A new study found that some people with chronic COVID have lasting nerve damage caused by infection-triggered immune failure, which can be addressed.
Even in mild situations, COVID symptoms might continue for at least three months after recovery. Symptoms include trouble doing daily tasks, fainting, an increased heart rate, difficulty breathing, cognitive difficulties, chronic discomfort, sensory irregularities, and muscular weakness.
COVID-19 and its ramifications for the neurological system
Scientists from Massachusetts General Hospital and the National Institutes of Health led the study, which was published today in Neurology: Neuroimmunology & Neuroinflammation.
There was evidence of peripheral neuropathy in 59 percent of the patients. As per The Harvard Gazette.
Typical neuropathic symptoms include weakness, sensory anomalies, and pain in the hands and feet, as well as internal problems including fatigue.
According to lead author Anne Louise Oaklander, a researcher in the Department of Neurology at MGH, it is one of the first publications to investigate the causes of chronic COVID, which will gradually acquire importance as acute COVID diminishes.
Her findings suggest that certain long-term COVID patients have proximal nerve fiber injury, with small-fiber nerve cell loss being the most common.
Oaklander suggests that if people have long-COVID symptoms that aren't explained by other means and aren't improving, they should talk to their doctor about neuropathy or consult a neurologist or neuromuscular expert.
Read more: Protein May Promote Nerve Regeneration
Autoimmune reactions that are abnormal
Harvard Medical School researchers recently studied individuals who developed neuropathic symptoms after recovering from a SARS-CoV-2 infection but had no prior history of neuropathy.
They observed that some people with long-term COVID have long-term nerve damage caused by an infection-induced immune dysfunction.
According to Dr. Mary Kelley, one of the study's authors, the knowledge helps us better understand the pathophysiology that may underpin some chronic COVID symptoms, which might lead therapies to offer symptomatic relief and validation to patients.
The researchers indicate that one-quarter of human dorsal root ganglia (DRG) cells, which link the peripheral nerves to the spinal cord, have mRNA that may attach to SARS-CoV-2 spike receptors.
This might stimulate the creation of antibodies that attack both neurons and SARS-CoV-2.
The study's relatively small size according to Michael Lipton, Ph.D., the Albert Einstein College of Medicine radiology and psychiatry and behavioral sciences professor who has not been involved in the study, makes understanding the underlying principle and reasons challenging.
​​Dr. Seth Congdon, co-director of the COVID-19 Recovery (CORE) Clinic at Montefiore Medical Center and not involved in the study, emphasized that the study left many unknown factors that need to be investigated further. It is uncertain how best to treat tiny fibre neuropathy. It is critical to test for and treat disorders that might develop or worsen neuropathy, such as diabetes, vitamin B12 deficiency, thyroid dysfunction, strong alcohol use, and autoimmune illnesses.
The researchers go on to say that the late initial symptoms of COVID for a long period of time, as well as the lengthy post-infectious courses and evident responses, suggest that those mechanisms are the result of a defective immune response.
They also point out some of their work's shortcomings, such as referral biases and limited sample size.
They go on to add that the first examinations occurred at a variety of stages during the disease and treatment, but that longitudinal tests at regular intervals are always preferable.
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