Research Article
Dement Geriatr Cogn Disord Received: January 7, 2021
Accepted: February 22, 2021
DOI: 10.1159/000515575 Published online: April 14, 2021
Hyposmia Is Associated with Reduced
Cognitive Function in COVID-19: First
Preliminary Results
Agnes Pirker-Kees a, b Kirsten Platho-Elwischger a Sebastian Hafner a
Kurt Redlich c Christoph Baumgartner a, b, d
aDepartment of Neurology, Clinic Hietzing, Vienna, Austria; bKarl Landsteiner Institute for Clinical Epilepsy Research
and Cognitive Neurology, Vienna, Austria; cDepartment of Rheumatology, Klinik Hietzing, Vienna, Austria; dMedical
Faculty, Sigmund Freud University, Vienna, Austria
Key words 10 ± 1 p = 0.028, r = 0.58). Total MoCA score was significant-
Coronavirus disease 2019 · Severe acute respiratory distress ly lower in COVID-19 patients than in controls (20 ± 5 vs. 26
syndrome coronavirus-2 · Hyposmia · Cognition ± 3, p = 0.042, r = 0.54). Cognitive performance indicated by
MoCA was associated with number of correctly identified
odors in COVID-19 patients and controls (COVID-19: p =
Abstract 0.018, 95% CI = 9–19; controls: p = 0.18, r = 0.63, 95% CI =
Background: Hyposmia is frequently reported as an initial 13–18.5 r = 0.64). Discussion/Conclusion: OD is associated
symptom in coronavirus disease 2019 (COVID-19). Objec- with cognitive impairment in controls and mild COVID-19.
tive: As hyposmia accompanies cognitive impairment in OD may represent a potentially useful clinical biomarker for
several neurological disorders, we aimed to study whether subtle and even subclinical neurological involvement in se-
hyposmia represents a clinical biomarker for both neurolog- vere acute respiratory distress syndrome coronavirus-2 in-
ical involvement and cognitive impairment in mild CO fection. © 2021 S. Karger AG, Basel
VID-19. We aimed to study whether olfactory dysfunction
(OD) represents a clinical biomarker for both neurological
involvement and cognitive impairment in mild COVID-19.
Methods: Formal olfactory testing using the Sniffin’Sticks® Introduction
Screening test, neuropsychological assessment using the
Montreal Cognitive Assessment (MoCA), and detailed neuro- Olfactory dysfunction (OD) is increasingly reported as
logical examination were performed in 7 COVID-19 patients a frequent initial symptom in mild to severe coronavirus
with mild disease course and no history of olfactory or cogni- disease 2019 (COVID-19) that arises from the severe
tive impairment, and 7 controls matched for age, sex, and acute respiratory distress syndrome coronavirus-2
education. Controls were initially admitted to a dedicated (SARS-CoV-2) [1, 2]. OD can be considered as a well-
COVID-19 screening ward but tested negative by real-time documented clinical biomarker for cognitive impairment
PCR. Results: The number of correctly identified odors was in several neurodegenerative disorders [3, 4]. In mild cog-
significantly lower in COVID-19 than in controls (6 ± 3, vs. nitive impairment, OD was associated with a faster rate
[email protected] © 2021 S. Karger AG, Basel Correspondence to:
www.karger.com/dem Agnes Pirker-Kees, agnes.pirker-kees @ gmx.at
of cognitive decline and might be predictive for progres- Materials and Methods
sion to dementia [4]. In Parkinson’s disease, OD is a well-
Patients
known premotor symptom [5], associated with dementia The study was conducted at the Clinic Hietzing, Vienna, Aus-
regardless of baseline cognitive function [6, 7]. The olfac- tria. Seven patients with confirmed SARS-CoV-2 infection admit-
tory mucosa represents a unique interface between the ted to a general ward, and 7 controls were included. Controls were
nervous and the immune system because olfactory recep- selected among all patients, who were admitted to a neurological
tor cells can transport various pathogens to the brain [8]. ward dedicated for COVID-19 screening, and then transferred to
a general neurological ward after COVID-19 was ruled out. Based
OD is present in 85% of moderate COVID-19 [2] and on age, sex, and years of education, controls were selected for each
