Neurological symptoms that could indicate peripheral nervous system dysfunction are relatively common in patients who have suffered a SARS-CoV-2 infection.
In our study we analyzed 23 patients with symptoms compatible with polyneuropathy after suffering a SARS-CoV2 infection. Of these patients, in eight we could detect alterations in the NPS. These findings were mild and even non-specific (alterations of F waves or SSR). However, in the appropriate clinical setting, these alterations may have a pathological value. Thus, two patients had an increase in the minimum latency of the F wave, three a decrease in its persistence, two more an absence of sympathetic-cutaneous response and, finally, another patient had a fall in the amplitude of the sensory action potentials.
Of these patients, three developed long COVID-19 syndrome, four had an acute, self-limiting course, probably a paucisymptomatic form of Guillain-Barré syndrome, as previously described5–7. One patient developed a relapsing-remitting form, with a tendency to progression, so with the suspicion of a CIDP he was treated with oral corticosteroids. In this last patient, it should be noted that so far flared ups of a CIDP have been described in patients already diagnosed10, but in our case COVID-19 would be the trigger for the disease.
While the number of patients is not important enough to make statistical comparisons, we can observe some differences between patients with an abnormal NPS and those in whom such a study is normal. First, patients with alterations in the NPS showed a delay (median of 17.5 days) from SARS-CoV-2 infection to the initial neurological symptoms compared to patients with a normal examination (median of 0 days), supporting a post-infectious pathophysiological mechanism of peripheral nervous system involvement (PNS)3. In all patients with reflexes decreased during the clinical examination, the NPS was pathological, demonstrating an involvement of the large myelinated fibers.
On the other hand, patients with a long COVID-19 syndrome had for the most part a normal NPS. So apparently, the sensitive neurological symptoms they present, do not have their origin in the PNS. It is true that the NPS were performed with a significant delay and we cannot rule out that there may be an initial alteration in the PNS that triggers a central sensitization mechanism that perpetuates the symptomatology as it occurs in other painful syndromes11,12. However, in our study the time of the NPS was similar in both groups (median 276 days vs 227 days).
The six patients who required hospitalization during acute infection by SARS-CoV-2 had a normal NPS. So these symptoms do not seem to be originated in the NPS and, therefore, in the PNS. The normality of this study would rule out a polyneuropathy of the critically ill patient, a dysimmune polyneuropathy or a toxic polyneuropathy secondary to the treatments prescribed during admission as the cause of their symptoms.
Finally, our work has a number of limitations. In the first place, the small number of patients that does not allow an adequate comparative study between patients with alterations in the NPS with those in whom it is normal. On the other hand, most of these patients were evaluated and followed by their primary care physician, so in most of them no other etiological studies have been carried out (cerebrospinal fluid analysis, antiganglioside antibodies,...) that allow a more accurate diagnosis. For this same reason, these patients have mild neurological symptoms and perhaps, with other more affected patients, the findings may vary. These mild symptoms could explain the mild alterations observed in the NPS. We cannot exclude the findings detected in NPS were present prior to SARS-CoV2- infection because in healthy people they can be seen. But prior to the infection, these patients do not complain about sensory symptoms. We recognized the findings observed in our patients are mild and non-specific, but in these mild symptoms they could play a role as marker of neurologic dysfunction.
In conclusion, we want to emphasize that, in patients with sensory symptoms compatible with a polyneuropathy, from the neurophysiological point of view we observed two patient profiles. On one hand, those who have alterations in the NPS are more likely to develop self-limiting symptoms, probably a paucisymptomatic Guillain-Barré syndrome. On the other hand, patients with a normal study more frequently suffer from a chronicity of their symptoms in the setting of a long COVID-19 syndrome.