The Laryngoscope

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Postinfectious Olfactory Loss: A Retrospective Study on 791 Patients

Annachiara Cavazzana, PhD ; Maria Larsson, PhD; Marcus M€ €hner, MD;

unch, MD; Antje Ha
Thomas Hummel, MD

Objectives/Hypothesis: Postinfectious olfactory loss is among the most common causes of olfactory impairment and
has substantial negative impact on patients’ quality of life. Recovery rates have been shown to spontaneously improve in
most of patients, usually within 2 to 3 years. However, existing studies are limited by small sample sizes and short follow-up.
We aimed to assess the prognostic factors for recovery in a large sample of 791 patients with postinfectious olfactory
disorders.
Study Design: Retrospective cohort.
Methods: We performed a retrospective analysis of 791 patients with postinfectious olfactory loss. Olfactory functions
were assessed using the Sniffin’ Sticks test at the first and final visits (mean follow-up 5 1.94 years).
Results: Smell test scores improved over time. In particular, patient’s age and the odor threshold (T), odor discrimina-
tion (D), and odor identification (I) (TDI) score at first visit were significant predictors of the extent of change. The percent-
age of anosmic and hyposmic patients exhibiting clinically significant improvement was 46% and 35%, respectively.
Conclusions: This study provides new evidence within the postinfectious olfactory loss literature, shedding light on the
prognostic factors and showing that recovery of olfactory function is very frequent, even many years after the infection.
Key Words: Postinfectious olfactory loss, recovery, smell disorders, Sniffin’ Sticks.
Level of Evidence: 4
Laryngoscope, 00:000–000, 2017

INTRODUCTION recovery, usually within 2 to 3 years after the infectious

Various etiologies are associated with olfactory loss,
including upper respiratory tract infection (URTI) (18%–
45% of the clinical population), nasal/sinus disease (7%–
56%), head trauma (8%–20%), toxic exposure (2%–6%),
and congenital anosmia (0%–4%).1 Postinfectious olfacto-
ry loss is among the most common causes leading to
olfactory disorders.2–4 It is characterized by a sudden
loss of olfactory functions after an infection of the upper
respiratory airway, typically associated with a common
cold or influenza.4 Usually, anosmia is present in 36% to
53% of the patients and hyposmia in 47% to 64%.5,6
Although the literature reports that topical steroids,7,8
vitamin B,7 acupuncture,9,10 zinc,11 and a-lipoid acid12
can be used to treat postinfectious olfactory loss, no
effective therapy is available to date3 except olfactory
training.13,14 However, it has been estimated that about
one-third of patients may experience spontaneous
From the Smell and Taste Clinic (A.C., M.M., A.H., T.H.), Technical
University of Dresden, Dresden, Germany; and the G€ osta Ekman Labo-
ratory, Department of Psychology (A.C., M.L.), Stockholm University,
Stockholm, Sweden.
Editor’s Note: This Manuscript was accepted for publication
March 9, 2017.
This research was supported by a grant from the Deutsche For-
schungsgemeinschaft to T.H. (DFG HU411/18-1) and the Swedish Foun-
dation for Humanities and Social Sciences to M.L. (M14-0375:1).
The authors have no other funding, financial relationships, or con-
flicts of interest to disclose.
Send correspondence to Annachiara Cavazzana, PhD, Smell and
Taste Clinic, Department of Otorhinolaryngology, Technical University of
Dresden, Fetscherstrasse 74, 01307 Dresden, Germany. E-mail: anna-
chiara.cavazzana@uniklinikum-dresden.de
DOI: 10.1002/lary.26606
event.6,15–19 Reden and coworkers15 tested 262 patients
using Sniffin’ Sticks, and they showed improvement in
32% within the first 13 months. A similar percentage
has been reported in different reviews. Hummel16
described spontaneous recovery in one-third of patients,
and Hendriks17 observed that out of 26 untreated
patients, 34.6% showed a complete recovery of olfactory
functions over a period of 12 months. Mott and Leo-
pold,18 in a longitudinal study of 40 patients, observed
that 15% showed improvement in olfactory test scores
after an average of 26 months (for similar results see
also Rombaux et al.19). Interestingly, other works have
demonstrated even higher rates of recovery. For exam-
ple, London and colleagues,20 using the University of
Pennsylvania Smell Identification Test (UPSIT),
reported that 56.7% of initially anosmic and 42.8% of
initially hyposmic patients improved significantly over
time. Similarly, Duncan and Seiden6 monitored 21
patients with URTI-related smell loss for 3 years. After
this period, 19 patients had a significantly improved
UPSIT score, and 13 patients reported subjective
improvement of olfactory performance (see also Lee
et al.21 with improving rates of 85.7%). Even though
olfactory recovery has been demonstrated, knowledge
regarding the percentage of improvement shows large
variation. Therefore, more research is needed, especially
considering the fact that most of the studies are based
on small sample sizes, and olfactory change is assessed
only in the short term and with different testing proce-
dures. Another problem, that probably cannot be solved,
relates to the fact that most data are collected in

