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Introduction: There are described differences in coagulation between females and males. Specifically, female sex is associated with greater platelet activation and stronger clotting characteristics. It is unclear whether there are relevant coagulation differences identifiable between female and male patients suffering from intracerebral hemorrhage (ICH). Hypothesis: Female sex will be associated with stronger clotting characteristics on whole blood viscoelastic hemostatic assay testing. Methods: Spontaneous ICH patients admitted and enrolled into a prospective observational ICH cohort study between 2009-2020 and who received baseline viscoelastic hemostatic assay testing (Rotational Thromboelastometry: ROTEM) were assessed. Patients with prior anticoagulant use, patients receiving hemorrhage control therapies prior to ROTEM, and secondary etiologies of ICH were excluded from the analysis. Female sex was assessed as the primary exposure variable. The following ROTEM clotting parameters were assessed as the outcome: Coagulation Time (CT) and Maximum Clot Firmness (MCF). We assessed relationships of female sex with these separate ROTEM parameters using multivariable linear regression analyses after adjusting for relevant covariates. Results: Of 57 ICH patients included for analyses, mean age was 65 (SD 14.1), 47% were female, and the median ICH volume was 20.6 mL (IQR 10.1-43.3). There were no baseline intergroup sex differences in demographics, age, or ICH characteristics. Female sex was associated with increased EXTEM MCF (ß 0.323, p Conclusions: We identified that female sex was associated with stronger clotting characteristics on ROTEM viscoelastic testing. Further work is required to clarify the clinical significance of these findings and their potential specific impacts on radiographic, complication, and clinical outcomes after ICH.

Introduction: Biological sex is known to impact cerebrovascular disease characteristics and clinical outcomes. While in intracerebral hemorrhage (ICH) it is known that biological sex impacts ICH incidence, it is less clear whether biological sex impacts ICH outcomes. Hypothesis: Female sex will be associated with ICH characteristics and clinical outcomes. Methods: Spontaneous ICH patients enrolled into a prospective observational ICH cohort study between 2009-2020 were assessed. Patients with prior anticoagulant use and secondary etiologies of ICH were excluded from the analysis. Female sex was assessed as the primary exposure variable. Primary analyses assessed relationships of female sex with radiographic outcomes: ICH location, ICH volume, hematoma expansion (>33% and/or >6mL). Secondary analyses assessed relationships of female sex with clinical outcomes: poor discharge neurological outcome (modified Rankin 4-6), and poor discharge disposition (skilled nursing facility, hospice, or inpatient death). Separate multivariable regression models assessed these relationships after adjusting for relevant covariates. Results: Of 504 ICH patients analyzed, mean age was 67 (SD 14.9), 46% were female, and median baseline ICH volume was 14.6 mL (IQR 4.98-35.0). In primary analyses, female sex was not associated with ICH volume or hematoma expansion but was associated with lobar ICH location (adjusted OR 1.72, 95% CI: 1.09-2.70). In secondary analyses, female sex was not associated with poor discharge neurological outcomes (adjusted OR 1.40, 95% CI: 0.74-2.64) after adjusting for race, ICH severity, and ICH location. However, there was an association of female sex with poor discharge disposition (adjusted OR 1.91, 95% CI: 1.15-3.16) after adjusting for similar covariates. Conclusions: While there were no clear intergroup sex differences in ICH severity or neurological outcomes, female sex was associated with worse discharge disposition. Further work is required to clarify whether these disposition differences are due to disease specific complications, characteristics, or if there are other social disparities responsible for these outcome differences.

