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Background Persistent cognitive symptoms have been reported following COVID-19 hospitalization. We investigated the relationship between demographics, social determinants of health (SDOH) and cognitive outcomes 6-months after hospitalization for COVID-19. Methods We analyzed 6-month follow-up data collected from a multi-center, prospective study of hospitalized COVID-19 patients. Demographic and SDOH variables (age, race/ethnicity, education, employment, health insurance status, median income, primary language, living arrangements, and pre-COVID disability) were compared between patients with normal versus abnormal telephone Montreal Cognitive Assessments (t-MOCA; scores

A 29-year-old man with no prior known medical diagnoses presented to the emergency department with 5 days of fevers, chills, vomiting, headache, and neck pain followed by voice changes, difficulty swallowing, and intractable hiccups. The patient denied vision changes, weakness, numbness, recent travel, new medications, or illicit drug use. He had no personal or family history of neurologic illness. On questioning concerning possible toxic exposure, he noted recent consumption of sushi and raw meat at a restaurant; a friend who had eaten with him also experienced gastrointestinal illness after that meal.

To describe cases of unilateral cone-rod dysfunction presenting in two middle-aged females.This case series highlights two middle-aged female patients with progressive visual decline in one eye. Fundus photography, fundus autofluorescence (FAF), spectral-domain optical coherence tomography (SD-OCT), multi-focal electroretinogram (mfERG), full-field electroretinogram(ffERG), and genetic testing were obtained.In the first patient, mfERG showed an extinguished response and ffERG demonstrated markedly reduced a-wave and b-wave amplitudes (more pronounced under photopic conditions) in the right eye. SD-OCT showed attenuation of the ellipsoid zone of the right eye. Similar findings were appreciated in the second patient. Genetic testing in the first patient identified three heterozygous variants in PRPH2, RCBTB1, and USH2A. The second patient was found to have heterozygous variants in BBS1 and ABCA4.These two cases add to the literature of case reports of unilateral cone-rod and rod-cone dystrophies. However, the underlying etiology of the unilateral pattern of cone-rod dysfunction and the significance of the heterozygous mutations found in both cases remains uncertain.

OBJECTIVE: To evaluate whether a retinal spectral-domain optical coherence tomography (SD-OCT) assessment at baseline is associated with long-term disability worsening in people with multiple sclerosis (PwMS), we performed SD-OCT and Expanded Disability Status Scale (EDSS) assessments among 132 PwMS at baseline and at a median of 10 years later. METHODS: In this prospective, longitudinal study, participants underwent SD-OCT, EDSS, and visual acuity (VA) assessments at baseline and at follow-up. Statistical analyses were performed using generalized linear regression models, adjusted for age, sex, race, multiple sclerosis (MS) subtype, and baseline disability. We defined clinically meaningful EDSS worsening as an increase of ≥2.0 if baseline EDSS score was

Background: Sideline diagnostic tests for concussion are vulnerable to volitional poor performance (“sandbagging”) on baseline assessments, motivated by desire to subvert concussion detection and p...

Objective We sought to review the literature on cerebrospinal fluid (CSF) testing in patients with COVID-19 for evidence of viral neuroinvasion by SARS-CoV-2. Methods We performed a systematic review of Medline and Embase between December 1, 2019 and November 18, 2020 to identify case reports or series of patients who had COVID-19 diagnosed based on positive SARS-CoV-2 polymerase chain reaction (PCR) or serologic testing and had CSF testing due to a neurologic symptom. Results We identified 242 relevant documents which included 430 patients with COVID-19 who had acute neurological symptoms prompting CSF testing. Of those, 321 (75%) patients had symptoms that localized to the central nervous system (CNS). Of 304 patients whose CSF was tested for SARS-CoV-2 PCR, there were 17 (6%) whose test was positive, all of whom had symptoms that localized to the central nervous system (CNS). The majority (13/17, 76%) of these patients were admitted to the hospital because of neurological symptoms. Of 58 patients whose CSF was tested for SARS-CoV-2 antibody, 7 (12%) had positive antibodies with evidence of intrathecal synthesis, all of whom had symptoms that localized to the CNS. Of 132 patients who had oligoclonal bands evaluated, 3 (2%) had evidence of intrathecal antibody synthesis. Of 77 patients tested for autoimmune antibodies in the CSF, 4 (5%) had positive findings. Conclusion Detection of SARS-CoV-2 in CSF via PCR or evaluation for intrathecal antibody synthesis appears to be rare. Most neurological complications associated with SARS- CoV-2 are unlikely to be related to direct viral neuroinvasion.

STRIVE was a 4-year, multicenter, observational, open-label, single-arm study of natalizumab treatment in anti-JC virus antibody-negative (JCV-negative) relapsing-remitting multiple sclerosis (RRMS) patients with disease duration ≤ 3 years. The objective of STRIVE was to examine no evidence of disease activity (NEDA) status and predictors of NEDA in natalizumab-treated patients with early RRMS.Proportions of patients with NEDA were evaluated along with baseline predictors of NEDA, annualized relapse rate, 24-week confirmed disability worsening (CDW), magnetic resonance imaging assessments (T2 and gadolinium-enhancing lesions), and serious adverse events.In years 1 and 2, 56.1% (95% confidence interval [CI] 48.7-63.4%) and 73.6% (95% CI 66.2-80.2%) of patients (intent-to-treat population [N = 222]), respectively, achieved NEDA. In years 3 and 4, 84.6% (95% CI 78.0-89.9%) and 91.9% (95% CI 86.4-95.8%) of patients, respectively, achieved Clinical NEDA (no relapses or 24-week CDW). Baseline predictors of NEDA in year 4 were Expanded Disability Status Scale score ≤ 2.0 (odds ratio [OR] = 3.85 [95% CI 1.54-9.63]; p = 0.004) and T2 lesion volume 4 cc (OR = 0.39 [95% CI 0.15-0.98]; p = 0.046), with the latter also predicting Clinical NEDA in year 4 (OR = 0.21 [95% CI 0.05-0.92]; p = 0.038). The cumulative probability of CDW at year 4 was 19.3%. Serious adverse events were reported in 11.3% of patients.These results support the long-term safety and effectiveness of natalizumab. Baseline predictors of NEDA help to inform benefit-risk assessments of natalizumab treatment in JCV-negative patients with early RRMS.ClinicalTrials.gov identifier NCT01485003.

