Smelling things that aren't there could be a sign of potential problems: Study

About one in 15 people reported the "phantom smells" that didn't go away.

Imagine smelling something that isn’t there. Now imagine if these smells were always around, persisting through everyday life without any apparent reason.

These "phantom odors" occur when someone smells something, but there is nothing in the environment that corresponds to the often unpleasant odors. Though it may seem like a minor irritation, a persistent problem with smells can come with some risks and indicate other health issues, according to a new study published in the Journal of the American Medical Association.

About one in 15 people in the study smelled phantom odors, according to researchers from the National Institute on Deafness and Other Communication Disorders who looked at national health survey records between 2011 and 2014 from more than 7,400 people over 40 years old.

Who is most at risk

A particularly striking find in the thousands of records: About twice as many women as men reported phantom odors, especially those under age 60.

There may be several explanations. Prior research suggests that women are generally better than men at naming odors, and women are more often negatively affected by odors around them. They may also have a heightened sense of smell and more likely to report a problem with phantom smells, according to past research.

Other factors also affect whether people report phantom odors, such as head injury, dry mouth, poor overall health, among a list of other possible issues.

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"Chronic nasal inflammation, deviated nasal septum, nasal polyps, and even having a bad cold can cause issues with our sense of smell," Dr. Benjamin S. Bleier, associate professor of otolaryngology and director of endoscopic skull base surgery at Harvard Medical School, told ABC News.

Another surprising factor seemed to be socio-economic status. Researchers think people with lower socio-economic status may be more commonly exposed to environmental pollutants and toxins, or have health conditions that contribute to phantom odors -- and medications treating those health conditions could also cause the phenomenon.

How phantom odors happen

The reasons behind phantom odors are a mystery.

“The condition could be related to overactive odor sensing cells in the nasal cavity or perhaps a malfunction in the part of the brain that understands odor signals,” Dr. Kathleen Bainbridge of the epidemiology and biostatistics program at the National Institute on Deafness and Other Communication Disorders, part of the National Institutes of Health, said in a statement.

Genetic variation may also play a role. Several genes have been implicated this condition. However, further studies are needed to look at potential genetic factors associated with it.

"A good first step in understanding any medical condition is a clear description of the phenomenon," she added. "From there, other researchers may form ideas about where to look further for possible causes and ultimately for ways to prevent or treat the condition."

This study didn't include information on other health conditions that could have helped explains the age, sex and income patterns that were described. It also did not look at anyone below the age of 40. Because it was limited to looking at data only from a specific survey and time period, it could not determine if other issues had occurred before or were diagnosed separately.

Why phantom odors shouldn't be ignored

Phantom odors can decrease quality of life if left untreated.

"Problems with the sense of smell are often overlooked, despite their importance. They can have a big impact on appetite, food preferences and the ability to smell danger signals such as fire, gas leaks and spoiled food," Dr. Judith A. Cooper, acting director the NIDCD said in a statement.

This can especially be problematic for those who work in places that rely on our sense of smell, including those in the food and service industries.

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Phantom odors may also be a sign of a more serious health problem. Recent studies show that phantom odors can be an early marker of severe neurological conditions, which highlights the importance of seeking early intervention.

The study found only 11 percent of people who report phantom odors have actually discussed a taste or smell problem with a doctor."Most people who have this condition don’t go to a physician," Bleier said. "The value of these studies is that they reveal findings of certain disease states that were not as previously well known."

The authors hope that increased awareness of phantom odors could prompt doctors to ask about them more, too, which could help more people with the problem receive accurate diagnosis and treatment.

Ryan Guinness M.D., M.P.H., is an internal and preventive medicine resident physician, currently in the ABC News Medical Unit.

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phantom smells from childhood

Memory and smell are intertwined; it’s through memory that we learn to remember smells, and disorders that take away memory also take away the ability to distinguish scents. Some of this learning starts even before we are born, when fetuses learn about their mother’s preferences through the amniotic fluid.

Flavor, like that described by Proust, is what happens when taste and smell come together. Technically, “taste” refers only to the senses that are associated with receptors on the tongue: sweet, sour, bitter, salty, and — some people argue — umami.

“What everybody calls ‘smell’ is when you sniff through your nostrils to get an odorant. That’s technically ‘orthonasal olfaction,’ ” says Linda Bartoshuk, a past president of APS and director of human research at the University of Florida Center for Smell and Taste. Volatile organic molecules come into your nose, where they meet receptors in the cells in the nose. From those receptors, the message travels to the brain. The other kind of olfaction, retronasal olfaction, works similarly. “You can illustrate this yourself with a jelly bean,” says Bartoshuk. All you have to do is pinch your nose with your fingers, put the jelly bean in your mouth, and chew it up. It shouldn’t taste like anything in particular — just sweet, and maybe a little bit sour. But, says Bartoshuk, when you “open your nose and swallow, that will be the first time you know what flavor the jellybean was.” Air rushes up behind the palate, into the nose from the back, carrying the jelly bean’s aromatic molecules along. Like smells coming from the front of the nose, those molecules meet the receptors and spread the news that the jelly bean in your mouth is popcorn or licorice or watermelon. The same is true for real food: “When you enjoy roast beef and lemon and rhubarb and chocolate, most of those are smells,” Bartoshuk says.

Getting back to Proust’s madeleines, Maria Larsson studies how smell evokes autobiographical memories at Stockholm University. She was trained in the study of memory, but became interested in smell when she realized that “there are a range of descriptions and stories from novelists like Marcel Proust and others.”  But, when she turned to the scientific literature, she says, “We found there was very little scientific evidence of this.” So she set out to find out whether smells really do evoke emotional memories.

Other researchers have found that the formation of autobiographical memory peaks between the ages of 15 and 30. This trend makes sense, Larsson says; it’s when people are going to college, getting married, and starting to establish themselves in the world. She modeled her work after that literature, exposing older adults to different smells and interviewing them about a memory evoked by the smell. “What we found was really amazing,” she says. For visual and verbal cues, people’s memories came from their teens and 20s, as expected. But for smells, the peak was around age 5. “It was really, totally clear that when they recollected a specific memory, that memory was localized to the childhood period,” she says. The memories were also more emotional and more vivid than memories brought up by visual or verbal cues.

Just finding the smells to test people with was tricky, Larsson says. She quickly learned that she couldn’t offer people smells like coffee, because they smell coffee all the time and it wouldn’t evoke particular early memories. Instead, she settled on scents that are less common in daily life, such as lily of the valley, mulled wine, chlorine, cloves, and tar. For example, “Tar is an odor that is related to wood and to springtime,” Larsson says. Even people who had smelled those scents in the intervening years didn’t think of later memories. “They pick one of the first times when they experienced this event,” she says. With other types of memories, memory researchers have found a phenomenon called retroactive interference, in which newer memories mingle with older memories and may change them. But this phenomenon doesn’t seem to happen with memories that are called up by a smell. “When it comes to odors, this is like an imprint that really lasts and is not disturbed by later experiences,” Larsson says. “Why this is, we don’t know.”

She speculates that this persistence of early memories could come from one of the functions of smell: to warn us away from things that are dangerous. If you eat something with a particular smell or flavor and immediately get sick, it would make sense to avoid that smell forever. Maybe it’s important for the brain to quickly and permanently learn to associate a particular smell with a particular experience, she says. “Maybe it’s a one-trial learning system and it’s very important that you remember the first time.” Or maybe smells are so important in early memories because the chemical senses of taste and smell are extremely active. After all, everything within reach goes into a baby’s mouth or past its nose. “As we get older — maybe luckily so — we stop exploring the world by putting things into our mouths, and we end up being more visually and auditorily-driven animals,” Larsson says.

Researchers like Larsson who study behavior have found a tight connection between smell, emotion, and memory. Those connections can also be seen in the brain, says Johan Lundstrom, an APS Fellow at the Monell Chemical Senses Center in Philadelphia. For every other sense, the message travels first to the brain stem and the thalamus before going out to the primary sensory areas. “Olfaction is completely differently wired,” Lundstrom says. First, odor molecules bind to receptors in the nose. Signals from the receptors travel up to the olfactory bulb, a Q-tip-like structure roughly above the eyes. From there, some signals go to the primary olfactory cortex and on to the higher-order parts of the brain. But there are also connections from the olfactory bulb directly to the amygdala, an area that is relevant to emotions and salience, and the hippocampus, which is involved in memory. That puts the receptors in the nose only one synapse away from emotion and memory.

Lundstrom suspects there is something special about how the brain learns about odors. It takes many trials to get people to associate some visual cue with negative feedback like an electric shock. “When we do this for odors, it takes just a few pairings — two or three, even one, for the system to react very strongly the next time you sense an odor,” Lundstrom says. Among other projects, he is working on understanding how classical conditioning works in odor — whether the brain acts differently when it’s learning to pair odors with negative stimuli.

The close connections to emotions and memory, rather than to the parts of the brain that put words on things, may help explain why humans are so bad at identifying smells. Studies have found that people can identify fewer than half of the odors of household items they use daily. But if you give them a list of a few possibilities, they can usually choose the right one. Or, if the odor is paired with a visual clue, it makes instant sense.

Just as we know a chair is a chair whether it’s red, blue, upholstered, plastic, in a living room, or in a dumpster, we know that coffee smells like coffee whether it’s from Starbucks, Dunkin’ Donuts, or a church coffeemaker. Coffee has hundreds of volatile molecules, each of which may have several components that activate receptors. These form part of the idea of coffee, but not the whole thing. “It looks as if those sort of feelings and contexts and memories can actually become tied into this object you call ‘coffee,’ ” says Donald Wilson, a neurobiologist at New York University. “That may be one reason why odors can be so evocative. You have these very strong other kinds of information that hit you at the same time you smell the odor.”

Research in animals is keeping pace with research in humans on how smell and memory work together, says Wilson, who works mostly with rodents. He has found that if you give a rat or mouse a drug to disrupt its memory, it gets worse at telling the difference between different odors.

This result could explain another connection between smell and memory. The sense of smell is often dull in people who have other cognitive impairments, like Alzheimer’s disease, Parkinson’s disease, schizophrenia, or Down syndrome. “If memory is critical for perception, then it starts to make sense,” Wilson says, that a decline in memory would mean a decline in smell, while other senses remain intact. Smell is a complex sense that requires people to learn and remember these “odor objects,” he says.  As memory fails, those odor objects may also start to fall apart.

In fact, deficiencies in smell seem to appear years before other symptoms of Alzheimer’s disease. A sense of smell that’s not so sharp may be an early sign of brain damage. Of course, it could also be a sign of a cold. But if a smell test is combined with one or two other measures, such as a cognitive test or an imaging test, it may be possible to diagnose Alzheimer’s disease much earlier than is currently possible. Wilson was a coauthor on a paper published in Science in which researchers gave the cancer drug bexarotene to mice that had a mouse version of Alzheimer’s disease and found that it rapidly cleared plaques from the brain — and the mice regained their sense of smell.

Wilson is also working on learning how smell memories are formed. Scientists already know that sleep is vital for cementing some kinds of memories. For example, when a rat is learning to run through a maze, particular neurons in its brain fire at particular locations in the maze. Then, when it goes back to its cage, curls up, and falls asleep, those same neurons can be seen firing in the same order, in quick succession. Wilson and his colleagues are trying to find out if the same process happens with olfactory memories by stimulating receptors in a rat’s nose and introducing a “smell” to a rat electronically. Initial results suggest that encouraging this replay in sleep helps rats learn smells better.

The process of learning about smells starts very early — even, research has shown, before babies are born. In the 1990s, APS Fellow Julie Mennella at the Monell Chemical Sciences Center suspected that smells made their way into amniotic fluid. She designed a study in which 10 pregnant women took either a garlic pill or a placebo 45 minutes before a routine amniocentesis. Samples of the women’s amniotic fluid were presented in pairs to people who were asked to pick the one that smelled more like garlic. For most of the pairs, the volunteers were able to tell the difference. So the environment that a fetus inhabits is full of smells that filter through from the mother’s diet. Smell seems to work the same way before birth that it does after birth. “Memories are formed from the experiences with flavors in amniotic fluid,” Mennella says. That means a fetus is already learning about the foods it’s likely to encounter in the outside world.

Benoist Schaal, a behavioral scientist at CNRS in France who also studies how babies respond to smells, tried an experiment with anise, the scent associated with licorice. In France, anise-flavored snacks are popular. Schaal and his colleagues worked with pregnant women who already habitually ate anise and had them eat more anise. As a control, they asked women who didn’t eat anise to continue avoiding anise at the end of their pregnancies. If their mothers had eaten anise-flavored cookies before birth, “these babies had very clear appetitive responses to the odor of anise,” Schaal says. In one test, the babies were offered the smell of anise and another odor. “When the head was placed between two pads, they turned their head toward the odor they had in the womb,” he says.

When a mother eats, ultrasounds have shown that babies speed up their pseudorespiration, inhaling and exhaling more quickly. “We do not really know how they learn in the womb,” Schaal says. “What we know is that the glucose in the brain is a promoter of memory.” One possibility is that babies are learning to associate the aromas of their mother’s food with the glucose that arrives at the same time.

And those associations last for a long time. About 10 years ago, around the same time Schaal was plying pregnant women with anise, Mennella did a study in which women drank either carrot juice or water during the last trimester of their pregnancy and the first two months of breastfeeding. Soon after each mother started feeding her baby cereal — but before the youngster had ever been offered carrots — the baby was offered cereal made with water and with carrot juice, in two different sessions. The babies who’d had prenatal exposure to carrot juice made fewer nasty faces while eating the carroty cereal and seemed to eat more, too. Mennella has done several studies that have shown that eating vegetables and fruit while breastfeeding makes babies more enthusiastic about them when they’re weaned.