Little is known about the natural history of comatose patients with brain injury, as in many countries most of these patients die in the context of withdrawal of life-sustaining therapies (WLSTs). The accuracy of predicting recovery that is used to guide goals-of-care decisions is uncertain. We examined long-term outcomes of patients with ischemic or hemorrhagic stroke predicted by experienced clinicians to have no chance of meaningful recovery in Japan, where WLST in patients with isolated neurological disease is uncommon.We retrospectively reviewed the medical records of all patients admitted with acute ischemic stroke, intracerebral hemorrhage, or nontraumatic subarachnoid hemorrhage between January 2018 and December 2020 to a neurocritical care unit at Toda Medical Group Asaka Medical Center in Saitama, Japan. We screened for patients who were predicted by the attending physician on postinjury day 1-4 to have no chance of meaningful recovery. Primary outcome measures were disposition at hospital discharge and the ability to follow commands and functional outcomes measured by the Glasgow Outcome Scale-Extended (GOS-E), which was assessed 6 months after injury.From 860 screened patients, we identified 40 patients (14 with acute ischemic stroke, 19 with intracerebral hemorrhage, and 7 with subarachnoid hemorrhage) who were predicted to have no chance of meaningful recovery. Median age was 77 years (interquartile range 64-85), 53% (n = 21) were women, and 80% (n = 32) had no functional deficits prior to hospitalization. Six months after injury, 17 patients were dead, 14 lived in a long-term care hospital, 3 lived at home, 2 lived in a rehabilitation center, and 2 lived in a nursing home. Three patients reliably followed commands, two were in a vegetative state (GOS-E 2), four fully depended on others and required constant assistance (GOS-E 3), one could be left alone independently for 8 h per day but remained dependent (GOS-E 4), and one was independent and able to return to work-like activities (GOS-E 5).In the absence of WLST, almost half of the patients predicted shortly after the injury to have no chance of meaningful recovery were dead 6 months after the injury. A small minority of patients had good functional recovery, highlighting the need for more accurate neurological prognostication.

Background Impaired consciousness is common in intensive care unit (ICU) patients, and an individual’s degree of consciousness is crucial to determining their care and prognosis. However, there are no methods that continuously monitor consciousness and alert clinicians to changes. We investigated the use of physiological signals collected in the ICU to classify levels of consciousness in critically ill patients. Methods We studied 61 patients with subarachnoid hemorrhage (SAH) and 178 patients with intracerebral hemorrhage (ICH) from the neurological ICU at Columbia University Medical Center in a retrospective observational study of prospectively collected data. The level of consciousness was determined on the basis of neurological examination and mapped to comatose, vegetative state or unresponsive wakefulness syndrome (VS/UWS), minimally conscious minus state (MCS−), and command following. For each physiological signal, we extracted time-series features and performed classification using extreme gradient boosting on multiple clinically relevant tasks across subsets of physiological signals. We applied this approach independently on both SAH and ICH patient groups for three sets of variables: (1) a minimal set common to most hospital patients (e.g., heart rate), (2) variables available in most ICUs (e.g., body temperature), and (3) an extended set recorded mainly in neurological ICUs (absent for the ICH patient group; e.g., brain temperature). Results On the commonly performed classification task of VS/UWS versus MCS−, we achieved an area under the receiver operating characteristic curve (AUROC) in the SAH patient group of 0.72 (sensitivity 82%, specificity 57%; 95% confidence interval [CI] 0.63–0.81) using the extended set, 0.69 (sensitivity 83%, specificity 51%; 95% CI 0.59–0.78) on the variable set available in most ICUs, and 0.69 (sensitivity 56%, specificity 78%; 95% CI 0.60–0.78) on the minimal set. In the ICH patient group, AUROC was 0.64 (sensitivity 56%, specificity 65%; 95% CI 0.55–0.74) using the minimal set and 0.61 (sensitivity 50%, specificity 80%; 95% CI 0.51–0.71) using the variables available in most ICUs. Conclusions We find that physiological signals can be used to classify states of consciousness for patients in the ICU. Building on this with intraday assessments and increasing sensitivity and specificity may enable alarm systems that alert physicians to changes in consciousness and frequent monitoring of consciousness throughout the day, both of which may improve patient care and outcomes.

This study evaluated intradialytic cerebral hemodynamics measured by transcranial Doppler (TCD) in intermittent hemodialysis (iHD) versus nightly peritoneal dialysis (NIPD). Intradialytic TCD was serially performed in chronic dialysis patients receiving iHD ( n = 10) and NIPD ( n = 10). A linear mixed model was used to model mean flow velocity (MFV), pulsatility index (PI), and mean arterial pressure (MAP) as functions of time and treatment group. Intradialytic cerebral volatility (IDCV) was calculated using the coefficient of variation (CV) and mean absolute value of change (AVC) of each patient’s MFV, PI, and MAP values over time. Mixed model analyses found no significant difference between MFV, PI, and MAP treatment groups in change over time, though volatility differed significantly. Mean CV values for MFV, PI, and MAP were higher in iHD than NIPD (MFV 0.22 vs. 0.10, p = 0.005; PI 0.14 vs. 0.08, p = 0.003; MAP 0.057 vs. 0.032, p = 0.009). AVC values were similarly higher in iHD compared to NIPD (MFV 8.26 vs. 4.43, p = 0.04; PI 0.17 vs. 0.084, p < 0.001; MAP 6.05 vs. 2.9, p = 0.003). PI, MFV, and MAP were more stable in NIPD than iHD, as measured by intradialytic TCD monitoring. This study identifies IDCV as a unique TCD metric for intradialytic cerebral hemodynamics.