Background Evolution of brain magnetic resonance imaging (MRI) findings in critically ill patients with coronavirus disease 2019 (COVID-19) is unknown. Methods We retrospectively reviewed 4530 critically ill patients with COVID-19 admitted to three tertiary care hospitals in New York City from March 1 to June 30, 2020 to identify patients who had more than one brain MRI. We reviewed the initial and final MRI for each patient to (1) measure the percent change in the bicaudate index and third ventricular diameter and (2) evaluate changes in the presence and severity of white matter changes. Results Twenty-one patients had two MRIs separated by a median of 22 [Interquartile range (IQR) 14–30] days. Ventricle size increased for 15 patients (71%) between scans [median bicaudate index 0.16 (IQR 0.126–0.181) initially and 0.167 (IQR 0.138–0.203) on final imaging (p

Coronavirus disease 2019 (COVID-19) is associated with a high inflammatory burden that can induce severe respiratory disease among other complications; vascular and neurological damage has emerged as a key threat to COVID-19 patients. Risk of severe infection and mortality increases with age, male sex, and comorbidities including cardiovascular disease, hypertension, obesity, diabetes, and chronic pulmonary disease. We review clinical and neuroradiological findings in five patients with COVID-19 who suffered severe neurological disease and illustrate the pathological findings in a 7-year-old boy with COVID-19-induced encephalopathy whose brain tissue sample showed angiocentric mixed mononuclear inflammatory infiltrate. We summarize the structural and functional properties of the virus including the molecular processes that govern the binding to its membrane receptors and cellular entry. In addition, we review clinical and experimental evidence in patients and animal models that suggests coronaviruses enter into the central nervous system (CNS), either via the olfactory bulb or through hematogenous spread. We discuss suspected pathophysiological mechanisms including direct cellular infection and associated recruitment of immune cells and neurovirulence, at least in part, mediated by cytokine secretion. Moreover, contributing to the vascular and neurological injury, coagulopathic disorders play an important pathogenic role. We survey the molecular events that contribute to the thrombotic microangiopathy. We describe the neurological complications associated with COVID-19 with a focus on the potential mechanisms of neurovascular injury. Our thesis is that following infection, three main pathophysiological processes-inflammation, thrombosis, and vascular injury-are responsible for the neurological damage and diverse pathology seen in COVID-19 patients.

Highlights • Multiple neuro-ophthalmological manifestations have been described in association with COVID-19. • These include optic neuritis, cranial nerve palsies, eye movement abnormalities and visual field defects. • The mechanisms of involvement tend to fall within three general categories – a post-viral inflammatory syndrome, sequelae of a proinflammatory state, and the result of systemic abnormalities including hypoxia and severe hypertension., Multiple neuro-ophthalmological manifestations have been described in association with COVID-19. These symptoms and signs may be the result of a range of pathophysiological mechanisms throughout the course from acute illness to recovery phase. Optic nerve dysfunction, eye movement abnormalities and visual field defects have been described.

Dr. Dinkin et al. reported 2 cases with MRI confirmation of cranial nerve inflammation within several days of systemic symptoms of the novel coronavirus disease 2019 (COVID-19). Both patients tested positive for SARS-CoV-2 by PCR from a nasal swab, and both were treated with hydroxychloroquine (one also with intravenous immunoglobulin), with mild short-term improvement. The authors suggest the inflammatory cranial neuropathies could have been because of a postviral immune-related response. Dr. Machado wonders whether the cranial neuropathies could have resulted from direct viral invasion, given their onset shortly after the viral symptoms started. As noted by Gutierrez-Ortiz et al. (Dinkin et al., reference 2 below) 2 patients developed evidence of cranial nerve inflammation and autoimmune neuropathy within 3–5 days of COVID-19 symptom onset. Each of these 4 cases highlight the accelerated time course of inflammatory cranial neuropathies after systemic manifestations of COVID-19, which seems to be more rapid than has been typically reported for variants of Guillain-Barre syndrome after other infectious illnesses. These observations may also support that there is an asymptomatic phase of this viral infection during which an immune response may be generated. Dr. Dinkin et al. reported 2 cases with MRI confirmation of cranial nerve inflammation within several days of systemic symptoms of the novel coronavirus disease 2019 (COVID-19). Both patients tested positive for SARS-CoV-2 by PCR from a nasal swab, and both were treated with hydroxychloroquine (one also with intravenous immunoglobulin), with mild short-term improvement. The authors suggest the inflammatory cranial neuropathies could have been because of a postviral immune-related response. Dr. Machado wonders whether the cranial neuropathies could have resulted from direct viral invasion, given their onset shortly after the viral symptoms started. As noted by Gutierrez-Ortiz et al. (Dinkin et al., reference 2 below) 2 patients developed evidence of cranial nerve inflammation and autoimmune neuropathy within 3–5 days of COVID-19 symptom onset. Each of these 4 cases highlight the accelerated time course of inflammatory cranial neuropathies after systemic manifestations of COVID-19, which seems to be more rapid than has been typically reported for variants of Guillain-Barre syndrome after other infectious illnesses. These observations may also support that there is an asymptomatic phase of this viral infection during which an immune response may be generated.

In an effort to grow our understanding of the neurologic complications of the novel human coronavirus, SARS-CoV-2, Drs. Gutierrez-Ortiz et al. reported a patient with the Miller Fisher syndrome and another patient with polyneuritis cranialis. Several days earlier, both patients manifested respiratory and systemic symptoms consistent with the coronavirus disease 2019 (COVID-19) and confirmed by oropharyngeal swab. Drs. Ni and Xu found this report of autoimmune-related peripheral neuropathy consistent with known complications of the Zika virus—a single-stranded RNA virus similar to coronavirus but actually a member of the genus Flavivirus. They inquired whether the authors tested the patients for other common viruses and evaluated for the presence of antibodies to SARS-CoV-2 in the CSF. In response, the authors indicated they did not test the CSF for antibodies to SARS-CoV-2 because of the lack of validity for the assay. Owing to healthcare limitations during the pandemic, only the first patient had their CSF tested for other CNS pathogens (negative for enterovirus, herpes simplex virus type 1 and 2, varicella zoster virus, and neurosyphilis). This patient also had a negative PCR test for SARS-CoV2 in the CSF. The temporal relationship between symptom onset of COVID-19 in these patients and the development of neurologic manifestations—within 3–5 days—argue for a strong association of SARS CoV-2 and autoimmune-related peripheral neuropathy. In an effort to grow our understanding of the neurologic complications of the novel human coronavirus, SARS-CoV-2, Drs. Gutierrez-Ortiz et al. reported a patient with the Miller Fisher syndrome and another patient with polyneuritis cranialis. Several days earlier, both patients manifested respiratory and systemic symptoms consistent with the coronavirus disease 2019 (COVID-19) and confirmed by oropharyngeal swab. Drs. Ni and Xu found this report of autoimmune-related peripheral neuropathy consistent with known complications of the Zika virus—a single-stranded RNA virus similar to coronavirus but actually a member of the genus Flavivirus. They inquired whether the authors tested the patients for other common viruses and evaluated for the presence of antibodies to SARS-CoV-2 in the CSF. In response, the authors indicated they did not test the CSF for antibodies to SARS-CoV-2 because of the lack of validity for the assay. Owing to healthcare limitations during the pandemic, only the first patient had their CSF tested for other CNS pathogens (negative for enterovirus, herpes simplex virus type 1 and 2, varicella zoster virus, and neurosyphilis). This patient also had a negative PCR test for SARS-CoV2 in the CSF. The temporal relationship between symptom onset of COVID-19 in these patients and the development of neurologic manifestations—within 3–5 days—argue for a strong association of SARS CoV-2 and autoimmune-related peripheral neuropathy.