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specialized centers that are probably not seen by many
people with milder symptoms. These factors limit the
generalizability of clinical prognostic features and the
possibility of recovery in these patients.
The aim of this retrospective study was to localize
significant predictors for olfactory recovery in a large
sample of patients with postinfectious olfactory loss (N
5 791) based on standardized objective testing methods
(i.e., the Sniffin’ Sticks test22). In so doing, we hope to
comprehensively provide useful clinical information to
counsel patients in a meaningful way.
MATERIALS AND METHODS
Subjects
The retrospective study group was composed of 791
patients presenting to the Interdisciplinary Centre for Smell
and Taste of the Technical University of Dresden between 1998
and 2010, with postinfectious olfactory disturbances (mean age
5 58.9 years, standard deviation [SD] 5 10.2 years, range 5
15–84 years, 224 males). The inclusion criteria included a histo-
ry of URTI immediately before olfactory loss and a sudden onset
of olfactory loss. The exclusion criteria included all the other
conditions associated with olfactory dysfunctions, such as a his-
tory of head trauma, acute or chronic rhinosinusitis, allergic
rhinitis, neurodegenerative diseases, or abnormal nasal anato-
my. Patients did not receive any specific and standardized treat-
ment protocol at our clinic. They were usually sent from other
medical centers for outside consultations. Regarding treatment,
3.2% reported that they had taken different types of vitamins
(e.g., A, B, and E), 15.4% steroids, 2.1% a-lipoic acid, and 3.5%
declared to having been treated with acupuncture. The majority
(75.8%) declared no treatment history. The study complied with
the Declaration of Helsinki and had been approved by the
ethics committee of the Technical University of Dresden. Writ-
ten informed consent was obtained from all participants prior to
the study.
Procedure
The patients were tested on two occasions (first visit [T1]
and second visit [T2]), with a follow-up variation in time rang-
ing from 13 to 4,251 days (mean 5 708.8 days, SD 5 929.4
days, median 5 338 days). Patients came to the first visit after
an average time period of 565 days after URTI (SD 5 957.8
days, range 5 6–11,073 days, median 5 281 days). At the first
visit, they underwent a structured interview where medical his-
tory was taken and parosmia and phantosmia were assessed.23
Psychophysical testing of olfactory function was performed both
at T1 and T2 with the validated Sniffin’ Sticks test.22 Odors
were presented to the patients in felt-tip pens. For birhinal
stimulation, the pen’s tip was placed approximately 2 cm below
both nostrils. Three different olfactory functions were assessed.
First, odor thresholds were determined for phenylethyl alcohol
(PEA), which has a rose-like odor,24 with 16 stepwise dilutions.
Thresholds were determined using the single staircase tech-
nique based on a three-alternative forced choice (3-AFC) task.
Second, odor discrimination was assessed over 16 trials. For
each discrimination, three pens were presented, two containing
the same odor and the third containing the target odorant (3-
AFC task). Third, odor identification was assessed by present-
ing 16 odors presented with four verbal descriptors in a multi-
ple forced-choice format (three distractors and one target).
Functional anosmia (i.e., anosmia below) was diagnosed if the
sum score of the three tests (odor threshold (T), odor
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2
discrimination (D), and odor identification (I) [TDI] score) was
less than 16.5. A TDI score between 16.5 and 30.5 was catego-
rized as hyposmia. A score above 30.5 was considered within
the normosmic range.
Dependent Variables and Statistical Analysis
For the regression analyses, the dependent variables were:
1) the numerical change in the TDI score from the first to the
second assessment (i.e., delta TDI); 2) a clinical change in the
TDI score by 6 points coded as 11 for TDI scores improved by
6 or more points, 0 for changes fewer than 6 points, and 21 for
clinical decline25; and 3) the final diagnosis at T2 (i.e., anosmic,
hyposmic, normosmic). Candidate predictors chosen as poten-
tially affecting changes in olfactory functions were: 1) TDI score
at the first assessment (TDI at T1), 2) duration of olfactory loss
until the first assessment (disease duration), 3) presence or
absence of parosmia, 4) presence or absence of phantosmia, 5)
interval between the first and the second assessment (T1–T2
interval), and 6) demographic factors including age at the first
visit and sex. Pearson’s v2 test was applied to analyze the cate-
gorical variables. All of the statistical analyses were performed
using a commercially available software package, SPSS version
22.0 (IBM, Armonk, NY). Any P values <.05 were considered to
be statistically significant.
RESULTS
The result section is organized as follows. First, the
patients’ demographic characteristics and baseline olfac-
tory functions are reported. Second, the results from the
three separate regression analyses are reported (i.e., del-
ta TDI, clinical change, and final diagnosis as the depen-
dent variables).
Baseline Olfactory Functions
At the first visit, 39.6% (N 5 313) of the patients
were diagnosed as anosmic, 57.9% (N 5 458) as hypos-
mic, and 2.5% (N 5 20) as normosmic. No differences
were observed between males and females with respect
to age, TDI score, or in threshold and identification
measurements (all P > .05). However, females outper-
formed males in odor discrimination (t790 5 2.01, P 5
.045). Age correlated weakly, but significantly with the
TDI score (r 5 20.09, P 5 .006), discrimination (r 5
20.10, P 5 .004), and identification (r 5 20.07, P 5 .04),
but not with thresholds (r 5 20.04, P 5 .20).
Regression Analyses
Predictors for the delta TDI. As a first step, a
multiple linear regression was performed to determine
whether the predictor variable would influence the
numerical change in the TDI scores (mean 5 4.7, SD 5
0.2, range 5 217.5–28, median 5 4.2). The results
showed that baseline TDI score (P < .001) and the
patients’ age at the first test occasion (P 5 .016) were
the only significant predictors of patients’ delta TDI.
Specifically, higher TDI score (b 5 20.35) and higher
age (b 5 20.07) at the first visit were related to lower
delta TDI scores (Fig. 1 and Table I). Including only
these two variables in the model, they accounted for
16.6% of the explained variability (F2, 790 5 78.43, P <
Cavazzana et al.: Postinfectious Olfactory Loss
Fig. 1. Scatterplot of the relationship between the delta TDI score and the TDI at the first visit (A) and the age of patients at the first visit
(B). (C) A scatterplot depicting the positive relationship between TDI scores at the first and second visits. TDI 5 odor threshold (T), odor
discrimination (D), and odor identification (I).

