Olfactory Bulb Atrophy in a Case of COVID-19 with Hyposmia.

Galougahi et al reported a patient with coronavirus disease 2019 (COVID-19) who presented with isolated anosmia and was found to have normal signal intensity in the olfactory bulb and tract on magnetic resonance imaging (MRI) (1). Although patients infected with COVID-19 not uncommonly develop anosmia/hyposmia, the pathogenesis of severe acute respiratory syndrome coronavirus -2 (SARS-CoV-2)-induced loss of olfactory function has not been fully studied nor have the image findings of olfactory bulb been fully described (2).

We recently studied a 16-year-old girl, who was confirmed with COVID-19 by both clinical symptoms of fever, rhinorrhea, headache, and hyposmia and real-time reverse transcription polymerase chain reaction (RT-PCR) testing on a nasopharyngeal swab. Although all the other symptoms resolved, her hyposmia persisted, even after being discharged from the hospital with three negative RT-PCR tests for SARS-CoV-2. Furthermore, the coronal brain 3D turbo spin echo T2-weighted MRI images with a slice thickness of 1mm on day 38 of COVID-19 onset disclosed small right olfactory blub and olfactory tract hyperintensity (Fig 1 ). Since her sense of smell had not returned, a follow-up MRI was done on day 121, which showed no change in the olfactory bulb and tract.

Figure 1

The coronal brain 3D turbo spin echo (TSE) MRI images (38 days after the symptoms onset) disclosed right olfactory bulb (white arrow) and tract (white arrowhead) neuropathy with atrophy (contrast by normal olfactory bulbs in white-boxes).

Many studies have showed that olfactory bulb volume decreased with postinfectious olfactory dysfunction. In patients with parosmia, a smaller olfactory bulb volume was found (3). Visual analyses of olfactory bulb atrophy by MRI can be used to objectively diagnose olfactory loss with flattening, thinning or loss of the normal oval or J-shape of the olfactory bulb, or an asymmetric decrease in the olfactory bulb size compared with the contralateral side (4). This correlation between structure and function was based on the theory that the degree of afferent neural activity is reflected by bulbar neurogenesis. Lesser activity level of sensory inputs from the olfactory epithelium would lead to lesser synaptogenesis of the olfactory bulb, and a further decrease in the olfactory bulb volume (3). Besides, some studies have suggested the reduction of olfactory bulb volume after certain infections resulted from peripheral damage rather than direct destruction and degeneration of olfactory bulb (3). Taken together, SARS-CoV-2 may infect non-neural cells of olfactory epithelium and disrupt olfactory sensory neurons function, further decreasing sensory input and causing olfactory bulb atrophy.

To the best of our knowledge, this is the first report of olfactory bulb atrophy in SARS-CoV-2 related hyposmia. A case report from Taiwan showed a smaller olfactory bulb from a patient with COVID-19 and partial recovery from anosmia (5), while another reported negative MRI findings in a patient with COVID-19 and hyposmia (6). Timing of image and severity of diseases may contribute to the differences among our case and previous reports. The original case received MRI in the early phase (1), and the other didn't mention the timing (6). MRI in our case was performed on day 38 and day 121. It may take weeks to see structural changes at the bulb level in patients of COVID-19. Besides, our case suffered from prolonged hyposmia for more than four months, which might suggest that not only epithelial support cells but also stem cells in olfactory epithelium were involved, and may cause severe olfactory dysfunction and olfactory bulb atrophy. Olfactory bulb MRI may be a useful diagnostic technique for cases of COVID-19 with hyposmia. Future studies discussing clinical features and pathogenesis of olfactory function are warranted.