Chronic kidney disease (CKD) independently increases the risk of stroke and small vessel disease (SVD). This study compared SVD and a transcranial Doppler (TCD)-based marker of intracranial vascular resistance (pulsatility index, PI) in post-stroke patients with and without CKD. Between January 2015 and December 2017, 118 individuals with stable eGFR (50 with CKD) had cerebral MRI and TCD within three months of a stroke. The means of bilateral PI in anterior (anterior cerebral [ACA] and middle cerebral arteries [MCA]) and posterior vessels (posterior cerebral [PCA] and vertebral arteries [VA]) were computed. CKD strongly correlated with higher distal resistance (median CKD ACA PI 1.2, IQR 1.0 to 1.35 vs. controls 0.91 IQR 0.79 to 1.1 [ p 4 IQR 2.66 to 7.76 × 104 voxels vs. controls median SVD 6.7 × 103 IQR 2.4 to 24.0 × 103 [ p

Patients with acute brain injury are at heightened risk for dialysis-associated neurovascular injury (DANI), a clinical syndrome associated with worsening cerebral edema and impaired cerebral blood flow during dialysis ([1][1]). Acute brain injury itself is commonly associated with cerebral edema

Intracerebral hemorrhage (ICH) accounts for only 10 to 15% of all strokes but remains a significant cause of morbidity and mortality. Despite lengthy stays in critical care units, only one-half of those experiencing an ICH survive after 30 days, and those who do are often left with considerable disability. Treatment has traditionally focused on minimizing the hemorrhage expansion and reducing clot volume through both medical and surgical means. Management of ICH is a complex and multidisciplinary process. This review will discuss a few common etiologies, explore the pathophysiology of secondary neuronal injury after ICH, review the basics of ICH imaging with computed tomography and magnetic resonance imaging, and highlight latest practices in medical and surgical management. Secondary injury mechanisms such as perihematomal edema and disordered cerebral autoregulation are discussed as potential targets for new treatment modalities. Emergent treatment in the “golden hour” after ictus provides a template of measures to adopt from initial contact with emergency medical services, to the emergency department, and thereafter, triage to the intensive care unit. Medical management including blood pressure control, hemostasis, and coagulopathy reversal are discussed and evidence from trials such as INTERACT 2, ATACH 2, and ANNEXA-4 are given a clinical context. Surgical management including intracranial pressure monitoring, surgical evacuation with open craniotomy, and minimally invasive approaches such as stereotactic-guided aspiration and thrombolysis, ultrasound-induced thrombolysis, image-guided stereotactic endoscopic aspiration, and stereotactic ICH underwater blood aspiration are enumerated. The outcomes and relevance of STICH, MISTIE, and CLEAR trials to present surgical care are elaborated. The review summarizes the current guidelines for the treatment of ICH and the latest literature in the field they are based upon. It aims to provide a concise article beneficial to the emergency physicians and neurointensivists/neuroanesthesiologists.

Background: Given the increasing worldwide prevalence of chronic kidney disease (CKD), it is critical to decrease the associated risk of debilitating vascular complications, including stroke, congestive heart failure, myocardial infarction, and peripheral vascular disease. Treatment options for reducing the risk of all subtypes of stroke in patients with CKD remain limited. For patients with end-stage kidney disease (ESKD), novel applications of noninvasive imaging may help personalize the type of dialysis and dialysis prescription for patients at high-risk. Summary: This manuscript reviews the heightened risk of stroke in patients with nephropathy, including ischemic and hemorrhagic subtypes. Mechanisms associated with increased risk include alterations in cardiac output, platelet function, regional cerebral perfusion, accelerated systemic atherosclerosis, altered blood brain barrier, and disordered neurovascular coupling. There is great potential for noninvasive monitoring of the cerebral vasculature using transcranial Doppler (TCD) to reduce stroke risk, particularly in patients with ESKD. Key Messages: Compared to the general population, patients with CKD are at heightened risk for all subtypes of stroke. This is due to a multitude of mechanisms linking nephropathy with altered cerebral perfusion, cerebral neurovascular coupling, and blood vessel integrity. Intracranial imaging is not currently standard of care practice in patients with CKD or ESKD. TCD may provide clinicians real-time and noninvasive measurement of brain perfusion. This could be useful for assessing risk of stroke in patients’ initiating dialysis, individualizing dialysis prescriptions, and potentially reducing rates of cerebrovascular disease and stroke in high-risk patients.