98% of overall patients [1, 9]. Compared to influenza-like COVID-19 patient on a 1:1 basis. For patient characteristics, see
symptoms, patients with OD were ten times more likely Table 1. Inclusion criteria were i) 18–99 years and ii) able to per-
to have COVID-19 [10]. The occurrence of OD as an ear- form olfactory and cognitive assessment. Exclusion criteria were
ly symptom of cognitive dysfunction in several neurode- i) not able to perform olfactory and cognitive assessment, ii) his-
tory of or present ear-nose-throat disease with preexisting and/or
generative diseases [3, 4] raises the question whether such current hyposmia, and iii) history of or present neurological disease
an association also exists in COVID-19 and whether OD with known alterations of olfactory sense or cognitive decline (e.g.,
could be an early biomarker of subtle central nervous sys- dementia, Parkinson’s disease, and frontal lobe lesions). None of
tem (CNS) involvement in COVID-19. the patients was admitted to an intensive care unit (ICU) during
Indeed, neurological symptoms, such as headache, al- disease course, none had oxygen (O2) supply, and patients were in-
vestigated between days 8 and 22 after diagnosis of COVID-19.
terations of consciousness, delirium, vertigo, seizures, or
ataxia, have been reported in 36% (unselected) up to 84% Neurological Examination
(severely affected) COVID-19 patients [11, 12]. In mild Neurological examination was performed by an experienced
infection, a high prevalence of headache (70%), visual dis- neurologist. Patients were asked for any neurological complains
turbances, vertigo, nerve pain, ataxia, or fatigue was also since COVID-19. Findings on physical examination were classi-
fied into meningism, cranial nerve abnormalities, brainstem signs,
reported [13]. CNS involvement might emerge within the pyramidal signs, coordination abnormalities, sensory signs, and
context of severe COVID-19: ischemic stroke, sinus vein gait abnormalities.
thrombosis, encephalitis, transverse myelitis, or encepha-
lopathy is reported [11, 14, 15]. Besides the occurrence of Olfactory Assessment
pronounced neurological symptoms in severely affected To get an impression, if participants were aware of their OD,
they were asked to semi-quantify their subjective olfactory func-
COVID-19 patients, subtle alterations of cognitive func- tion in general prior to the infection (worse than others, normal,
tions in mild COVID-19 infections have not been inves- or better than others) and their subjective alterations of olfactory
tigated systematically, to the best of our knowledge. sense at beginning of the actual disease (1: no change of olfactory
Despite initially mild symptoms, the condition of function and 5: severe alteration of olfactory function/anosmia).
some patients can suddenly deteriorate dramatically with Olfactory function was assessed using Sniffin’Sticks® (www.smell-
test.eu), a widely used olfactory test battery in Europe [20], consist-
the need for prolonged mechanical ventilation [16]. One ing of 12 pen-shaped sticks with different odors (orange, leather,
possible explanation for this unfavorable clinical course cinnamon, peppermint, banana, lemon, liquorice, coffee, cloves,
could be CNS involvement. Indeed, transsynaptic trans- pineapple, rose, and fish) to be identified.
fer of various coronaviruses is well documented, and an-
tigens of the other coronaviruses have been detected in Cognitive Assessment
The Montreal Cognitive Assessment (MoCA) was performed
the nucleus ambiguous and the nucleus of the solitary to assess cognitive functions. This test assesses the domains atten-
tract, which belong to the cardiorespiratory center [17– tion and concentration, executive functions, memory, language,
19]. SARS-CoV-2 virus RNA has been isolated in the ce- visuoconstructional skills, conceptual thinking, calculations, and
rebrospinal fluid of one patient [15]. Early identification orientation. A maximum of 30 points can be achieved; scores
of patients with subtle neurological and neurocognitive above 23–25 are considered normal, depending on age and educa-
tion [21, 22].
