Genetics of Chronic Traumatic Encephalopathy.

Although chronic traumatic encephalopathy (CTE) garners substantial attention in the media and there have been marked scientific advances in the last few years, much remains unclear about the role of genetic risk in CTE. Two athletes with comparable contact-sport exposure may have varying amounts of CTE neuropathology, suggesting that other factors, including genetics, may contribute to CTE risk and severity. In this review, we explore reasons why genetics may be important for CTE, concepts in genetic study design for CTE (including choosing controls, endophenotypes, gene by environment interaction, and epigenetics), implicated genes in CTE (including APOE, MAPT, and TMEM106B), and whether predictive genetic testing for CTE should be considered.

Mononeuropathy Multiplex After Severe SARS-CoV-2 Infection: A Case Series and Literature Review.

INTRODUCTION: Peripheral nerve injuries are being increasingly recognized in patients recovering from severe SARS-CoV-2 infections. Axonal neuropathies can occur, leading to lasting and disabling deficits. CASE REPORTS: We present the cases of 3 patients who developed weakness and sensory symptoms after severe SARS-CoV-2 pneumonia. The clinical deficits revealed various patterns of injury including a mononeuropathy multiplex (MNM) in the first patient, a brachial plexopathy with superimposed MNM in the second patient, and a mononeuropathy superimposed on a polyneuropathy in the third patient. Electrodiagnostic studies revealed axonopathies. The patients with MNM were left with severe disability. The third patient returned to his baseline level of functioning. CONCLUSIONS: Severe SARS-CoV-2 infections can result in disabling axonopathies. Possible explanations include ischemic nerve damage from the profound inflammatory response and traumatic nerve injuries in the ICU setting. Preventing severe disease through vaccination and antivirals may therefore help reduce neurologic morbidity.

A machine learning eye movement detection algorithm using electrooculography.

STUDY OBJECTIVES: Eye movement quantification in polysomnograms (PSG) is difficult and resource intensive. Automated eye movement detection would enable further study of eye movement patterns in normal and abnormal sleep, which could be clinically diagnostic of neurologic disorders, or used to monitor potential treatments. We trained a long short-term memory (LSTM) algorithm that can identify eye movement occurrence with high sensitivity and specificity. METHODS: We conducted a retrospective, single-center study using one-hour PSG samples from 47 patients 18-90 years of age. Team members manually identified and trained an LSTM algorithm to detect eye movement presence, direction, and speed. We performed a 5-fold cross validation and implemented a "fuzzy" evaluation method to account for misclassification in the preceding and subsequent 1-second of gold standard manually labeled eye movements. We assessed G-means, discrimination, sensitivity, and specificity. RESULTS: Overall, eye movements occurred in 9.4% of the analyzed EOG recording time from 47 patients. Eye movements were present 3.2% of N2 (lighter stages of sleep) time, 2.9% of N3 (deep sleep), and 19.8% of REM sleep. Our LSTM model had average sensitivity of 0.88 and specificity of 0.89 in 5-fold cross validation, which improved to 0.93 and 0.92 respectively using the fuzzy evaluation scheme. CONCLUSION: An automated algorithm can detect eye movements from EOG with excellent sensitivity and specificity. Noninvasive, automated eye movement detection has several potential clinical implications in improving sleep study stage classification and establishing normal eye movement distributions in healthy and unhealthy sleep, and in patients with and without brain injury.