The most obvious theory of the neurological effects of the COVID-19 virus is the mechanism of ACE2, which is identified as a functional receptor of SARS-CoV-2. The virus reaches host cells via ACE2 receptor. This enzyme receptor is found mostly in type II alveolar cells in the lungs . It is also produced by many cells, including glial cells and neurons. The presentation and distribution of ACE2 suggests that the COVID-19 virus may cause neurological-neural involvement through direct or indirect mechanisms. Studies have shown that the virus enters the central nervous system through the olfactory nerve, another pathway, and can spread from neuron to neuron via axonal transport . Apart from direct neurological system invasion of the virus, neurological complications associated with COVID-19 may occur as a result of widespread cardiopulmonary insufficiency and metabolic abnormalities induced by SARS-CoV-2 infection or mechanisms of autoimmunity . Neurological complications associated with COVID-19 can be divided into two: central and peripheral nervous system complications. While common central nervous system complications include headache, cerebrovascular events, encephalitis, and imbalance, the most common findings of peripheral nervous system complications are anosmia/hyposmia and chemosensory dysfunctions . Furthermore, cases reported in the literature in terms of peripheral nerve involvement associated with COVID-19 virus are Guillain-Barré syndrome, facial nerve palsy, abducens nerve paralysis, optic neuritis and phrenic nerve involvement [8, 9, 10].
In the present case, the patient had a complaint of hoarseness that started concurrently with the COVID-19 infection. The examination performed following the COVID-19 positivity revealed left VCP, and there was no other reason to explain this condition in the etiology of the disease. The absence of pneumonia in the thorax CT findings of the patient suggested that it was due to vagal neuritis caused by nerve invasion of the virus, rather than the nerve being affected with possible mediastinal involvement. Furthermore, cadaveric position of the vocal cord and the presence of additional cranial nerve involvement findings supported the mononeuritis picture.
The literature review has shown that there are no unilateral or bilateral VCP cases in which varicella-zoster virus, cytomegalovirus and herpes zoster virus play a role in the etiology . Although coronaviruses are a diverse family of viruses, they can lead to different symptoms in cases infected with COVID-19 as they are associated with high rates of neurological involvement. Altought we do not have objective data to prove definitively this situation, when we consider other possible viral etiologies the most likely factor that could explain idiopathic VCP in our patient was the COVID-19 virus. Moreover, the present case will be thought-provoking for evaluating the movements of the vocal cords and changes in the voice quality in patients being infected with COVID-19 during the pandemic.