symptoms could be crucial for further patient manage-
ment and appropriate resource allocation. Statistical Analysis
We systematically studied the association of olfactory For statistical analysis, SPSS version 26 was used. Data were
function, cognitive performance, and neurological symp- analyzed as seven case-control matched pairs. Due to small sam-
ples, nonparametric tests for paired samples were used: Wilcoxon
toms in COVID-19 patients. We hypothesized that olfac-
sign-rank was used for discrete and categorical variables, and effect
tory functions and cognitive functions were impaired in size was estimated as r (r > 0.5 indicates a strong effect). McNe-
COVID-19 as compared to non-COVID-19 patients. mar’s test was used for dichotomous variables. p < 0.05 was con-
sidered statistically significant.
2 Dement Geriatr Cogn Disord Pirker-Kees/Platho-Elwischger/Hafner/
DOI: 10.1159/000515575 Redlich/Baumgartner
Table 1. Baseline characteristics and neurological findings of COVID-19 patients and non-COVID-19 controls
Pat ID Age, Sex Days since Days in Years of Neurological Neurological
years infection ICU education complaints examination
COVID-19 patients
C1 70 M 21 0 18 Visual hallucinations Normal
C2 78 M 8 0 8 Headache Normal
C3 79 M 20 0 8 None Normal
C4 73 M 22 0 12 None Normal
C5 96 F 10 0 12 None Normal
C6 76 F 19 0 8 Sensory disturbance lower Reflex-attenuation
extremities Lower extremities
C7 82 F 9 0 8 Headache Normal
Controls
H1 77 M 18 Headache Normal
H2 71 M 18 Headache Normal
H3 86 M 8 None Normal
H4 80 M 8 Lower back pain Normal
H5 79 F 12 None Normal
H6 79 F 12 None Normal
H7 92 F 8 none Normal
COVID-19, coronavirus disease 2019; ICU, intensive care unit.
Results VID-19. Although not statistically significant, we want to
mention the odors “lemon” and “clove” identified by 2/7
The study population consisted of 7 COVID-19 pa- (28%) COVID-19 patients but 6/7 (85%) controls.
tients (3 females) and 7 controls (3 females). Patients and None of the patients and controls reported about
controls did not differ significantly regarding age (pa- memory or other cognitive problems in the past, none
tients 79 ± 8 vs. controls 80 ± 7, p > 0.05), sex, and years had a known history of MCI or dementia, and none re-
of education (patients 11 ± 4 vs. controls 12 ± 5, p > 0.05). ported subjective cognitive impairment at the time of ex-
COVID-19 was mild in all patients, and none of them had amination. Total MoCA score was significantly lower in
to be admitted to an ICU during disease course. For base- COVID-19 patients than in controls (20 ± 5 vs. 26 ± 3,
line characteristics, see Table 1. All patients and 6/7 con- p = 0.042, r = 0,54). MoCA was indicative of MCI 6/7 CO-
trols rated their subjective olfactory function in general as VID-19 patients (median 21/30, range 10–27) and in 1/7
normal or excellent. At the time of evaluation, olfactory controls (median 25/30, range 21–30).
sense was self-reported to be reduced in 6/7 (85%) of CO- None of the MoCA subtests and domains was signifi-
VID-19 patients (hyposmia in 4 and anosmia in 2 pa- cantly different between patients and controls.