.001) (Table II). To provide a descriptive and clinical
overview of the data, we decided to divide groups
approximately according to decades of age. We explored
the numerical change in the TDI score (i.e., the delta
TDI) from the first to the second assessment according
to decades of age. Eighty percent of patients (8 out of 10)
in age group 15 to 30 years (mean age 5 25.8 years, SD
5 4.59 years, four females), 83.9% (26 out of 31) in age
group 31 to 40 years (mean age 5 35.9 years, SD 5 2.39
years; 24 females), 89.4% (93 out of 104) in age group 41
to 50 years (mean age 5 46.45 years, SD 5 2.64 years,
71 females), 82.9% (208 out of 251) in age group 51 to 60
years (mean age 5 55.88 years; SD 5 2.75 years; 185
females), 81.5% (265 out of 325) in age group 61 to 70
years (mean age 5 64.75 years, SD 5 2.95 years, 236
females), and 77.1% (54 out of 70) in age group 71 to 85
years (mean age 5 75.41 years, SD 5 3.55 years, 47
females) showed improvement in the TDI delta score.
The percentage of improvement was above 80% in all
age groups, except in the oldest group of patients. Nev-
ertheless, the percentage of improvement or decline did
not differ across the age groups (v2 [5] 5 5.18, P 5 .39).
Data regarding the predictors T1–T2 interval and dis-
ease duration were not normally distributed, but skewed

TABLE I.
Multiple Linear Regression Analysis of the Delta TDI in Postinfectious Patients.
Predictors No. B SE B b t Significance 95% CI (Lower) 95% CI (Upper)

