Anesthetic Considerations for Patients with Hereditary Neuropathy with Liability to Pressure Palsies: A Narrative Review.

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant demyelinating neuropathy characterized by an increased susceptibility to peripheral nerve injury from trauma, compression, or shear forces. Patients with this condition are unique, necessitating distinct considerations for anesthesia and surgical teams. This review describes the etiology, prevalence, clinical presentation, and management of HNPP and presents contemporary evidence and recommendations for optimal care for HNPP patients in the perioperative period.

Severe Neurologic Complications of SARS-CoV-2.

Purpose Of Review: This review presents an overview of the known neurocritical care complications of severe acute respiratory virus 2 (SARS-CoV-2). We present readers with a review of the literature of severe neurologic complications of SARS-CoV-2 and cases from our institution to illustrate these conditions.

Recent Findings: Neurologic manifestations are being increasingly recognized in the literature.

Acute Cerebrovascular Events With COVID-19 Infection.

Background And Purpose: Coronavirus disease 2019 (COVID-19) has been associated with an increased incidence of thrombotic events, including stroke. However, characteristics and outcomes of COVID-19 patients with stroke are not well known.

Methods: We conducted a retrospective observational study of risk factors, stroke characteristics, and short-term outcomes in a large health system in New York City.

ER Protein Processing Under Oxidative Stress: Implications and Prevention.

Elevated levels of mitochondrial nitrosative stress have been associated with the pathogenesis of both Parkinson's and Alzheimer's diseases. The mechanism involves catalytic poisoning of the endoplasmic reticulum (ER)-resident oxidoreductase chaperone, protein disulfide isomerase (PDI), and the subsequent accumulation of ER-processed substrate proteins. Using a model system to mimic mitochondrial oxidative and nitrosative stress, we demonstrate a PDI-independent mechanism whereby reactive oxygen species (ROS) compromise regeneration rates of disulfide bond-containing ER-processed proteins.