tients) and as usual in controls. When tested systemati- MoCA was directly associated with number of correct-
cally using Sniffin’Sticks®, hyposmia was present in 6/7 ly identified odors in COVID-19 patients and controls
COVID-19 patients (moderate 28%, severe 42%, and an- (COVID-19: p = 0.018, 95% CI = 9–19, r = 0.63; controls:
osmia 14%), whereas mild hyposmia was present in 1/7 p = 0.18, 95% CI = 13–18.5, r = 0.64). Neurological his-
of controls (14%). tory revealed headache in 2/7 COVID-19 patients and in
The number of correctly identified odors was signifi- 1/7 controls. None reported vertigo or dizziness. One
cantly lower in COVID-19 patients than in controls (6 ± highly educated man with COVID-19 without any psy-
3, vs. 10 ± 1 p = 0.028, r = 0.58). One patient identified all chiatric history reported visual hallucinations from day
odors correctly but reported a complete loss of gustatory 18 (colored waves and flowers, occurring when eyes
sense since the infection with COVID-19. opened and closed, no association to circadian rhythm).
In addition to the overall number of correctly identi- He was fully communicable, orientated, and presented no
fied odors, we were interested, if any particular odor was symptoms of delirium. One female patient reported onset
identified significantly less frequently depending on CO- of sensory disturbances in her legs since day 15 after in-
COVID-19 Cognition Dement Geriatr Cogn Disord 3
DOI: 10.1159/000515575
fection, vibration sense was 6/8, and deep tendon reflexes or fatigue [13]. However, OD is a typical and well-de-
were slightly attenuated. Lumbar puncture was not per- scribed feature in COVID-19 [10]. It is reported in up to
formed because of mild symptoms only. Headache was 85% of mild [2] and 98% of severe COVID-19 [1].
present in 2 of the controls and lower back pain in one In the light of our novel findings, cognitive dysfunc-
control. None of the other patients or controls had neu- tion and OD in mild COVID-19 might represent one end
rological abnormalities on clinical neurological examina- of a spectrum of subtle CNS involvement – with the olfac-
tion. Frequency of any symptom did not differ signifi- tory system as the entry port. Delirium, confusion, and
cantly between patients and controls. alterations of consciousness in severe COVID-19 might
represent the other end of the spectrum with severe CNS
involvement. However, the exact pathophysiological
Discussion/Conclusion mechanism remains speculative, and the long-term cog-
nitive outcome after subtle or severe CNS involvement in
This appears to be the first study demonstrating an as- COVID-19 cannot yet be predicted.
sociation of olfactory and cognitive dysfunction in mild In terms of OD, post-viral anosmia has been reported
COVID-19. Cognitive dysfunction was documented in in previous studies [9, 27, 28]. SARS-CoV-2 has the abil-
association with OD in all but one COVID-19 patient, ity to enter epithelial cells, depending on their expression
and in only one individual in the control group, despite of angiotensin converting receptor 2 and the TMPRSS2-
no one had a history of dementia or subjective memory protease. The nasal epithelial cells and the olfactory bulb
complaints. [29] showed the highest expression and therefore are the
These findings are in line with our study hypothesis. It main gate for SARS-CoV-2 entrance [30]. Viral invasion
is well known that the olfactory system represents a key of those regions is supposed to be responsible for OD in
entry port for pathogens including viruses and environ- COVID-19 [29].
mental toxins to the CNS [4]. OD is known as occasional In terms of CNS involvement and possible cognitive
presymptomatic sign of various neuroimmunological decline, angiotensin converting receptor 2 is also ex-
and neurodegenerative disorders [8], and it is predictive pressed on astrocytes, oligodendrocytes, and neurons
of cognitive decline in mild cognitive impairment, Alz [31], which might bear the potential to promote CNS in-
heimer’ disease, Parkinson’s disease [7], multiple sclero- volvement. This is in accordance with increasing reports
sis [23], and in dementia-free older adults [4]. The pos- of meningoencephalitis [15], myelitis [32], or encepha-
sible contribution of inflammation and viral infections lopathy [14, 16] leading to alterations of consciousness or
(e.g., human herpesviruses and cytomegalovirus) in the delirium in severe COVID-19 [33].