Dialysis-associated neurovascular injury (DANI) is a significant contributor to secondary neurologic injury for patients with acute brain injury undergoing renal replacement therapy (RRT). This manuscript reviews the multi-faceted pathophysiologic aspects of DANI and focuses on options for neuro-monitoring and RRT prescription modification to prevent DANI. We consider DANI a clinical syndrome encompassing cerebral edema, impaired cerebral blood flow, and cerebrospinal fluid metabolic alterations during RRT, all of which may lead to secondary brain injury. Neurological monitoring in dialysis, particularly non-invasive methods such as near-infrared spectroscopy and transcranial Doppler ultrasonography, are emerging tools for dialysis medicine in acute brain injury and DANI prevention. Treatment options such as dialysate sodium modeling, limited solute clearance, weight-based ultrafiltration rates, cooled dialysate, and combination ultrafiltration and dialysis treatments may be helpful in limiting secondary neurologic injury from DANI. This manuscript is intended to inform neurocritical care providers about components of DANI pathophysiology, and potential preventative and treatment strategies for at-risk patients.

PURPOSE OF REVIEW: This review focuses on the relationships between diabetes, cognitive impairment and the contribution of kidney disease. RECENT FINDINGS: We review the independent contributions of parameters of kidney disease, including albuminuria, glomerular filtration, bone/mineral metabolism and vitamin D synthesis, on cognitive performance in patients with diabetes. Potential pathophysiologic mechanisms underlying these associations are discussed highlighting gaps in existing knowledge. Finally, effects of the dialysis procedure on the brain and cognitive performance are considered. Emphasis is placed on novel non-invasive screening tools with the potential to preserve cerebral perfusion during hemodialysis and limit cognitive decline in patients with diabetic ESKD. SUMMARY: Patients with type 2 diabetes and advanced chronic kidney disease suffer a higher prevalence of cognitive impairment. This is particularly true in patients with diabetes and end-stage kidney disease (ESKD).

Objectives Acute kidney injury (AKI) is common after cardiac arrest (CA). Few data exist on survival and neurological outcomes measured at hospital discharge of patients with severe AKI requiring renal replacement therapy (RRT) within the first 72 hours (i.e., duration of post-CA syndrome). Methods Single-center, prospective, observation cohort of patients with in- or out-of-hospital CA who survived to intensive care unit admission and were considered for targeted temperature management between 2010 and 2016 were reviewed. After excluding preexisting RRT history, patients with new RRT requirements within the first 72 hours after CA were included. Primary outcome of survival and secondary outcome of good neurological recovery defined as cerebral performance category score of 1 to 2, were compared between patients with and without RRT. Within 24 hours of initiating RRT, illness severity, as measured by Sequential Organ Failure Assessment score, Acute Physiology and Chronic Health Evaluation–II, and Charlson Comorbidity Index, was compared between survivors and nonsurvivors. Results Of 524 patients, 65 (12.4%) had new RRT requirements within 72 hours. Survival rates and good neurological recovery at discharge were comparable between RRT and non-RRT groups (19 of 65 [29%] vs. 162 of 459 [35%], P = 0.3, and 8 of 19 [42%] vs. 73 of 162 [45%], respectively). Sixty-three percent (12 of 19) of survivors requiring RRT did not need dialysis on discharge. Among patients requiring RRT, prognostic factors, including illness severity scores and indications for RRT, did not differ between survivors and nonsurvivors. Conclusions Patients with severe AKI requiring RRT during the post-CA syndrome period were not associated with any significant reduction in survival or poor neurological recovery, compared with those without RRT. Among those requiring RRT, none of the known prognostic factors predicted survival., Graphical abstract

