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Accurate, automated extraction of clinical stroke information from unstructured text has several important applications. ICD-9/10 codes can misclassify ischemic stroke events and do not distinguish acuity or location. Expeditious, accurate data extraction could provide considerable improvement in identifying stroke in large datasets, triaging critical clinical reports, and quality improvement efforts. In this study, we developed and report a comprehensive framework studying the performance of simple and complex stroke-specific Natural Language Processing (NLP) and Machine Learning (ML) methods to determine presence, location, and acuity of ischemic stroke from radiographic text. We collected 60,564 Computed Tomography and Magnetic Resonance Imaging Radiology reports from 17,864 patients from two large academic medical centers. We used standard techniques to featurize unstructured text and developed neurovascular specific word GloVe embeddings. We trained various binary classification algorithms to identify stroke presence, location, and acuity using 75% of 1,359 expert-labeled reports. We validated our methods internally on the remaining 25% of reports and externally on 500 radiology reports from an entirely separate academic institution. In our internal population, GloVe word embeddings paired with deep learning (Recurrent Neural Networks) had the best discrimination of all methods for our three tasks (AUCs of 0.96, 0.98, 0.93 respectively). Simpler NLP approaches (Bag of Words) performed best with interpretable algorithms (Logistic Regression) for identifying ischemic stroke (AUC of 0.95), MCA location (AUC 0.96), and acuity (AUC of 0.90). Similarly, GloVe and Recurrent Neural Networks (AUC 0.92, 0.89, 0.93) generalized better in our external test set than BOW and Logistic Regression for stroke presence, location and acuity, respectively (AUC 0.89, 0.86, 0.80). Our study demonstrates a comprehensive assessment of NLP techniques for unstructured radiographic text. Our findings are suggestive that NLP/ML methods can be used to discriminate stroke features from large data cohorts for both clinical and research-related investigations.

Purpose To determine the temporal evolution, clinical correlates, and prognostic significance of electroencephalographic (EEG) patterns in post-cardiac arrest comatose patients treated with hypothermia. Methods Prospective cohort study of consecutive post-anoxic patients receiving hypothermia and continuous EEG monitoring between May 2011 and June 2014 ( n  = 100). In addition to clinical variables, 5-min EEG clips at 6, 12, 24, 48, and 72 h after return of spontaneous circulation (ROSC) were reviewed. EEG background was classified according to the American Clinical Neurophysiological Society critical care EEG terminology. Clinical outcome at discharge was dichotomized as good [Glasgow outcome scale (GOS) 4–5, low to moderate disability] vs. poor (GOS 1–3, severe disability to death). Results Non-ventricular fibrillation/tachycardia arrest, longer time to ROSC, absence of brainstem reflexes, extensor or no motor response, lower pH, higher lactate, hypotension requiring >2 vasopressors, and absence of reactivity on EEG were all associated with poor outcome (all p values ≤0.01). Suppression-burst at any time indicated a poor prognosis, with a 0 % false positive rate (FPR) [95 % confidence interval (CI) 0–10 %]. All patients (54/54) with suppression-burst or a low voltage (<20 µV) EEG at 24 h had a poor outcome, with an FPR of 0 % [95 % CI 0–8 %]. Normal background voltage ≥20 µV without epileptiform discharges at any time interval carried a positive predictive value >70 % for good outcome. Conclusions Suppression-burst or a low voltage at 24 h after ROSC was not compatible with good outcome in this series. Normal background voltage without epileptiform discharges predicted a good outcome.

BackgroundCentral retinal artery occlusion (CRAO) is an ophthalmological emergency, the retinal analog of a stroke. To date there is no consensus or national guidelines on how this disorder should be managed. As academic neurologists and ophthalmologists treat CRAO frequently, we set out to understand how these clinicians approach patients with CRAO with a national survey.MethodsWe identified university-associated teaching hospitals offering vascular neurology, neuro-ophthalmology and/or retina fellowships in the US and asked the directors of the programs to respond to questions in an open response format to profile the acute management of CRAO at their institution.ResultsWe found remarkable heterogeneity in the approach to acute treatment of patients with CRAO among the 45 institutions that responded to the survey. Only 20% had a formal policy, guideline or white paper to standardize the approach to treatment. The primary treating physician was an ophthalmologist, neurologist, or neuro-ophthalmologist 44, 27, and 4% of the time, respectively; 24% were co-managed acutely by neurology and ophthalmology. Intravenous fibrinolysis was offered to selected patients in 53% of institutions, and was the preferred initial treatment in 36%. When the acute treatment team involved a vascular neurologist, fibrinolysis was more likely to be considered a first-line treatment (p < 0.05). Anterior chamber paracentesis, ocular massage and hyperbaric oxygen therapy were offered 42, 66 and 7% of the time, respectively, while 9% of institutions offered no treatment. Anterior chamber paracentesis was more likely to be offered at programs where neurologists were not involved in treating CRAOs (p < 0.001). At 35% of institutions, patients with acute CRAO were not routinely referred to a general emergency room for initial evaluation and treatment. Carotid imaging was routinely obtained by 89% of programs, magnetic resonance imaging of the brain by 69%, echocardiogram by 62%, laboratory screening for an inflammatory state by 27% and retinal angiography by 30%. The thoroughness of vascular risk factors’ screening was greater in programs that routinely referred acute CRAO cases to the emergency department.ConclusionsThis survey shows that there is significant variability in treatment practices for acute CRAO in the US. Because of the high cerebrovascular and cardiovascular risk reported in this population of patients, it is notable that the approach to risk factor screening is also highly variable and many programs do not routinely refer patients to an emergency department for urgent evaluation. Finally, there appears to be equipoise among treatment teams regarding the efficacy of systemic fibrinolysis, as 53% of programs report a willingness to treat at least some patients with this modality.