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Objective Investigations have found associations of homonymous thinning of the macular ganglion cell/ inner-plexiform layer (GCIPL) with demyelinating lesions in the post-chiasmal visual pathway among patients with multiple sclerosis (MS). Retinal thinning may also occur through retrograde trans-synaptic degeneration, a process by which lesions in post-geniculate visual pathway structures lead to thinning of the GCIPL across thalamic synapses. The purpose of our study was to determine the frequency of homonymous hemimacular thinning that occurs in association with post-chiasmal visual pathway demyelinating lesions in patients with MS and other demyelinating diseases. Methods Adult patients with demyelinating diseases (MS, neuromyelitis optica spectrum disorder [NMOSD], myelin oligodendrocyte glycoprotein antibody disease (anti-MOG)) who were participants in an ongoing observational study of visual pathway structure and function were analyzed for the presence of hemimacular GCIPL thinning on OCT scans. Brain MRI scans were examined for the presence of post-geniculate visual pathway demyelinating lesions. Results Among 135 participants in the visual pathway study, 5 patients (3.7%) had homonymous hemimacular GCIPL thinning. Eleven patients (8.1%) had a whole+half pattern of GCIPL thinning, characterized by hemimacular thinning in one eye and circumferential macular thinning in the contralateral eye. All but one patient with homonymous hemimacular thinning had demyelinating lesions in the post-geniculate visual pathway; however, these lesions were located in both cerebral hemispheres. Conclusion Homonymous hemimacular thinning in the GCIPL by OCT is associated with post-chiasmal visual pathway demyelinating lesions but it appears to be a relatively uncommon contributor to GCIPL loss. Patients with this pattern of GCIPL often fail to complain of hemifield visual loss. Future studies with prospective and detailed MR imaging may be able to more closely associate demyelinating lesions in anatomically appropriate regions of the post-chiasmal visual pathways with homonymous hemimacular thinning.

ObjectiveTo outline changes made to a neurology residency program in response to coronavirus disease 2019 (COVID-19).MethodsIn early March 2020, the first cases of COVID-19 were announced in the United States. New York City quickly became the epicenter of a global pandemic, and our training program needed to rapidly adapt to the increasing number of inpatient cases while being mindful of protecting providers and continuing education. Many of these changes unfolded over days, including removing residents from outpatient services, minimizing the number of residents on inpatient services, deploying residents to medicine services and medical intensive care units, converting continuity clinic patient visits to virtual options, transforming didactics to online platforms only, and maintaining connectedness in an era of social distancing. We have been able to accomplish this through daily virtual meetings among leadership, faculty, and residents.ResultsOver time, our program has successfully rolled out initiatives to service the growing number of COVID-related inpatients while maintaining neurologic care for those in need and continuing our neurologic education curriculum.ConclusionIt has been necessary and feasible for our residency training program to undergo rapid structural changes to adapt to a medical crisis. The key ingredients in doing this successfully have been flexibility and teamwork. We suspect that many of the implemented changes will persist long after the COVID-19 crisis has passed and will change the approach to neurologic and medical training.

Struggling trainees exist in all residency programs across all fields. Remediation, the act of improving deficiencies in struggling trainees, is necessary to promote the graduation of competent physicians. Deficiencies may be primarily cognitive or behavioral, and occasionally physical limitations do arise during residency. Remediation is challenging for all parties involved, and there is a paucity of literature to help guide the most effective process. In this review, we outline key principles of effective remediation of a struggling trainee in the modern era of medical education. A systematic approach that begins early, is consistent, and remains sensitive to a trainee's need for self-reflection in a nonjudgmental culture is essential for successfully remediating a trainee.

A 41-year-old man with a history of low testosterone on androgen therapy presented to the emergency department complaining of acute onset of the worst headache of his life. He reported being well until 6 hours earlier, when he was resting in his hotel room and experienced a thunderclap headache. The headache was initially described as retro-orbital, left-sided, associated with vomiting, and extending to the occiput. It was maximal within moments of onset. There were no associated visual complaints, weakness, numbness, or tingling. On initial examination, he was noted to have preserved mental status. The cranial nerve examination showed intact visual fields, normal extraocular motility, and no evidence of papilledema. Sensorimotor function was intact and symmetric throughout, and his gait was stable and narrow-based. Initial laboratory studies including blood count and metabolic panel were unremarkable. He was administered oxygen via nasal cannula, metoclopramide, and diphenhydramine without improvement.

OBJECTIVE: Measures of rapid automatized naming (RAN) have been used for over 50 years to capture vision-based aspects of cognition. The Mobile Universal Lexicon Evaluation System (MULES) is a test of rapid picture naming under investigation for detection of concussion and other neurological disorders. MULES was designed as a series of 54 grouped color photographs (fruits, random objects, animals) that integrates saccades, color perception and contextual object identification. Recent changes to the MULES test have been made to improve ease of use on the athletic sidelines. Originally an 11 × 17-inch single-sided paper, the test has been reduced to a laminated 8.5 × 11-inch double-sided version. We identified performance changes associated with transition to the new, MULES, now sized for the sidelines, and examined MULES on the sideline for sports-related concussion. METHODS: We administered the new laminated MULES to a group of adult office volunteers as well as youth and collegiate athletes during pre-season baseline testing. Athletes with concussion underwent sideline testing after injury. Time scores for the new laminated MULES were compared to those for the larger version (big MULES). Results: Among 501 athletes and office volunteers (age 16 ± 7 years, range 6–59, 29% female), average test times at baseline were 44.4 ± 14.4 s for the new laminated MULES (n = 196) and 46.5 ± 16.3 s for big MULES (n = 248). Both versions were completed by 57 participants, with excellent agreement (p < 0.001, linear regression, accounting for age). Age was a predictor of test times for both MULES versions, with longer times noted for younger participants (p < 0.001). Among 6 athletes with concussion thus far during the fall sports season (median age 15 years, range 11–21) all showed worsening of MULES scores from pre-season baseline (median 4.0 s, range 2.1–16.4). CONCLUSION: The MULES test has been converted to an 11 × 8.5-inch laminated version, with excellent agreement between versions across age groups. Feasibly administered at pre-season and in an office setting, the MULES test shows preliminary evidence of capacity to identify athletes with sports-related concussion.