Introduction: Cerebral venous sinus thrombosis (CVST) represents an important cause of both ischemic and hemorrhagic strokes in young people. While recent guidelines recommend management in a stroke unit, the impact of Neurocritical care in this condition has not been studied. We aimed to assess whether the introduction of a Neurocritical Care program influenced clinical outcomes in CVST patients. Methods: We retrospectively reviewed electronic medical records of adult patients admitted to Yale New Haven Hospital’s Neuroscience ICU (NICU) between 2010 and 2017 with a diagnosis of CVST. Demographics, vascular risk factors, comorbidities, length of stay and discharge modified Rankin scale (mRS) were collected. Patients were excluded for transfer after 24 hours of initial presentation. We compared two time periods, before (epoch 1, 2010-2012) and after (epoch 2, 2013-2017) the introduction of continuous staffing of CVST cases by neurointensivists in the NICU. Univariable and multivariable logistic regression were utilized to model the odds of poor outcome (dichotomized mRS 0-2 vs 3-6). Results: Fifty-three patients with CVST met the inclusion criteria during the study period (mean age 39 (+/- 17) years, 51 % female). 20 patients were identified for Epoch 1 and 33 patients for Epoch 2. Overall, 40 patients (76%) had a good (mRS 0-2) outcome. For epochs 1 and 2, good outcomes were observed in 12 (60%) and 28 (85%) patients, respectively (p=0.04). In both univariable and multivariable regression analysis (adjusted for age and sex), admission during epoch 2 was associated with a significantly reduced odds of a poor outcome (OR 0.27, CI 0.07 - 0.98; p =0.048) and (OR 0.27, CI 0.07- 1; p=0.05), respectively. Conclusions: In this small, single-center cohort of patients with CVST, most patients experienced a good outcome. The institution of continuous neurointensivist coverage was independently associated with better outcomes. Further validation in prospective, multicenter cohort studies is needed.

Although detailed practice parameters have been developed to help guide physicians in brain death determination, guidelines based on these parameters widely vary. The recent case of Jahi McMath not only highlights social misconceptions but also serves as a call to action to decrease medical variability and confusion regarding brain death determination. This review discusses common sources of variations in brain death determination - we divide these sources into before, during, and after brain death declaration.We use four key studies to elucidate variable practice in brain death determination. Poor training of examiners and patient qualifications for brain death examination prior to testing, incomplete apnea testing, repeat examinations during testing, and the sometimes unjustified use of ancillary testing are highlighted as main areas for improvement. Improved physician training and certification, as well as better standardization of hospital protocols, may be answers to more universal practice.Diagnosing brain death is confusing because of numerous variations in practice, but this variation can be improved. Improved and standardized physician training can help create a formal certification process for examiners and help create uniformity in brain death determination. National standards will also help decrease variability of practice.

See Ghoshal and Claassen (doi:10.1093/brain/awx226) for a scientific commentary on this article.

Delirium is sometimes defined as acute onset of either overactivity or underactivity. This article reviews the nature and clinico-anatomical locations of lesions in patients with reduced activity. The term abulia is used to describe global underactivity. Abulia is customarily explained by interruptions in frontal-subcortical circuitry. These interruptions can occur with lesions in the frontal lobes, caudate nuclei, midbrain, and thalamus. The article describes the anatomy of frontal and subcortical circuits and reviews in detail individual cases and series of patients with reduced initiative and activity who have had localized central nervous system lesions.

Objectives To describe a case and review literature for intracerebral hemorrhage caused by migraine. Design Case report. Setting Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. Patient A 54-year-old truck driver with a 2-year history of atypical headaches. Results A 54-year-old right-handed truck driver was seen in consultation with a 2-year history of atypical headaches. The headaches were dull, throbbing, gradually progressive, and limited over the left occipital area. They were accompanied by right visual field deficit, diplopia, and, at times, confusion. These headaches were notably different from the usual migraine headaches he had been having for more than 20 years. Brain imaging revealed left parieto-occipital lobar hemorrhage. Further investigations ruled out arteriovenous malformations. He did not have any vascular risk factors, including hypertension. Migraine-associated intracerebral hemorrhage was considered to be the most likely diagnosis. Conclusions Intracerebral hemorrhage associated with migraine is believed to result from vasoconstriction leading to ischemia of the walls of blood vessels, making them leaky and porous. It is important to be aware of this phenomenon because vasoactive medications used to treat migraine can further aggravate the vasoconstriction and hence the intracerebral bleed.