TDI at T1 233 20.35 0.06 20.39 26.3 <.001 20.46 20.24

Age at T1 233 20.07 0.03 20.16 22.44 .016 20.13 20.01
Sex 233 0.52 0.69 0.05 0.75 .456 20.86 1.9
Presence of phantosmia 233 21.03 0.71 20.1 21.45 .147 22.43 0.37
Presence of parosmia 233 1.05 0.72 0.1 1.46 .146 20.37 2.48
Disease duration 233 <0.001 0.00 20.05 20.87 .386 20.001 0.001
T1–T2 interval 233 <0.001 0.00 0.05 0.79 .432 <0.001 0.001

R2 5 0.17. Model: F7,232 5 6.43, P < .001. When considering all of the predictors, the sample size is reduced to 233 patients, because it was possible
in only some of them to collect information regarding the presence/absence of parosmia/phantosmia.
B 5 beta; CI 5 confidence interval; SE B 5 standard error of beta; T1 5 first visit; T2 5 second visit; TDI 5 odor threshold (T), odor discrimination (D),
and odor identification (I).

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Multiple Linear Regression Analysis of the Delta TDI in Postinfectious Patients.
No. B SE B
TDI T1 791 20.37 0.03
Age T1 791 20.09 0.02
B 5 beta; SE B 5 standard error of beta; T1 5 first visit; TDI 5 odor threshold (T), odor discrimination (D), and odor identification (I).
to the right. For this reason, we decided to split the sam-
ple according to 1) the median time between the first
and the second visit, which was 338 days (i.e., 11
months) and 2) the median time between the onset of
the disease and the first visit, which was 281 days (i.e.,
9 months). A Mann-Whitney test was then run to com-
pare the delta TDI between the two groups (T1–T2 inter-
val: U 5 68214.5, Z 5 23.1, P 5 .002; disease duration:
U 5 65830, Z 5 23.8, P < .001). Delta TDI in patients
with a shorter T1–T2 interval (median 5 4.7) and dis-
ease duration (median 5 5.4) differed significantly from
delta TDI in patients with longer T1–T2 interval (medi-
an 5 3.7) and disease duration (median 5 3.5).
Predictors for a significant clinical change in
olfactory functions. Of the 791 patients, 306 (38.7%)
exhibited a clinical improvement in having a TDI score
of more than six points, indicating a significant improve-
ment of olfactory functions, whereas 137 patients
(17.3%) exhibited a decrease in olfactory function. The
vast majority (N 5 348, 44%) exhibited no clinical
change. The multinomial logistic regression analysis
identified that clinical changes in TDI scores (more than
six points) depended on the initial TDI score; as TDI at
T1 increases by a unit, the odds of declining, as com-
pared to clinically improving, increases by 25.3%. In oth-
er words, patients whose olfactory acuity worsened had
initially higher TDI scores, whereas those who clinically
improved had the lowest initial scores (b 5 0.226, Wald
v2 (1) 5 26.15, P < .001) (Fig. 2 and Table III). A univar-
iate analysis of variance (ANOVA) showed a significant
difference between the TDI score at T1 and the level of
clinical change (F2,790 5 33.78, P < .001). Patients who
clinically improved had lower initial TDI scores (mean 5
15.52, SD 5 5.57) as compared to both patients who
remained stable (mean 5 18.71, SD 5 6.07, P < .001)
and who decreased (mean 5 21.45, SD 5 6.39, P < .001).
On the other hand, patients who decreased had higher
initial TDI score as compared to those who improved
and remained stable (P < .001).
Predictors of the final olfactory diagnosis. At
follow-up testing, the number of anosmic patients signif-
icantly decreased as compared to T1 (from 39.6% to
18.3%), whereas the number of normosmic people
increased (from 2.5% to 14.4%); 67.3% were hyposmic
versus 57.9% at T1. Specifically, among the anosmia
patients at T1, 22.1% became hyposmic and 1.5% nor-
mosmic, whereas 11.0% developed normosmia from an
initial diagnosis of hyposmia. Only 3.1% worsened in
their olfactory diagnosis, and the other 62.3% remained
stable (15.9% remained anosmic, 44.5% hyposmic, and
1.9% normosmic). Logistic regression analysis identified
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TABLE II.
b t Significance 95% CI (Lower) 95% CI (Upper)
20.39 211.93 <0.001 20.43 20.31
20.16 24.94 <0.001 20.13 20.06
the age at first visit and the baseline TDI score as signif-
icant predictors for the final olfactory diagnosis (v2[4] 5
281.02, P < .001; R2 5 .29 [Cox & Snell]; R2 5 .37
[Nagelkerke]). Increasing age at T1 was related to a
worse olfactory diagnosis at T2 (univariate ANOVA:
F2,790 5 14.21; P < .001; mean initial age [SD]: final
anosmia, 60.83 [9.93]; final hyposmia, 59.25 [9.9]; final
normosmia, 54.44 [10.9]; significant differences between
normosmia and both hyposmia and anosmia groups at P
< .001; no significant difference between hyposmia and
anosmia, P 5 .09). However, higher baseline TDI scores
were related to a better diagnosis outcome at T2 (univar-
iate ANOVA: F2,790 5 151.98; P < .001; mean initial TDI
scores [SD]: final anosmia, 12.81 [3.75]; final hyposmia,
18.59 [5.34]; final normosmia, 24.21 [6.38]; significant
differences between all groups at P < .001).
DISCUSSION
To our knowledge, this is the first study that com-
prises a large population of postinfectious olfactory loss
patients who have been followed up in the long term (up
to 11 years). The main purpose was to determine the sig-
nificant predictors for patients’ spontaneous olfactory
recovery. In particular, recovery was assessed along
three dimensions: 1) simple improvement (the delta TDI
score, the numerical change in the TDI score from the
first to the second visit); 2) clinical improvement
(changes in TDI scores by a relevant clinical degree, by
6 points); and 3) the final diagnosis.
The principal factor identified as potentially affect-
ing the three dimensions of olfactory recovery was the
initial TDI score. The presence of residual olfactory
Fig. 2. Mean TDI at first visit with respect to the change in olfacto-
ry functions. Bars represent the standard error of the mean. Sig-
nificant differences are seen between all groups at P < .001. TDI
5 odor threshold (T), odor discrimination (D), and odor identifica-
tion (I).
Cavazzana et al.: Postinfectious Olfactory Loss
 TABLE III.
Results for Multinomial Logistic Regression Models With Clinical Change as the Outcome.
B SE B Wald Significance Odds Ratio 95% CI (Lower) 95% CI (Upper)