BACKGROUND: The King-Devick (K-D) test of rapid number naming is a reliable visual performance measure that is a sensitive sideline indicator of concussion when time scores worsen (lengthen) from preseason baseline. Within cohorts of youth athletes

The 2010 McDonald criteria for the diagnosis of multiple sclerosis are widely used in research and clinical practice. Scientific advances in the past 7 years suggest that they might no longer provide the most up-to-date guidance for clinicians and researchers. The International Panel on Diagnosis of Multiple Sclerosis reviewed the 2010 McDonald criteria and recommended revisions. The 2017 McDonald criteria continue to apply primarily to patients experiencing a typical clinically isolated syndrome, define what is needed to fulfil dissemination in time and space of lesions in the CNS, and stress the need for no better explanation for the presentation. The following changes were made: in patients with a typical clinically isolated syndrome and clinical or MRI demonstration of dissemination in space, the presence of CSF-specific oligoclonal bands allows a diagnosis of multiple sclerosis; symptomatic lesions can be used to demonstrate dissemination in space or time in patients with supratentorial, infratentorial, or spinal cord syndrome; and cortical lesions can be used to demonstrate dissemination in space. Research to further refine the criteria should focus on optic nerve involvement, validation in diverse populations, and incorporation of advanced imaging, neurophysiological, and body fluid markers.

To evaluate the performance of the EyeTribe compared to the EyeLink for eye movement recordings during a rapid number naming test in healthy control participants.With the increasing accessibility of portable, economical, video-based eye trackers such as the EyeTribe, there is growing interest in these devices for eye movement recordings, particularly in the domain of sports-related concussion. However, prior to implementation there is a primary need to establish the validity of these devices. One current limitation of portable eye trackers is their sampling rate (30-60 samples per second, or Hz), which is typically well below the benchmarks achieved by their research-grade counterparts (e.g., the EyeLink, which samples at 500-2000 Hz).We compared video-oculographic measurements made using the EyeTribe with those of the EyeLink during a digitized rapid number naming task (the King-Devick test) in a convenience sample of 30 controls.EyeTribe had loss of signal during recording, and failed to reproduce the typical shape of saccadic main sequence relationships. In addition, EyeTribe data yielded significantly fewer detectable saccades and displayed greater variance of inter-saccadic intervals than the EyeLink system.Caution is advised prior to implementation of low-resolution eye trackers for objective saccade assessment and sideline concussion screening.

Objective We reviewed the literature on cerebrospinal fluid (CSF) testing in patients with altered olfactory/gustatory function due to COVID-19 for evidence of viral neuroinvasion. Methods We performed a systematic review of Medline and Embase to identify publications that described at least one patient with COVID-19 who had altered olfactory/gustatory function and had CSF testing performed. The search ranged from December 1, 2019 to November 18, 2020. Results We identified 51 publications that described 70 patients who met inclusion criteria. Of 51 patients who had CSF SARS-CoV-2 PCR testing, 3 (6%) patients had positive results and 1 (2%) patient had indeterminate results. Cycle threshold (Ct; the number of amplification cycles required for the target gene to exceed the threshold, which is inversely related to viral load) was not provided for the patients with a positive PCR. The patient with indeterminate results had a Ct of 37 initially, then no evidence of SARS-CoV-2 RNA on repeat testing. Of 6 patients who had CSF SARS-CoV-2 antibody testing, 3 (50%) were positive. Testing to distinguish intrathecal antibody synthesis from transudation of antibodies to the CSF via breakdown of the blood-brain barrier was performed in 1/3 (33%) patients; this demonstrated antibody transmission to the CSF via transudation. Conclusion Detection of SARS-CoV-2 in CSF via PCR or evaluation for intrathecal antibody synthesis appears to be rare in patients with altered olfactory/gustatory function. While pathology studies are needed, our review suggests it is unlikely that these symptoms are related to viral neuroinvasion.

A 4-year-old girl presented to an outside hospital after waking up with inability to stand or walk. She had a viral prodrome with fever for several days. Brain and spine MRIs revealed lesions in the left caudate, bilateral insular cortex, right thalamus, and right temporal cortex as well as longitudinally extensive cervical and thoracic cord lesions. Spinal fluid showed pleocytosis with 200 white blood cells (mixed neutrophils and lymphocytes), elevated CSF protein (103 mg/dL), and negative bacterial and viral cultures and PCR. Oligoclonal bands were negative. During the hospitalization, she developed encephalopathy and was diagnosed with acute disseminated encephalomyelitis (ADEM). She received a course of IV steroids followed by an oral steroid taper, and her neurologic symptoms resolved fully. However, within 2 weeks, she experienced painless bilateral vision loss. A repeat brain and orbit MRI revealed swelling in the bilateral optic nerves and decrease in size or resolution of prior brain lesions. Optic neuritis (ON) was diagnosed based on clinical and radiographic presentation. She was given a course of IV immunoglobulin, followed by IV steroids, and a longer steroid taper.

Background Given that post-traumatic headache is one of the most prevalent and long-lasting post-concussion sequelae, causes significant morbidity, and might be associated with slower neurocognitive recovery, we sought to evaluate the use of concussion screening scores in a concussion clinic population to assess for post-traumatic headache. Methods This is a retrospective cross-sectional study of 254 concussion patients from the New York University (NYU) Concussion Registry. Data on the headache characteristics, concussion mechanism, concussion screening scores were collected and analyzed. Results 72% of the patients had post-traumatic headache. About half (56.3%) were women. The mean age was 35 (SD 16.2). 90 (35%) patients suffered from sport-related concussions (SRC). Daily post-traumatic headache patients had higher Sport Concussion Assessment Tool (SCAT)-3 symptom severity scores than the non-daily post-traumatic headache and the headache-free patients (50.2 [SD 28.2] vs. 33.1 [SD 27.5] vs. 21.6 SD23], p

Low-contrast letter acuity (LCLA) has emerged as the leading outcome measure to assess visual disability in multiple sclerosis (MS) research. As visual dysfunction is one of the most common manifestations of MS, sensitive visual outcome measures are important in examining the effect of treatment. Low-contrast acuity captures visual loss not seen in high-contrast visual acuity (HCVA) measurements. These issues are addressed by the MS Outcome Assessments Consortium (MSOAC), including representatives from advocacy organizations, Food and Drug Administration (FDA), European Medicines Agency (EMA), National Institute of Neurological Disorders and Stroke (NINDS), academic institutions, and industry partners along with persons living with MS. MSOAC goals are acceptance and qualification by regulators of performance outcomes that are highly reliable and valid, practical, cost-effective, and meaningful to persons with MS. A critical step is elucidation of clinically relevant benchmarks, well-defined degrees of disability, and gradients of change that are clinically meaningful. This review shows that MS and disease-free controls have similar median HCVA, while MS patients have significantly lower LCLA. Deficits in LCLA and vision-specific quality of life are found many years after an episode of acute optic neuritis, even when HCVA has recovered. Studies reveal correlations between LCLA and the Expanded Disability Status Score (EDSS), Multiple Sclerosis Functional Composite (MSFC), retinal nerve fiber layer (RNFL) and ganglion cell layer plus inner plexiform layer (GCL + IPL) thickness on optical coherence tomography (OCT), brain magnetic resonance imaging (MRI), visual evoked potential (VEP), electroretinogram (ERG), pupillary function, and King-Devick testing. This review also concludes that a 7-point change in LCLA is clinically meaningful. The overall goal of this review is to describe and characterize the LCLA metric for research and clinical use among persons with MS.

