Discussion: 
We are learning to understand the COVID-19 disease, an emerging infection that resulted in a global pandemic. Initially, respiratory symptoms are most distinctively seen in COVID-19 patients. It is believed that pro-inflammatory cytokine release, known as ‘cytokine storm,’ causes pulmonary damage, and it is the likely mechanism of CNS damage.  ACE2 is the functional receptor for the SARS-CoV-2 virus, present in multiple organs such as the lungs, heart, nervous system, skeletal muscles, blood vessels, kidney, liver, and gastrointestinal tract. The ACE2 receptor is found remarkably in the epithelial lining of lung alveoli, enterocytes of the small intestine, the endothelial lining of arteries and veins, and arterial smooth muscles of all organs.4 Hence, COVID-19 can affect any of the organs, as mentioned above. SARS-CoV-2 enters the CNS through either a hematogenous or retrograde neuronal route; the neural invasion mechanism is mainly through the cribriform plate, olfactory nerve, thalamus brainstem. Thus, resulting in the suppression of central cardiorespiratory drive.5 Mao et al., in a study in Wuhan published in April 2020, mentioned that the neurological manifestations are seen in critically ill patients.6Later, it is noticed that many patients with few or no symptoms of COVID-19 disease also had neurological symptoms.7Further, Mao et al. classified neurological manifestations as dizziness, headache, impaired consciousness, ataxia, seizure, and acute cerebrovascular disease into central nervous system manifestations. Nerve pain, taste, smell, and vision impairment into peripheral nervous system manifestations and skeletal muscular injury manifestations.6
Our patient presented with features of peripheral nerve involvement (anosmia and dysgeusia), cranial nerve involvement (hemifacial spasms and vestibular neuritis), and Raynaud’s phenomenon. Peri- and post-infectious anosmia and dysgeusia could be secondary to olfactory nerve lesion or apparatus damage from viral infection. The majority of patients presented at the same time or a few days after the onset of other COVID-19 symptoms.8 Hemifacial spasm is a neuromuscular movement disorder with slight intermittent contractions or twitching of the muscles innervated by the facial nerve (cranial nerve VII). Though twitching is irregular initially, it may be severe, more persistent, and can spread to the muscles of facial expression in the following months. Sometimes, a mild peripheral weakness can develop. The spasms are due to compression of the facial nerve by the artery at the root exit of the brainstem. The clinical features are essential in diagnosing the disease; electromyography and magnetic resonance imaging (MRI) are additional diagnostic modalities to determine the underlying cause.9 A case report by Hutchins et al. described the association of bilateral facial paralysis with paresthesia, a subtype of Guillain- Barre syndrome, and COVID-19.10 Few studies describe facial nerve involvement, causing Bell’s palsy but relatively do not know much about the hemifacial spasms in COVID-19.
Acute vestibular neuritis (VN), or peripheral vestibulopathy (PVP), is defined as a lesion of the eighth cranial nerve’s vestibular component without auditory deficits. It is a clinical entity with the features of vertigo or dizziness along with nausea or vomiting, gait instability, head motion intolerance, and nystagmus, which is developed over minutes or hours. The most common cause is the reactivation of latent herpes simplex virus, especially herpes simplex virus type 1 (HSV-1).11 But a case report by Malayala et al. mentioned that COVID-19 infection could cause vestibular neuritis in susceptible populations.12 The possible source of vestibular neuritis in our patient is post-viral inflammation of the vestibular nerve, probably due to HSV-1 or COVID-19 infection. Considering the pandemic, the cause of VN is perhaps due to COVID-19 infection, given that VN’s features were seen after a week of negative COVID-19 test. As pathophysiology is uncertain in most cases, symptomatic treatment with antiemetics, antihistamines, anticholinergic agents, antidopaminergic agents, and benzodiazepines are given.13 Sometimes, methylprednisolone shows significant improvement of peripheral vestibular function recovery in severe cases. 14 Resumption of regular activity and vestibular rehabilitation with Cawthorne and Cooksey exercises promotes central vestibular compensation.15
COVID-19 has also been associated with various cutaneous manifestations like a morbilliform rash, urticaria, vesicular eruptions, acral lesions, petechiae, chilblains, Livedo racemosa, and distal necrosis.3,16 The possible mechanisms for cutaneous manifestations are the lymphocytic vasculitis induced by blood immune complexes activated by cytokines due to viral particles in the cutaneous blood vessels in patients with COVID-19.17 A few case reports noted that cutaneous findings are present before developing respiratory symptoms. In contrast, a few case reports found that these findings are seen several days after the onset of symptoms.16 Our patient presented with Raynaud’s phenomenon (RP) during the disease and urticarial rash several weeks later despite no previous history. Kolivras et al. described the first case of COVID-19 induced chilblains due to the delayed expression of the IFN-inducible genes, further exacerbating hypercytokinemia.18 Chilblains and RP are related to circulation but do not necessarily mean to have both. Chilblains are an inflammatory skin reaction to an abnormal vascular response to cold. They present as tender, pruritic, red lesions on the dorsal aspect of fingers or toes. 19 In contrast, RP is the triphasic color change with initial pallor, followed by cyanosis and erythema due to abnormal vasoconstriction of the digital arterioles when exposed to cold. RP’s diagnosis is mainly made with history, and physical examination mainly affects hands, and the thumb is often spared. RP is primarily associated with systemic lupus erythematosus and CREST (Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia) syndrome. Hence, the autoantibodies and nail fold capillary microscopy together give a clue to the diagnosis. Most of the patients with RP will respond well with general measures like smoking cessation, avoidance of cold exposure, repeated trauma, and vasoconstricting drugs. Few patients who do not respond to general measures will require pharmacological treatment that includes a calcium channel blocker, losartan, an angiotensin II receptor blocker.20
Our case report mentioned the neurological and cutaneous manifestations in a patient with COVID-19 with an excellent prognosis. To our knowledge, this is the first case report of COVID-19 induced hemifacial spasms and Raynaud’s phenomenon. Until further validation by other studies, we would like to alert the clinicians to various disease presentations in COVID-19, who are immediately tested and treated. Respiratory symptoms remain the hallmark of early identification and management of COVID-19; the treatment should not be delayed while keeping in mind the other manifestations.