Objective: Traumatic brain injury (TBI) and repetitive head impacts (RHI) related to blasts or contact sports are commonly reported among military service members. However, the clinical implications of remote TBI and RHI in veterans remains a challenge when evaluating older veterans at risk of neurodegenerative conditions including Alzheimer's disease (AD) and Chronic Traumatic Encephalopathy (CTE). This study aimed to test the hypothesis that veterans in a memory disorders clinic with remote head injury would be more likely to have neurodegenerative clinical diagnoses, increased rates of amyloid PET positivity, higher prevalence of cavum septum pellucidi/vergae, and alterations in event-related potential (ERP) middle latency auditory evoked potentials (MLAEPs) and long latency ERP responses compared to those without head injuries. Methods: Older veterans aged 50-100 were recruited from a memory disorders clinic at VA Boston Healthcare system with a history of head injury (n = 72) and without head injury history (n = 52). Patients were classified as reporting prior head injury including TBI and/or RHI exposure based on self-report and chart review. Participants underwent MRI to determine presence/absence of cavum and an ERP auditory oddball protocol. Results: The head injury group was equally likely to have a positive amyloid PET compared to the non-head injury group. Additionally, the head injury group were less likely to have a diagnosis of a neurodegenerative condition than those without head injury. P200 target amplitude and MLAEP amplitudes for standard and target tones were decreased in the head injury group compared to the non-head injury group while P3b amplitude did not differ. Conclusions: Veterans with reported remote head injury evaluated in a memory disorders clinic were not more likely to have a neurodegenerative diagnosis or imaging markers of neurodegeneration than those without head injury. Decreased P200 target and MLAEP target and standard tone amplitudes in the head injury group may be relevant as potential diagnostic markers of remote head injury.

To understand the long-term neurological outcomes resultant of West Nile virus (WNV) infection, participants from a previously established, prospective WNV cohort were invited to take part in a comprehensive neurologic and neurocognitive examination. Those with an abnormal exam finding were invited for MRI to evaluate cortical thinning and regional brain atrophy following infection. Correlations of presenting clinical syndrome with neurologic and neurocognitive dysfunctions were evaluated, as well as correlations of neurocognitive outcomes with MRI results. From 2002 to 2012, a total of 262 participants with a history of WNV infection were enrolled as research participants in a longitudinal cohort study, and 117 completed comprehensive neurologic and neurocognitive evaluations. Abnormal neurological exam findings were identified in 49% (57/117) of participants, with most abnormalities being unilateral. The most common abnormalities included decreased strength (26%; 30/117), abnormal reflexes (14%; 16/117), and tremors (10%; 12/117). Weakness and decreased reflexes were consistent with lower motor neuron damage in a significant proportion of patients. We observed a 22% overall rate of impairment on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), with impairments observed in immediate (31%) and delayed memory (25%). On MRI, participants showed significant cortical thinning as compared to age- and gender-matched controls in both hemispheres, with affected regions primarily occurring in the frontal and limbic cortices. Regional atrophy occurred in the cerebellum, brain stem, thalamus, putamen, and globus pallidus. This study provides valuable new information regarding the neurological outcomes following WNV infection, with MRI evidence of significant cortical thinning and regional atrophy; however, it is important to note that the results may include systemic bias due to the external control group. Considering no effective treatment measures are available, strategies to prevent infection are key.

Background: Decreased brainstem raphe (BR) echogenicity detected by transcranial parenchymal sonography (TCS) is associated with depression in psychiatric and neurologic diseases. However, previous studies focusing on the relationship between motor and non-motor symptoms and echogenicity changes in BR in patients with PD yielded controversial results. Objectives: To investigate the relationship between echogenicity changes in BR detected by TCS and motor and a series of non-motor symptoms in patients with PD. Methods: Consecutive PD patients were recruited from the Second Affiliated Hospital of Soochow University. Demographic information and Motor and non-motor symptoms for all subjects were collected. TCS was used to detect the echogenicity changes in BR in PD patients. Results: One hundred and thirty-five consecutive patients with PD were enrolled in the study. The BR abnormal rate was significantly higher in PD patients with anxiety (p = 0.003) or depression (p = 0.022) than patients without. Spearman correlation analyses showed that Hamilton Rating Scale for Depression(HRSD) (r = 0.274, p = 0.002) and Parkinson's Disease Questionnaire 39-item(PDQ-39) (r = 0.208, p = 0.034) scores were positively correlated with abnormal BR echogenicity. Multivariate logistic regression analyses showed that HRSD and HAMA scores were associated with BR hypoechogenicity, the corresponding odds ratios (confidence intervals) were 1.07 (95% CI, 1.01-1.13) and 1.10(1.01-1.18), respectively. However, the PDQ-39 score was not associated with BR hypoechogenicity. Conclusion: The abnormal reduction in BR echogenicity detected by TCS is associated with depression and anxiety, but not motor symptoms in PD patients.