Now Mennella is working on experiments to figure out if there’s some sensitive period when it’s best to expose babies to a new food through breast milk. “We’re trying to really get into the sensory world of the baby to look at the potency of these really early experiences and later behaviors, and also looking at the mother and her liking for these foods,” she says. These experiences may last. A preference for green beans might be passed from mother to child and carry on into adulthood. Or, like Proust’s narrator, the young children in Mennella’s studies could one day find themselves tasting an unusual flavor and being transported back through their lives.

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I was wondering what is the scientific term for the relationship between the sense of smell and how it can help recall emotional memories.

Thank you for any help you can provide.

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i remember a taste from when i was 9 years of age now i’am 14 i was offered soda then i remember the taste from this trip from Haiti.

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Hello, I’ve a strange phenomenon with my lost of smell. I don’t smell odors from 4 years ago and I could have this sense back just after taking corticoides. My problem is I still remember the smells even I don’t smell and they cross my mind suddenly without thinking about that smells!!! I’ve a sister which have the same problem I’ve asked her if smells crosses her mind from time to time she answers me no. Sometime I have the smell but I don’t recognise it’s the smell of what!! I hope to find an explanation to this or at least find peaople who have the same case of me. thanks

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Hi Assia…I have my sense of smell, but this happens to me too. It’s a scent I really love; Green Tea with Ginseng and Honey. I can be anywhere and I’ll just smell it, even though the tea is not around. It makes me smile and I’ve always wondered how/why…..

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It’s awesome to visit this website and reading the views of all colleagues regarding this article, while I am also eager of getting know-how.

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I seem to remember some classic work on this by Rachel Herz.

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A month and a half ago, I stayed in a hotel with a very unpleasant smell and I haven’t been able to shake it off. The odor seems to just appear at random times and locations. I could be anywhere and will randomly smell the bad odor. I’ve tried scented candles, perfumes and food that have scents that I love and evoke good memories, but the bad odor just keeps re-appearing. What could be the cause of this and how can I get rid of this odor memory?

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I have had this since i was younger. If i smell anything (such as cologne,deodorant,)while im eating, it makes me gagged.

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I have been having a thing happen to me lately that I can only describe as ‘phantom’ smells. I have a memory of a smell pop into my head even though I am not currently smelling the scent and it is always associated with an old memory although the association in my brain is sometimes so quick and fleeting that I only have time to identify as a scent that reminds me of a certain time period in my life but not a specific memory. Anyone ever heard of this?

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me too….i always get a familiar smell sometimes…and it also take me to some memories but it is very short lived..that i can’t remember anything…and i get this scent often.

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i’ve been experiencing this exact thing too!! it’s so quick that you like can’t re“smell” it!! I was clueless on how to explain this weird phenomenon

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I’ve had this happen too periodically throughout my life and the scent is pleasant, reminds me of my childhood but I can’t place the scent nor does it tie to a specific memory. It’s very fleeting – lasts may be a second or two. I’ve always wished I could figure out what it is …. or how or what triggers it.

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I’ve had only three instances of this,ever,all close together. A sharp, dark,unpleasant smell, alongside clear memory of an aunt, long dead. There was no connection or event, to my knowledge.I was 77, and she had died many decades ago.

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I get the same exact thing…. mostly when I get close to people or objects, it reminds me of my past when I was with my family… it is as if I am there again and that I’m with them.. for a couple of years I thought I was the only one that had that reaction, now I know I’m not. And this really helped me

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I “recall” smells vividly…. I’ll smell lily of the valley or lilac or cedar when I see a picture. Just now the person I was talking to on the phone told me that it was time for them to take the oatmeal raisin cookies out of the oven, and my nose is smelling them right here, right now. (I also “hear” voices, however, like the smells, I define them as imagined!)

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There’s a lot of talk about smells bringing memories before us but what about the other way around? Since smell and memory are linked I’d guess that would be the case. Not long ago I heard a few chords of a 60s song and immediately knew what the name of the song – then immediately and ‘simultaneously’ pictured a college scene where the song would have been played and smelled incense burning.

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This has been so helpful the information & comments, i am 46yrs old I have been struggling for a while with trying to understand why I can smell things from my childhood such as my Nan’s perfume 4711 so I had to buy it to smell it again then it was a Corning ware coffee stove top perculator that my mum would have on the stove when I came home from school, yesterday it was buttercream cupcakes my nan made so I had to bake some I thought it was to do with my age or something bizarre going on with me

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phantom smells from childhood

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Phantom Smells: Prevalence and Correlates in a Population-Based Sample of Older Adults

Sara sjölund.

1 Gösta Ekman’s Laboratory, Department of Psychology, Stockholm University, Frescati Hagväg 9 A, 10691 Stockholm, Sweden

Maria Larsson

Jonas k. olofsson, janina seubert.

2 Department of Clinical Neuroscience, Psychology Division, Karolinska Institutet, Nobels väg 9, 17165 Stockholm, Sweden

3 Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Gävlegatan 16, 11330 Stockholm, Sweden

Erika J. Laukka

Loss of olfactory function is common in old age, but evidence regarding qualitative olfactory dysfunction in the general older population is scarce. The current study investigates the prevalence and correlates of phantom smell experiences (phantosmia) in a population-based study (Swedish National Study on Aging and Care in Kungsholmen [SNAC-K]) of Swedish adults ( n = 2569) aged between 60 and 90 years. Phantosmia was assessed through a standardized interview and defined as reporting having experienced an odor percept in the absence of any stimuli in the surrounding environment that could emit the odor. The relationships between phantosmia and demographic, genetic, health-related, and behavioral variables were analyzed with hierarchical logistic regression analyses. The overall prevalence of phantom smells was 4.9%, and was associated with female gender, carrying the met allele of the BDNF gene, higher vascular risk burden, and reporting distorted smell sensations (parosmia). Olfactory dysfunction was, however, not related to phantosmia. The most frequently reported phantom smell was smoky/burnt. A novel finding was that some individuals reported phantom smells with an autobiographical connotation. The results from this study indicate that the prevalence of phantosmia in the general older population is not negligible and that some factors that are beneficial for preserved olfactory function, such as female gender and the BDNF met allele, are also associated with the occurrence of phantom smells.


Olfactory dysfunction is common, especially among older individuals. Between 32% and 62% of the older population are estimated to have an impaired sense of smell compared with 6–17% in younger age groups ( Murphy et al. 2002 ; Brämerson et al. 2004 ; Landis et al. 2004 ; Wehling et al. 2011 ). Olfactory dysfunction significantly impacts on quality of life; individuals with an impaired sense of smell often report nutritional and interpersonal problems as well as negative mood changes and depression ( Temmel et al. 2002 ; Hummel and Nordin 2005 ). Age-related olfactory impairments are also associated with cognitive decline and can predict later occurrence of dementia in elderly adults ( Olofsson et al. 2009 ; Stanciu et al. 2014 ; Devanand et al. 2015 ).

Previous research has mainly focused on quantitative olfactory dysfunctions in old age, such as reduced olfactory sensitivity and identification ability. However, olfactory dysfunctions may also involve qualitatively distorted odor sensations such as parosmia and phantosmia. Individuals with parosmia experience odors that are incongruent with the olfactory environment. Fresh fruit smells may, for example, be perceived as rotten. An individual with phantosmia suffers from olfactory “hallucinations,” experiences of odors when no odor source is present ( Leopold 2002 ; Frasnelli et al. 2004 ). Qualitative olfactory dysfunctions are in fact often experienced as more disturbing than a reduction of smell function because the individual is repeatedly reminded of the problem ( Leopold 2002 ). A person with a reduced sense of smell, on the other hand, may remain unaware of the olfactory deficit ( Mackay-Sim et al. 2006 ).

Phantosmia has previously been documented in individuals with epileptic seizures, schizophrenia, depression, migraine, and otorhinolaryngology problems ( Fuller and Guiloff 1987 ; Nordin et al. 1996 ; Leopold 2002 ; Chen et al. 2003 ; Frasnelli et al. 2004 ; Landis et al. 2004 ; Coleman et al. 2011 ). The prevalence has been estimated to range between 0.8% and 25% depending on the clinical group studied ( Nordin et al. 1996 ; Landis et al. 2004 ), yet little is known about the prevalence of phantosmia in healthy individuals. One study on self-reported chemosensory alterations in a population-based US sample of adults 40 years and older found the prevalence of phantosmia to be 6% ( Rawal et al. 2016 ). In another study investigating the frequency of various hallucinations (olfactory, gustatory, visual, auditory, haptic, out-of-body experiences, hypnopompic, and hypnagogic) in samples of healthy participants in 3 different countries, olfactory hallucinations were the most common hallucination, reported by 8.6% of the participants, with 3.5% experiencing phantosmia at least once a month ( Ohayon 2000 ).

A related area of research addresses olfactory dreams, which also constitute a subjective experience of smell in the absence of actual stimulation. In one study, 31.7% of the sample reported having had olfactory sensations in a dream ( Stevenson and Case 2004 ). The olfactory sensations described were often related to odors frequently encountered in the environment such as food, drinks, body odors, and odors occurring in nature. A large proportion (21%) of those experiencing olfactory sensations in dreams reported odors with a “smoky” or “burnt” quality ( Stevenson and Case 2004 ). This is in line with the olfactory experiences reported by phantosmic patients. Phantom smells are frequently reported to be negative in valence and are often described as burnt, foul, unpleasant, spoiled, or rotten ( Leopold 2002 ; Chen et al. 2003 ; Velakoulis 2006 ; Coleman et al. 2011 ), although neutral and positive phantom smells have also been reported ( Acharya et al. 1998 ).

Olfactory hallucinations and phantosmias are reported more often by women than men ( Ohayon 2000 ; Leopold 2002 ). Typically, the first episode occurs between the ages of 15 and 30 years, lasts for about 5–20 min and resolves spontaneously with no lingering effects. Also, evidence indicates that the hallucinations often become gradually more frequent and persistent following the year of onset ( Leopold 2002 ).

Phantosmia occurs in a variety of clinical conditions, and its causes are yet unknown. Prior accounts have suggested that the phantosmic sensations originate either in the peripheral olfactory nervous system or in central brain regions ( Stevenson and Langdon 2012 ), such as the amygdala ( Acharya et al. 1998 ; Chen et al. 2003 ) and the orbital frontal cortex ( Arguedas et al. 2012 ). A recent study showed that patients who experienced phantosmia following head trauma were characterized by left frontal atrophy, suggestive of a cortical origin ( Lötsch et al. 2016 ). However, a patient study reported successfully resolving phantosmia in 7 out of 8 patients through excision of the olfactory epithelium, suggesting also peripheral olfactory system involvement ( Leopold et al. 2002 ). It is thus likely that phantosmias may originate from disruptions in the functional interactions of central and peripheral olfactory circuits.

Although aging is associated with diminished olfactory function ( Brämerson et al. 2004 ; Landis et al. 2004 ; Larsson et al. 2004 ; Mackay-Sim et al. 2006 ), little is known about the role of aging in the occurrence of phantosmia or whether phantosmia is related to any of the variables that are typically associated with olfactory impairments. Genetic variation is one factor that may modulate olfactory ability. For example, Hedner et al. (2010) reported that carriers of the BDNF val allele exhibited a higher age-related olfactory decline compared with met allele carriers, perhaps due to the gene’s role in neural plasticity ( Poo 2001 ). Further, the apolipoprotein E ( APOE ) ε4 allele has been linked to olfactory deficits in older adults ( Olofsson et al. 2010 ; Larsson et al. 2016 ; Olofsson et al. 2016 ). Olfactory impairments have also been associated with a number of other demographic, clinical, and behavioral variables ( Murphy et al. 2002 ; Brämerson et al. 2004 ; Mackay-Sim et al. 2006 ). As phantosmia might be related to impaired olfaction ( Frasnelli et al. 2004 ), it is important to further investigate variables that are known to play a role in old-age olfactory dysfunction and whether these may account for phantosmia.

The primary aim of this study was thus to investigate the prevalence of phantosmia in the general older population, and how phantosmia correlates with demographic, genetic, clinical, behavioral, olfactory, and cognitive variables. Furthermore, the qualitative (type of odor) and quantitative (e.g., duration, frequency) features of phantosmia in old age were examined.

Materials and methods


Participants were derived from the population-based longitudinal Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). This study originally recruited 3363 randomly selected residents of the area of Kungsholmen in central Stockholm, Sweden, belonging to predefined age cohorts (60, 66, 72, 78, 81, 84, 87, 90, 93, 96, and 99 years or older). They took part in extensive baseline assessments of medical, psychological, and social factors. A subgroup of 2848 participants underwent cognitive assessment ( Laukka et al. 2013 ), which included an interview on olfactory functions and an olfactory testing protocol. For the present study, 77 participants who did not respond to the questions regarding phantosmia were excluded. In addition, individuals with dementia ( n = 81), Parkinson’s disease ( n = 21), and developmental disorder ( n = 1), as well as individuals above 90 years of age ( n = 79) or scoring < 24 ( n = 20) on the Mini-Mental State Examination (MMSE) were excluded (see Figure 1 ). The final study sample included 2569 participants (61.6% women, mean age = 72.05 years, SD = 9.52). The SNAC-K study has been approved by the ethical committee at Karolinska Institutet. All participants provided written informed consent, and the study was performed in accordance with the ethical standards stated in the 1964 Declaration of Helsinki.

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Exclusion flowchart. MMSE, Mini-Mental State Examination; SNAC-K, Swedish National Study on Aging and Care in Kungsholmen.

