The benefits of hypothermia for the treatment of subarachnoid hemorrhage (SAH) remain controversial. In 1999, we initiated brain hypothermia treatment (BHT) in the hyperacute phase to mitigate the evolution of early brain injury in patients with World Federation of Neurological Surgeons (WFNS) grade V SAH. In June 2014, we introduced endovascular cooling to maintain normothermia for seven days following the initial BHT period. Immediately after the decision to treat the sources of bleeding, cooling was initiated, with a target temperature of 33-34°C. Bleeding sources were extirpated primarily by clipping with decompressive craniectomy. Patients were rewarmed at a rate of ≤1°C/day after ≥48 hours of surface cooling. After being rewarmed to 36°C, temperatures were controlled with antipyretic (chronologically divided into groups A-C with 47, 46, and 46 patients, respectively) or endovascular (group D, 38 patients) cooling. Overall, 177 patients (median age, 62 [52-68] years; 94 [53.1%] women; onset-to-arrival time, 36 minutes [28-50]) were included. The median Glasgow Coma Scale (GCS) score upon admission was 4 (3-6). Median core body temperature was 36 (35.3-36.6)°C on arrival, 34.6 (34.0-35.3)°C on entering the operating room, 33.8 (33.4-34.3)°C upon starting the microsurgical or interventional radiology procedure, and 33.7 (33.3-34.2)°C upon admission to the intensive care unit. There were no significant differences in age, sex, GCS score, pupillary findings, location of bleeding sources, or treatment methods. There were 69 (39.0%) overall favorable outcomes (modified Rankin Scale score of 0-3) at 6 months and 11 (23.4%), 18 (39.1%), 17 (37.0%), and 23 (60.5%) in groups A-D, respectively (p = 0.0065). The outcomes of patients with WFNS grade V SAH improved over time. Herein, we report our experience using BHT for severe SAH through a narrative review.

The incidence of aging-related neurodegenerative disorders and neurocritical care diseases is increasing worldwide. Microglia, the main inflammatory cells in the brain, could be potential viable therapeutic targets for treating neurological diseases. Interestingly, mitochondrial functions, including energy metabolism, mitophagy and transfer, fission and fusion, and mitochondrial DNA expression, also change in activated microglia. Notably, mitochondria play an active and important role in the pathophysiology of neurodegenerative disorders and neurocritical care diseases. This review briefly summarizes the current knowledge on mitochondrial dysfunction in microglia in neurodegenerative disorders and neurocritical care diseases and comprehensively discusses the prospects of the application of neurological injury prevention and treatment targets by mitochondria.

Background: The protocols and therapeutic guidance established for treating traumatic brain injury (TBI) in neurointensive care focus on managing cerebral blood flow (CBF) and brain tissue oxygenation based on pressure signals. The decision support process relies on assumed relationships between cerebral perfusion pressure (CPP) and blood flow, pressure-flow relationships (PFRs), and shares this framework of assumptions with mathematical intracranial hemodynamics models. These foundational assumptions are difficult to verify, and their violation can impact clinical decision-making and model validity. Methods: A hypothesis- and model-driven method for verifying and understanding the foundational intracranial hemodynamic PFRs is developed and applied to a novel multi-modality monitoring dataset. Results: Model analysis of joint observations of CPP and CBF validates the standard PFR when autoregulatory processes are impaired as well as unmodelable cases dominated by autoregulation. However, it also identifies a dynamical regime -or behavior pattern-where the PFR assumptions are wrong in a precise, data-inferable way due to negative CPP-CBF coordination over long timescales. This regime is of both clinical and research interest: its dynamics are modelable under modified assumptions while its causal direction and mechanistic pathway remain unclear. Conclusion: Motivated by the understanding of mathematical physiology, the validity of the standard PFR can be assessed a) directly by analyzing pressure reactivity and mean flow indices (PRx and Mx) or b) indirectly through the relationship between CBF and other clinical observables. This approach could potentially help to personalize TBI care by considering intracranial pressure and CPP in relation to other data, particularly CBF. The analysis suggests a threshold using clinical indices of autoregulation jointly generalizes independently set indicators to assess CA functionality. These results support the use of increasingly data-rich environments to develop more robust hybrid physiological-machine learning models.