Identifying concussion and initiating removal from play is challenging for even the most diligent youth sports organizations. Empowering parents to implement removal from play protocols and sideline testing may be the most practical plan at community levels to protect young athletes. We developed paradigms for community-based youth sports teams that incorporated both standard concussion protocols and research investigations. The research studies were designed to determine how sideline tests of vision, cognition and balance augment the capacity for parents and other responsible adults to identify youth athletes with concussion in ice hockey, football, lacrosse and cheerleading. Research-based sideline tests were performed at pre-season baseline sessions and during the season at the time of injury or as soon as symptoms were recognized by trained volunteer parent team testers. The combination of standard concussion protocols and research studies were performed for 510 athletes, aged 5-17 years, over 2.5 years through 5 athletic seasons. To implement the protocols and studies, approximately 80 student volunteers and parents were educated and trained on early concussion recognition and on baseline and sideline test administration. Over 80% of parent-identified head injuries were physician-confirmed concussions. Of the sideline tests performed, over two-thirds were administered within 24 hours of injury; the rest were performed within an average of 2.6 days post-injury since some athletes had delayed development of symptoms. Removal from play guidelines and standard concussion evaluation protocols were maintained in the context of the sideline testing research investigations. Based on this observational study, parents of youth athletes can be successfully empowered to perform rapid sideline tests in the context of existing concussion protocols. Implementation of objective testing may improve concussion identification and shift the culture of advocacy and responsibility towards parent groups to promote safety of young athletes. Ongoing investigations will further examine the impact of these programs on concussion management in youth sports.

This study introduces a rapid picture naming test, the Mobile Universal Lexicon Evaluation System (MULES), as a novel, vision-based performance measure for concussion screening. The MULES is a visual-verbal task that includes 54 original photographs of fruits, objects and animals. We piloted MULES in a cohort of volunteers to determine feasibility, ranges of picture naming responses, and the relation of MULES time scores to those of King-Devick (K-D), a rapid number naming test.A convenience sample (n=20, age 34±10) underwent MULES and K-D (spiral bound, iPad versions). Administration order was randomized; MULES tests were audio-recorded to provide objective data on temporal variability and ranges of picture naming responses.Scores for the best of two trials for all tests were 40-50s; average times required to name each MULES picture (0.72±0.14s) was greater than those needed for each K-D number ((spiral: 0.33±0.05s, iPad: 0.36±0.06s, 120 numbers), p0.0001, paired t-test). MULES scores showed the greatest degree of improvement between trials (9.4±4.8s, p0.0001 for trials 1 vs. 2), compared to K-D (spiral 1.5±3.3s, iPad 1.8±3.4s). Shorter MULES times demonstrated moderate and significant correlations with shorter iPad but not spiral K-D times (r=0.49, p=0.03).The MULES test is a rapid picture naming task that may engage more extensive neural systems than more commonly used rapid number naming tasks. Rapid picture naming may require additional processing devoted to color perception, object identification, and categorization. Both tests rely on initiation and sequencing of saccadic eye movements.

Opsoclonus consists of bursts of involuntary, multidirectional, back-to-back saccades without an intersaccadic interval. We report a 60-year-old man with post-concussive headaches and disequilibrium who had small amplitude opsoclonus in left gaze, along with larger amplitude flutter during convergence. Examination was otherwise normal and brain MRI was unremarkable. Video-oculography demonstrated opsoclonus predominantly in left gaze and during pursuit in the left hemifield, which improved as post-concussive symptoms improved. Existing theories of opsoclonus mechanisms do not account for this eye position-dependence. We discuss theoretical mechanisms of this behavior, including possible dysfunction of frontal eye field and/or cerebellar vermis neurons; review ocular oscillations in traumatic brain injury; and consider the potential relationship between the larger amplitude flutter upon convergence and post-traumatic ocular oscillations.

Objective To determine the underlying etiology in a patient with progressive dementia with extrapyramidal signs and chronic inflammation referred to the National Institutes of Health Undiagnosed Diseases Program. Methods Extensive investigations included metabolic profile, autoantibody panel, infectious etiologies, genetic screening, whole exome sequencing, and the phage-display assay, VirScan, for viral immune responses. An etiological diagnosis was established postmortem. Results Using VirScan, enrichment of dengue viral antibodies was detected in cerebrospinal fluid as compared to serum. No virus was detected in serum or cerebrospinal fluid, but postmortem analysis confirmed dengue virus in the brain by immunohistochemistry, in situ hybridization, quantitative polymerase chain reaction, and sequencing. Dengue virus was also detectable by polymerase chain reaction and sequencing from brain biopsy tissue collected 33 months antemortem, confirming a chronic infection despite a robust immune response directed against the virus. Immunoprofiling and whole exome sequencing of the patient did not reveal any immunodeficiency, and sequencing of the virus demonstrated wild-type dengue virus in the central nervous system. Interpretation Dengue virus is the most common arbovirus worldwide and represents a significant public health concern. Infections with dengue virus are usually self-limiting, and chronic dengue infections have not been previously reported. Our findings suggest that dengue virus infections may persist in the central nervous system causing a panencephalitis and should be considered in patients with progressive dementia with extrapyramidal features in endemic regions or with relevant travel history. Furthermore, this work highlights the utility of comprehensive antibody profiling assays to aid in the diagnosis of encephalitis of unknown etiology. ANN NEUROL 2019;86:695-703.

OBJECTIVES: Using optic coherence tomography (OCT), to determine relationships with visual function (VF) and disability in patients with multiple sclerosis (MS) and a) ganglion cell-inner plexiform layer (GCIPL) b) peripapillary retinal nerve fiber layer (pRNFL); and c) Bruch’s membrane opening minimum rim width (BMO-MRW) thicknesses. METHODS: Sixty-eight MS patients and 22 healthy controls (HCs) underwent spectral-domain OCT, and 100%-contrast visual acuity (VA), 2.5%-, and 1.25%-contrast letter-acuity (LA), and Expanded Disability Status Scale (EDSS) testing. Mixed-effects linear regression models, accounting for within-subject, inter-eye correlations, were used to assess relationships. RESULTS: The MS cohort exhibited significantly lower BMO-MRW (p=0.01), pRNFL at 3.7 mm, 4.1 mm, and 4.7 mm diameters surrounding the optic disc (p

