Knox, Molly G.

Introduction CAR T‐cell therapy is an immunotherapy essential in treating blood and plasma cancers. A common side effect of CAR T‐cell therapy is ICANS (Immune Effector Cell‐Associated Neurotoxicity Syndrome), with mechanism including excessive cytokine response resulting in endothelial dysfunction and blood brain barrier (BBB) disruption with CART cell migration to the CNS. Manifestations of ICANS includes aphasia, dysgraphia, tremor and other features of encephalopathy. PRES (posterior reversible encephalopathy syndrome) has a similar proposed mechanism of endothelial dysfunction and BBB breakdown while acute ischemic stroke can present similarly with aphasia. This is a case report of a patient who developed ICANS grade 3 found to have PRES on neuro imaging with initial improvement before again decompensating and found to have acute ischemic stroke. Methods N/A Results This was a 63‐year‐old female with multiple myeloma who underwent CAR T‐cell therapy. She developed encephalopathy and tremors consistent with grade 3 neurotoxicity with MR brain showing findings of mild PRES. She improved with ICANS treatment of steroids, Anakinra, tocilizumab, IT methotrexate/hydrocortisone and management of PRES with SBP control. Unfortunately, she had acute decompensation a week after these treatments with aphasia concerning for relapsed ICANS or PRES, however MR brain revealed a hyperacute left MCA stroke, not a candidate for treatment due to lack of LVO and thrombocytopenia. Subsequently she went into atrial fibrillation with RVR and was noted to have HfrEF. Repeat neuro imaging with CT head revealed multifocal strokes and R ICA occlusion. No obvious vasospasm on vessel imaging to support co‐existing RCVS given prior findings of PRES. Conclusion As CAR T‐cell therapy becomes widely utilized, it is important to be aware of the presentation of ICANS and remain diligent in ruling out ICAN mimics such as PRES and acute ischemic stroke. image image

The Neurohospitalist Core Competencies comprise a set of competency-based learning objectives that encapsulate the knowledge, skills, and attitudes of neurohospitalitists who specialize in the care of hospitalized patients with neurologic conditions. These competencies serve to characterize the rapidly expanding field of neurohospitalist medicine. The 27 chapters are divided into 3 sections entitled: neurological conditions, clinical interventions and interpretation of ancillary studies, and neurohospitalist role in the healthcare system. Each individual learning objective in the chapters describes a specific concept with an action verb to illustrate the behavior that the neurohospitalist exhibits. The individual neurohospitalist may not exhibit mastery in each of the topics included as individual practices vary in scope and practice pattern. A few examples of how the complete set of competencies may be used include in the creation of curricula for neurohospitalist fellowships, to assist in defining the scope of practice of neurohospitalists for administrative leaders of hospitals and departments, and in influencing the direction of further research and quality improvement in the field.

Objective: The objective of this study was to critically assess current evidence regarding the role of prophylactic antiseizure medication in patients presenting with acute intracerebral hemorrhage (ICH). Methods: The objective was addressed through the development of a structured critically appraised topic. This included a clinical scenario with a clinical question, literature search strategy, critical appraisal, results, evidence summary, commentary, and bottom-line conclusions. Participants included resident neurologists, a medical librarian, and content experts in the fields of epilepsy, stroke neurology, neurohospitalist medicine, and neurocritical care. Results: A randomized clinical trial was selected for critical appraisal. The trial assessed whether prophylactic levetiracetam (LEV) use reduced the risk of acute seizures in patients with ICH, as defined by clinical or electrographic seizure, captured by continuous electroencephalogram 72 hours after enrollment. A total of 42 patients were included in the final analysis (19 in the LEV group and 23 in the placebo group). There was a significantly higher occurrence of seizures in the placebo versus LEV group (LEV 16% vs placebo 43%, P = 0.043). There were no differences in functional outcomes between the groups at 3, 6, or 12 months (P > 0.1). Conclusions: The role of prophylactic treatment with antiseizure medication in ICH remains unclear.

Usually used in emergency settings, bedside sonographic measurement of optic nerve sheath diameter can aid in diagnosing elevated intracranial pressure. We report a case of a 26-year-old male hospitalized for CAR T-cell therapy with Axicabtagene Ciloleucel for treatment of relapsed diffuse large B-cell lymphoma, who developed progressive symptoms of immune effector cell-associated neurotoxicity syndrome. Fundoscopic examination suggested the presence of blurred optic disc margins. Bedside ocular ultrasound revealed wide optic nerve sheath diameters and bulging optic discs bilaterally. The patient had a ventriculostomy placed for monitoring and received treatment with steroids and mannitol, as well as tocilizumab. After 7 days in the ICU, the patient recovered with no evidence of long-term neurological deficits.

Abstract Usually used in emergency settings, bedside sonographic measurement of optic nerve sheath diameter can aid in diagnosing elevated intracranial pressure. We report a case of a 26-year-old male hospitalized for CAR T-cell therapy with Axicabtagene Ciloleucel for treatment of relapsed diffuse large B-cell lymphoma, who developed progressive symptoms of immune effector cell-associated neurotoxicity syndrome. Fundoscopic examination suggested the presence of blurred optic disc margins. Bedside ocular ultrasound revealed wide optic nerve sheath diameters and bulging optic discs bilaterally. The patient had a ventriculostomy placed for monitoring and received treatment with steroids and mannitol, as well as tocilizumab. After 7 days in the ICU, the patient recovered with no evidence of long-term neurological deficits.

AbstractObjectiveThere are few neuropathological studies on Parkinson's disease with mild cognitive impairment (PD‐MCI). Those published reveal coexisting Lewy body and Alzheimer's disease pathology. Our objective is to determine the pathology that underlies PD‐MCI.MethodsWe used data from the Arizona Study of Aging and Neurodegenerative Disorders, a longitudinal clinicopathological study. Of 736 autopsied subjects with standardized movement and cognitive assessments, 25 had PD‐MCI. Neuropathological findings, including Lewy body and Alzheimer's disease pathology, were compared in PD subjects with amnestic MCI (A‐MCI) and nonamnestic MCI (NA‐MCI).ResultsSignificant pathological heterogeneity within PD‐MCI was found. This included varying Lewy body stages, Alzheimer's disease pathology, and cerebral amyloid angiopathy. There was a significant increase in the severity of Lewy body pathology (meeting The Unified Staging System for Lewy Body disorders neocortical stage) in nonamnestic MCI (7/1, 63%) when compared with amnestic MCI (3/14, 21%, P = 0.032).ConclusionAlthough a small study, distinct pathological changes may contribute to PD‐MCI phenotype. © 2020 International Parkinson and Movement Disorder Society