Letter to the Editor

With interest, we read the article by Krasnodebska et al. on a study of six patients with laryngeal sensory neuropathy (LSN) as a manifestation of long-COVID syndrome (LCS) [1]. A neuropathic pattern on needle electromyography (EMG) of the crico-thyroid or the thyro-ari-thyroid muscle was recorded in five patients [1]. It was concluded that LSN can be a manifestation of long-COVID syndrome and that the severity of dysphonia correlates with the severity of the neuropathic EMG pattern [1]. The study is excellent but has limitations that are cause of concerns and should be discussed.

The first limitation is that the title is contradictory and misleading. LSN cannot be assessed by needle EMG. Needle EMG assesses motor but not sensory modalities. Neuropathy affecting motor fibers can be assessed by needle EMG but not neuropathy due to affection of sensory fibers. This discrepancy should be addressed. If the needle EMG showed a neurogenic pattern, this indicates motor but not sensory neuropathy.

Another limitation is that various differential diagnoses of LSN were not adequately ruled out. To rule out central nervous system (CNS) disease such as infectious or autoimmune encephalitis (AIE), in particular, rhombencephalitis, brainstem Bickerstaff encephalitis, and cerebellitis [2], it is crucial that each included patient had undergone cerebral MRI with contrast medium and cerebrospinal fluid (CSF) studies. CSF studies should not only include cell count, protein level, glucose level, and oligoclonal bands, but also measurement of intrathecal immunoglobulins, neopterin, neurofilament light chain, tau, antibodies related to AIE and levels of cytokines, chemokines, 14-3-3, and glial factors [3].

To rule out cranial nerve involvement in Guillain–Barre syndrome (GBS), it is crucial that all patients had undergone not only nerve conduction studies (NCSs) of peripheral nerves and the facial nerve, but also CSF investigations and cerebral MRI. GBS is a common complication of SARS-CoV-2 infections [4] and commonly goes along with involvement of one or several cranial nerves, including the glossopharyngeal and the vagal nerves.

Another limitation is that thyroid dysfunction was not adequately ruled out in the six included patients. We should know if any of the six patients had thyroid dysfunction or required adequate therapy.

There is no mention if sicca syndrome (e.g., Sjögren syndrome) was adequately ruled out in each patient.

Another differential diagnosis that needs to be ruled out is spasmodic dysphonia.

Depression is a common cause of LSN. A limitation here is that the included patients were not tested with any of the depression scales.

Because patient-5 was regularly taking pregabalin and pregabalin can cause nasopharyngitis, it is crucial to know the dosage this patient was taking and whether or not it caused LSN.

Patient-1 had a myogenic EMG [1]. We should know whether this patient had any indications for myopathy, such as weakness, wasting, fasciculations, elevation of creatin-kinase, LDH, myoglobin, or aldolase, or a myogenic EMG from muscles other than the laryngeal ones.

It is contradictory to state in the method section that asthma was an exclusion criterion and to include patient-1 who had exacerbation of asthma. This discrepancy should be solved.

Overall, the interesting study has limitations that call the results and their interpretation into question. Addressing these issues would strengthen the conclusions and could improve the status of the study. Before interpreting LCN as a long-term complication of COVID-19 various differential diagnoses need to be adequately ruled out.

The vagal nerve carries motor, sensitive, sensory, and autonomic qualities. We should know if all these different qualities were adequately tested in the glossopharyngeal and vagal nerve. We should know if neuropathy of these cranial nerves was adequately ruled out.