Comparisons with other studies
Prior investigations on the prevalence rates of parosmia and phantosmia in patients with various causes of smell loss showed difference between study centers.6–9 Since symptoms of isolated qualitative dysfunctions are hardly ever spontaneously reported by patients23, the heterogeneity of methods and questionnaires used has been suggested to be one major reason for this discrepancy.24 In addition, qualitative olfactory dysfunction is – like in the present investigation – typically assessed in terms of the presence or absence. This lack of granularity may oversimplify a complex symptom. Nevertheless, our finding that parosmia was most commonly present in the postinfectious group was altogether not surprising. It has been previously reported that parosmia is most prevalent in postinfectious smell loss and one possible explanation might relate to its pathophysiology. Although the exact mechanism is only partly delineated, there is at least preliminary evidence that the number of olfactory sensory neurons (OSN) is reduced in these patients.25 Considering the mechanism of olfactory coding26, it is tempting to speculate that loss of OSN leads to incomplete patterns of afferent sensory information, resulting in distorted odour perceptions.
The role and clinical course of idiopathic phantosmia has been outlined in detail.27 It has been suggested that idiopathic phantosmia can be seen as a harmless symptom rather than an early predictor of neurodegenerative diseases. Likewise, our results showed that phantosmia was not associated with clinically relevant recovery of olfactory function, hence was also not a relevant predictor for olfactory recovery after OT. Various theories have been postulated on the neurobiological causes of odour perceptions in the absence of an apparent source (olfactory hallucinations).28 However, a previous study on the prevalence of phantosmia provided a first link between olfactory hallucinations and the presence of the BDNF met allele, which accounts for neuronal survival and synaptic plasticity.29