Neuro-imaging in intracerebral hemorrhage: updates and knowledge gaps.

Intracerebral hemorrhage (ICH) is characterized by hematoma development within the brain's parenchyma, contributing significantly to the burden of stroke. While non-contrast head computed tomography (CT) remains the gold standard for initial diagnosis, this review underscores the pivotal role of magnetic resonance imaging (MRI) in ICH management. Beyond diagnosis, MRI offers invaluable insights into ICH etiology, prognosis, and treatment. Utilizing echo-planar gradient-echo or susceptibility-weighted sequences, MRI demonstrates exceptional sensitivity and specificity in identifying ICH, aiding in differentiation of primary and secondary causes. Moreover, MRI facilitates assessment of hemorrhage age, recognition of secondary lesions, and evaluation of perihematomal edema progression, thus guiding tailored therapeutic strategies. This comprehensive review discusses the multifaceted utility of MRI in ICH management, highlighting its indispensable role in enhancing diagnostic accuracy as well as aiding in prognostication. As MRI continues to evolve as a cornerstone of ICH assessment, future research should explore its nuanced applications in personalized care paradigms.

Case report: Invasive neuromonitoring in status epilepticus induced hypoxic ischemic brain injury.

Objectives: Literature on invasive neuromonitoring and bilateral decompressive craniectomies (BDC) in patients with refractory status epilepticus (RSE)-mediated hypoxic-ischemic brain injury (HIBI) is limited. Neuromonitoring can guide decision making and treatment escalation. Methods and results: We report a case of a 17 years-old male who was admitted to our hospital's intensive care unit for RSE. HIBI was detected on neuroimaging on this patient's second day of admission after he developed central diabetes insipidus (DI). Invasive neuromonitoring revealed raised intracranial pressure (ICP) and brain hypoxia as measured by reduced brain tissue oxygen tension (PbtO2). Treatments were escalated in a tiered fashion, including administration of hyperosmolar agents, analgesics, sedatives, and a neuromuscular blocking drug. Eventually, BDC was performed as a salvage therapy as a means of controlling refractory ICP crisis in the setting of diffuse cerebral edema (DCE) following HIBI. Discussion: SE-mediated HIBI can result in refractory ICP crisis. Neuromonitoring can help identify secondary brain injury (SBI), guide treatment strategies, including surgical interventions, and may lead to better outcomes.

Safety and efficacy of peripheral nerve blocks to treat refractory headaches after aneurysmal subarachnoid hemorrhage - A pilot observational study.

Objectives: Headache after aneurysmal subarachnoid hemorrhage (HASH) is common, severe, and often refractory to conventional treatments. Current treatment standards include medications including opioids, until the pain is mitigated. Peripheral nerve blocks (PNBs) may be an effective therapeutic option for HASH. We conducted a small before-and-after study of PNBs to determine safety, feasibility, and efficacy in treatment of HASH. Methods: We conducted a pilot before-and-after observational study and collected data for 5 patients in a retrospective control group and 5 patients in a prospective intervention PNB group over a 12-month period. All patients received a standard treatment of medications including acetaminophen, magnesium, gabapentin, dexamethasone and anti-spasmodics or anti-emetics as needed. Patients in the intervention group received bilateral greater occipital, lesser occipital, and supraorbital PNBs in addition to medications. The primary outcome was pain severity, measured by Numeric pain rating scale (NPRS). All patients were followed for 1 week following enrollment. Results: The mean ages in the PNB group and control group were 58.6 and 57.4, respectively. One patient in the control group developed radiographic vasospasm. Three patients in both groups had radiographic hydrocephalus and IVH, requiring external ventricular drain (EVD) placement. The PNB group had an average reduction in mean raw pain score of 2.76 (4.68, 1.92 p = 0.024), and relative pain score by 0.26 (0.48, 0.22 p = 0.026), compared to the control group. The reduction occurred immediately after PNB administration. Conclusion: PNB can be a safe, feasible and effective treatment modality for HASH. Further investigations with a larger sample size are warranted.

Neuromonitoring in Critically Ill Patients.

OBJECTIVES: Critically ill patients are at high risk of acute brain injury. Bedside multimodality neuromonitoring techniques can provide a direct assessment of physiologic interactions between systemic derangements and intracranial processes and offer the potential for early detection of neurologic deterioration before clinically manifest signs occur. Neuromonitoring provides measurable parameters of new or evolving brain injury that can be used as a target for investigating various therapeutic interventions, monitoring treatment responses, and testing clinical paradigms that could reduce secondary brain injury and improve clinical outcomes. Further investigations may also reveal neuromonitoring markers that can assist in neuroprognostication. We provide an up-to-date summary of clinical applications, risks, benefits, and challenges of various invasive and noninvasive neuromonitoring modalities. DATA SOURCES: English articles were retrieved using pertinent search terms related to invasive and noninvasive neuromonitoring techniques in PubMed and CINAHL. STUDY SELECTION: Original research, review articles, commentaries, and guidelines. DATA EXTRACTION: Syntheses of data retrieved from relevant publications are summarized into a narrative review. DATA SYNTHESIS: A cascade of cerebral and systemic pathophysiological processes can compound neuronal damage in critically ill patients. Numerous neuromonitoring modalities and their clinical applications have been investigated in critically ill patients that monitor a range of neurologic physiologic processes, including clinical neurologic assessments, electrophysiology tests, cerebral blood flow, substrate delivery, substrate utilization, and cellular metabolism. Most studies in neuromonitoring have focused on traumatic brain injury, with a paucity of data on other clinical types of acute brain injury. We provide a concise summary of the most commonly used invasive and noninvasive neuromonitoring techniques, their associated risks, their bedside clinical application, and the implications of common findings to guide evaluation and management of critically ill patients. CONCLUSIONS: Neuromonitoring techniques provide an essential tool to facilitate early detection and treatment of acute brain injury in critical care. Awareness of the nuances of their use and clinical applications can empower the intensive care team with tools to potentially reduce the burden of neurologic morbidity in critically ill patients.

