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Neurological complications among hospitalized COVID-19 patients may be associated with elevated neurodegenerative biomarkers.Among hospitalized COVID-19 patients without a history of dementia (N = 251), we compared serum total tau (t-tau), phosphorylated tau-181 (p-tau181), glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), ubiquitin carboxy-terminal hydrolase L1 (UCHL1), and amyloid beta (Aβ40,42) between patients with or without encephalopathy, in-hospital death versus survival, and discharge home versus other dispositions. COVID-19 patient biomarker levels were also compared to non-COVID cognitively normal, mild cognitive impairment (MCI), and Alzheimer's disease (AD) dementia controls (N = 161).Admission t-tau, p-tau181, GFAP, and NfL were significantly elevated in patients with encephalopathy and in those who died in-hospital, while t-tau, GFAP, and NfL were significantly lower in those discharged home. These markers correlated with severity of COVID illness. NfL, GFAP, and UCHL1 were higher in COVID patients than in non-COVID controls with MCI or AD.Neurodegenerative biomarkers were elevated to levels observed in AD dementia and associated with encephalopathy and worse outcomes among hospitalized COVID-19 patients.

Limited data exists evaluating predictors of long-term outcomes after hospitalization for COVID-19.We conducted a prospective, longitudinal cohort study of patients hospitalized for COVID-19. The following outcomes were collected at 6 and 12-months post-diagnosis: disability using the modified Rankin Scale (mRS), activities of daily living assessed with the Barthel Index, cognition assessed with the telephone Montreal Cognitive Assessment (t-MoCA), Neuro-QoL batteries for anxiety, depression, fatigue and sleep, and post-acute symptoms of COVID-19. Predictors of these outcomes, including demographics, pre-COVID-19 comorbidities, index COVID-19 hospitalization metrics, and life stressors, were evaluated using multivariable logistic regression.Of 790 COVID-19 patients who survived hospitalization, 451(57%) completed 6-month (N = 383) and/or 12-month (N = 242) follow-up, and 77/451 (17%) died between discharge and 12-month follow-up. Significant life stressors were reported in 121/239 (51%) at 12-months. In multivariable analyses, life stressors including financial insecurity, food insecurity, death of a close contact and new disability were the strongest independent predictors of worse mRS, Barthel Index, depression, fatigue, and sleep scores, and prolonged symptoms, with adjusted odds ratios ranging from 2.5 to 20.8. Other predictors of poor outcome included older age (associated with worse mRS, Barthel, t-MoCA, depression scores), baseline disability (associated with worse mRS, fatigue, Barthel scores), female sex (associated with worse Barthel, anxiety scores) and index COVID-19 severity (associated with worse Barthel index, prolonged symptoms).Life stressors contribute substantially to worse functional, cognitive and neuropsychiatric outcomes 12-months after COVID-19 hospitalization. Other predictors of poor outcome include older age, female sex, baseline disability and severity of index COVID-19.

Background and ObjectiveLittle is known about trajectories of recovery 12 months after hospitalization for severe COVID-19.MethodsWe conducted a prospective, longitudinal cohort study of patients with and without neurologic complications during index hospitalization for COVID-19 from March 10, 2020, to May 20, 2020. Phone follow-up batteries were performed at 6 and 12 months after COVID-19 onset. The primary 12-month outcome was the modified Rankin Scale (mRS) score comparing patients with or without neurologic complications using multivariable ordinal analysis. Secondary outcomes included activities of daily living (Barthel Index), telephone Montreal Cognitive Assessment (t-MoCA), and Quality of Life in Neurologic Disorders (Neuro-QoL) batteries for anxiety, depression, fatigue, and sleep. Changes in outcome scores from 6 to 12 months were compared using nonparametric paired-samples sign test.ResultsTwelve-month follow-up was completed in 242 patients (median age 65 years, 64% male, 34% intubated during hospitalization) and 174 completed both 6- and 12-month follow-up. At 12 months, 197/227 (87%) had ≥1 abnormal metric: mRS >0 (75%), Barthel Index p = 0.037). Significant improvements in outcome trajectories from 6 to 12 months were observed in t-MoCA scores (56% improved, median difference 1 point; p = 0.002) and Neuro-QoL anxiety scores (45% improved; p = 0.003). Nonsignificant improvements occurred in fatigue, sleep, and depression scores in 48%, 48%, and 38% of patients, respectively. Barthel Index and mRS scores remained unchanged between 6 and 12 months in >50% of patients.DiscussionAt 12 months after hospitalization for severe COVID-19, 87% of patients had ongoing abnormalities in functional, cognitive, or Neuro-QoL metrics and abnormal cognition persisted in 50% of patients without a history of dementia/cognitive abnormality. Only fatigue severity differed significantly between patients with or without neurologic complications during index hospitalization. However, significant improvements in cognitive (t-MoCA) and anxiety (Neuro-QoL) scores occurred in 56% and 45% of patients, respectively, between 6 and 12 months. These results may not be generalizable to those with mild or moderate COVID-19.