Assessment of phantosmia

Subjective assessments of olfactory abilities were acquired through a modified version of a standardized interview ( Nordin et al. 2004 ), including questions regarding different olfactory functions and dysfunctions. Phantosmia was defined to the participants as an odor percept in the absence of any stimuli in the surrounding environment that could emit the odor. Specifically, phantosmia was assessed by the question “Have you in the last year experienced so called phantom smells?”. The question was answered on a 5-point Likert-type scale, where 0 = “Never” and 4 = “Always.” Participants were grouped as phantosmic (1–4) and nonphantosmic (0 = never). In instances where a participant reported phantosmia, follow-up questions regarding the quality of the phantom smell were asked. The participants were first asked to indicate what type of phantom smell they had experienced. Seven predefined types of smells were provided: infected tissue, smoke, feces, rotten, musk, mold, and metallic. The participants could also generate their own label if the phantom smell did not match any of the predefined alternatives. They were allowed to select several categories if they had experienced more than one type of phantom smell. The answers generated by the participants were later grouped into 11 additional categories, consisting of similar responses. The grouping was conducted by 2 experts and was then compared and revised until a consensus was reached.

Another follow-up question addressed the intensity of the phantom smell (“How strong is the phantom smell?”). The participants indicated whether the phantom smell was perceived as faint, medium, or strong. They were also asked to assess for how long they had experienced the phantom smell (0 = “less than a year,” 1 = “1–3 years,” 2 = “4–5 years,” 3 = “6–10 years,” 4 = “more than 10 years,” and 5 = “whole life”) and how often the phantom smell appeared (0 = “every month,” 1 = “every week,” 2 = “daily,” 3 = “always,” and 4 = “other”). The duration of the phantom smell was assessed by the question “How long does the phantom smell last?” (0 = “fleeting,” 1 = “a few minutes,” 2 = “a few hours,” and 3 = “all day”). Finally, the participants were asked to specify when the phantom smell last occurred (0 = “more than 6 months ago,” 1 = “1–6 months ago,” 2 = “2–4 weeks ago,” 3 = “in the last few days,” or 4 = “it is present right now”).

Correlates of phantosmia

Demographic variables.

Demographic variables included age, gender, and educational background. Age was dichotomized into 2 age groups; young-old (<75 years) and old-old (≥75 years). Educational background was measured as the number of years of formal schooling and was dichotomized into higher (≥12 years) and lower (<12 years) education.

Genetic variables

Genotyping was conducted via DNA extraction from peripheral blood samples. APOE (rs429358) and BDNF (rs6265) were genotyped using MALDI-TOF analysis on the Sequenom MassARRAY platform at the Mutation Analysis Facility, Karolinska Institutet ( Darki et al. 2012 ). Hardy Weinberg Equilibrium was confirmed for both polymorphisms ( P ’s ≥ 0.10). For APOE , participants were grouped as carriers or noncarriers of the ε4 allele, and for BDNF , participants were dichotomized into homozygous val/val carriers and carriers of any met allele.

Vascular variables

Information on vascular variables was collected through self-report, clinical examination, medication lists, laboratory data, and the computerized Stockholm inpatient register ( Welmer et al. 2014 ). Vascular conditions included in the study were cerebrovascular disease (stroke), number of cardiovascular diseases (heart failure, atrial fibrillation, and coronary heart disease), and number of cardiovascular risk factors (diabetes, hypertension, and high cholesterol). The indexes of both cardiovascular disease and cardiovascular risk burden ranged from 0 to 3.

Other clinical variables

Other clinical variables that potentially could be related to phantosmia included current diagnosis of depression (ICD-10 criteria), as well as self-reported lifetime history of head trauma, migraine, epilepsy, any form of cancer, hypothyroidism, and schizophrenia. Furthermore, dementia (DSM IV criteria) was diagnosed at each testing occasion. The potential effect of dementia conversion up to 6 years after baseline could therefore be investigated. Due to more rapid changes and higher attrition rates in the older cohorts, the follow-up interval was 3 years for older (>78 years of age) and 6 years for younger cohorts (60–72 years of age). Dementia conversion was treated as a dichotomous variable (dementia vs. no dementia).

Behavioral variables

Current smoking and alcohol consumption were assessed through a standardized interview conducted by a nurse. Alcohol consumption was based on self-rated estimations of frequency and amount of drinks on a typical drinking day, and categorized into no or occasional, light-to-moderate (1–14 drinks/week for men and 1–7 drinks/week for women), and heavy (>14 drinks/week for men and >7 drinks/week for women). No or occasional and light-to-moderate consumption were collapsed in the analysis. Physical activity was assessed by a self-administered questionnaire regarding both intensity and frequency. Physical inactivity refers to light, moderate, or intense exercise less or equal to 2–3 times per month and was compared with physical exercise more than 3 times per month. Furthermore, the longest held profession was assessed to investigate the differences between unskilled or skilled manufacturing work (“blue collar”) and intermediate or highly trained professionals (“white collar”). Weight and length for all participants were assessed and used to calculate their body mass index (BMI). Obesity was classified as BMI > 30.

Olfactory functions

Olfactory performance was assessed using Sniffin’ Sticks, a standardized 16-item odor identification test. The Sniffin’ Sticks test battery is a well-validated and norm-referenced test set with high test−retest reliability ( Hummel et al. 1997 ; Croy et al. 2015 ). The testing procedure has been described in detail elsewhere ( Larsson et al. 2016 ). In short, odors were presented using felt tip-pens containing the following odors: apple, banana, cinnamon, cloves, coffee, fish, garlic, leather, lemon, licorice, mushroom, peppermint, petrol, pineapple, rose, and turpentine. Participants were first instructed to freely identify the odors. If they were unable to correctly identify an odor, they were asked to select 1 of 4 written response alternatives of which 1 was correct. The score of interest here was the proportion of correctly identified odors with free or cued identification. Participants with a score of 10 points or lower were classified as having olfactory dysfunction according to established clinical practice ( Hummel et al. 2001 ).

Parosmia was defined as distorted odor perception where known odors are experienced as qualitatively different compared with how they are usually perceived (e.g., orange smells like mud). Parosmia was measured through self-reports with the question “Have you during the last year experienced a distorted sense of smell?”. The question was answered on a 5-point scale, where 0 = “never” and 4 = “always.” Participants were grouped as parosmic (1–4) and nonparosmic (0 = never).

Cognitive function

As a measure of global cognitive ability, MMSE ( Folstein et al. 1975 ) was included.

Statistical analysis

Chi-square tests and t -tests were used to examine potential differences in the demographic, genetic, clinical, behavioral, olfactory, and cognitive variables between those with phantosmia and those without. The relationships between phantosmia and the included variables were analyzed by hierarchical logistic regression analyses. In the first step, gender, age group, and educational level were entered in the regression model (block 1). Subsequently, blocks containing genetic variables (block 2), vascular diseases and risk factors (block 3), other clinical variables (block 4), behavioral variables (block 5), olfactory functions (block 6), and cognitive ability (block 7) were entered. As a measure of model fit, Nagelkerke’s pseudo- R 2 is reported for each step. The omnibus chi-square test of model coefficients was used to test whether entering a new block resulted in significantly improved model fit. Odds ratios (OR) including 95% confidence intervals and P -values for each contrast are reported. Potential interaction effects between individually contributing factors were assessed. Only statistically significant interaction effects ( P < 0.05) were included in the final regression model.

An additional analysis was conducted to investigate whether participants with rare occurrences of phantosmia modulated the observed statistical associations. Here, the reported frequency of the phantom smell was used to separate between those with mild and more severe phantosmia. Those who experienced phantosmia at least once a month were compared with a reference group consisting of nonphantosmic individuals and individuals who experienced phantosmia less than once a month, using the same statistical procedure as above.

Prevalence and correlates of phantosmia

The overall prevalence of phantosmia was 4.9% ( n = 125). The prevalence of phantosmia across the demographic, genetic, vascular, clinical, behavioral, olfactory, and cognitive factors is presented in Table 1 . Individuals with phantosmia were more likely to be women ( P = 0.038), and BDNF met allele carriers ( P = 0.019). They were also more likely to have parosmia ( P < 0.001). No other significant differences between the 2 groups were observed. To reduce the number of variables in the regression analyses, variables that were nonsignificant at the univariate level and had few observations in the phantosmic group ( n < 10, Table 1 ) were not included in the subsequent analyses.

Prevalence of phantosmia as a function of potential correlates ( n = 2569)

SD, standard deviation.

Results from the blockwise hierarchical logistic regressions are presented in Table 2 . The first block, with the demographic variables only, was not significantly associated with phantosmia ( P = 0.091). Adding a genetic (Nagelkerke’s pseudo- R 2 = 0.02; P = 0.009) and a vascular (Nagelkerke’s pseudo- R 2 = 0.04; P = 0.034) block significantly improved model fit. Although overall model fit was better in the final model, including all 7 blocks (Nagelkerke’s pseudo- R 2 = 0.06, χ 2 (19) = 39.48, P = 0.004), adding blocks including clinical, behavioral, olfactory, and cognitive variables did not result in significant model improvements.

Blockwise hierarchical logistic regression analysis for correlates of phantosmia ( n = 2003)

CVD, cardiovascular disease; CVR, cardiovascular risk.

In the final regression model, a number of significant individual correlates were identified. Among the demographic variables, only female gender showed an association with phantosmia. Independent of demographic information, a significant association was also observed with the BDNF met allele. Furthermore, cardiovascular risk burden, but none of the other clinical, behavioral, or cognitive variables, contributed significantly to phantosmia. Olfactory dysfunction was not related; however, prevalent parosmia showed a strong association to phantosmia. Examinations of potential interactions between variables revealed no significant effects and are therefore not included in Table 2 .

In a follow-up analysis, we investigated the prevalence of severe phantosmia (defined as phantosmia experiences at least once a month) and found that it was experienced by 1.7% (48 individuals) of the sample. Adopting the same statistical procedure as above, we found that the final model resulted in a comparatively high model fit (Nagelkerke’s pseudo- R 2 = 0.12, χ 2 (19) = 39.99, P = 0.003). In this analysis, female gender was no longer significantly related to phantosmia (OR = 1.78, P = 0.140, 95% CI = 0.83–3.83). However, the BDNF met allele (OR = 3.45, P < 0.001, 95% CI = 1.74–6.81), cardiovascular risk burden (OR = 1.77, P = 0.020, 95% CI = 1.09–2.87), head trauma (OR = 2.39, P = 0.031, 95% CI = 1.08–5.28), and parosmia (OR = 5.95, P = 0.032, 95% CI = 1.17–30.40) were all significantly related to severe phantosmia in the final model. Hence, the results indicate that the correlates of severe phantosmia are largely similar to those of overall phantosmia.

Qualitative descriptions of phantom smells

Qualitative descriptions of frequency and intensity of phantom smell perception are summarized in Figure 2A–E . Among the individuals with phantosmia ( n = 125), 16% had experienced phantosmia their entire life, 16% had experienced phantosmia for more than 10 years, and 17% had experienced phantosmia for less than a year. The majority of the phantosmics reported that the intensity of the phantom smell was faint (48%) or of medium strength (43%); 9% experienced strong phantom smells. Phantom smells were experienced at least once a week by 20% of the phantosmic sample. However, a majority of those who selected the response alternative “other” reported that the phantom smell occurred less than once a month (54%). Phantom smells within the last few days were reported by 24% of the phantosmic group. The phantom smell was most commonly reported to last for a few minutes (43%) or to appear fleetingly (39%).

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 The distribution of answers to the following questions regarding the qualitative features of the phantom smell ( n = 125). (A) How long have you had the phantom smell? (B) How strong is the phantom smell? (C) How often does the phantom smell appear? (D) When did the phantom smell last appear? (E) How long does the phantom smell last?

The different types of reported phantom smells are described in Figure 3 . The most frequently reported phantom smell was smoky or burnt, reported by 54 of the 117 phantosmic individuals who had specified the type of the smell they had experienced. Other smell qualities reported were rotten ( n = 5), mold ( n = 8), metallic ( n = 6), cooked food ( n = 5), perfume ( n = 6), flower ( n = 6), and dusty and/or dirty ( n = 6). Twenty-eight participants reported more than one type of phantom smell.

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Type of phantom smells reported by the participants. Y axis represents the number of individuals who reported the smell.

Nine individuals reported phantom smells with an autobiographical connotation. The autobiographical descriptions linked to each phantom smell are summarized in Table 3 . Phantom smells that were associated with childhood memories were reported by 3 individuals, and 2 individuals reported smells that had been perceived during an incident of fire in their homes several years ago. Furthermore, 2 individuals reported phantom smells that were associated with their deceased spouses.

Personal descriptions of phantom smells with an autobiographical connotation

To investigate whether any specific feature of the phantom smell was associated with other features, Spearman’s rank correlation coefficients were calculated. This revealed a significant positive correlation between the last occurrence of the phantom smell and how often the phantom smell is perceived ( r = 0.40, n = 91, P < 0.001). This indicates that individuals who have experienced their phantom smell more recently also tend to experience the smell more often. An association was also observed between how often the smell occurs and how long it lasts ( r = 0.24, n = 91, P = 0.022), indicating that the phantom smell lasts longer in individuals who experience phantom smells more often. The associations between duration, frequency, and recency indicate that the severity of phantosmia varies systematically among affected individuals. Correlation coefficients between all variables are presented in Table 4 .

Spearman rank correlation coefficients between the phantosmia-related questions

Although qualitative perceptual distortions, or hallucinations, have been investigated in the auditory and visual senses, less is known about qualitative distortions in the olfactory sense. This is one of the first studies to investigate the experiences of phantosmia, the perception of an odor where the odor source is not present, in a large population-based sample of older adults. The overall prevalence of phantosmia was 4.9% and was mainly associated with female gender, the BDNF met allele, vascular risk burden, and reported experience of parosmia, another qualitative odor distortion.

Overall, the prevalence of phantosmia corresponds with prior reports conducted in healthy individuals, where phantosmia was reported by 6.0–8.5% of the sample ( Ohayon 2000 ; Rawal et al. 2016 ). Studies of clinical groups have reported a wider range of prevalent phantosmia. Nordin et al. (1996) reported a prevalence of phantosmia of 25.6% in a group of chemosensory and nasal/sinus patients. However, Landis et al. (2004) investigated phantosmia in relatively healthy otorhinolaryngology outpatients and found that only 0.8% of those without olfactory loss experienced phantom smells. One explanation for the discrepancy could be ascribed to differences in how phantosmia has been operationalized and described to the participants. Another explanation could be that previous work has focused on different groups of patients with mixed pathogenesis.