Clinical decline vs. clinical improvement

Intercept 27.58 1.83 17.20 <.001
TDI at T1 0.23 0.04 26.14 <.001 1.25 1.15 1.37
Age at T1 0.04 0.02 3.19 .07 1.04 1.00 1.09
Sex, male 0.12 0.48 0.06 .81 1.12 0.44 2.88
Presence of phantosmia, no 20.55 0.51 1.18 .28 0.58 0.22 1.55
Presence of parosmia, no 0.75 0.50 2.20 .14 2.11 0.79 5.67
Disease duration <0.001 <0.001 0.42 .52 1.00 1.00 1.00
T1–T2 interval <0.001 <0.001 0.73 .39 1.00 1.00 1.00
No change vs. clinical improvement
Intercept -0.92 1.08 0.74 .39
TDI at T1 0.23 0.04 26.14 <.001 1.25 1.15 1.37
Age at T1 0.01 0.01 0.55 .46 1.01 0.98 1.04
Sex, male 0.15 0.34 0.19 .66 1.16 0.60 2.24
Presence of phantosmia, no 20.65 0.34 3.57 .06 0.52 0.27 1.03
Presence of parosmia, no 0.27 0.35 0.59 .44 1.31 0.66 2.60
Disease duration <0.001 <0.001 1.00 .32 1.00 1.00 1.00
T1–T2 interval <0.001 <0.001 0.47 .49 1.00 1.00 1.00

R2 5 0.17 (Cox & Snell), R2 5 0.2 (Nagelkerke). Model: v2(14) 5 43.26, P < .001.
B 5 beta; CI 5 confidence interval; SE B 5 standard error of beta; T1 5 first visit; T2 5 second visit; TDI 5 odor threshold (T), odor discrimination (D),
and odor identification (I).

