To the Editor:We read with interest the article by Lee et al.[1] about a 73-year old man with Parkinson disease who developed severe, prolonged dysphagia 26 days after onset of a severe SARS-CoV-2 infection initially requiring high-flow oxygen supplementation via a nasal cannula. Feeding was possible only via a nasogastric tube.[1] After self-removal of the nasogastric tube, he aspirated and required mechanical ventilation for 3 days because of respiratory insufficiency. Consecutively, a percutaneous endoscopic gastrostomy tube was inserted.[1] Despite intensive swallowing therapy during 8 wks, dysphagia only marginally improved why the percutaneous endoscopic gastrostomy tube could not be removed at the 21-wk follow-up after onset of dysphagia.[1] The study is appealing but raises several comments and concerns.The main limitation of the study is that the cause of dysphagia remained unexplained. Although it was speculated that the virus could have destroyed dopaminergic neurons, the dosages of levodopa, carbidopa, entacapone, and ropinirol were not increased.[1] Neuritis of cranial nerves IX and X was excluded upon the clinical presentation and a cerebral computed tomography with contrast medium. Because COVID-19 can be complicated by Guillain-Barre syndrome (GBS), it is crucial that all subtypes of GBS were excluded or confirmed upon application of the Brighton criteria.[2] To diagnose or exclude GBS according to the Brighton criteria, a thorough neurological examination, cerebrospinal fluid investigations, and nerve conduction studies are a prerequisite. Subtypes of GBS that could explain intractable dysphagia include Bickerstaff brainstem encephalitis; pharyngo-cervico-brachial subtype of GBS; polyneuritis cranialis; and acute, inflammatory demyelinating polyneuropathy; or acute, motor, axonal neuropathy with concomitant affection of the IXth and Xth cranial nerves. Diagnosing Bickerstaff brainstem encephalitis requires the presence of ophthalmoparesis and ataxia in addition to dysphagia and application of an magnetic resonance imaging with contrast medium. Thus, we should know if ocular motility was disturbed, if the patient complained about double vision, if the clinical examination revealed ataxia, and if ever a cerebral magnetic resonance imaging had been carried out. Affection of the IXth and Xth cranial nerve roots may be visible on cerebral magnetic resonance imaging as hyperintensity on T1-weighted images with gadolinium.[3] The latency of 26 days between onset of COVID-19 and onset of dysphagia is no argument against GBS, as post–COVID-19 GBS may develop up to at least 1 month after onset of the viral infection.[2]A second differential explaining dysphagia not considered is ischemic stroke in the brainstem. Because of immune-mediated hypercoagulability SARS-CoV-2, patients are at an increased risk of experiencing not only venous thrombosis but also occlusion of arteries. A small brainstem ischemia that could explain prolonged dysphagia may not be visible on cerebral computed tomography. A multimodal cerebral magnetic resonance imaging together with magnetic resonance angiography is mandatory to confirm or exclude brainstem ischemia.A third differential not considered is focal or pandysautonomia. Parasympathetic innervation may be disturbed as a complication of the infection leading to small fiber neuropathy. Thus, we should be told if autonomic dysfunctions other than swallowing were additionally affected. Autonomic denervation can be investigated by several simple or sophisticated tests, upon which the extension of the autonomic denervation can be assessed.Last, it would be interesting to know whether noninvasive neurostimulation therapies such as repetitive, transcranial magnetic stimulation, transcranial direct current stimulation, surface neuromuscular electrical stimulation, or pharyngeal electrical stimulation were ever applied during the 8 wks of swallowing therapy.Overall, the elegant study has limitations that should be addressed to eventually unravel the etiology of post–COVID-19 dysphagia.