The Mobile Universal Lexicon Evaluation System (MULES) is a test of rapid picture naming under investigation. Measures of rapid automatic naming (RAN) have been used for over 50 years to capture aspects of vision and cognition. MULES was designed as a series of 54 grouped color photographs (fruits, random objects, animals) that integrates saccades, color perception and contextual object identification. We examined MULES performance in youth, collegiate and professional athletes at pre-season baseline and at the sidelines following concussion.Our study teams administered the MULES to youth, collegiate and professional athletes during pre-season baseline testing. Sideline post-concussion time scores were compared to pre-season baseline scores among athletes with concussion to determine degrees and directions of change.Among 681 athletes (age 17 ± 4 years, range 6-37, 38% female), average test times at baseline were 41.2 ± 11.2 s. The group included 280 youth, 357 collegiate and 44 professional athletes; the most common sports were ice hockey (23%), soccer (17%) and football (11%). Age was a predictor of MULES test times, with longer times noted for younger participants (P .001, linear regression). Consistent with other timed performance measures, significant learning effects were noted for the MULES during baseline testing with trial 1 test times (mean 49.2 ± 13.1 s) exceeding those for trial 2 (mean 41.3 ± 11.2 s, P .0001, paired t-test). Among 17 athletes with concussion during the sports seasons captured to date (age 18 ± 3 years), all showed increases (worsening) of MULES time scores from pre-season baseline (median increase 11.2 s, range 0.6-164.2, P = .0003, Wilcoxon signed-rank test). The Symptom Severity Score from the SCAT5 Symptom Evaluation likewise worsened from pre-season baseline following injury among participants with concussion (P = .002).Concussed athletes demonstrate worsening performance on the MULES test compared to their baseline time scores. This test samples a wide network of brain pathways and complements other vision-based measures for sideline concussion assessment. The MULES test demonstrates capacity to identify athletes with sports-related concussion.

A 17-year-old man was brought to the emergency department with several weeks of irritability, insomnia, and depression, followed by 1 week of nonsensical speech and visual, nonthreatening hallucinations. His medical history included depression and Sydenham chorea diagnosed when he was aged 12 years with positive ASO titer and anti-DNAse B antibodies. The National Multiple Sclerosis Society Case Conference Proceedings are both a live educational Webinar, in conjunction with a peer review publishing initiative from the monthly “Diagnostic and Treatment Challenges in MS and Neuroimmunology Webinars”; sponsored by the National Multiple Sclerosis Society Fellowship Training Program; and Directed by Elliot M. Frohman, MD, PhD, and Teresa C. Frohman, MPAS, MSCS, PA-C, from the Dell Medical School at the University of Texas at Austin. The authors wish to express their gratitude to their medical illustrator, Mr. Jason Ooi, for his evidence-based rendition of the putative mechanisms underlying the development of anti-NMDAR mediated encephalitis.

Functional (nonorganic) visual loss is frequently encountered in ophthalmic and neurologic practice, occurring in 0.5–5% of patients presenting with vision loss. Patients with functional visual loss may be misdiagnosed because of the paucity of objective findings on examination. Identifying such patients is extremely important to avoid unnecessary laboratory testing and to facilitate secondary gain. Likewise, it is also imperative to be able to identify those patients with organic vision loss with superimposed functional vision loss. Although the characterization of the psychological profile of patients with functional vision loss is helpful, for the ophthalmologist or neurologist, a familiarity with diagnostic strategies used to identify functional vision loss is more important. In this chapter, terminology is clarified, then patient types and their potential interactions with the examiner are described. The methods used to diagnose functional vision loss are reviewed in detail, followed by a brief description of other neuro-ophthalmologic manifestations of nonorganic disease.

Opsoclonus consists of bursts of involuntary, multidirectional, back-to-back saccades without an intersaccadic interval. We report a 60-year-old man with post-concussive headaches and disequilibrium who had small amplitude opsoclonus in left gaze, along with larger amplitude flutter during convergence. Examination was otherwise normal and brain MRI was unremarkable. Video-oculography demonstrated opsoclonus predominantly in left gaze and during pursuit in the left hemifield, which improved as post-concussive symptoms improved. Existing theories of opsoclonus mechanisms do not account for this eye position-dependence. We discuss theoretical mechanisms of this behavior, including possible dysfunction of frontal eye field and/or cerebellar vermis neurons; review ocular oscillations in traumatic brain injury; and consider the potential relationship between the larger amplitude flutter upon convergence and post-traumatic ocular oscillations.

The time-sensitive nature of acute ischemic stroke diagnosis and treatment with IV tissue plasminogen activator (tPA) presents a unique set of challenges for obtaining informed consent. Despite guideline recommendations that informed consent is indicated for thrombolysis,1 there is no accepted standardized consent process for thrombolytic administration and wide variability has been reported.2 Refusal of IV-tPA based on incorrect or incomplete understanding of its risks and benefits has the potential to affect morbidity after ischemic stroke, particularly for minority race/ethnic groups.3

BackgroundLittle is known regarding long-term outcomes of patients hospitalized with COVID-19.MethodsWe conducted a prospective study of 6-month outcomes of hospitalized COVID-19 patients. Patients with new neurological complications during hospitalization who survived were propensity score-matched to COVID-19 survivors without neurological complications hospitalized during the same period. The primary 6-month outcome was multivariable ordinal analysis of the modified Rankin Scale(mRS) comparing patients with or without neurological complications. Secondary outcomes included: activities of daily living (ADLs;Barthel Index), telephone Montreal Cognitive Assessment and Neuro-QoL batteries for anxiety, depression, fatigue and sleep.ResultsOf 606 COVID-19 patients with neurological complications, 395 survived hospitalization and were matched to 395 controls; N=196 neurological patients and N=186 controls completed follow-up. Overall, 346/382 (91%) patients had at least one abnormal outcome: 56% had limited ADLs, 50% impaired cognition, 47% could not return to work and 62% scored worse than average on ≥1 Neuro-QoL scale (worse anxiety 46%, sleep 38%, fatigue 36%, and depression 25%). In multivariable analysis, patients with neurological complications had worse 6-month mRS (median 4 vs. 3 among controls, adjusted OR 2.03, 95%CI 1.22-3.40, P=0.01), worse ADLs (aOR 0.38, 95%CI 0.29-0.74, P=0.01) and were less likely to return to work than controls (41% versus 64%, P=0.04). Cognitive and Neuro-QOL metrics were similar between groups.ConclusionsAbnormalities in functional outcomes, ADLs, anxiety, depression and sleep occurred in over 90% of patients 6-months after hospitalization for COVID-19. In multivariable analysis, patients with neurological complications during index hospitalization had significantly worse 6-month functional outcomes than those without.

Objective The Mobile Universal Lexicon Evaluation System (MULES) is a rapid picture naming task that captures extensive brain networks involving neurocognitive, afferent/efferent visual, and language pathways. Many of the factors captured by MULES may be abnormal in sleep-deprived residents. This study investigates the effect of sleep deprivation in post-call residents on MULES performance. Methods MULES, consisting of 54 color photographs, was administered to a cohort of neurology residents taking 24-hour in-hospital call (n = 18) and a group of similar-aged controls not taking call (n = 18). Differences in times between baseline and follow-up MULES scores were compared between the two groups. Results MULES time change in call residents was significantly worse (slower) from baseline (mean 1.2 s slower) compared to non-call controls (mean 11.2 s faster) (P, Highlights • MULES is a rapid picture naming test that captures extensive brain networks. • MULES performance is impaired in sleep deprived residents. • Subjective sleepiness may also affect MULES performance. • MULES may serve as an assessment tool for sleep deprivation in residents.