In our sample, which included individuals between 60 and 90 years, age was not associated with the prevalence of phantosmia. Our finding that 32% of the phantosmics reported that they had experienced phantom smells for more than 10 years indicates that, at least for some individuals, phantosmia persists from middle age until old age. We observed a higher prevalence of phantosmia in women, which is in line with previous research. As women in general are better than men at naming odors ( Larsson et al. 2004 ), and more often than men are negatively affected by environmental odors ( Nordin et al. 2013 ), their heightened olfactory sensitivity might make them more prone to experiencing phantom smells. However, women were not more likely to experience phantom smells when only considering those with severe phantosmia. These results might be explained by a gender difference in criterion, such that women report phantosmia at a lower threshold compared to men.

Although the neurobiological basis of phantosmia is unknown, the present study suggests that phantosmia is linked to the presence of the BDNF met allele. This statistical relationship remained stable after all other variables had been accounted for. The BDNF (rs6265) gene is mainly responsible for neuronal survival, transmission, and synaptic plasticity ( Poo 2001 ), and previous studies have reported that BDNF is implicated in cognitive and olfactory function. Most studies targeting the effect of BDNF on cognitive function suggests that met allele carriers are more cognitively impaired than homozygote val carriers (see for example Hariri et al. 2003 ). However, some studies have found the opposite relationship, indicating that met allele carriers exhibited less age-related cognitive decline ( Erickson et al. 2008 ). We previously reported that the met allele might be protective against age-related decline in olfactory function ( Hedner et al. 2010 ). The BDNF gene expression is high in various parts of the central nervous system involved in olfaction, including the hippocampus and olfactory bulb ( Zigova et al. 1998 ; Poo 2001 ; Hariri et al. 2003 ). Although not conclusive, our results are consistent with the notion that the met allele is associated with increased levels of plasticity in the olfactory system, which might result in preserved olfactory function, but also in an increased risk of “false alarms” when no odors are present.

In the present study, prevalent parosmia was associated with phantosmia. It is possible that the same biological mechanisms underlie these 2 qualitative olfactory distortions. In the study by Nordin et al. (1996) , 9.6% of the participants reported both parosmia and phantosmia. In contrast to previous findings, olfactory impairments were not related to phantosmia in the current sample. Prior work on clinical populations has observed an association between smell loss and phantosmia, and these results have been interpreted as supporting a peripheral account of the origin of phantosmia ( Leopold 2002 ; Hong et al. 2012 ). The lack of such an association in our sample suggests that previous findings might not generalize to the population of older individuals.

Furthermore, the present study revealed a significant relationship between the number of vascular risk factors and phantosmia. One possible explanation to this finding might be that certain medication alters the olfactory functions and changes olfactory perception ( Doty and Bromley 2004 ). No relationship was observed between other clinical variables and phantosmia, suggesting that phantosmia is specifically linked to vascular conditions.

The relatively low value (0.06) of Nagelkerke’s pseudo- R 2 for the final model suggest that a large proportion of the variance remained unexplained and that other variables, not covered by this study, are of importance for the occurrence of phantosmia. However, it should be noted that this value was comparatively larger (0.12) in the model for severe phantosmia. Restricting the sample of phantosmics to individuals with more frequent experiences of phantosmia resulted in more distinct group differences, where gender was no longer of importance and head trauma appeared as a correlate of phantosmia ( Lötsch et al. 2016 ).

The present study also investigated qualitative descriptions of prevalent phantosmia, making it one of the first studies to investigate the perceived qualities of the phantom smells. The most commonly experienced phantom smells were unpleasant, specifically smoky or burnt sensations. This confirms previous findings regarding phantom smells as well as reports of smell sensations in dreams ( Leopold 2002 ; Chen et al. 2003 ; Stevenson and Case 2004 ). Why negative odors are overrepresented is not yet known, but could be the result of an evolutionary history where detecting and avoiding fire smoke would be of particular adaptive value. It has been shown that combat veterans with posttraumatic stress disorder are sensitive to fire odors, which suggests an exaggerated response to threat-related odors as a result of previous experiences ( Cortese et al. 2015 ). It has also been suggested that negative odor sensations are easier to access in memory ( Konstantinidis et al. 2006 ; Larsson et al. 2009 ). However, a number of individuals in the present study reported positive phantom smell qualities such as flower, perfume, and fruit. Intriguingly, 9 individuals reported smells with an autobiographical connotation. This suggests that the phantom smells should not be characterized as merely neural noise originating in the peripheral olfactory system, but instead might be linked to personal and meaningful events or memories. These findings should be viewed in the context of autobiographical memories, which often are more vivid and emotional when generated by an odor compared with other sensory cues ( Larsson and Willander 2009 ; Larsson et al. 2014 ).

Among the strengths of the present study are the population-based sample selection and the large sample size. This allows robust inferences to the general population. The study, however, also has some limitations to consider. Given that the results are based on cross-sectional data, the direction of the associations among the variables cannot be established, and any causal inferences on risk factors for phantosmia cannot be determined. Also, because the age range of the sample was restricted to 60–90 years of age, our findings cannot be generalized beyond this age span. Despite the large sample size, phantosmia is a relatively rare condition, which reduces the power and makes it difficult to clearly establish potential relationships between the variables of interest.

The subjective and retrospective nature of phantosmia assessment poses certain challenges. In the present study, data were collected through a structured interview. An advantage of this method over surveys is that it enables the interviewer to clarify potential uncertainties. However, it is difficult to exclude the possibility that some of the participants did not understand the meaning of phantosmia. As people’s experiences are subjective, 2 individuals might classify the same olfactory sensation as 2 different types of phantom smells. A further limitation of the present study, and other studies, is that the information regarding phantosmia relies on retrospective self-reports. The participant might have forgotten or overestimated or underestimated how frequent and how intense their phantom smells were. To limit this type of bias, future studies should investigate phantosmia by using prospective diaries in which participants can write information about their phantom smell continuously. It should also be noted that it cannot be ruled out that a source of the odor was in fact present at the time the participant experienced the phantom smell. This is especially the case for odors where the source of smell might not be visible, for example, mold.

To conclude, the present findings suggest that the prevalence of phantosmia in the elderly general population is not negligible as about 5% reports such experiences. Phantosmia is mainly associated with female gender, the BDNF met allele, vascular risk factors, and parosmia. It is of interest to note that variables that are frequently reported to be beneficial for olfactory function, such as female gender and the BDNF met allele, are also associated with the experience of phantosmia. Given this pattern of results, it would be of interest for future research to determine whether olfactory experts (e.g., perfumers, wine experts) are more susceptible to phantosmia than nonexperts. Our results complement those of prior work on phantosmia in clinical populations with olfactory deficits. Further studies are needed to address the epidemiology and underlying biological mechanisms of phantosmia in healthy individuals as well as in clinical groups.

SNAC-K is financially supported by the Swedish Ministry of Health and Social Affairs, the participating County Councils and Municipalities, and the Swedish Research Council. This work was further funded by grants from the Swedish Research Council (M.L., J.S., E.L.), the Swedish Foundation for Humanities and Social Sciences (M.L.: M14-0375:1), and the Swedish Council for Working Life and Social Research (E.L.).


We thank the participants as well as all staff involved in the data collection and management of the SNAC-K study.

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Phantom smells may be a sign of trouble

A health worker administers a Covid-19 test in Amsterdam on Dec. 2, 2021

Problems with our sense of smell, including phantom odors or a loss of smell, can be a warning sign of serious illness.

Since the beginning of the pandemic, Covid infection has been the main culprit for causing a loss of smell or taste. Although most recover within a month or so, about 5% of people with a confirmed case of Covid report smell and taste dysfunction six months later, according to a study published in July.

Before a full recovery, many patients who have Covid-related loss of smell describe a period when they experience phantom smells like burning rubber or smoke or other foul odors that aren't really there, the researchers report. Covid is also linked to a condition known as parosmia, which turns a pleasant odor such as coffee into an unpleasant one.

For people who have mostly recovered from Covid but are still coping with a loss of smell, scientists from Duke Health found some new clues from biopsies taken deep inside nasal cavities. There's evidence of continued inflammation and an immune response persisting months after an infection.

Normally, we experience smell when the olfactory sensory neurons in the nose pick up an odor and then transmit a message to the brain, which identifies the odor. Another way for the brain to receive information about an odor is through a channel that connects the top of the throat to the nose. When we chew food, aromas are released that pass through the channel to the olfactory sensory neurons, then to the brain. 

Viruses including flu, parainfluenza and other coronaviruses, along with other health issues, can lead to smell dysfunction, said rhinology expert Dr. Jonathan Overdevest, an assistant professor of otolaryngology and head and neck surgery at Columbia University Irving Medical Center in New York.

“Alterations in one’s sense of smell can be the result of chronic sinusitis,” said Overdevest. "The ongoing inflammation can in time impair the sense of smell or cause smell loss. If a dental infection is causing the sinusitis, people may sense a foul smell.”

Beyond Covid, smelling something that isn't there can indicate a serious condition.

A 2018 study found that millions of Americans may have some kind of olfactory disorder, reporting unpleasant, bad or burning odor when no actual odor is there. The researchers from the National Institute on Deafness and Communication Disorders, part of the National Institutes of Health, found a link to depression, migraine auras and head trauma.

“A head trauma that shears the connection between the brain and the peripheral nerves in the nose can lead to a loss of smell," Overdevest said.

Neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, can also lead to problems with smell, including phantosmia, according to the National Institute on Deafness and Communication Disorders (NIDCD).

“When someone is smelling something and there is no source of that smell, similar to when people have phantom limb pain, it’s called phantosmia,” said Stephanie Hunter, a postdoctoral fellow at the Monell Chemical Senses Center in Philadelphia. “It’s thought that this might be caused by overactive neurons."

People who suffer with a smell disorder may lose weight, since smell and taste are so closely linked, although others may eat too much and gain weight or use too much salt.

Commonly reported phantom smells are bad, such as rotten eggs or burning hair.

Types and causes of smell disorders

The causes of smell disorders are not well understood, but women seem to be affected twice as often as men, according to the NIDCD study. Normal aging is also associated with some loss of smell or taste.

About 2% of Americans have some type of olfactory problem, including:

  • Anosmia, the inability to smell.
  • Hyposmia, a decreased ability to smell.
  • Parosmia, a distorted perception. Coffee may smell like sewage, for example.
  • Phantosmia , sensing an odor that isn't there.

Loss of taste comes when a person loses the sense of smell and then is left only with the basics that come through the tongue: sweet, sour, salty, bitter and umami. Some of the taste disorders, include:

  • Ageusia, the inability to taste.
  • Hypogeusia, a decreased ability to taste.
  • Dysgeusia, a distorted ability to taste.

Sometimes, people with a smell disorder can interpret something like urine or feces as a pleasant odor.

"We don’t hear about this as much as unpleasant smells," said Hunter. "Maybe people smelling pleasant smells are less likely to look for help.”

Smell disorders can be diagnosed and treated by an otolaryngologist, or ENT, who specializes in ear, nose, throat, head and neck diseases.

Smell training can help someone with a disorder get back to normal, Hunter said. During the training, which should last at least three months, the patient is introduced to four strong odors — rose, eucalyptus, lemon and cloves.

"You smell the odor and then try to remember what it smelled like before you lost your sense of smell," Hunter said. "It can be really frustrating and a lot of people give up. But it’s important to stick with it.”

Linda Carroll is a regular health contributor to NBC News. She is coauthor of "The Concussion Crisis: Anatomy of a Silent Epidemic" and "Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings." 

phantom smells from childhood

Jane Weaver is managing editor of the health and medical unit at NBC News. 


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​ Download PDF

Phantosmia is the smelling of an odour that isn’t there. It is also called ‘olfactory hallucination’. Hyposmia/anosmia means

reduced/loss of sense of smell. Parosmia is when people have an altered sense of smell for something that other people can smell.

Phantosmia is a surprisingly common reason for referral to our neurology outpatient service. This was the case even before Covid-19 and we anticipate that there will be an increase in the problem which is why we made this factsheet.

Most people with phantosmia report it as an intermittent smell of something burnt, foul or unpleasant. Cigarette smoke and petrol are common but olfactory experiences can be varied. Sometimes it can be persistent.

What causes Phantosmia?

There are many potential causes of phantosmia although most are ‘idiopathic’. In a population study of 2569 Swedish adults over the age of 60, 5% had this symptom. Smoky/Burnt – was the runaway “smell” in this study.

Idiopathic – by far the commonest cause

Structural – much rarer. Just as people can develop Charles Bonnet visual hallucinations when they can’t see, or musical hallucinations when they can’t hear, so olfactory hallucinations can occur whenever the usual olfactory pathways, either in the nose or brain, are disrupted.

Should I be worried about neurological disease?

The answer is ‘hardly ever’, especially if 1 in 20 people already have it.

• Migraine – there is a statistical relationship with migraine, this included migraine olfactory aura but also relates to

generalised brain hypersensitivity seen in people with migraine.

• Head injury – head injury like any process associated with loss of sense of smell can trigger phantosmia.

• Other – there are case reports associating phantosmia with virtually every brain disease. But they are all rare.

Do they need to see a Neurologist or Psychiatrist?

The answer is ‘hardly ever’. If your patient has this as an isolated symptom, without other focal neurological symptoms and signs, they need reassurance not investigation or treatment. If they have had a head injury you can explain the mechanism to them. Have a think about whether there are features of Parkinson’s disease or migraine.