Severe Wernicke's Encephalopathy Associated with Cortical Ribboning and Intracranial Hemorrhage.

Wernicke's encephalopathy (WE) is a neurological emergency that results from thiamine deficiency. It is most commonly associated with chronic alcohol consumption but can result from any cause of impaired thiamine absorption or dietary intake. The classic triad of ophthalmoparesis, ataxia, and altered sensorium is rarely seen in toto, and while certain radiographic findings strongly correlate with the disease, one should have a low threshold to suspect (and promptly treat) patients in order to mitigate the risk of morbidity and mortality. However, atypical presentations can result in delayed or missed diagnoses. In this report, we describe a case of severe non-alcoholic WE associated with atypical brain Magnetic resonance imaging (MRI) manifestations of both cortical diffusion restriction and intracranial hemorrhage, which have previously been associated with poor outcomes. Early treatment with high-dose parenteral thiamine resulted in rapid improvement in ocular motility and reversal of MRI abnormalities, and on long-term follow up, the patient had made a marked functional improvement. This case highlights the importance of recognizing these unusual imaging features of WE in a patient with a compatible clinical syndrome in order to make a timely diagnosis and initiate treatment, as there is potential for a good clinical outcome despite these imaging findings.

Hierarchical Cluster Analysis Identifies Distinct Physiological States After Acute Brain Injury.

BACKGROUND: Analysis of intracranial multimodality monitoring data is challenging, and quantitative methods may help identify unique physiological signatures that inform therapeutic strategies and outcome prediction. The aim of this study was to test the hypothesis that data-driven approaches can identify distinct physiological states from intracranial multimodality monitoring data. METHODS: This was a single-center retrospective observational study of patients with either severe traumatic brain injury or high-grade subarachnoid hemorrhage who underwent invasive multimodality neuromonitoring. We used hierarchical cluster analysis to group hourly values for heart rate, mean arterial pressure, intracranial pressure, brain tissue oxygen, and cerebral microdialysis across all included patients into distinct groups. Average values for measured physiological variables were compared across the identified clusters, and physiological profiles from identified clusters were mapped onto physiological states known to occur after acute brain injury. The distribution of clusters was compared between patients with favorable outcome (discharged to home or acute rehab) and unfavorable outcome (in-hospital death or discharged to chronic nursing facility). RESULTS: A total of 1704 observations from 20 patients were included. Even though the difference in mean values for measured variables between patients with favorable and unfavorable outcome were small, we identified four distinct clusters within our data: (1) events with low brain tissue oxygen and high lactate-to-pyruvate ratio-values (consistent with cerebral ischemia), (2) events with higher intracranial pressure values without evidence for ischemia (3) events which appeared to be physiologically "normal," and (4) events with high cerebral lactate without brain hypoxia (consistent with cerebral hyperglycolysis). Patients with a favorable outcome had a greater proportion of cluster 3 (normal) events, whereas patients with an unfavorable outcome had a greater proportion of cluster 1 (ischemia) and cluster 4 (hyperglycolysis) events (p < 0.0001, Fisher-Freeman-Halton test). CONCLUSIONS: A data-driven approach can identify distinct groupings from invasive multimodality neuromonitoring data that may have implications for therapeutic strategies and outcome predictions. These groupings could be used as classifiers to train machine learning models that can aid in the treatment of patients with acute brain injury. Further work is needed to replicate the findings of this exploratory study in larger data sets.

Cerebrovascular pressure reactivity and intracranial pressure are associated with neurologic outcome after hypoxic-ischemic brain injury.