ABSTRACTThe ascending reticular activating system (ARAS) mediates arousal, an essential component of human consciousness. Lesions of the ARAS cause coma, the most severe disorder of consciousness. Because of current methodological limitations, including of postmortem tissue analysis, the neuroanatomic connectivity of the human ARAS is poorly understood. We applied the advanced imaging technique of high angular resolution diffusion imaging (HARDI) to elucidate the structural connectivity of the ARAS in 3 adult human brains, 2 of which were imaged postmortem. High angular resolution diffusion imaging tractography identified the ARAS connectivity previously described in animals and also revealed novel human pathways connecting the brainstem to the thalamus, the hypothalamus, and the basal forebrain. Each pathway contained different distributions of fiber tracts from known neurotransmitter-specific ARAS nuclei in the brainstem. The histologically guided tractography findings reported here provide initial evidence for human-specific pathways of the ARAS. The unique composition of neurotransmitter-specific fiber tracts within each ARAS pathway suggests structural specializations that subserve the different functional characteristics of human arousal. This ARAS connectivity analysis provides proof of principle that HARDI tractography may affect the study of human consciousness and its disorders, including in neuropathologic studies of patients dying in coma and the persistent vegetative state.

Macrophages are a source of both proinflammatory and restorative functions in damaged tissue through complex dynamic phenotypic changes. Here, we sought to determine whether monocyte-derived macrophages (MDMs) contribute to recovery after acute sterile brain injury. By profiling the transcriptional dynamics of MDMs in the murine brain after experimental intracerebral hemorrhage (ICH), we found robust phenotypic changes in the infiltrating MDMs over time and demonstrated that MDMs are essential for optimal hematoma clearance and neurological recovery. Next, we identified the mechanism by which the engulfment of erythrocytes with exposed phosphatidylserine directly modulated the phenotype of both murine and human MDMs. In mice, loss of receptor tyrosine kinases AXL and MERTK reduced efferocytosis of eryptotic erythrocytes and hematoma clearance, worsened neurological recovery, exacerbated iron deposition, and decreased alternative activation of macrophages after ICH. Patients with higher circulating soluble AXL had poor 1-year outcomes after ICH onset, suggesting that therapeutically augmenting efferocytosis may improve functional outcomes by both reducing tissue injury and promoting the development of reparative macrophage responses. Thus, our results identify the efferocytosis of eryptotic erythrocytes through AXL/MERTK as a critical mechanism modulating macrophage phenotype and contributing to recovery from ICH.

Key Points Therapeutic hypothermia (TH) influences the time course of neurological recovery after cardiac arrest, and the influence of added sedation is also of paramount importance Standard modalities for assessing prognosis might be influenced by the use of TH Promising tools for prognostication in the era of TH include certain blood biomarkers, brainstem reflexes, somatosensory evoked potentials, EEG reactivity, and neuroimaging findings Clinicians should use a multimodal approach to prognosticate for individual patients To improve generalizability of prognostic modalities, future studies should record, in a standardized fashion, the time before return of spontaneous circulation, the fraction of patients with out-of-hospital arrest, and other patient characteristics Standardization of terminology, procedures and outcome measures using common data elements in future prospective research investigations will improve comparisons—and potentially allow pooling of data—across studies Neurological prognostication in patients who remain in hypoxic–ischaemic coma after cardiac arrest has always been challenging, and has become even more so since the advent of therapeutic hypothermia (TH). In this Review, Greer et al . consider how neurological outcomes and prognostic indicators might be influenced by the use of TH, and discuss advances in neuroimaging and electrophysiology that are expected to aid neuroprognostication in this patient population. Neurological prognostication after cardiac arrest has always been challenging, and has become even more so since the advent of therapeutic hypothermia (TH) in the early 2000s. Studies in this field are prone to substantial biases—most importantly, the self-fulfilling prophecy of early withdrawal of life-sustaining therapies—and physicians must be aware of these limitations when evaluating individual patients. TH mandates sedation and prolongs drug metabolism, and delayed neuronal recovery is possible after cardiac arrest with or without hypothermia treatment; thus, the clinician must allow an adequate observation period to assess for delayed recovery. Exciting advances have been made in clinical evaluation, electrophysiology, chemical biomarkers and neuroimaging, providing insights into the underlying pathophysiological mechanisms of injury, as well as prognosis. Some clinical features, such as pupillary reactivity, continue to provide robust information about prognosis, and EEG patterns, such as reactivity and continuity, seem promising as prognostic indicators. Evoked potential information is likely to remain a reliable prognostic tool in TH-treated patients, whereas traditional serum biomarkers, such as neuron-specific enolase, may be less reliable. Advanced neuroimaging techniques, particularly those utilizing MRI, hold great promise for the future. Clinicians should continue to use all the available tools to provide accurate prognostic advice to patients after cardiac arrest.