There is a condition called ‘Olfactory reference syndrome’ which is a form of obsessive compulsive disorder. In this

condition the patient becomes convinced that they smell bad to other people.

Should they go to ENT?

The answer is ‘hardly ever’. If there are nasal symptoms, then it may be worthwhile, but very unlikely if there are not.

Essentially, therefore, like a neurological referral, make the referral based on the associated symptoms rather than

phantosmia. A clue to a nose problem may be that the problem is in one nostril.

What treatments can I give and what can I tell my patient about the likely outcome?

Treatment studies only consist of case series of a handful of patients. There is no evidence based treatment.

The good news is that studies of idiopathic phantosmia are reassuring. In a study that followed 44 patients over 6 years,

30% resolved, 25% improved and 40% stayed the same. Worsening was rare and NONE developed a serious condition like

Parkinson’s disease. So, unless red flags, we would suggest simply explain how common and benign it is to your patient.

There are some links here –

Jon Stone, Richard Davenport (Neurology) and Gillian Macdougall (ENT), NHS Lothian

February 2021

Landis BN, Reden J, Haehner A. Idiopathic phantosmia: Outcome and clinical significance. Orl 2010; 72: 252–255.

Saltagi MZ, et al . Management of long-lasting phantosmia: a systematic review. Int Forum Allergy Rhinol 2018; 8: 790–796.

Sjölund S,et al Phantom smells: Prevalence and correlates in a population-based sample of older adults. Chem Senses 2017; 42: 309–318

Phantosmia – advice for primary care ( Download PDF form )

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Case report article, first-episode olfactory hallucination in a patient with anxiety disorder: a case report.

phantom smells from childhood

  • 1 Mental Health Center, West China Hospital, Sichuan University, Chengdu, China
  • 2 Sichuan Clinical Medical Research Center for Mental Disorders, Chengdu, China
  • 3 The Third Department of Clinical Psychology, Karamay Municipal People’s Hospital, Karamay, China

Background: Olfactory hallucination refers to olfactory perception in the absence of chemical stimuli. Although it has been associated with many neurological and psychotic disorders, it has rarely been reported as the first and only symptom in patients with anxiety disorder, and its treatment remains inadequate.

Case summary: A 66-year-old woman who had been experiencing gradually worsening olfactory hallucinations for almost 4 years was diagnosed with generalized anxiety disorder. Olfactory hallucination disappeared after treatment with anti-anxiety drugs.

Conclusion: Olfactory hallucination can be the first and only symptom in patients with anxiety disorder and may be effectively treated with anti-anxiety medication. In fact, it can precede the diagnosis of anxiety disorder by several years.

Olfactory hallucination is an uncommon type of hallucination in which the individual reports olfactory perceptions in the absence of chemical stimuli. Olfactory hallucination has been reported in 4.2–14.5% of the general population ( 1 , 2 ). In more than half of affected individuals, olfactory hallucination occurs together with auditory, visual, or tactile hallucinations ( 2 ). Olfactory hallucinations, similar to other psychotic-like experiences, are more common in young individuals (< 40 years) with less education who have been exposed to alcohol and drugs or who have experienced stressful and traumatic events ( 2 ). Olfactory hallucinations have been observed in various neurological disorders, such as Alzheimer’s disease ( 3 ), Parkinson’s disease ( 4 ), epilepsy ( 5 ), and migraine ( 6 ), as well as in psychological disorders, such as schizophrenia ( 7 ), depression ( 8 ), bipolar disorder ( 9 ), and substance abuse ( 10 ). Changes in olfactory sensitivity have also been observed in patients with anorexia, post-traumatic stress disorder ( 11 ), bulimia ( 12 ), and autism ( 13 ). Olfactory hallucinations have been significantly associated with self-reported anxiety symptoms and stressful life events ( 14 ). Several studies have specifically indicated an increased sensitivity to internal and external sensory cues in patients with panic disorder ( 15 , 16 ). The previous study also found that panic disorder patients appeared to be highly sensitive, reactive and aware of odors relative to healthy controls ( 17 ). The majority of research reported that anxiety disorders have detrimental effects on neuropsychological performance, such as executive function, memory, attention, and learning ( 18 ). People having health anxiety are mainly worried about and inaccurate interpret their body symptoms and might present psychotic-like symptoms, such as hypochondria ( 19 ). Furthermore, olfactory hallucinations may increase the likelihood of developing psychopathology: patients with olfactory hallucination develop symptoms of mood disorders whose severity correlates with severity of olfactory loss ( 2 ).

No consistent effective treatment strategies have been reported for olfactory disorders ( 20 , 21 ), and such hallucinations have rarely been identified as the initial symptom of anxiety disorders. Here, we present a rare case of an elderly woman who experienced olfactory hallucination that worsened over a period of almost 4 years. After admission to our hospital, she was diagnosed with generalized anxiety disorder and treated with anti-anxiety medication, which effectively eliminated the olfactory hallucination.

Case presentation

Chief complaints.

A 66-year-old Chinese woman was referred to our hospital in June 2021 due to olfactory hallucination. In 2004 the patient had been admitted to our hospital due to insomnia and nightmares. She had difficulty in initiating sleep and frequently awaked almost every night. The sleep disturbance caused her distress in daily life. She was diagnosed with insomnia disorder. Administration of 12.5 mg doxepin per night improved her sleep, and the patient reported stable mood and good social function during follow-up. However, in May 2017 she gradually manifested olfactory hallucinations, claiming that she could smell some Chinese medicines, even in wide open spaces on mountains. She did well in her job as a storekeeper and took good care of her grandson. At first, she went to the otorhinolaryngologic department, but the nasal endoscopy revealed normal structural nasal cavity or nasopharynx, axial and coronal computed tomography of the nose did not show abnormalities, so she did not get any treatment but psychiatric consultation was recommended. She was diagnosed with brief psychotic disorder after 20 days of olfactory hallucination onset in a local hospital, and she denied manic, depressive or anxious mood, denied unexpected panic attacks, denied psychotic symptoms except olfactory hallucination. The psychological tests administered by clinicians indicated a Hamilton Depression Scale (HAMD) score of 5, Hamilton Anxiety Scale (HAMA) score of 3. She received olanzapine (10 mg/night) for 2 months, followed by aripiprazole (20 mg/day) for 1 month, but her symptoms continued.

When the patient was admitted to our hospital in June 2021, she reported that 6 months before, her olfactory hallucinations had worsened and that the phantom smells had changed to something like a mixture of scallion, ginger, and garlic. At the same time, she reported being unable to smell normal scents, being unable to fall asleep at night, feeling restless and fatigued, having difficulty concentrating on daily activities, and often feeling limb muscle tension and sweating. She worried a lot about her daughter’s marriage, feared that some accidents would happen to her family members. She can still take care of her grandson. She denied depressed mood, unexpected panic attacks, and phobic avoidance.

Personal history and family history

The patient had completed primary school and had worked as a storekeeper until her retirement. She reported having grown up in a strict family environment and having a bad relationship with her ex-husband. She brought up her daughter alone and she lives alone since her daughter got married.

History of past illness

She had a history of tuberculosis and cholecystectomy. In 2011 she had been diagnosed with hyperlipidemia and since then she had been taking 5 mg atorvastatin every night. The patient and her family members denied any drug abuse, smoking or drinking. She had no family history of mental disorders.

Physical examination and laboratory examinations

In light of the patient’s long history of olfactory hallucination, the otorhinolaryngology department was asked to examine her, and those clinicians suggested the possibility of phantom olfactory perception. To exclude organic lesions, auxiliary examination and nasal endoscopy were performed. Endoscopy failed to reveal obvious structural auxiliary abnormalities, or abnormalities in the nasal cavity or nasopharynx (see Figure 1 ). Axial and coronal computed tomography of the nose showed only paranasal sinusitis (see Figure 2 ). And brain magnetic resonance imaging only showed a few ischemic foci in the brain parenchyma and paranasal sinusitis (see Figure 3 ). Chest computed tomography showed soft tissue nodules in the anterior basal segment of the lower lobe of the right lung, while both lungs showed multiple, scattered, small inflammatory nodules as well as mild chronic inflammation. Bilateral pleural thickening and adhesion, enlarged mediastinal lymph nodes, and aortic wall calcification were also observed. Thyroid color Doppler ultrasonography revealed bilateral lobular thyroid nodules suggestive of nodular goiter, while conventional color ultrasonography of the abdomen and urinary system indicated the presence of fatty liver, liver cyst, dilated common bile duct, and enlarged spleen. Electrocardiography and electroencephalography were unremarkable.

Figure 1. Endoscopy failed to reveal obvious structural auxiliary abnormalities, or abnormalities in the nasal cavity or nasopharynx.

Figure 2. Axial and coronal computed tomography of the nose showed only paranasal sinusitis.

Figure 3. Brain magnetic resonance imaging only showed a few ischemic foci in the brain parenchyma and paranasal sinusitis.

Neurological examination showed no obvious abnormalities, and her apolipoprotein E genotype was E3/E3, suggesting low risk of Alzheimer’s disease. In addition, no obvious abnormalities were found in routine blood or urine indices, liver or kidney function, electrolytes, blood lipids or glucose, coagulation or thyroid function, tumor markers, or glycosylated hemoglobin.

Further diagnostic work-up

Assessment of symptoms was based on a Chinese version of HAMD and HAMA administered by a psychiatrist. HAMD score of 8, HAMA score of 22. Chinese version of Childhood Trauma Questionnaire score 33 (emotional abuse score 9, physical abuse score 5, sexual abuse score 5, emotional neglect score 9, and physical neglect score 5) which indicated without childhood trauma ( 22 ). Mini-mental State Examination score25, and Montreal Cognitive Assessment score of 24, indicating no obvious abnormalities in cognitive function.

Final diagnosis

Based on the patient’s reported symptoms and the tests, the patient was diagnosed at our hospital with generalized anxiety disorder based on the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition ( 23 ).

After diagnosis, the patient was treated with paroxetine (20 mg/day), tandospirone (10 mg three times a day), and lorazepam (0.5 mg/night) to relieve anxiety and control sleep disorders, as well as atorvastatin calcium (5 mg/night) to control hyperlipidemia. This medication was combined with electroencephalographic biofeedback training and repetitive transcranial magnetic stimulation once a day. After 4 days of this therapy, the patient started to smell strong odor of ammonia in the restroom, especially in the afternoon. Therefore, we adjusted the medication to tandospirone (10 mg three times a day), paroxetine (40 mg/day), and lorazepam (0.25 mg/noon and 0.5 mg/night). After 6 days on the modified drug regime, the patient claimed that the odor became mild, but she still had hyposmia for normal smells, especially in the afternoon. After 10 days on the physiotherapy and modified drug regime, the patient reported feeling relaxed and sleeping well at night, with no olfactory hallucination. After a total of 20 days hospitalization, transcranial magnetic stimulation sessions were stopped. She was discharged on tandospirone at 10 mg three times a day, paroxetine at 40 mg/day, and lorazepam 0.5 mg/night. She scored 7 on the HAMD and 8 on the HAMA. A timeline of treatment is shown in Figure 4 .

Figure 4. The timeline of treatment.

Outcome and follow-up

At 3-month follow-up, she reported no olfactory hallucination, and she slept well. She scored 5 on the HAMD and 4 on the HAMA. She lived with her daughter and took good care of her grandson every day. She denied anxious and her mood was relatively easy to maintain a smooth. She also had good tolerability of the medication.

Discussion and conclusion

Olfactory dysfunction can be quantitative or qualitative, and the latter type is also known as olfactory hallucination (phantosmia) or parosmia (troposmia) ( 1 ). Olfactory dysfunction has an obvious negative impact on mental health, social skills, relationships, wellbeing, and life quality ( 24 ), yet most affected individuals are unaware of the disorder. The majority of the research reported that anxiety disorders have detrimental effects on neuropsychological performance, such as executive function, memory, attention, and learning, which adversely affecting patients’ lives ( 18 ). Several diseases have been shown to impair olfactory function, such as upper respiratory infection, nasal and paranasal sinus disease, head trauma, neurodegenerative disease, epilepsy, and psychiatric disorders ( 25 ). However, we are unaware of reports that olfactory dysfunction can be the first symptom of anxiety disorder. Our case indicates that such hallucination may be a prodromal symptom in patients with anxiety disorder, and that it can be effectively treated with anti-anxiety medication.

The previous studies suggest that paranasal sinusitis may cause olfactory hallucinations ( 26 ). But the nasal endoscopy and the axial and coronal computed tomography of the nose did not show any abnormity when the first-time olfactory appeared in 2017, and this time we did not do any targeted treatment about paranasal sinusitis, and after the only antianxiety therapy, the odor disappeared. So, the olfactory hallucination may not be caused by paranasal sinusitis.

Since smell dysfunction is one of the first signs of neurodegenerative diseases ( 27 ), we also performed neurological examinations. The patient did not show characteristic Alzheimer’s symptoms such as ecmnesia, or characteristic Parkinson’s symptoms such as static tremor, bradykinesia, muscle rigidity, or abnormal posture or gait. In addition, only a few ischemic foci were detected in the brain parenchyma and paranasal sinusitis, and the patient showed a E3/E3 genotype for apolipoprotein E, indicating low risk of Alzheimer’s disease. Furthermore, no abnormalities were observed by electroencephalography, and the patient denied any seizures, allowing us to exclude neurodegenerative disease as a cause of the olfactory hallucination.

The patient’s symptoms led us to examine whether she might have anxiety disorder. Olfactory dysfunction is a marker for depression ( 8 ) and it may be associated with schizophrenia ( 7 ), bipolar disorder ( 9 ), anorexia ( 12 ), bulimia ( 12 ), post-traumatic stress disorder ( 11 ), and autism ( 13 ). Indeed, low scores on olfactory tests have been found useful for early diagnosis of such diseases ( 28 ). Our patient had refused to take olfactory tests in the past, and she again refused at admission to our hospital. She also denied other psychotic symptoms, such as delusion and abnormal behavior, and her earlier treatment with antipsychotics was ineffective. She claimed no depression or elevation in mood at admission to our hospital, she reported symptoms consistent with anxiety syndrome, and her HAMA score was 22, confirming the presence of generalized anxiety disorder.