Background: Previous reported neurologic sequelae associated with SARS-CoV-2 infection have mainly been confined to hospital-based patients in which viral detection was restricted to nasal/throat swabs or to IgM/IgG peripheral blood serology. Here we describe seven cases from Brazil of outpatients with previous mild or moderate COVID-19 who developed subacute cognitive disturbances. Methods: From June 1 to August 15, 2020, seven individuals 18 to 60 years old, with confirmed mild/moderate COVID-19 and findings consistent with encephalopathy who were observed >7 days after respiratory symptom initiation, were screened for cognitive dysfunction. Paired sera and CSF were tested for SARS-CoV-2 (IgA, IgG ELISA, and RT-PCR). Serum and intrathecal antibody dynamics were evaluated with oligoclonal bands and IgG index. Cognitive dysfunction was assessed by the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and the Clock Drawing Test (CDT). Results: All but one of our patients were female, and the mean age was 42.6 years. Neurologic symptoms were first reported a median of 16 days (IQR 15-33) after initial COVID-19 symptoms. All patients had headache and altered behavior. Cognitive dysfunction was observed mainly in phonemic verbal fluency (MoCA) with a median of six words/min (IQR 5.25-10.75) and altered visuospatial construction with a median of four points (IQR 4-9) (CDT). CSF pleocytosis was not detected, and only one patient was positive for SARS-Co Conclusions: A subacute cognitive syndrome suggestive of SARS-CoV-2-initiated damage to cortico-subcortical associative pathways that could not be attributed solely to inflammation and hypoxia was present in seven individuals with mild/moderate COVID-19.

Introduction: Polyneuropathy (PN) complaints are common, prompting many referrals for neurologic evaluation. To improve access of PN care in distant community clinics, we developed a telemedicine service (patient-clinician interactions using real-time videoconference technology) for PN. The primary goal of this study was to construct a remote exam for PN that is feasible, reliable, and concordant with in-person assessments for use in our tele-PN clinics. Methods: To construct the VA Neuropathy Scale (VANS), we searched the literature for existing, validated PN assessments. From these assessments, we selected a parsimonious set of exam elements based on literature-reported sensitivity and specificity of PN detection, with modifications as necessary for our teleneurology setting (i.e., a technician examination under the direction of a neurologist). We recruited 28 participants with varying degrees of PN to undergo VANS testing under 5 scenarios. The 5 scenarios differed by mode of VANS grading (in-person vs. telemedicine) and by the in-person examiner type (neurologist vs. technician) in telemedicine scenarios. We analyzed concordance between the VANS and a person's medical chart-derived PN status by modeling the receiver operating characteristic (ROC) curve. We analyzed reliability of the VANS by mixed effects regression and computing the intraclass correlation coefficient (ICC) of scores across the 5 scenarios. Results: The VA Neuropathy Scale (VANS) tests balance, gait, reflexes, foot inspection, vibration, and pinprick. Possible scores range from 0 to 50 (worst). From the ROC curve, a cutoff of >2 points on the VANS sets the sensitivity and specificity of detecting PN at 98 and 91%, respectively. There is a small (1.3 points) but statistically significant difference in VANS scoring between in-person and telemedicine grading scenarios. For telemedicine grading scenarios, there is no difference in VANS scores between neurologist and technician examinations. The ICC is 0.89 across all scenarios. Discussion: The VANS, informed by existing PN instruments, is a promising clinical assessment tool for diagnosing and monitoring the severity of PN in telemedicine settings. This pilot study indicates acceptable concordance and reliability of the VANS with in-person examinations.