Immune cell-associated neurotoxicity syndrome (ICANS) and cytokine release syndrome (CRS) are both common adverse effects of chimeric antigen receptor (CAR) T-cell therapy. Blinatumomab is a commonly used CAR T-cell treatment in patients with B-cell acute lymphoblastic leukemia (B-ALL). Our patient presented with an extensive past medical history, including refractory B-ALL, and developed CRS and ICANS following treatment with blinatumomab CAR-T cell therapy. Early clinical detection of ICANS, monitoring using immune effector cell encephalopathy scores, following the appropriate protocol for ICANS grade, and adding anakinra (IL-1 receptor antagonist) were crucial steps in managing his condition. The approach to managing and monitoring this patient was unique in that we added anakinra to the standard treatment regimen. With this report, we emphasize the need for further research regarding CAR T-cell therapeutic regimens and how to decrease the morbidity and mortality of its adverse effects.

BACKGROUND: Volatile anesthetics have shown neuroprotective effects in preclinical studies, but clinical data on their use after aneurysmal subarachnoid hemorrhage (aSAH) are limited. This study aimed to analyze whether the use of volatile anesthetics for neurocritical care sedation affects the incidence of delayed cerebral ischemia (DCI), cerebral vasospasm (CVS), DCI-related infarction or functional outcome.
METHODS: Data were retrospectively collected for ventilated aSAH patients (2016-2022), who received sedation for at least 180 hours. For comparative analysis patients were assigned to a control and a study group according to the sedation used (intravenous vs. volatile sedation). Logistic regression analysis was performed to identify independent predictors of DCI, CVS, DCI-related infarction, and functional outcome.
RESULTS: 99 patients with a median age of 58 years (IQR 52-65 years) were included. 47 patients (47%) received intravenous sedation, while 52 patients (53%) received (additional) volatile sedation with isoflurane (n=30, 58%) or sevoflurane (n=22, 42%) for a median duration of 169 hours (range 5-298 hours). There were no significant differences between the two groups regarding the occurrence of DCI, angiographic CVS, DCI-related infarction, or functional outcome. In a multivariable logistic regression analysis, the use of volatile anesthetics had no impact on the incidence of DCI-related infarction or the patients\' functional outcome.
CONCLUSIONS: Volatile sedation in aSAH patients is not associated with the incidence of DCI, CVS, DCI-related infarction or functional outcome. Although we could not demonstrate neuroprotective effects of volatile anesthetics, our results suggest that volatile sedation after aSAH has no negative effect on patient\'s outcome.

OBJECTIVE: Targeting single monitoring modalities such as intracranial pressure (ICP) or cerebral perfusion pressure alone has shown to be insufficient in improving outcome after traumatic brain injury (TBI). Multimodality monitoring (MMM) allows for a more complete description of brain function and for individualized management. Transcranial Doppler (TCD) represents the gold standard for continuous cerebral blood flow velocity assessment, but requires high levels skill and time. In TBI, the practical aspects of conducting extended TCD monitoring sessions have yet to be evaluated.
METHODS: Patients with acute moderate-to-severe TBI admitted to the neurocritical care unit between March 2022 and December 2023 receiving invasive ICP measurements were evaluated for inclusion. Exclusion criteria included trauma incompatible with TCD monitoring and if MMM was unwarranted. Daily MMM sessions (in addition to regular monitoring) were performed using TCD (Delica EMS 9D System or the DWL Doppler Box) for ≤5 d. Quantitative and qualitative feasibility, safety, and quality metrics were assessed.
RESULTS: Of 74 patients, 36 (75% male; mean age, 44 ± 17 y) were included. Common reasons for exclusion were skull fractures (n = 12) and decompressive craniectomy (n = 9). We acquired 88 recordings (mean, 275 ± 88 min). Overall monitoring times increased, and set-up times decreased. Physiologic variables (including ICP/brain temperature) did not change with TCD application. A single adverse event (dislodging of a microdialysis catheter) occurred.
CONCLUSIONS: Implementing extended TCD monitoring in MMM protocols is feasible and safe. Considering these results, inclusion of long-term TCD as part of the MMM is strongly encouraged to allow for in-depth description and direct evaluation of hemodynamic changes after TBI.

