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Long COVID link to corneal nerve damage

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Nerve fibre loss and an increase in key immune cells on the cornea may be an identifying feature of ‘long COVID’, suggests a small study published in the British Journal of Ophthalmology.

These changes – identified through corneal confocal microscopy (CCM) – were particularly evident among those with neurological symptoms, such as loss of taste and smell, headache, dizziness, numbness, and neuropathic pain, following COVID-19 infection, the findings show.

The study was conducted by researchers from Necmettin Erbakan University Meram Medical Faculty Hospital in Turkey and Weill Cornell Medicine-Qatar in Doha.

“To the best of our knowledge, this is the first study reporting corneal nerve loss and an increase in [dendritic cell] density in patients who have recovered from COVID-19, especially in subjects with persisting symptoms consistent with long COVID,” the researchers said.

“We show that patients with long COVID have evidence of small nerve fibre damage which relates to the severity of long COVID and neuropathic as well as musculoskeletal symptoms.

“Corneal confocal microscopy may have clinical utility as a rapid objective ophthalmic test to evaluate patients with long COVID.”

According to the study, long COVID is characterised by several potentially debilitating symptoms that continue for more than four weeks after the acute phase of the infection has passed and aren’t explained by an alternative diagnosis.

Around one in 10 of all infected people will develop symptoms, and it has been suggested that small nerve fibre damage may underlie its development.

To explore this further, the researchers used a real time CCM to identify nerve damage in the cornea. Forty people who had recovered from confirmed COVID-19 infection between one and six months earlier completed a National Institute of Health and Clinical Excellence (NICE) questionnaire to find out if they had longer term symptoms arising from their disease.

It consisted of 28 items in nine domains including generalised, respiratory, cardiovascular, neurological, musculoskeletal, psychological/psychiatric, gastrointestinal, dermatological, and ear, nose and throat symptoms, with a total score ranging from 0 to 28.

Neurological symptoms were present at four and 12 weeks in 22 out of 40 (55%) and 13 out of 29 (45%) patients, respectively.

Participants’ corneas were then scanned using CCM to look for small nerve fibre damage and the density of dendritic cells. These cells have a key role in the primary immune system response by capturing and presenting antigens from invading organisms.

The corneal scans were compared with those of 30 healthy people who hadn’t had COVID-19 infection.

Twenty-two (55%) of the 40 COVID-19 patients had no clinical signs of pneumonia; 11 (28%) had clinical signs of pneumonia not requiring oxygen therapy; four (10%) had been admitted to hospital with pneumonia and received oxygen therapy; and three (8%) with pneumonia had been admitted to the intensive care.

The corneal scans revealed that patients with neurological symptoms four weeks after they had recovered from acute COVID-19 had greater corneal nerve fibre damage and loss, with higher numbers of dendritic cells, than those who hadn’t been infected.

Those without neurological symptoms had comparable numbers of corneal nerve fibres as those who hadn’t been infected with COVID-19, but higher numbers of dendritic cells.

The questionnaire responses indicative of long COVID symptoms correlated strongly with corneal nerve fibre loss.

The researchers pointed out this was an observational study, so it couldn’t establish cause. They also acknowledge several limitations, including the relatively small number of study participants, the absence of longer term monitoring, and reliance on questionnaires to establish the severity of neurological symptoms rather than more objective measures.

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