We report four patients with monocular visual loss for whom optical coherence tomography (OCT) was helpful in distinguishing the sequelae of retinal artery occlusion from those of primary optic neuropathy. Determinations of the peripapillary retinal nerve fiber layer (RNFL) thickness as well as macular retinal layer thicknesses and architecture were used. The major findings in our patients show that changes in the inner retinal layers (including ganglion cell and inner plexiform layer) with disruption of normal macular architecture supports a diagnosis of retinal artery occlusion. Our results support the use of OCT imaging for patients with monocular visual loss of uncertain etiology; macular imaging as well as peripapillary RNFL thickness measurement can be helpful in differentiating primary retinal disease or ischemia from primary disorders of the optic nerve.

Objective Concussion is a major public health problem and considerable efforts are focused on sideline-based diagnostic testing to guide return-to-play decision-making and clinical care. The King–Devick (K–D) test, a sensitive sideline performance measure for concussion detection, reveals slowed reading times in acutely concussed subjects, as compared to healthy controls; however, the normal behavior of eye movements during the task and deficits underlying the slowing have not been defined. Methods Twelve healthy control subjects underwent quantitative eye tracking during digitized K–D testing. Results The total K–D reading time was 51.24 (± 9.7) seconds. A total of 145 saccades (± 15) per subject were generated, with average peak velocity 299.5°/s and average amplitude 8.2°. The average inter-saccadic interval was 248.4 ms. Task-specific horizontal and oblique saccades per subject numbered, respectively, 102 (± 10) and 17 (± 4). Subjects with the fewest saccades tended to blink more, resulting in a larger amount of missing data; whereas, subjects with the most saccades tended to make extra saccades during line transitions. Conclusions Establishment of normal and objective ocular motor behavior during the K–D test is a critical first step towards defining the range of deficits underlying abnormal testing in concussion. Further, it sets the groundwork for exploration of K–D correlations with cognitive dysfunction and saccadic paradigms that may reflect specific neuroanatomic deficits in the concussed brain.

Mild head injury such as concussions and subconcussive repetitive impact may lead to subtle changes in brain function and it is imperative to find sensitive and reliable tests to detect such changes. Tests involving the visual system, in particular eye movements, can incorporate higher cortical functioning and involve diffuse pathways in the brain, including many areas susceptible to head impact. With concussions, the clinical neuro-ophthalmic exam is important for detecting abnormalities in vergence, saccades, pursuit, and visual fixation. On the sidelines, the King–Devick test has been used as a visual performance measure that incorporates eye movements and increases the sensitivity in detecting possible concussions in conjunction with standard sideline tests of cognition, symptom checklists, and balance. Much promise lies in the eye movement laboratory to quantitate changes in saccades and pursuit with concussions using video-oculography. A combination of eye movement tasks coupled with neuroimaging techniques and other objective biomarkers may lead to a better understanding of the anatomical and physiological consequences of concussion and to better understand the natural history of this condition.

In the article, “Neurologic complications of coronavirus infections,” Dr. Nath discussed the central (CNS) and peripheral nervous system (PNS) complications associated with coronaviruses, including what we may encounter with coronavirus disease 2019 (COVID-19). The article prompted several interesting responses from our readers. Dr. Umapathi highlights 5 patients with large artery stroke in the context of severe acute respiratory syndrome (SARS) who were seen in Singapore in 2003, 4 of whom were critically ill with SARS-coronavirus-1 (SARS-CoV-1) and 3 of whom died. Prompted by the findings of venous and pulmonary emboli and sterile vegetations at autopsy in one patient, subsequent critically ill patients apparently received low-molecular-weight heparin (LMWH), yet thromboembolic events continued to be reported. Besides possible direct prothrombotic effects of SARS-CoV-1, Dr. Umapathi postulates that intravenous immunoglobulin (IVIg) use may have contributed to thromboembolic risk in some patients and encourages physicians to be vigilant about such complications with the use of IVIg in critically ill patients with COVID-19, especially in the setting of sedation and iatrogenic paralysis where stroke may be easily missed. The editors note that large controlled clinical trials are now underway to examine the role of full-dose anticoagulation and antiplatelet therapy in patients with COVID-19 who are critically ill with high D-dimers, supporting the observation that a significant amount of the neurologic disability in this disorder may result from vascular complications. In another response, Dr. Machado wonders whether respiratory distress in COVID-19 can be partly explained by CNS infection—specifically brainstem dysfunction—noting that the SARS-CoV-1—similar to SARS-CoV-2, the cause of COVID-19—has been reported in the brainstems of infected patients and experimental animals, potentially invading the brainstem by synaptic routes to the medullary respiratory center. Dr. Machado therefore notes that therapeutic efforts against acute respiratory distress in COVID-19 may benefit from the involvement of neurologists and neurointensivists. In addition, Dr. Serrano-Castro highlights the relatively understudied question of medium- or long-term consequences of COVID-19 in patients with neurodegenerative diseases (NDDs). Noting that chronic neuroinflammation is noted in the pathophysiology of NDDs, Dr. Serrano-Castro wonders whether such sustained neuroinflammation may follow the cytokine storms of SARS-CoV-2 infections, particularly if the virus can remain latent in the CNS, with uncertain repercussions for populations vulnerable to NDDs. Furthermore, Drs. Steyger et al. emphasize the importance of anticipating other neurologic morbidities that may be experienced by COVID-19 survivors in the aftermath of the acute inflammatory response, with sensory system targets potentially including the ear. They note that certain experimental treatments for COVID-19 may carry risks of inner ear toxicity, particularly if coadministered in critical care settings, with the attendant costs of chronic hearing or vestibular dysfunction. They suggest capturing such symptoms and relevant signs during a review of systems and physical examination because systematic clinical observations may not only inform public health and research efforts but also help improve patient outcomes. These responses give us a glimpse of the wide range of potential neurologic considerations with COVID-19, while also underscoring the enduring need for systematically gathered evidence for the incidence, characteristics, natural history, and management of these presentations. In the article, “Neurologic complications of coronavirus infections,” Dr. Nath discussed the central (CNS) and peripheral nervous system (PNS) complications associated with coronaviruses, including what we may encounter with coronavirus disease 2019 (COVID-19). The article prompted several interesting responses from our readers. Dr. Umapathi highlights 5 patients with large artery stroke in the context of severe acute respiratory syndrome (SARS) who were seen in Singapore in 2003, 4 of whom were critically ill with SARS-coronavirus-1 (SARS-CoV-1) and 3 of whom died. Prompted by the findings of venous and pulmonary emboli and sterile vegetations at autopsy in one patient, subsequent critically ill patients apparently received low-molecular-weight heparin (LMWH), yet thromboembolic events continued to be reported. Besides possible direct prothrombotic effects of SARS-CoV-1, Dr. Umapathi postulates that intravenous immunoglobulin (IVIg) use may have contributed to thromboembolic risk in some patients and encourages physicians to be vigilant about such complications with the use of IVIg in critically ill patients with COVID-19, especially in the setting of sedation and iatrogenic paralysis where stroke may be easily missed. The editors note that large controlled clinical trials are now underway to examine the role of full-dose anticoagulation and antiplatelet therapy in patients with COVID-19 who are critically ill with high D-dimers, supporting the observation that a significant amount of the neurologic disability in this disorder may result from vascular complications. In another response, Dr. Machado wonders whether respiratory distress in COVID-19 can be partly explained by CNS infection—specifically brainstem dysfunction—noting that the SARS-CoV-1—similar to SARS-CoV-2, the cause of COVID-19—has been reported in the brainstems of infected patients and experimental animals, potentially invading the brainstem by synaptic routes to the medullary respiratory center. Dr. Machado therefore notes that therapeutic efforts against acute respiratory distress in COVID-19 may benefit from the involvement of neurologists and neurointensivists. In addition, Dr. Serrano-Castro highlights the relatively understudied question of medium- or long-term consequences of COVID-19 in patients with neurodegenerative diseases (NDDs). Noting that chronic neuroinflammation is noted in the pathophysiology of NDDs, Dr. Serrano-Castro wonders whether such sustained neuroinflammation may follow the cytokine storms of SARS-CoV-2 infections, particularly if the virus can remain latent in the CNS, with uncertain repercussions for populations vulnerable to NDDs. Furthermore, Drs. Steyger et al. emphasize the importance of anticipating other neurologic morbidities that may be experienced by COVID-19 survivors in the aftermath of the acute inflammatory response, with sensory system targets potentially including the ear. They note that certain experimental treatments for COVID-19 may carry risks of inner ear toxicity, particularly if coadministered in critical care settings, with the attendant costs of chronic hearing or vestibular dysfunction. They suggest capturing such symptoms and relevant signs during a review of systems and physical examination because systematic clinical observations may not only inform public health and research efforts but also help improve patient outcomes. These responses give us a glimpse of the wide range of potential neurologic considerations with COVID-19, while also underscoring the enduring need for systematically gathered evidence for the incidence, characteristics, natural history, and management of these presentations.

