Discussion

Acute invasive fungal sinusitis caused by Mucorales, termed as sinonasal mucormycosis, is a rapidly progressive devastating infection of the nose and paranasal sinuses, with a tendency for contiguous spread to the orbits, infratemporal fossa, brain and skin. Optimal treatment involves surgical debridement of necrotic tissues followed by medical management with liposomal amphotericin B, regarded as the first-line medical management in such patients.^{Reference Cornely, Alastruey-Izquierdo, Arenz, Chen, Dannaoui and Hochhegger1}

Coronavirus disease 2019 associated mucormycosis has taken the form of an epidemic in the Indian subcontinent. Along with the common presentation of nasal blockage, facial hypoesthesia, proptosis, chemosis, dental pain and palatal ulcer in mucormycosis, several clinicians have noticed the presence of facial paralysis in Covid-19-associated mucormycosis patients. The available literature has reports of facial paralysis in rhino-cerebral mucormycosis; however, the exact pathophysiology of facial nerve involvement has not been explored. We evaluated the potential route of facial nerve involvement in Covid-19-associated mucormycosis through clinico-radiological correlation.

Facial paralysis has been reported in few isolated cases of mucormycosis. Mane et al. reported facial nerve paralysis in four patients with mucormycosis.^{Reference Mane, Patil, Mohite and Mohanty2} All patients were diabetic, and underwent surgical debridement followed by liposomal amphotericin B treatment. Two patients expired during ongoing treatment, while the other two showed improvement in facial nerve function following the completion of treatment. The authors speculated the pterygopalatine fossa to be the reservoir of infection in mucormycosis, with the spread of infection proceeding to the inferior orbital fissure, orbital apex and infratemporal fossa, as was described by Hosseini and Borghei.^{Reference Hosseini and Borghei3}

In our study, involving four patients, disease in the sinonasal cavity travelled through the pterygopalatine fossa towards the infratemporal fossa via the pterygomaxillary fissure, and led to fibro-fasciitis of the lateral pterygoid muscle. Lateral extension along the lateral pterygoid muscle, resulting in inflammatory spread to the deep lobe of the parotid and the facial nerve at the exit from the mastoid (stylomastoid foramen), seems the most plausible explanation of facial palsy.

In a similar case scenario, Shekar et al. reported sinonasal orbital mucormycosis in a 75-year-old man with lower motor neuron facial paralysis and no alteration or loss of taste sensation.^{Reference Shekar, Sikander, Rangdhol and Naidu4} Facial nerve palsy has been reported in cases with isolated involvement of the parotid gland by mucormycosis, leading to Mucor parotitis.^{Reference Chandu, MacIsaac, MacGregor, Campbell, Wilson and Bach5,Reference Gochhait, Alexender, Dehuri, Rangarajan, Jacob and Siddaraju6}

Invasion of the peripheral nerves in mucormycosis has also been reported in the literature, and the organism may travel along the peripheral nerves.^{Reference Margo, Linden, Strickland-Marmol, Denietolis, McCaffrey and Kirk7–Reference McLean, Ginsberg and Stanton9} The authors of these papers identified ascending neuritis of the trigeminal nerve on radiological evaluation, which was confirmed on histopathological assessment. Facial nerve involvement at the stylomastoid foramen through similar ascending neuritis is a strong possibility.

Some authors have hypothesised similar involvement of the Vidian nerve by the organism and ascending involvement of the geniculate ganglion.^{Reference Mane, Patil, Mohite and Mohanty2,Reference Aloosi10} In our case series of four patients, this explanation seems unlikely. There was no radiological enhancement along the Vidian nerve. In order to further validate our hypothesis, we performed Schirmer's test in two patients and both had normal lacrimation.

Another possible explanation for facial palsy is the reactivation of latent ‘viral’ infection, given the considerable immune compromise in such cases. Facial nerve involvement in diabetic patients has been described previously in Bell's palsy. It is hypothesised to be due to the pathology of resistance arteries, leading to facial nerve oedema and ischaemia.^{Reference Mane, Patil, Mohite and Mohanty2} The clear demonstration of intense inflammation on MRI and the uniform involvement of extratemporal facial nerve areas in all cases makes direct inflammation of the nerve by fungal elements a more likely explanation. Although middle-ear effusion was present in three of our patients, the involvement of the facial nerve in the intra-temporal segment by the effusion does not seem plausible, as the facial nerve is a robust nerve with good protection within a bony fallopian canal. In addition, middle-ear effusion is a common disease and does not usually cause facial palsy.

To the best of our knowledge, ours is the first study to elucidate the route of facial nerve involvement in Covid-19-associated mucormycosis. Familiarity with this route may better enhance our understanding of the pathogenesis of this manifestation.