ObjectiveTo determine the prevalence and associated mortality of well-defined neurologic diagnoses among patients with coronavirus disease 2019 (COVID-19), we prospectively followed hospitalized severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)–positive patients and recorded new neurologic disorders and hospital outcomes.MethodsWe conducted a prospective, multicenter, observational study of consecutive hospitalized adults in the New York City metropolitan area with laboratory-confirmed SARS-CoV-2 infection. The prevalence of new neurologic disorders (as diagnosed by a neurologist) was recorded and in-hospital mortality and discharge disposition were compared between patients with COVID-19 with and without neurologic disorders.ResultsOf 4,491 patients with COVID-19 hospitalized during the study timeframe, 606 (13.5%) developed a new neurologic disorder in a median of 2 days from COVID-19 symptom onset. The most common diagnoses were toxic/metabolic encephalopathy (6.8%), seizure (1.6%), stroke (1.9%), and hypoxic/ischemic injury (1.4%). No patient had meningitis/encephalitis or myelopathy/myelitis referable to SARS-CoV-2 infection and 18/18 CSF specimens were reverse transcriptase PCR negative for SARS-CoV-2. Patients with neurologic disorders were more often older, male, white, hypertensive, diabetic, intubated, and had higher sequential organ failure assessment (SOFA) scores (all p < 0.05). After adjusting for age, sex, SOFA scores, intubation, history, medical complications, medications, and comfort care status, patients with COVID-19 with neurologic disorders had increased risk of in-hospital mortality (hazard ratio [HR] 1.38, 95% confidence interval [CI] 1.17–1.62, p < 0.001) and decreased likelihood of discharge home (HR 0.72, 95% CI 0.63–0.85, p < 0.001).ConclusionsNeurologic disorders were detected in 13.5% of patients with COVID-19 and were associated with increased risk of in-hospital mortality and decreased likelihood of discharge home. Many observed neurologic disorders may be sequelae of severe systemic illness.

Objective To investigate whether paresthesia of the lower extremities following exposure to the World Trade Center (WTC) disaster was associated with signs of neuropathy, metabolic abnormalities, or neurotoxin exposures. Methods Case-control study comparing WTC-exposed paresthesia cases with "clinic controls" (WTC-exposed subjects without paresthesias), and "community controls" (WTC-unexposed persons). Results Neurological histories and examination findings were significantly worse in cases than controls. Intraepidermal nerve fiber densities were below normal in 47% of cases and sural to radial sensory nerve amplitude ratios were less than 0.4 in 29.4%. Neurologic abnormalities were uncommon among WTC-unexposed community controls. Metabolic conditions and neurotoxin exposures did not differ among groups. Conclusions Paresthesias among WTC-exposed individuals were associated with signs of neuropathy, small and large fiber disease. The data support WTC-related exposures as risk factors for neuropathy, and do not support non-WTC etiologies.

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

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

Both type 1 diabetes (T1D) and celiac disease (CD) have been linked to an increased risk of neuropathy. This study examined the risk of neuropathy in patients with T1D compared with patients with both T1D and CD.In a nationwide population-based cohort, T1D was defined as having a diagnosis of diabetes between 1964 and 2009 recorded in the Swedish National Patient Register in individuals ≤30 years of age. CD was defined as having villous atrophy (Marsh histopathology stage III) on small intestinal biopsy. CD cases were identified through biopsies examined between 1969 and 2008 at any of Sweden's 28 pathology departments. Nine hundred fifty-eight patients had both T1D and CD and were matched for sex, age, and calendar period with 4590 controls who only had T1D. Through Cox regression analysis, with CD as the time-dependent covariate, we estimated the risk of neuropathy in T1D patients with CD.Fifty-four individuals with T1D and CD had later neuropathy (expected: n = 42). This corresponded to an adjusted hazard ratio of 1.27 (95% confidence interval = 0.95-1.71) compared with those who had T1D alone. The hazard ratio was statistically significant in the first 5 years with CD (1.67; 95% confidence interval = 1.13-2.47) but decreased to neutrality thereafter. Risk estimates were similar in men and women, and did not differ by age at CD onset.CD does not seem to influence the risk of neuropathy in individuals with T1D, although a small excess risk cannot be ruled out.

