and Reliability of Bedside, Single Burr Hole Technique for Intracranial Multimodality Monitoring in Severe Traumatic Brain Injury.

The Epilepsy Bioinformatics Study for Anti-epileptogenic Therapy (EpiBioS4Rx) is a longitudinal prospective observational study funded by the National Institute of Health (NIH) to discover and validate observational biomarkers of epileptogenesis after traumatic brain injury (TBI). A multidisciplinary approach has been incorporated to investigate acute electrical, neuroanatomical, and blood biomarkers after TBI that may predict the development of post-traumatic epilepsy (PTE). We plan to enroll 300 moderate-severe TBI patients with a frontal and/or temporal lobe hemorrhagic contusion. Acute evaluation with blood, imaging and electroencephalographic monitoring will be performed and then patients will be tracked for 2 years to determine the incidence of PTE. Validation of selected biomarkers that are discovered in planned animal models will be a principal feature of this work. Specific hypotheses regarding the discovery of biomarkers have been set forth in this study. An international cohort of 13 centers spanning 2 continents will be developed to facilitate this study, and for future interventional studies.

The epilepsy bioinformatics study for anti-epileptogenic therapy (EpiBioS4Rx) clinical biomarker: Study design and protocol.

Traumatic brain injury (TBI) has been associated with adverse mental health outcomes, such as posttraumatic stress disorder (PTSD) and major depressive disorder (MDD), but little is known about factors that modify risk for these psychiatric sequelae, particularly in the civilian sector.

Brandon Foreman

Department of Neurology and Rehabilitation Medicine

University of Cincinnati

A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury

Brandon Foreman

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Neurology and Rehabilitation Medicine

University of Cincinnati

A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury

Department of Neurology and Rehabilitation Medicine