Earlier epidemiologic studies have shown that olfactory dysfunction and anxiety occur more often in women younger than 40 years ( 29 ) who have less education and poor mental health, who have been exposed to alcohol and drugs, and/or who have experienced stressful and traumatic events ( 2 ). Although our patient was older and was not taking alcohol or drugs when olfactory hallucination appeared, she was still clearly suffering from anxiety, highlighting the need to pay attention to anxiety disorder in the elderly.

The association of olfactory dysfunction with anxiety disorder could be attributed to negative life experiences. Our patient reported having grown up in a strict family and an unpleasant childhood but without childhood trauma. She also reported having a bad marriage, and a stressful everyday life. These chronic stress may have led to changes in neural circuits, including the olfactory system, as already reported for animal models and humans ( 30 ). Moreover, anxiety and olfaction may have common cerebral substrates. Earlier studies have reported a close relationship between olfactory and emotional processing, as they share a common brain pathway ( 31 ). The hippocampus ( 32 ) and amygdala ( 33 ) in the primary olfactory cortex, as well as the insula ( 34 ) and the orbitofrontal cortex ( 35 ) in the secondary olfactory cortices, may play key roles in encoding, learning, and regulating emotions, especially negative emotions such as sadness, unhappiness, and rage ( 33 ). Functional magnetic resonance imaging of patients with generalized anxiety disorder has confirmed the involvement of the prefrontal lobe and amygdala in disease pathogenesis ( 36 ), while abnormal activation of the amygdala and the orbitofrontal region has been observed in mood disorder ( 37 ). Thus, generalized anxiety disorder and olfactory disorders may have the same neuropathogenesis involving lesions in the prefrontal lobe and amygdala. In fact, anxiety patients have shown deficits in odor discrimination and altered odor perception ( 38 ), suggesting that olfactory hallucination may be a symptom of anxiety disorder.

There is evidence of the increased olfactory sensitivity among anxiety disorders and even the association with joint hypermobility syndrome (JHS), which is a benign heritable collagen condition that is featured by increased laxity of the joints, resulting in enhanced distensibility in passive movements and hypermobility in active movements of joint ( 39 , 40 ). The previous study found that suffering from JHS in patients with panic disorder showed higher odor acuity, greater reactivity to smells and also increased odor awareness ( 16 ). A 15-year follow-up study indicated that JHS was a risk factor in the development of panic disorder, highlighting the importance of assessing JHS among patients with anxiety disorders ( 41 ). Individuals suffering from JHS frequently report symptoms associated with autonomic nervous system abnormalities and stress-sensitive illnesses ( 39 , 42 ). Although our patient did not present the obvious abnormalities of joint movements and autonomic nervous system, such as syncope, fatigue, chest discomfort and orthostatic hypotension, it suggested that a detail physical examination by using the Hospital del Mar criteria to assess JHS symptoms in patients with anxiety disorder was required ( 43 ). Phantosmia has been clinically related to schizophrenia and mood disorders: these mental diseases and perception of phantom smells have been linked to abnormal levels of several neurotransmitters such as acetylcholine, dopamine, and norepinephrine ( 27 ). It has been difficult to isolate the effects of each neurotransmitter on olfactory hallucination because affected patients show cell losses within the cholinergic nucleus basalis of Meynert, the noradrenergic locus coeruleus, the serotonergic raphe nuclei, and the dopaminergic ventral tegmental area, suggesting that all these neurotransmitters interact with one another ( 27 ). Abnormal levels of 5-hydroxytryptamine and norepinephrine have also been found in patients with anxiety ( 44 ), suggesting further implicating neurotransmitters in the link between phantom smells and anxiety disorder.

Clinical treatment of olfactory disorders has not yet been standardized ( 20 , 21 ). Our patient showed no inflammation or head injury, and her treatment with antipsychotic drugs at a local hospital had no effect on olfactory hallucination. Considering the patient’s severe anxiety symptoms, we provided her with anti-anxiety medication, which completely eliminated the olfactory hallucination. This experience indicates that anti-anxiety drugs may treat this symptom effectively in patients with generalized anxiety disorder.

Assessing a patient’s perspective on treatment is part of an integrated approach to treatment optimization ( 45 , 46 ). The previous study also found that seeking help for emotional concerns is challenging due to stigma and unfamiliar symptoms ( 47 ). High psychological distress was associated with low satisfaction with provider–patient interactions and the presence of an anxiety disorder was associated with low satisfaction in adequacy of care ( 48 ). Our patient did not know where to get help and how to cope with the olfactory hallucination. She prefers to hear positive information from other people who have experienced the same symptom. However, she felt distressed when she heard neurodegenerative diseases or psychotic disorder maybe suffered. For this treatment, we provided information about the nature and causes of anxiety disorder and olfactory hallucination, medication, side effects and how to cope with the daily problems. She was satisfied with the treatment and had good compliance. The previous study also suggested the need for increased attention when delivering care to older adults with mental health problems ( 48 ).

In summary, our findings clearly support that olfactory hallucination can be the first and only symptom of anxiety disorder, preceding diagnosis of the disorder by several years, even in elderly individuals who have experienced stressful life events but have never consumed drugs or alcohol. We also found that anti-anxiety medication maybe an effective approach to treating olfactory hallucination in such patients. Further studies should investigate the mechanisms underlying the association of olfactory hallucination with anxiety.

Data availability statement

The original contributions presented in this study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.

Ethics statement

Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author contributions

XJ was the major contributor in writing and revising the manuscript. YY and ZXL interpreted the patient data. YO collected the patient data. ZL made the substantial contribution to the conception and design of the work. All authors read and approved the final manuscript.

This study was supported by the Science and Technology Project of Health Commission of Sichuan Province (20PJ027) to ZL, Applied Psychology Research Center of Sichuan Province (CSXL-202A08) to ZL, Department of Human Resources and Social Security of Sichuan Province [(2020) 291-20] to ZL, Science and Technology Bureau of Chengdu (2021-YF05-01336-SN) to ZL, and Science and Technology Department of Sichuan Province (2022YFS0349) to ZL. The above funding agencies had no role in the design of the study, collection, analysis, and interpretation of the data, or in the writing of the manuscript.


We are grateful to the patient in the study.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


HAMD, Hamilton Depression Scale; HAMA, Hamilton Anxiety Scale.

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Keywords : anxiety disorder, anti-anxiety treatment, case report, first-episode, olfactory hallucination

Citation: Jiang X, Yuan Y, Li Z, Ou Y and Li Z (2022) First-episode olfactory hallucination in a patient with anxiety disorder: A case report. Front. Psychiatry 13:990341. doi: 10.3389/fpsyt.2022.990341

Received: 09 July 2022; Accepted: 02 September 2022; Published: 20 September 2022.

Reviewed by:

Copyright © 2022 Jiang, Yuan, Li, Ou and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Zhe Li, [email protected]

This article is part of the Research Topic

Case Reports in Anxiety and Stress

  • Published: 29 September 2022

Phantom smells: a prevalent COVID-19 symptom that progressively sets in

  • Christophe Bousquet   ORCID: 1   na1 ,
  • Kamar Bouchoucha 1   na1 ,
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  • Camille Ferdenzi   ORCID: 1   na2  

European Archives of Oto-Rhino-Laryngology volume  280 ,  pages 1219–1229 ( 2023 ) Cite this article

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One of the long-term symptoms of COVID-19 is phantosmia, a type of Olfactory Disorder (OD) that has deleterious impacts on patients’ quality of life. The aim of this article was to study how this poorly understood qualitative OD manifests itself in the COVID-19.

4691 patients with COVID-19 responded to our online questionnaire focusing on COVID-19-related OD. We first analyzed the prevalence of phantosmia in this population. Then, with the help of Natural Language Processing techniques, we investigated the qualitative descriptions of phantom smells by the 1723 respondents who reported phantosmia.

The prevalence of phantosmia was of 37%. Women were more likely to report phantosmia than men, as well as respondents for whom OD was described as fluctuating rather than permanent, lasted longer, was partial rather than total and appeared progressively rather than suddenly. The relationship between OD duration and phantosmia followed a logarithmic function, with a prevalence of phantosmia increasing strongly during the first 2 months of the disease before reaching a plateau and no decrease over the 15 months considered in this study. Qualitative analyses of phantosmia descriptions with a sentiment analysis revealed that the descriptions were negatively valenced for 78% of the respondents. Reference to “tobacco” was more frequent in non-smokers. Source names and odor characteristics were used differently according to age and OD duration.

The results of this descriptive study of phantosmia contribute to the current efforts of the medical community to better understand and treat this rapidly increasing COVID-19-related OD.

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Quantitative Olfactory Disorders (ODs) are some of the earliest symptoms of COVID-19 [ 1 , 2 ], as well as one of the longest lasting once acute symptoms of the disease have been cured [ 3 , 4 ], inducing a reduction in the quality of life of patients [ 5 ]. Besides quantitative ODs, qualitative ones are also reported. These are parosmia (when olfactory sources smell differently than usual) and phantosmia: phantom smells are strange subjective experiences—olfactory hallucinations—occurring when no odor source is present in the environment [ 6 ]. These qualitative disorders often have an even more deleterious impact on daily life than the quantitative partial (i.e., hyposmia) or total (i.e., anosmia) loss of smell [ 6 , 7 ], even though patients rarely seek medical support [ 8 ]. Research on COVID-19-induced OD reports that both parosmia and phantosmia become more prevalent as OD duration increases [ 9 , 10 , 11 ]. It has even been found that they can appear after a period of apparent recovery from COVID-19-induced OD [ 12 ].

Before the wake of the COVID-19 pandemic, research on phantosmia was not very advanced, potentially due to the subjective nature of this sensory phenomenon. However, coupled with research on other forms of sensory hallucinations, a few findings have emerged. First, the prevalence of phantosmia varies depending on the studies and the populations investigated (from 6.5% of the general population in , to 10% of Parkinson’s patients in , and 25.6% of patients with chemosensory and nasal/sinus complaints in ). This figure rises to 50% for patients suffering from head trauma or post-viral upper respiratory infections [ 14 ]. In COVID-19 patients, the prevalence of phantosmia also fluctuates between studies, from 10% [ 15 ] to 34% when OD is still present up to 11 months after the acute phase of the disease [ 11 ]. Second, the underlying mechanisms responsible for phantosmia and other sensory hallucinations are far from being understood, but typically involve peripheral and central causes [ 6 , 16 ]. Third, phantom smells vary widely in their forms from subject to subject [ 16 ]: they may have different durations and frequencies of occurrence, and may be associated or not with other ODs. They are also more often reported by women than by men [ 8 , 16 ], but not always [ 10 ]. Besides, contrary to quantitative ODs that increase with age, experiencing phantom smells was found to be not affected by age [ 17 , 18 ], or even to be more frequent in younger individuals [ 8 , 16 ].

While quantitative ODs can be assessed objectively with psychophysiological methods [ 19 ], the subjectivity of phantom smells invites to study them by letting participants fill in questionnaires about their experiences. This can even be done online, which is particularly convenient when patients cannot be approached, as was the case at the start of the COVID-19 pandemic. Usually, phantom smells are preconceived as negative by the investigators based on past experience with patients [ 8 , 10 , 14 , 16 ]. Instead, in this article we present data obtained from an online questionnaire in which we framed questions about phantom smells in such a way that participants can describe them freely. The diversity of answers obtained with this approach called for an analysis based on Natural Language Processing (NLP), a set of techniques enabling, among other things, to reveal the valence contained in human language [ 20 ].

Given the extent of reported OD following COVID-19 (43% of COVID-19 patients worldwide according to a meta-analysis [ 21 ]) and the millions of cases over the world since the SARS-CoV-2 appeared, it is mathematical that the number of people suffering from phantosmia will increase significantly in the coming months. It is therefore important to characterize this phenomenon in order to provide the most comprehensive descriptive model possible and to better inform patients and practitioners. We further focused on how different individual characteristics could influence phantom smell perception. For instance, women are often found to react more emotionally to odors and are better at identifying odors [ 22 ]. In addition, older adults tend to report fewer emotional experiences (positive or negative) than younger adults [ 23 ]. When describing a smell, older adults also appear to use references to its characteristics more often than to its source [ 24 ]. As phantom smells are often related to something burning, smoking status may also play a role. Finally, all aspects of the associated quantitative OD (type, onset speed, persistence and duration) could impact how the phantosmia is described. With this in mind, our study has four main objectives. Firstly, we determine the prevalence of phantosmia in COVID-19 patients with OD. Secondly, we seek to identify factors modulating this prevalence, including gender, age and smoking status of the participants as well as the characteristics of their OD (type, onset speed, persistence and duration). Thirdly, we refine the study of the dynamics of the occurrence of phantosmia after contracting COVID-19 by comparing different models (linear, quadratic and logarithmic). Fourthly, we investigate the words used in the descriptions of the phantosmia, both quantitatively and qualitatively. In particular, we look at whether the number of keywords used varies between participants and at the variables that influence the valence of the descriptions or the use of certain categories of words.


Participants in an online survey ( ) answered questions about their sociodemographic status, their COVID-19 status and their OD status (see details in [ 5 ]) between 8 April 2020 and 20 April 2021. To be included in the analysis, participants had to complete the entire questionnaire for the first time, have been positive for COVID-19 (either via a PCR test or, for participants at the beginning of the pandemic, based on their symptoms as it was a common way to detect COVID-19 due to limited access to PCR tests), and have reported having an OD. For the full inclusion criteria and inclusion tree, see Fig. S1. The final sample consisted of 4691 participants: 3763 women (80.2%) and 928 men (19.8%), with an average age of 40.4 ± 12.5 years-old (mean ± sd). Among them, 1723 were considered to have phantosmia (i.e., their descriptions fitted the definition of phantom smells).