functions (i.e., TDI at first visit) has already been
reported in literature as one of the most important fac-
tors determining the outcome.19,20,26,27 This has been
demonstrated for olfactory psychophysical testing
results.20,26 London et al.,20 for example, reported that
microsmic patients were more than twice as likely to
improve into the normal range than anosmic patients, a
result also confirmed by Hummel and L€otsch,26 showing
that higher initial scores were associated with higher
probability of normosmia. Interestingly, literature also
reports that both olfactory bulb volume27 and olfactory
event-related potentials19 are important predictors for
recovery of the sense of smell. Similarly, our data
showed that higher baseline TDI scores were related to
less improvement.26 Patients who obtained a high TDI
score at T1 might have regained functions by the time of
their first visit. Therefore, at T2, their olfactory func-
tions probably remained stable, without significantly
impacting on the final TDI score. When the final diagno-
sis was targeted, higher baseline TDI scores were associ-
ated with higher probability of final normosmia.20,26
Hence, patients with postinfectious olfactory loss in the
hyposmic range can therefore expect a better outcome
(i.e., diagnosis) compared to anosmic patients, although
the latter might present a higher TDI score difference
(i.e., delta TDI) between T1 and T2 without reaching the
normosmic range. Also, patient’s age at the first visit
was a significant prognostic factor that confirms obser-
vations from previous studies,15,16,20 but only when con-
sidering the delta TDI scores and the final diagnosis.
Here, older age was related to less improvement and a
worsening in the final diagnosis. It is well known that
postinfectious olfactory loss is caused by a damage to
olfactory receptor neurons in the olfactory epithelium.28
Such damage becomes more evident in older people who
are more vulnerable to infections as they are character-
ized by a decrease in the size of the olfactory epithelium
and a consequent loss of the number of olfactory recep-
tor neurons.29,30 Such cumulative insult, together with
the fact that the challenge of regeneration in advanced
age is significantly reduced, might be the reason why
the recovery of olfactory functions after postinfectious
olfactory loss decreases with increasing age. When it
comes to the sex of the participants, in line with other
studies6,10,15,20, this predictor was not significantly asso-
ciated with the outcome. Intriguingly, the interval
between the first and the second assessment6,15,20 and
the duration of disease until the first baseline test did
not play a significant role in the model. The reason
behind this lack of statistical significance might be
explained by taking into consideration the high T1–T2
interval and disease duration variability, which in turn
has probably influenced the normality of the data distri-
bution. For this reason, patients were divided into two
groups according to the median values T1–T2 interval
and disease duration (see Predictors for the Delta TDI
Section). Regarding the predictor T1–T2 interval, our
data indicate that although both groups improved their
delta TDI (positive values), patients who came to our
clinic for the second visit after a shorter time period
improved better as compared to those who waited longer.
It is likely that these patients, perceiving their situation
as concretely improved, felt more prone to volunteer for
retesting, eager to test whether their olfactory abilities
really improved. On the contrary, patients who did not
perceive that their olfactory functions showed

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5
improvement lost their motivation to be retested again.
This might have shifted their decision to be tested only
later in time, when they started to realize that their olfac-
tory abilities were somewhat reduced. Regarding the role
played by the disease duration, studies in literature are
contradictive. Some results show that a longer disease
duration is associated with less subsequent improve-
ment,2,6,14,15,20 although others10,21 observed that longer
periods after onset of olfactory loss were positively related
to recovery. At odds with previous work, disease duration
was unrelated to outcome, although the b value was nega-
tive, suggesting that the longer the disease, the lower the
olfactory recovery (Table I). By dividing patients accord-
ing to the median value between the onset of the disease
and the first visit (i.e., 281 days), results showed that
patients who came to the first visit after a shorter time
from the disease had a higher chance to exhibit improve-
ment of overall olfactory function, expressed as the change
of TDI score. This might indicate that, within a specific
time window, the recovery is higher. After this period,
recovery still happens but in a lesser amount. Therefore,
it seems that functional regenerative processes in periph-
eral olfactory epithelium might be effective, although to a
lesser extent, also after a relatively long latency.
Although this study provides evidence for factors that
affect recovery, it should be noted that the patient popula-
tion here described is disproportionately represented by per-
sons with more long-standing dysfunctions and probable
irreversible olfactory damage, who do not represent the
whole postinfectious olfactory loss community. In addition,
these patients usually visited our clinic many years after
the onset of the infectious event, assuming that the symp-
tom will eventually disappear; therefore, all the information
they provided depends on their recollection and accuracy.
CONCLUSION
In clinical practice, patients with postinfectious
olfactory disorders are informed that recovery of smell
function occurs, usually within 2 to 3 years. However,
available evidence is mixed and prevents clinicians from
correctly informing the patients about the rate of success
in regaining olfactory functions. For the first time, we
demonstrate that olfactory recovery occurs many years
after the viral event, underlining that olfactory functions
may change over a long period of time. Hence, the pre-
sent findings favor a good prognosis for postinfectious
olfactory loss patients, especially for those with initially
poor olfactory function and younger age.
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Cavazzana et al.: Postinfectious Olfactory Loss