Identify if SARS-CoV-2 virus is triggering and/or worsening dysautonomia by reviewing the function of autonomic patients pre-COVID-19 and post-COVID-19 infection, as well as new onset autonomic patients post-COVID-19 infection.

Autonomic dysfunction may be part of acute and long COVID-19 infection.

Six participants were enrolled and divided into two groups. The first group of 4 volunteers reported worsened autonomic symptoms post-COVID-19 infection. These individuals had first autonomic test prior to COVID-19 pandemic outbreak (July 2019-December 2019). Autonomic function testing was repeated in these participants, 6 months to 1-year post-COVID-19 infection (June, 2021). The second group of 2 volunteers reported new-onset autonomic symptoms post-COVID-19 infection and were tested March-May, 2021. All participants were screened for known causes of autonomic dysfunction and had normal neurophysiological studies (EMG/NCS), no hypertension/hyperlipidemia or thyroid dysfunction, no diabetes/prediabetes, no vitamin deficiencies, no history of HIV, hepatitis, or syphilis, no prior radiation or chemical exposure and no evidence of monoclonal gammopathy, or autoimmune condition. Participants were diagnosed with COVID-19 via PCR testing, and tested again via SARS-CoV-2 capsid-antibody test.

All volunteers were female (age: 21-37y) and endorsed orthostatic intolerance. Gastrointestinal symptoms (5/6), new-onset paresthesias, drier skin (3/6), and sexual dysfunction (2/6) were reported. Dysgeusia reported in 50%, but was not demonstrated on neurological examination. Parasympathetic autonomic function remained stable 6-months to 1-year post-COVID-19 infection and not demonstrated in participants with new-onset symptoms. Sympathetic-adrenergic dysfunction as new-onset orthostatic hypotension and abnormalities on blood-pressure response to Valsalva was found in 50% of participants. Sympathetic cholinergic (sudomotor) dysfunction was demonstrated in ALL participants. Worsened, or new-onset, sudomotor dysfunction was demonstrated in those with mild or normal sudomotor function on pre-COVID-19 autonomic testing.

Sudomotor dysfunction was demonstrated as worsened or new-sequelae to COVID-19 infection. COVID-19 may be responsible for new-onset or worsened small-fiber neuropathy in this sample.