BACKGROUND: Interventions to reduce intracranial pressure (ICP) in patients with traumatic brain injury (TBI) are multimodal but variable, including sedation-dosing strategies. This article quantifies the different sedation intensities administered in patients with moderate to severe TBI (msTBI) using the therapy intensity level (TIL) across different intensive care units (ICUs), including the use of additional ICP-lowering therapies.
METHODS: Within the prospective Transforming Research and Clinical Knowledge in TBI (TRACK-TBI) study, we performed a retrospective analysis of adult patients with msTBI admitted to an ICU for a least 5 days from seven US level 1 trauma centers who received invasive ICP monitoring and intravenous sedation. Sedation intensity was classified prospectively as one of three ordinal levels as part of the validated TIL score, which were collected at least once a day.
RESULTS: A total of 127 patients met inclusion criteria (mean age 41.6 ± 17.7 years; 20% female). The median Injury Severity Score was 27 (interquartile range 17-33), with a median admission Glasgow Coma Score of 3 (interquartile range 3-7); 104 patients had severe TBI (82%), and 23 patients had moderate TBI (18%). The sedation intensity score was highest on the first ICU day (2.69 ± 1.78), independent of patient severity. Time to reaching each sedation intensity level varied by site. Sedation level I was reached within 24 h for all sites, but sedation levels II and III were reached variably between days 1 and 3. Sedation level III was never reached by two of seven sites. The total TIL score was highest on the first ICU day, with a modest decrease for each subsequent ICU day, but there was high site-specific practice-pattern variation.
CONCLUSIONS: Intensity of sedation and other therapies for elevated ICP for patients with msTBI demonstrate large practice-pattern variation across level 1 trauma centers within the TRACK-TBI cohort study, independent of patient severity. Optimizing sedation strategies using patient-specific physiologic and pathoanatomic information may optimize patient outcomes.

How to cite this article: Salhotra R. Transient Cerebral Circulation Arrest in SAH. Indian J Crit Care Med 2024;28(6):620-621.

Paradoxical herniation is a dreadful neurosurgical complication often underdiagnosed, which typically becomes evident over the course of weeks to months after the initial intervention. Here we present a unique case with manifestations in the post-operative period. A patient initially referred to neurosurgery for a meningioma underwent an uneventful surgical excision, followed by the transient placement of a lumbar drain for 48 hours. On the first post-operative day, the patient exhibited progressively altered neurological status, with corresponding imaging revealing a transfalcine herniation, necessitating emergent decompressive craniectomy. Despite the medical and surgical interventions, there were continuous signs of neurological and imaging worsening, with increase in herniation, which led to the diagnosis suspicion of a paradoxical brain herniation. Consequently, a rapid reversal of neurological deficits was observed after applying maneuvers to augment the intracranial pressure, followed by cranioplasty. This case illustrates the utmost importance of clinical suspicion for the uncommon complications of neurointerventions.

Hypoxic-ischemic encephalopathy is the most common cause of neonatal seizures. Continuous electroencephalographic monitoring is recommended given high rates of subclinical seizures. Prompt diagnosis and treatment of seizures may improve neurodevelopmental outcomes. International League Against Epilepsy guidelines indicate that (1) phenobarbital remains the first-line treatment of neonatal seizures and (2) early discontinuation of antiseizure medications following resolution of acute provoked seizures, and prior to discharge home, is recommended. Long-term follow-up of these infants is necessary to screen for postneonatal epilepsy and support neurodevelopment.