Share on Pinterest New research sheds light on neuropathies in long COVID, suggesting immune dysfunction may be to blame for the nerve damage. Photo Editing by Steve Kelly; Ildar Imashev/Getty Images In a recently published study, researchers investigated the reasons behind neuropathic symptoms in long COVID.
They found that neuropathic symptoms in long COVID may arise from immune system dysfunction.
Larger studies can build on these findings to help scientists better understand the underlying mechanisms. More than half of the individuals who recover from SARS-CoV-2 experience long-term disability, including mental health conditions and pulmonary and neurological disorders. The authors of the current study note that there is an overlap between long COVID symptoms and those of small-fiber polyneuropathy (SFN) , which affects the small nerve fibers in the skin. Investigations into the relationship between long COVID and neuropathy could help clinicians better evaluate and treat patients. Recently, researchers from Harvard Medical School examined individuals with no prior neuropathy history who developed neuropathic conditions after recovering from a SARS-CoV-2 infection. They found that some people with long COVID have long lasting nerve damage resulting from infection-triggered immune dysfunction. “The information helps us better understand the pathophysiology that may underlie some long COVID symptoms, which can guide treatments to bring symptomatic relief and validation to patients,” Dr. Mary Kelley, one of the authors of the study, told Medical News Today. The authors published their study in Neurology: Neuroimmunology & Neuroinflammation.
Patient recruitment For the study, the researchers recruited 17 people with a confirmed SARS-CoV-2 infection, no prior history of neuropathy, and a neuromuscular referral. The participants met the criteria for having long COVID, according to the World Health Organization’s (WHO’s) definition. Of the participants, 69% were female, 19% were of Latinx ethnicity, and 94% were white. The researchers tracked standardized symptoms, clinical examinations, objective neurodiagnostic test results, and outcomes for each participant over an average of 1.4 years. As most of the participants had received symptom-relieving medications, the researchers examined potential preventive treatments, too. Among the 17 people in the study, 16 had mild COVID-19, while one was in intensive care with ventilatory support for a month. Diagnostic tests for neuropathy revealed that 62.5% of lower leg skin biopsies and 50% of upper thigh biopsies and autonomic function tests confirmed SFN. The treatments included IV immunoglobulins (IVIg) — the primary treatment for inflammatory neuropathy, with early evidence for treating SFN — and corticosteroids. Most of those who received the IVIg treatment perceived improvement in their symptoms, and the same was true for some of those on corticosteroids. The researchers noted that some of the participants also made a spontaneous recovery. Due to this, they acknowledge in their paper the need to individualize treatment decisions for patients.
Dysfunctional immune response To explain their findings, the researchers write that one-quarter of human dorsal root ganglia (DRG) neurons — that is, neurons that communicate between the peripheral nervous system and the spinal cord — express mRNA that is susceptible to attaching to SARS-CoV-2 spike proteins. This may promote the formation of antibodies that target neurons as well as SARS-CoV-2. The researchers further explain that the delayed onset of symptoms that occurs in long COVID, alongside prolonged postinfectious courses and apparent responses, suggests that mechanisms arise from a dysfunctional immune response. “Given the nature and design of the small nerve fibers, they are particularly vulnerable to damage by things like inflammation, illness, and immunological derangements, generally speaking,” said Dr. Kelley. Although it seems that there are underlying immune causes, what lies behind these mechanisms remains unknown.