Evaluation of phantosmia

Unlike other studies focusing on phantosmia [ 8 , 14 , 16 , 18 ], we decided to ask an open-ended question with as little guidance as possible. In our opinion, this approach is justified by the fact that phantom smells are inherently a subjective experience. The exact formulation of our question was (originally in French): “In the last few days/weeks, have you had any olfactory hallucinations (phantom smells)?”. If the participants answered "Yes" to this question, they were then given the opportunity to freely describe these phantom smells.

Prevalence analysis

We assessed the prevalence of phantosmia in respondents with OD participating in our study (i.e., number of “yes” answers to the question about phantosmia), as well as the potential effect of seven factors on this frequency (age, gender, smoking status [smoker or non-smoker], OD type [partial/hyposmia or total/anosmia], OD onset speed [progressive or sudden], OD persistence [fluctuating or permanent] and OD duration). As the most prominent and informative effect in terms of dynamics of appearance of phantosmia was OD duration, we further explored the type of function that best fitted this relationship between phantosmia frequency and OD duration by performing a series of regression models (linear [increase or decrease?], quadratic [increase followed by decrease?], logarithmic [increase followed by plateau?]). This analysis was performed over a period of 1 to 60 weeks (i.e., 15 months) of OD duration.

Analysis of qualitative descriptions

We examined the descriptions of the phantom smells and how the seven factors cited above could modulate these descriptions.

First, we calculated the number of different keywords used by each participant to describe their phantom smell(s).

Second, in an attempt to summarize the verbal descriptions, we associated each keyword used by the participants to describe their phantom smells with one or two of the following overarching categories: “characteristic” (i.e., a characteristic of the odor, generally an adjective), “duration” (i.e., how long or how frequent the phantom smell lasts/is), “health” (i.e., health consequences of phantom smells), “location” (i.e., where the phantom smell occurs), “position” (i.e., the body position in which the phantom smell occurs) and “source” (i.e., the source of the odor). The “source” category was further divided into the following subcategories: “detergent” (i.e., toxic products), “fire” (i.e., something burning), “food” (i.e., a food item), “hydrocarbon” (i.e., fuel), “hygiene” (i.e., body hygiene), “tobacco” (i.e., tobacco use) and “others” (all remaining sources). The distribution of usage of each category shows that keywords pointing to the “source” of the phantom smell are the most frequent, followed by keywords describing a “characteristic” of the phantom smell (Fig. S2A). The 3 most common “source” subcategories are “fire”, “food” and “tobacco” (subcategory “others” aside; Fig. S2B). Therefore, we conducted analyses to determine whether these two categories (“source”, “characteristic”) and three subcategories (“fire”, “food”, “tobacco”) varied according to individual factors.

Third, we analyzed the keywords in detail by searching which keywords were more specifically used by particular groups of participants, using the tf-idf (term frequency-inverse document frequency) analysis detailed in the Supplementary Material.

Fourth, we focused on the qualitative content of the descriptions of phantosmia by following a Natural Language Processing approach. This approach allowed us to produce word clouds associated with phantosmia (Figs. S3 and S4), and to conduct a sentiment analysis of the valence (positive or negative) of the descriptions, using the R package sentimentr [ 25 ]. A sentiment analysis requires the mining of the text to be analyzed as well as an independent evaluation of the valence associated with the words used in the text, before combining these two components [ 26 ]. We first retrieved all the different keywords ( N  = 623 French keywords) used in the participants’ descriptions of phantom smells. Then, we conducted a new anonymous survey on a different panel of participants ( N  = 313 participants). This step was critical because no French lexicon based on the valence associated with odor descriptions was available. Each participant had to report its gender (women: 247 [78.9%] and men: 66 [21.1%]) and age (mean ± sd: 35.5 ± 13.7 years old) and to evaluate 30 keywords in a random order. Each keyword characterizing a phantom smell was evaluated on a valence scale ranging from − 10 (negative odor) to + 10 (positive odor). More details about the valence of the keywords can be found in the Supplementary Material.

Statistical analysis

The following analyses were performed in R.4.1.1 [ 27 ]. The statistical threshold for significance was set at α  = 0.01.

The factors influencing the prevalence of phantosmia were investigated using a logistic regression with the glm() function. The presence (1) or absence (0) of phantosmia was the response variable. The explanatory variables were: (i) age, (ii) gender (men or women), (iii) smoking status (smoker or non-smoker), (iv) OD type (partial [hyposmia] or total [anosmia]), (v) OD onset speed (progressive or sudden), (vi) OD persistence (fluctuating or permanent) and (vii) OD duration. The two numeric variables (age and OD duration) were scaled before the analyses to facilitate the interpretation of the estimates. We conducted backward elimination of non-significant variables until the minimal model containing only significant variables was reached.

Then we limited our analysis to the relationship between OD duration and phantosmia prevalence in order to determine more precisely its nature. Three different models (linear, quadratic and logarithmic) were fitted to the data and their associated Akaike Information Criteria (AIC) were recorded in order to determine which model had the lowest AIC (i.e., provided a better fit to our data).

The factors influencing the number of keywords used in describing phantosmia were investigated using a generalized linear model with a positive-Poisson distribution (as all descriptions had at least one keyword) with the vglm() function from the VGAM package [ 28 ]. The same seven explanatory variables as detailed above were used and non-significant variables were dropped one by one until the minimal model was reached.

The average sentiment score associated with the descriptions of phantosmia (resulting from the previously described sentiment analysis) was investigated using a linear model with the lm() function. Again, the same seven explanatory variables were fitted in the full model and the non-significant variables were removed one by one until the minimal model was reached.

To analyze the categories used to describe phantosmia, we focused on the two main categories, “source” and “characteristic” (because they are representing 90.8% of all categories) and ran a bivariate odds ratio model (i.e., a combination of two logistic regressions in a single model) with the function vglm(). The same model selection procedure as before was followed, starting with the same seven explanatory variables.

For the three subcategories that had enough occurrence to warrant further analysis (“fire”, “food” and “tobacco”), we ran three separate logistic regressions with the same model structure and selection as before.

Prevalence of phantosmia in COVID-19

Following the inclusion criteria (Fig. S1), 4691 respondents to our online questionnaire about ODs were retained and all reported OD. Among these participants, 2016 (43.0%) reported a phantosmia, while 2675 (57.0%) reported other types of OD. Based on a subjective analysis of the description of the reported phantosmia, we considered that 1723 (85.5%) truly described phantom smells (others confounded them with parosmia or their descriptions were too vague to be classified as a phantosmia). In our dataset, the prevalence of phantom smells in participants with COVID-related OD was thus 1723/4691 = 36.7%.

Factors modulating the prevalence of phantosmia

The prevalence of phantosmia was significantly affected by five of our explanatory variables (seven variables were considered: age, gender [man or woman], smoking status [smoker or non-smoker], OD type [partial/hyposmia or total/anosmia], OD onset speed [progressive or sudden], OD persistence [fluctuating or permanent] and OD duration), while two variables were non-significant (Fig.  1 ). Namely, the probability to report phantosmia was higher when OD was fluctuating rather than permanent ( β  = 0.75 ± 0.07, z  = 11.2, p  < 0.0001; OR [99% CI] 2.12 [1.86–2.42]), lasted longer ( β  = 0.44 ± 0.03, z  = 13.2, p  < 0.0001; OR [99% CI] 1.56 [1.46–1.67]), was partial rather than total ( β  = 0.39 ± 0.08, z  = 4.7, p  < 0.0001; OR [99% CI] 1.47 [1.25–1.73]) and appeared progressively rather than suddenly ( β  = 0.28 ± 0.09, z  = 3.1, p  < 0.01; OR [99% CI] 1.32 [1.11–1.58]). Furthermore, women were more likely to report phantosmia than men ( β  = 0.48 ± 0.09, z  = 5.65, p  < 0.0001; OR [99% CI] 1.62 [1.37–1.92]). The predicted probability to report phantosmia for a woman with a partial, fluctuating, long-lasting OD that appeared progressively was 92.9%, whereas the predicted probability to report phantosmia for a man with a total, permanent OD that appeared suddenly and did not last long was 15.4%.

figure 1

Results from the logistic regression on the probability to report phantosmia ( N  = 4691 participants). A Odds-ratios (OR) and 99% confidence intervals of the significant variables in the minimal model. Note that for continuous variables, OR are given for each standard deviation of the corresponding variable. Effects of B gender, C OD type, D OD onset speed, E OD persistence and F OD duration on the probability to report phantosmia. G Prevalence of phantosmia (in blue) as a function of OD duration. In F , circle size is proportional to the number of participants. In B , C , D and E , square size is proportional to the percent of participants reporting phantosmia for each corresponding category, respectively

Dynamics of the appearance of phantosmia in COVID-19

When we examined the relationship between OD duration and the prevalence of phantosmia in a window of about 15 months after OD onset, results showed that the logarithmic function had a better fit to the data (AIC = 5639) than the quadratic (AIC = 5727) or the linear (AIC = 5867) function (Fig.  2 ). The frequency of phantosmia strongly increases during the first 8 weeks of ODs approximately, before reaching a plateau.

figure 2

Relationship between the prevalence of phantosmia and the OD duration ( N  = 4691 participants). For visual clarity, OD duration has been binned per week prior to calculating the corresponding prevalence (the underlying model took into consideration the raw data). Black dots correspond to phantosmia prevalence for each week of OD duration and their size is proportional to the number of participants in this bin. The dotted red line corresponds to the linear relationship, the dashed green line corresponds to the quadratic relationship and the solid blue line [slightly bigger to underline its better fit] corresponds to the logarithmic relationship

Description of phantom smells in COVID-19

Number of descriptors.

The number of keywords used to describe phantosmia was 2.43 (sd: 1.37) on average, and was not affected by any of our explanatory variables at α  = 0.01: neither age, gender, smoking status nor any of the OD characteristics impacted the number of keywords used by participants to describe their phantosmia.

Keyword categories

When considering which categories of words participants used to describe their phantosmia, we found that most descriptions contained a reference to the source (51.9%; e.g., “smoke”, “cigarette”) or to a characteristic of the smell (41.2%; e.g., “burnt”, “unpleasant”) (Fig. S2A). Regarding how the use of these categories vary as a function of our seven factors of interest, we found that older participants used more frequently keywords referring to the source (in blue in Fig.  3 A, B; β  = 0.33 ± 0.06, z  = 5.2, p  < 0.001; OR [99% CI]: 1.39 [1.23–1.57]) and less frequently keywords describing a characteristic (in red in Fig.  3 A, B; β  = −0.23 ± 0.05, z  = −4.5, p  < 0.001; OR [99% CI] 0.80 [0.72–0.88]). Furthermore, participants with longer OD referred more frequently to a characteristic of their phantom smell (in red in Fig.  3 A, C; β  = 0.19 ± 0.05, z  = 3.7, p  < 0.001; OR [99% CI] 1.21 [1.09–1.34]) and less frequently to its source (in blue in Fig.  3 A, C; β  = − 0.27 ± 0.06, z  = -4.7, p  < 0.001; OR [99% CI] 0.76 [0.68–0.86]).

figure 3

Results from the bivariate odds ratio model ( N  = 1723 participants) on the probability to use a specific keyword category (either source or characteristic, excluding all other rarer categories, see “Methods”). A Odds-ratios (OR) and 99% confidence intervals of the significant variables in the minimal model. Effects of B age and C OD duration on propensity to use a keyword referring to the source (blue lines and shades) or to a characteristic (red lines and shades) of a phantom smell. Lines represent predicted probabilities of logistic regressions and shades represent their 99% confidence intervals

In a finer-grained analysis of the categories, we examined the most frequently cited subcategories of sources, namely “fire”, “food” and “tobacco” (Fig. S2B). None of the seven explanatory variables had an effect on the probability to make references to products or usages linked to “fire” or “food”. However, as for references to the “source” of the phantosmia, we found that older participants ( β  = 0.29 ± 0.06, z  = 4.6, p  < 0.001; OR [99% CI] 1.34 [1.14–1.58]; Fig.  4 A, B) and participants with shorter OD duration ( β  = −0.25 ± 0.07, z  = − 3.7, p  < 0.001; OR [99% CI] 0.78 [0.65–0.92]; Fig.  4 A, E) made more references to “tobacco” to describe their phantom smells. In addition, non-smokers made more references to “tobacco” than smokers ( β  = 0.55 ± 0.18, z  = 3.1, p  < 0.01; OR [99% CI] 1.74 [1.12–2.79]; Fig.  4 A, C). Finally, participants with fluctuating OD made more references to “tobacco” than participants with permanent OD ( β  = 0.35 ± 0.13, z  = 2.8, p  < 0.01; OR [99% CI] 1.42 [1.03–1.98]; Fig.  4 A, D).

figure 4

Results from the logistic regression on the probability to refer to tobacco to describe phantosmia ( N  = 1723 participants). A Odds-ratios (OR) and 99% confidence intervals of the significant variables in the minimal model. Note that for continuous variables, OR are given for each standard deviation of the corresponding variable. Effects of B age, C smoking status, D OD persistence and E OD duration on the probability to refer to tobacco. In B , F , circle size is proportional to the number of participants. In C , D , square size is proportional to the percent of participants referring to tobacco for each corresponding category, respectively

Individual keywords

The word cloud illustrating the keywords used to describe phantosmia shows that negatively-connoted keywords are more frequent (Fig. S3), with the most frequent being “burnt” (319 occurrences, 7.63%), “smoke” (208 occurrences, 4.97%) and “cigarette” (205 occurrences, 4.90%). As age and OD duration were found to be prominent factors of variation in the previous analyses by categories, we intended to better characterize the keywords used by younger and older participants, as well as by participants with a shorter and longer OD duration. As an illustration, specific word clouds associated with young vs old and short OD vs long OD can be found in Fig. S4. The tf-idf (term frequency-inverse document frequency) analysis revealed that the 4 keywords most specific of younger participants were: “imagination”, “blood”, “fluctuating” and “stinging”. For older participants, the 4 most specific keywords were: “cigarette smoke”, “chemical”, “grilled bread” and “exhaust pipe”. For participants with shorter OD duration, the 5 most specific keywords were (the last 3 were ex-aequo): “sensation”, “blood”, “bleach”, “chlorine” and “vomit”. Finally, for participants with longer OD duration, the 4 most specific keywords were: “chemical”, “sewer”, “spicy” and “fuel”.