AIM: We evaluated the association of physiological parameters measured by intracranial multimodality neuromonitoring with neurologic outcome in a consecutive series of patients with hypoxic-ischemic brain injury (HIBI). METHODS: We retrospectively identified all patients with HIBI who underwent combined invasive intracranial pressure (ICP) and brain tissue oxygen (PbtO2) monitoring over a 3 year period. Cerebrovascular pressure reactivity index (PRx) was calculated continuously as a surrogate of cerebral autoregulation. Favorable outcome was defined as recovery of consciousness (Glasgow Coma Scale motor score = 6). Differences in mean ICP, PRx and PbtO2 for the entire monitoring period across outcomes were measured. Logistic regression and area under receiver operating characteristic (AUROC) curve were used to assess the association of each monitoring parameter with neurologic outcome. RESULTS: We analyzed data from 36 patients. Most (89%) had an antecedent sudden cardiac arrest. Favorable outcome occurred in 8 (22%) patients. ICP and PRx were higher in patients with unfavorable outcome (ICP: 26 ±â€¯4.1 mmHg vs 7.5 ±â€¯2 mmHg, p = 0.0002; PRx: 0.51 ±â€¯0.05 vs 0.11 ±â€¯0.05, p < 0.0001). There was no significant difference in PbtO2 between groups (unfavorable: 20 ±â€¯2.4 mmHg vs favorable: 25 ±â€¯1.5 mmHg, p = 0.12). Both ICP (AUROC 0.84, 95%CI 0.72-0.98, p = 0.003) and PRx (AUROC 0.94, 95%CI 0.85-1, p = 0.0002) discriminated between favorable and unfavorable outcome, in contrast to PbtO2, (AUROC 0.59, 95%CI 0.39-0.78, p = 0.52). ICP > 15 mmHg, PRx > 0.2, and PbtO2 < 18 mmHg had sensitivity/specificity of 68%/100%, 89%/88%, and 40%/100% respectively for discriminating outcomes. CONCLUSION: Cerebrovascular pressure reactivity and intracranial pressure appear to be associated with neurologic outcome in patients with HIBI.

Physiological Signatures of Brain Death Uncovered by Intracranial Multimodal Neuromonitoring.

BACKGROUND: The physiological and neurochemical changes that accompany brain death are not well described. MATERIALS AND METHODS: A retrospective observational study of patients with acute brain injury who underwent intracranial multimodality neuromonitoring between October 2015 and June 2018. Patients were included for analysis either if brain death was diagnosed or refractory intracranial hypertension with persistent equalization of intracranial pressure (ICP) and mean arterial pressure (MAP) developed. RESULTS: Of 114 patients who underwent invasive neuromonitoring, 11 cases with MAP/ICP equalization were identified. Of those, 9 were declared brain dead based on accepted national and institutional criteria. An additional 2 cases with MAP/ICP equalization who died after withdrawal of life-sustaining therapies were identified. Of the 11 identified patients, 10 had continuous monitoring data available for analysis. Cerebral microdialysis data were available for 4 patients.In the 10 cases with available continuous data, ICP/MAP equalization was associated with marked reduction of cerebral blood flow and brain tissue oxygen tension to near zero levels as well as a significant decrease in brain temperature compared with body temperature. In the 4 patients with microdialysis monitoring, ICP/MAP equalization resulted in a near complete depletion of cerebral glucose and pyruvate, as well as a marked rise in cerebral glycerol. Finally, ICP/MAP equalization was accompanied by complete loss of cerebrovascular pressure reactivity, decrease in intracranial pulse pressure, and a paradoxical improvement of ICP waveform morphology. CONCLUSIONS: A characteristic set of changes in cerebrovascular physiology and neurochemistry occurs during brain death. These changes can be identified by intracranial neuromonitoring.

Defining a Taxonomy of Intracranial Hypertension: Is ICP More Than Just a Number?

Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension.

Differential effects of phosphodiesterase PDE-3/PDE-4-specific inhibitors on vasoconstriction and cAMP-dependent vasorelaxation following balloon angioplasty.

It is known that cAMP and cGMP are important for vasorelaxation, and cyclic nucleotide phosphodiesterases (PDEs) regulate their levels. Balloon angioplasty (BAL) is associated with reduced cAMP and cGMP levels, and inhibition of PDE-3 reduces restenosis. In this study, we found that BAL increased PDE-3 activity, which affected vasoreactivity of rat aortic rings 24-h post-BAL; these were compared with intact (INT) and ex vivo endothelium-denuded rings (RUB) from sham rats. In BAL and RUB rings, vasorelaxant responses to ACh were abolished. The EC(50) for phenylephrine (PE) was 1.8-fold less in RUB than in INT or BAL, whereas the maximal contractile effect of PE was greater in BAL than in INT or RUB. PDE-3 inhibitors reduced the maximal response to PE by >65% in BAL compared with 10-30% in INT and RUB; the reduction of the maximal response to U-46619 was 37% in BAL compared with 8% in INT with no reduction in RUB. PDE-4 inhibitors reduced PE-induced tone by <30% in an endothelium-dependent manner. Vasorelaxant responses to agonists that utilize cAMP were greatly impaired in BAL and RUB rings, and inhibition of PDE-3 enhanced the vasorelaxant responses in BAL or RUB. Inhibition of PDE-4 increased vasorelaxant responses to isoproterenol (ISO) to a much lesser degree. Thus PDE-3 and PDE-4 inhibitors exhibited differential effects on PE-induced tone and vasorelaxant responses to ISO. Inhibition of PDE-3 also produced a greater increase in cAMP in BAL than INT or RUB rings. These results suggest that increased PDE-3 activity after BAL may promote a vasospastic state and that the reduction in cAMP may, possibly, influence vessel remodeling.