We examined whether time to onset of paresthesia was associated with indicators of severity of World Trade Center (WTC) exposure. We analyzed data from 3411 patients from the Bellevue Hospital&mdash, WTC Environmental Health Center. Paresthesia was defined as present if the symptom occurred in the lower extremities with frequency &ldquo, often&rdquo, or &ldquo, almost continuous.&rdquo, We plotted hazard functions and used the log-rank test to compare time to onset of paresthesia between different exposure groups. We also used Cox regression analysis to examine risk factors for time-to-paresthesia after 9/11/2001 and calculate hazard ratios adjusted for potential confounders. We found significantly elevated hazard ratios for paresthesia for (a) working in a job that required cleaning of WTC dust in the workplace, and (b) being heavily exposed to WTC dust on September 11, 2001, after adjusting for age, race/ethnicity, depression, anxiety, post-traumatic stress disorder, and body mass index. These observational data are consistent with the hypothesis that exposure to WTC dust or some other aspect of cleaning WTC dust in the workplace, is associated with neuropathy and paresthesia. Further neurological evaluations of this and other WTC-exposed populations is warranted.

With an increasing focus on quality metrics, hospital length of stay (LOS) in the U.S. has garnered significant scrutiny. To help establish evidence-based benchmarks for epilepsy monitoring unit (EMU) metrics, we evaluated the impact of multiple variables on LOS through a retrospective analysis of 905 consecutive inpatient adult EMU admissions. The most common reasons for admission were event characterization (n=494), medication adjustment (n=189), and presurgical evaluation (n=96). Presurgical evaluations experienced a longer average LOS (aLOS) of 7.1days versus patients admitted for other indications (p

Background: Our aims were to: (1) estimate the prevalence of essential tremor (ET) in a community-based study in northern Manhattan, New York, N.Y., USA; (2) compare prevalence across ethnic groups, and (3) provide prevalence estimates for the oldest old. Methods: This study did not rely on a screening questionnaire. Rather, as part of an in-person neurological evaluation, each participant produced several handwriting samples, from which ET diagnoses were assigned. Results: There were 1,965 participants (76.7 ± 6.9 years, range = 66–102 years); 108 had ET [5.5%, 95% confidence interval (CI) = 4.5–6.5%]. Odds of ET were robustly associated with Hispanic ethnicity versus white ethnicity [odds ratio (OR) = 2.19, 95% CI = 1.03–4.64, p = 0.04] and age (OR = 1.14, 95% CI = 1.03–1.26, p = 0.01), i.e. with every 1 year advance in age, the odds of ET increased by 14%. Prevalence reached 21.7% among the oldest old (age ≥95 years). Conclusions: This study reports a significant ethnic difference in the prevalence of ET. The prevalence of ET was high overall (5.5%) and rose markedly with age so that in the oldest old, more than 1 in 5 individuals had this disease.

Objectives Bortezomib is a proteasome inhibitor that is frequently used for multiple myeloma and lymphoma. A sensory predominant axonal neuropathy is associated with bortezomib treatment but a demyelinating neuropathy is also described primarily based on electrodiagnostic findings. We report a series of patients treated with bortezomib who developed peripheral neuropathy and were found to have demyelinating features on electrodiagnostic testing. Methods Four patients who developed a bortezomib-induced peripheral neuropathy underwent electrophysiological testing, and 1 patient had a nerve biopsy. Results The four patients with bortezomib-induced peripheral neuropathy had demyelinating features on their electrophysiological testing. The nerve biopsy performed in 1 patient demonstrated a demyelinating component in a background of axonal degeneration. Conclusions Although most toxic neuropathies are symmetrical axonal neuropathies, bortezomib is part of a small list of agents that may cause a demyelinating polyneuropathy and axonal degeneration. These findings have been confirmed by nerve biopsy.

Background: Mild cognitive deficits, mainly in frontal-executive function and memory, have been reported in patients with essential tremor (ET). Furthermore, an association between ET and dementia has been reported in a single population-based study in Spain. This has not been confirmed elsewhere. Objective: To determine whether baseline ET is associated with prevalent and incident dementia in an ethnically diverse, community-based sample of elders. Methods: Community-dwelling elders in northern Manhattan were enrolled in a prospective cohort study. Baseline ET diagnoses were assigned from handwriting samples. Dementia was diagnosed at baseline and follow-up using DSM-III-R criteria. Results: In cross-sectional analyses, 31/124 (25.0%) ET cases had prevalent dementia vs 198/2,161 (9.2%) controls (odds ratio [OR]unadjusted = 3.31, 95% confidence interval [CI] = 2.15 - 5.09, p < 0.001; ORadjusted = 1.84, 95% CI = 1.13 - 2.98, p = 0.01). In prospective analyses, 17/93 (18.3%) ET cases vs 171/1,963 (8.7%) controls developed incident dementia (hazard ratio [HR]unadjusted = 2.78, 95% CI = 1.69 - 4.57, p < 0.001; HRadjusted = 1.64, 95% CI = 0.99 - 2.72, p = 0.055). Conclusions: In a second population-based study of elders, essential tremor (ET) was associated with both increased odds of prevalent dementia and increased risk of incident dementia. Presence of dementia, therefore, appeared to be greater than that expected for age (i.e., a disease-associated feature). Rather than attributing cognitive complaints in patients with ET to old age, assessment and possible treatment of dementia should be routinely incorporated into the treatment plan.