Sentiment analysis (valence of the descriptions)

In accordance with the nature of the keywords illustrated in the word cloud (Fig. S3), the sentiments associated with the descriptions of phantosmia (derived from the evaluation of each keyword’s valence by an independent group of participants, see Methods) were negative for 77.9% of the participants and neutral or positive for the other 22.1% (Fig.  5 ). The average sentiment score associated with the description of phantosmia was influenced by only one of our seven explanatory variables. Participants who had a fluctuating OD described their phantosmia slightly more negatively than participants with permanent OD ( β  = 0.05 ± 0.02, z  = 2.9, p  < 0.01; Fig. S5).

figure 5

Distribution of sentiments associated with the description of phantosmia (77.9% negative, 22.1% neutral or positive; N  = 1723 participants). Each line represents a participant and each dot represents a keyword used by the participant to describe his/her phantosmia (keywords used by the same participant are connected by thin grey lines). The bigger red (negative descriptions) and green (positive descriptions) dots represent the average sentiment score of each participant (participants are sorted based on this average score). The vertical blue line represents a neutral evaluation, while scores between − 1.0 and 0.0 represent negative descriptions and scores between 0.0 and + 1.0 represent positive descriptions. The sentiment value associated with each keyword was determined by an independent sample of participants on a scale from − 10 to + 10 (see “Methods”). The inset on the bottom right represents the density distribution of the average sentiment score of the participants (negative descriptions in red and positive descriptions in green)

COVID-19 has affected many people over the world, often with associated OD. This pandemic therefore represents a unique occasion to study a previously rare, but unfortunately increasing, qualitative OD: phantosmia. By analyzing the responses of more than 4500 individuals, we showed that the prevalence of phantosmia in COVID-19 patients with OD was very high (37% of 4691 people). This prevalence was influenced by the gender of the participants (more frequent in women), and the probability to report phantosmia differed as a function of OD characteristics (higher in fluctuating, long-lasting, partial ODs that progressively settled in). In particular, the prevalence of phantosmia ranged from 14% at the very beginning of the olfactory symptoms of COVID-19 to 56% after 6 months. The dynamics of the prevalence of phantosmia as a function of OD duration is best explained by a logarithmic relationship, with a strong increase at the beginning subsequently followed by a plateau.

The prevalence of phantosmia found in our study was in line with other studies using online questionnaires completed by participants of different countries: up to 34% of COVID-19 patients with OD [ 11 ] and 31% of patients with more varied etiologies of OD [ 29 ], for instance. Such a high percentage may result from a selection bias in our online questionnaire (among other limits of the approach, which are detailed in [ 5 ]). People who are the most affected by their ODs, including persons with phantosmia, may have been more likely to spontaneously participate to our study. However, this high prevalence may also stem from a known association of phantosmia with depression [ 30 ], the global prevalence of which has drastically increased during the pandemic [ 31 ]. The fact that women appeared to be more prone to phantom smells than men confirms some previous findings [ 8 , 16 ], but not all [ 10 ]. Age did not seem to be an influential factor in our study, while higher prevalence of phantosmia have been reported elsewhere in younger participants [ 8 , 16 ].

Of particular interest for the understanding of this olfactory phenomenon are the relationship between its occurrence and OD characteristics. First, evidence is pointing towards the necessity of having an at least partially functioning olfactory system to experience phantom smells. Indeed, we found that phantom smells were more frequently reported when OD appeared progressively than when it appeared suddenly. Phantom smells were more prevalent in hyposmic than in anosmic patients, and in fluctuating (vs. permanent) ODs. Second, as also showed in another group of COVID-19 participants [ 11 ], we found that the prevalence of phantosmia increases as the duration of the smell disorders associated with COVID-19 increases. While there were anecdotal reports of very brief episodes of phantosmia on the day preceding the total loss of smell in a few patients, in most cases phantosmia occurs in a delayed fashion, sometimes even after apparent recovery as this starts to be reported in case studies for other qualitative disorders [ 12 ]. This is consistent with Leopold [ 6 ]’s statement that olfactory distortions (including phantosmia) seem to occur either during olfactory receptor neuron death or regeneration. It is noteworthy that COVID-19 patients experiencing phantosmia often have an ability to smell (quantitatively) within the normal range (6 patients out of 9 with phantosmia were normosmic while the others were hyposmic in [ 9 ] and patients with phantosmia and/or parosmia did not differ in Sniffin’ Sticks test scores from patients without qualitative ODs in [ 32 ]).

Although studies are clearly needed to better characterize the pathophysiology of phantosmia, several hypotheses about peripheral and central mechanisms (which are not necessarily exclusive) of such a phenomenon have been formulated. At the peripheral level, lower number of olfactory neurons in the olfactory epithelium, higher number of immature neurons and disordered growth of olfactory axons have been found in patients with phantosmia [ 6 ]. Peripheral phantosmia is more often intermittent and worse on one side, relieved by nasal obstruction and anesthesia/resection of the olfactory epithelium [ 33 ]. Some reports in our study indicated that mechanical actions affecting the nasal cavity, such as yawning or blowing one’s nose, could trigger a phantom smell [ 5 ]. Central mechanisms may also occur, with manifestations that are constant, bilateral and not relieved by any of the options mentioned previously [ 33 ]. This is consistent with abnormally high brain activity in several frontal, insular and temporal regions [ 6 ], but also with some etiologies of phantosmia outside COVID-19 (psychiatric diseases, neurologic and neurodegenerative disorders). Consistent with the central hypothesis, the reports of several patients in our study were in favor of an effect of suggestion (like reading/talking about a smell, which would trigger the phantom smell) and of attention (phantosmia being more present during the peak periods of the epidemic waves, or disappearing during a limited period in which the patient has changed environment and directed her attention to a person to help). Representation of an odor can be elicited in people without pathological condition (imagined odor: [ 34 ]). Possible dysfunction or damage in the central olfactory pathways (olfactory bulb, olfactory tract and/or primary/secondary cortices) [ 33 ] could trigger such representations. It has been suggested that disinhibition of olfactory excitation could originate in these unwanted odor perceptions.

The shape of the prevalence curve (Fig.  2 ) suggests that there might be both peripheral and central phenomena in play. The prevalence of phantosmia reaches a plateau at a time (about 8 weeks) were neuronal regeneration in the olfactory epithelium is likely to take place: indeed, regeneration time of a healthy epithelium after axotomy (including olfactory bulb reinnervation) is about 30 days in mammals [ 35 , 36 ], but could be longer in a damaged epithelium. From this time on, the prevalence curve then illustrates what seems to be a rather installed phenomenon, since it does not decrease over 60 weeks after the beginning of the first COVID-19-related OD. This is particularly preoccupying first because, whereas parosmia seems to be a positive sign of recovery, phantosmia appears to be a poorer predictor of recovery in the most recent studies in COVID-19 patients [ 37 ] as well as in patients with varied etiologies [ 38 ] (but see [ 39 ] for contradictory findings that occurrence of parosmia or phantosmia has little prognostic value). And second, because to date there is not enough evidence in the literature to formulate treatment recommendations for phantosmia (or parosmia): only anecdotal evidence can be found for the local use of some medical therapies, such as antimigraines, antipsychotics or antiepileptic, with success rates depending on the patients’ etiology [ 33 ] (see also the recent study by [ 40 ] for an encouraging effect of intranasal sodium citrate in reducing phantosmia).

Additionally, with regards to the qualitative description of phantom smells, we found that 78% of the participants described their phantosmia as a negative experience, and this was more marked when the OD was fluctuating. Why phantom smells are more often unpleasant is an intriguing question, to which we can propose several possible answers. First, one of the main functions of olfaction, which has the most immediate consequences for survival, is the detection of threats. One can thus hypothesize that, (i) in the case of anarchic activation of olfactory neurons and (ii) assuming there is a central contribution to the generated olfactory percept, olfactory representations that are preferentially generated are those of odors that are the most relevant for survival (smoke, decay/fermentation…). The fact that the odor of a toxic substance, tobacco, was cited more often by non-smokers as a phantom smell is totally in line with this, given that the threatening value of tobacco products is likely to be stronger in this subgroup. Second, the dimensions of unexpectedness (phantom smells occurring in a non-predictable manner) and incongruency (phantom smells unrelated with the actual physical environment) may contribute significantly to the unpleasantness of this experience since they are significant determinants of the responses to smells [ 41 ]. Finally, fluctuation of the occurrence of phantom smells is likely to worsen the deleterious effect of unexpectedness, explaining why fluctuating OD is a significant predictor of negativity of phantosmia.

Another result of interest is that participants with OD of shorter duration and older participants tended to favor source names (i.e., descriptions of the olfactory experience). Conversely, participants with OD of longer duration and younger participants referred more to odor characteristics (i.e., more emotional descriptions of the olfactory experience). The fact that older participants used more words linked to the potential source of the phantom smell than to its characteristics contrasts with previous results [ 24 ], which found the opposite pattern when participants were asked to describe an actually perceived odorant. It could therefore be that semantic usage differs with age depending on whether participants have to describe a real or a mental construction of a smell. In addition, as elderly persons are typically less sensitive to emotions [ 23 ], it could be that older participants use less emotional descriptors and thus refer more to the source of the smell. The different usage of semantic categories with age may be linked to age-related changes in word representation and retrieval [ 42 ]. Regarding the effect of OD duration, it is possible that people with longer OD are more annoyed by the phantom phenomenon and use more adjectives to describe how they feel about it whereas people with shorter OD are still in the exploratory phase where they have a more analytical approach, trying to define what the odor is exactly. More broadly, it is worth mentioning that phantosmia is subjective and may be affected by the usage of a specific language. Future studies could therefore try to assess how phantom smells are described by respondents from different cultures and/or languages with different sizes of smell-related vocabularies [ 43 ].

Finally, we would like to stress the importance of studying phantosmia separately from parosmia. These qualitative ODs are often grouped together in the literature, but it has been suggested that this may be a mistake since they have different patterns of expression depending on demographic factors, etiologies and consequences on the quality of life [ 10 ]. Although adopting a questionnaire approach has limitations [ 5 ], it provides useful quantitative and qualitative elements to gain additional insights into previously rarely observed phenomena such as phantosmia. Future studies are needed to better understand this category of sensory hallucinations and its physiopathology. As well as parosmia, phantosmia has very deleterious consequences on the patients’ quality of life [ 44 ]. In spite of this, knowledge of these and other related ODs remains low amongst medical professionals [ 5 , 45 ] and the medical community is still lacking therapeutic options [ 29 ]. Hopefully, the number of studies on phantosmia, which already significantly increased in 2020 and 2021, will continue to grow in the future to better answer the needs of the many patients suffering from this long-term sequalae of COVID-19.

Conclusion on clinical relevance

By using a model of viral infection often associated with olfactory disorders, COVID-19, we pointed at the high frequency of the under-studied phenomenon of phantom smells in patients with post-infectious ODs. Indeed, using spontaneous reports of patients with an online questionnaire, we found that 37% of post-COVID patients with ODs experienced phantom smells. It is important to note that this figure is likely to overestimate the prevalence of this symptom on the ground, since people who suffer from their OD may be over-represented within the sample of volunteers who answered the online questionnaire. It may though be in line with the frequency observed by the clinicians because patients who decide to consult for their phantosmia are those who are adversely affected by their condition. The characteristics of phantom smells (i.e., which smells, (un)pleasantness of the smells) and their dynamics of occurrence after OD onset, as we report them in this article, are certainly well representative of the reality on the ground. To better inform patients, clinicians’ attention should be drawn to the factors associated with a higher probability to develop phantosmia, namely being a woman and displaying a fluctuating/long-lasting/progressively installed OD. Finally, it must be kept in mind by the medical and scientific community that research on the characteristics, mechanisms and remediation of phantosmia is dependent on patients’ verbal reports, since there is no objective way to measure sensory hallucinations.

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The authors wish to thank all the people who helped disseminate the questionnaire. This work was carried out with the financial support of the IDEXLYON Project of the University of Lyon as part of the Future Investments Program (ANR-16-IDEX-0005, CORODORAT project to CF and MB).

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Christophe Bousquet and Kamar Bouchoucha: co-first authors.

Moustafa Bensafi and Camille Ferdenzi: co-last authors.

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Lyon Neuroscience Research Center, CNRS UMR5292, INSERM U1028, University Claude Bernard Lyon 1, CH Le Vinatier, Bât. 462 Neurocampus, 95 boulevard Pinel, 69675, Bron Cedex, France

Christophe Bousquet, Kamar Bouchoucha, Moustafa Bensafi & Camille Ferdenzi

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Conceived and designed the study: MB, CF. Wrote the paper: CB, MB, CF. Data acquisition and curation: CB, KB, MB, CF. Performed analysis: CB, KB. Edited and approved the final manuscript: CB, KB, MB, CF.

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Bousquet, C., Bouchoucha, K., Bensafi, M. et al. Phantom smells: a prevalent COVID-19 symptom that progressively sets in. Eur Arch Otorhinolaryngol 280 , 1219–1229 (2023).

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