Background and Purpose Patients with the Coronavirus Disease of 2019 (COVID-19) are at increased risk for thrombotic events and mortality. Various anticoagulation regimens are now being considered for these patients. Anticoagulation is known to increase the risk for adverse bleeding events, of which intracranial hemorrhage (ICH) is one of the most feared. We present a retrospective study of 33 patients positive for COVID-19 with neuroimaging-documented ICH and examine anticoagulation use in this population. Methods Patients over the age of 18 with confirmed COVID-19 and radiographic evidence of ICH were included in this study. Evidence of hemorrhage was confirmed and categorized by a fellowship trained neuroradiologist. Electronic health records were analyzed for patient information including demographic data, medical history, hospital course, laboratory values, and medications. Results We identified 33 COVID-19 positive patients with ICH, mean age 61.6 years (range 37–83 years), 21.2% of whom were female. Parenchymal hemorrhages with mass effect and herniation occurred in 5 (15.2%) patients, with a 100% mortality rate. Of the remaining 28 patients with ICH, 7 (25%) had punctate hemorrhages, 17 (60.7%) had small- moderate size hemorrhages, and 4 (14.3%) had a large single site of hemorrhage without evidence of herniation. Almost all patients received either therapeutic dose anticoagulation (in 22 [66.7%] patients) or prophylactic dose (in 3 [9.1] patients) prior to ICH discovery. Conclusions Anticoagulation therapy may be considered in patients with COVID-19 though the risk of ICH should be taken into account when developing a treatment regimen.

Objective We discuss the psychosocial implications of the COVID-19 pandemic as self-reported by housestaff and faculty in the NYU Langone Health Department of Neurology, and summarize how our program is responding to these ongoing challenges. Methods During the period of May 1–4, 2020, we administered an anonymous electronic survey to all neurology faculty and housestaff to assess the potential psychosocial impacts of COVID-19. The survey also addressed how our institution and department are responding to these challenges. This report outlines the psychosocial concerns of neurology faculty and housestaff and the multifaceted support services that our department and institution are offering in response. Faculty and housestaff cohorts were compared with regard to frequencies of binary responses (yes/ no) using the Fisher's exact test. Results Among 130 total survey respondents (91/191 faculty [48%] and 37/62 housestaff [60%]), substantial proportions of both groups self-reported having increased fear (79%), anxiety (83%) and depression (38%) during the COVID-19 pandemic. These proportions were not significantly different between the faculty and housestaff groups. Most respondents reported that the institution had provided adequate counseling and support services (91%) and that the department had rendered adequate emotional support (92%). Participants offered helpful suggestions regarding additional resources that would be helpful during the COVID-19 pandemic. Conclusion COVID-19 has affected the lives and minds of faculty and housestaff in our neurology department at the epicenter of the pandemic. Efforts to support these providers during this evolving crisis are imperative for promoting the resilience necessary to care for our patients and colleagues., Highlights • The psychosocial impact of the COVID-19 pandemic on healthcare providers is enormous. • Neurology faculty and trainees are feeling anxiety and depression during this crisis. • Neurology departments must implement innovative support strategies in response.

Objective To investigate the incidence and spectrum of neuroimaging findings and their prognostic role in hospitalized COVID-19 patients in New York City. Methods This is a retrospective cohort study of 3218 COVID-19 confirmed patients admitted to a major healthcare system (three hospitals) in New York City between March 1, 2020 and April 13, 2020. Clinical data were extracted from electronic medical records, and particularly data of all neurological symptoms were extracted from the imaging reports. Four neuroradiologists evaluated all neuroimaging studies for acute neuroimaging findings related to COVID-19. Results 14.1% of admitted COVID-19 patients had neuroimaging and this accounted for only 5.5% of the total imaging studies. Acute stroke was the most common finding on neuro-imaging, seen in 92.5% of patients with positive neuro-imaging studies, and present in 1.1% of hospitalized COVID-19 patients. Patients with acute large ischemic and hemorrhagic stroke had much higher mortality risk adjusted for age, BMI and hypertension compared to those COVID-19 patients without neuroimaging. (Odds Ratio 6.02 by LR; Hazard Ratio 2.28 by CRR). Conclusions Our study demonstrates acute stroke is the most common neuroimaging finding among hospitalized COVID-19 patients. Detection of an acute stroke is a strong prognostic marker of poor outcome. Our study also highlights the fact there is limited use of neuroimaging in these patients due to multiple logistical constraints.