BACKGROUND

Postviral olfactory loss after upper respiratory tract infection (URI) is not uncommon. However, its exact location and nature are not fully understood. Although it is likely to be caused by a direct damage of olfactory epithelium, a damage of the central pathway has also been suspected as its possible mechanism. This study will show basal metabolism in the brain of patients with postviral olfactory loss using fluorodeoxyglucose-positron emission tomography (FDG PET).

METHODS

Nine patients with postviral olfactory dysfunction were enrolled. All of the patients had neither apparent sinusitis nor rhinitis. All of them recalled causative URI and temporal connection with development of their olfactory loss. After olfactory function tests using the butanol threshold test and smell identification test confirmed olfactory impairment, FDG PET studies were performed during a rest state. The cerebral metabolic abnormality was compared between the patients and age/gender-matched healthy controls using a voxel-wised analysis.

RESULTS

In comparison with healthy controls, the patients showed a significant hypometabolism in the right piriform cortex and bilateral amygdala and parahippocampal areas where the olfactory neurons primarily project. Furthermore, hypometabolism was also shown in the bilateral insular cortices, medial and lateral temporal cortex where the olfactory information is integrated to produce the sensation. Increased metabolism was not found in any brain area.

CONCLUSION

This study showed that the postviral olfactory loss is likely to be associated with decreased metabolism in the specific brain regions where the olfactory information is received and integrated.