pathogenesis of mild cognitive impairment and Alzhei Several limitations of our study need to be mentioned.
mer’s disease is worth mentioning [24, 25], but given the The number of patients in our study was rather small, but
high prevalence of those viruses, the meaning of these ep- sample size was limited due to strict hygienic measures in
idemiological data is difficult to interpret. Because of the the hospital. A confirmation of our significant results in
recency of COVID-19 pandemic, the association of OD a larger number of patients is needed. Even though pa-
and cognitive dysfunction in COVID-19 could serve as an tients negotiated cognitive problems, we cannot exclude
epidemiological and pathophysiological model, in terms slight subclinical cognitive impairment prior to SARS-
of the olfactory system as a gate to the CNS, and the as- CoV-2 infection. Structural brain imaging is not available
sociation of viral infections with neurodegenerative and because it was not indicated during hospital stay. O2 satu-
neuroinflammatory diseases. ration can be a long-term risk factor for cognitive decline
However, there is no systematic data about cognitive [34] but was not measured at time of investigation. All
performance in the course of COVID-19. It is well de- patients were on a normal ward, and no one needed O2
scribed that neurological symptoms in moderate to se- supply or had objective signs of dyspnea. There was no
vere COVID-19 include headache (14%), impaired con- indication for monitoring the O2 saturation. Silent hy-
sciousness (7.5% up to 22%), delirium/agitation (69%), poxia cannot be ruled out as a potential cofactor for cog-
confusion (10%), and seldom seizures [11, 12, 14, 16, 19, nitive impairment. This might be an important aspect to
26]. Some patients can suddenly develop severe encepha- consider in future studies. Patients were included in the
lopathy [11, 15]. In contrast, data about neurological in- study between days 8 and 22 after diagnosis, according to
volvement in the mild course are limited, to reports of the inclusion criteria of mild COVID-19, no ICU stay,
higher prevalence of headache (70%), vertigo, dizziness, and clinically stable. Hyposmia persists least 7 days in
4 Dement Geriatr Cogn Disord Pirker-Kees/Platho-Elwischger/Hafner/
DOI: 10.1159/000515575 Redlich/Baumgartner
COVID-19 [2]. All but one of our patients had OD, so we Conflict of Interest Statement
would not expect this time frame to affect our results.
The authors have no conflicts of interest to declare.
In conclusion, we documented cognitive dysfunction
in association with OD in mild to moderate affected CO-
VID-19 patients and an association of olfactory and cog-
Funding Sources
nitive dysfunction in these individuals. OD thus might be
considered as a clinical biomarker for CNS involvement No funding was raised for this study.
not apparent on routine clinical assessment. While olfac-
tory impairment due to viral infection is mostly reversible
[28], the long-term course of cognitive dysfunction in Author Contributions
COVID-19 needs to be studied systematically in the fu-
ture and might contribute to the understanding of the Pirker-Kees A.: substantial contribution to the conception,
role of the olfactory system as gatekeeper to the CNS. data acquisition, analysis, drafting, final approval, and agreement
to be accountable for all aspects of the work. Hafner S.: substantial
contribution to the data acquisition, drafting, final approval, and
agreement to be accountable for all aspects of the work. Platho-
Statement of Ethics Elwischger K.: substantial contribution to the conception, data ac-
quisition, drafting, final approval, and agreement to be account-
The study was approved by the local Ethics Committees “Ethik- able for all aspects of the work. Redlich K.: substantial contribution
Kommission der Stadt Wien” according to the Helsinki Declara- to the data acquisition, drafting, final approval, and agreement to
tion of 1975, and all patients gave written informed consent to be accountable for all aspects of the work. Baumgartner C.: sub-
participate in the study. stantial contribution to the conception, analysis, revising it criti-
cally for important intellectual content, final approval, and agree-
ment to be accountable for all aspects of the work.
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DOI: 10.1159/000515575 Redlich/Baumgartner