Substantial progress has been made over the past two decades in detecting, predicting and promoting recovery of consciousness in patients with disorders of consciousness (DoC) caused by severe brain injuries. Advanced neuroimaging and electrophysiological techniques have revealed new insights into the biological mechanisms underlying recovery of consciousness and have enabled the identification of preserved brain networks in patients who seem unresponsive, thus raising hope for more accurate diagnosis and prognosis. Emerging evidence suggests that covert consciousness, or cognitive motor dissociation (CMD), is present in up to 15–20% of patients with DoC and that detection of CMD in the intensive care unit can predict functional recovery at 1 year post injury. Although fundamental questions remain about which patients with DoC have the potential for recovery, novel pharmacological and electrophysiological therapies have shown the potential to reactivate injured neural networks and promote re-emergence of consciousness. In this Review, we focus on mechanisms of recovery from DoC in the acute and subacute-to-chronic stages, and we discuss recent progress in detecting and predicting recovery of consciousness. We also describe the developments in pharmacological and electrophysiological therapies that are creating new opportunities to improve the lives of patients with DoC.In this Review, the authors discuss recent progress in the detection and prediction of recovery of consciousness in patients with disorders of consciousness caused by severe brain injuries. They describe the ongoing development of pharmacological and electrophysiological therapies designed to enhance recovery.

The determination of brain death is typically made on the basis of clinical assessment (shown in a video) and requires demonstration of the permanent loss of all brain function, including brainstem function, in the absence of factors that may confound the assessment. If these factors cannot be eliminated, or if the examination cannot be safely or fully performed, ancillary testing is conducted.

Progressive secondary brain injury—induced by dysregulated neuroinflammation in spontaneous intracerebral hemorrhage (sICH)—underlies high sICH-mortality and remains without FDA-approved pharmacotherapy. Clinical insight that hematoma-directed interventions do not improve mortality prioritizes resolving acute secondary brain injury in sICH. As neutrophils are implicated in sICH secondary brain injury, we tested whether inhibition of a rogue neutrophil-subset expressing the dual endothelin-1/signal peptide receptor (DEspR) and associated with secondary tissue injury, DEspR+ CD11b+ immunotype, will attenuate mortality in a hypertensive-sICH (hsICH) rat model. We confirmed sICH-related deaths in hsICH-rats by T2*-weighted 9.4 T MRI and DEspR+ neutrophils in hsICH-rat brain perihematomal areas by immunostaining. At acute sICH, anti-DEspR muIgG1-antibody, mu10a3, treatment increased median survival in hsICH rats vs controls (p < 0.0001). In pre-stroke sICH, weekly 10a3-treatment did not predispose to infection and delayed sICH-onset vs controls (p < 0.0001). As potential sICH-therapeutic, we tested humanized anti-DEspR IgG4 S228P -mAb, hu6g8. In vitro, hu6g8 reversed delayed-apoptosis in DEspR+ CD11b+ neutrophils. In vivo, hu6g8 increased median survival and reduced neurologic symptoms in male/female hsICH-rats vs controls (p < 0.0001). Altogether, preclinical efficacy of inhibition of DEspR+ CD11b+ neutrophils in acute sICH—without infection complications, supports the potential of anti-DEspR therapy in sICH. Data provide basis for clinical study of DEspR+ CD11b+ neutrophil-subset in sICH patients.

Historically, investigators have not differentiated between patients with and without hemorrhagic transformation ( HT ) in large core ischemic stroke at risk for life-threatening mass effect ( LTME ) from cerebral edema. Our objective was to determine whether LTME occurs faster in those with HT compared to those without. We conducted a two-center retrospective study of patients with ≥ 1/2 MCA territory infarct between 2006 and 2021. We tested the association of time-to-LTME and HT subtype (parenchymal, petechial) using Cox regression, controlling for age, mean arterial pressure, glucose, tissue plasminogen activator, mechanical thrombectomy, National Institute of Health Stroke Scale, antiplatelets, anticoagulation, temperature, and stroke side. Secondary and exploratory outcomes included mass effect-related death, all-cause death, disposition, and decompressive hemicraniectomy. Of 840 patients , 358 (42.6%) had no HT, 403 (48.0%) patients had petechial HT, and 79 (9.4%) patients had parenchymal HT. LTME occurred in 317 (37.7%) and 100 (11.9%) had mass effect-related deaths. Parenchymal (HR 8.24, 95% CI 5.46–12.42, p < 0.01) and petechial HT (HR 2.47, 95% CI 1.92–3.17, p < 0.01) were significantly associated with time-to-LTME and mass effect-related death. Understanding different risk factors and sequelae of mass effect with and without HT is critical for informed clinical decisions.