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