Phantosmia

Last updated

Phantosmia (phantom smell), also called an olfactory hallucination or a phantom odor, [1] is smelling an odor that is not actually there. This is intrinsically suspicious as the formal evaluation and detection of relatively low levels of odour particles is itself a very tricky task in air epistemology. It can occur in one nostril or both. [2] Unpleasant phantosmia, cacosmia, is more common and is often described as smelling something that is burned, foul, spoiled, or rotten. [3] Experiencing occasional phantom smells is normal and usually goes away on its own in time. [4] When hallucinations of this type do not seem to go away or when they keep coming back, it can be very upsetting and can disrupt an individual's quality of life. [2]

Contents

Olfactory hallucinations can be caused by common medical conditions such as nasal infections, nasal polyps, or dental problems. It can result from neurological conditions such as migraines, head injuries, strokes, Parkinson's disease, seizures, or brain tumors. [4] It can also be a symptom of certain mental disorders such as depression, bipolar disorder, intoxication or withdrawal from drugs and alcohol, or psychotic disorders. [3] Environmental exposures are sometimes the cause as well, such as smoking, exposure to certain types of chemicals (e.g., insecticides or solvents), or radiation treatment for head or neck cancer. [4]

A physician can determine if the problem is with the sense of smell (olfactory system) or taste (gustatory system), or if it is caused by a neurological or psychiatric disorder. Phantosmia usually goes away on its own, though this can sometimes be gradual and occur over several years. [2] When caused by an illness (e.g., sinusitis), it should go away when the illness resolves. [4] If the problem persists or causes significant discomfort, a doctor might recommend nasal saline drops, antidepressant or anticonvulsant medications, anesthesia to parts of the nose, or in very rare circumstances, surgical procedures to remove the olfactory nerves or bulbs. [2] [3]

Symptoms

Other olfactory disorders such as hyposmia and anosmia have been found to be a symptom of mood disorders (depression). However, it is not known what olfactory disorders occur and if they are indeed a symptom of a depressive disorder. [5] It has been proposed that phantosmia may be an early sign of the neurodegenerative disease Parkinson's disease. [6] It may also be a sign of an intracranial hemorrhage [7] (brain tumours or epilepsy). [8] Other studies have also found that the symptoms of phantosmia have been alleviated after the patient has been treated for depression. [9] [10] Another case of a 70-year-old male reported that his first abnormal symptoms were irregular bowel movements. After this the patient developed irregular eye movements and had developed a sleep and behavior disorder. He subsequently developed phantosmia, in which what he smelled was described as "stinky and unpleasant". The patient did not display any of the following symptoms: loss of awareness; confusion; automatisms; convulsive seizures; auditory/visual hallucinations. [3]

Co-occurrence with other conditions

Phantosmia has been found to co-exist in patients with other disorders such as schizophrenia, epilepsy, alcoholic psychosis, and depression. It has also been found that many patients may begin to experience depression after the occurrence of phantosmia and have looked towards committing suicide. The occurrence of depression resulted from the severe symptoms of phantosmia as everything even food smelled spoilt, rotten and burnt for these patients. [3] By the age of 80, 80% of individuals develop an olfactory disorder. As well 50% of these individuals also have anosmia. [11]

Migraines

In 2011 Coleman, Grosberg and Robbins did a case study on patients with olfactory hallucinations and other primary headache disorders. In their 30-month long study, the prevalence rates for phantosmia turned out to be as low as 0.66%.

In their findings, it was observed that a typical hallucination period was of 5–60 minutes, occurred either before or with the onset of head pain, and typically consisted of an unpleasant odor. It was also noted that phantosmia occurs most commonly among women having a migraine complaint. [12] In their study, prophylactic therapy for headaches helped cure phantosmia in most of the patients.

This finding is consistent with the findings of Schreiber and Calvert in 1986 which also mentioned the olfactory hallucinations before the occurrence of a migraine attack in four of their subjects. [13]

Causes

The cause of phantosmia can be either peripheral or central, or a combination of the two. The peripheral explanation of this disorder is that rogue neurons malfunction and transmit incorrect signals to the brain or it may be due to the malfunction of the olfactory neurons. [14] The central explanation is that active or incorrectly functioning cells of the brain cause the perception of the disturbing odor. Another central cause is that the perception of the phantom odor usually follows after the occurrence of seizures. The time span of the symptoms usually lasts a few seconds. [15]

Other studies on phantosmia patients have found that the perception of the odor initiates with a sneeze, thus they avoid any nasal activity. It has also been found that the perception of the odor is worse in the nostril that is weaker in olfaction ability. It has also been noted that about a quarter of patients with phantosmia in one nostril will usually develop it in the other nostril as well over a time period of a few months or years. [3]

Several patients who have received surgical treatment have stated that they have a feeling or intuition that the phantom odor is about to occur, however it does not. This sensation has been supported by positron emission tomography, and it has been found that these patients have a high level of activity in their contralateral frontal, insular and temporal regions. The significance of the activity in these regions is not definitive as not a significant number of patients have been studied to conclude any relation of this activity with the symptoms. However the intensity of the activity in these regions was reduced by excising the olfactory epithelium from the associated nasal cavity. [15]

There are a few causes for phantosmia, but one of the most common and well-documented involves brain injury or seizures in the temporal lobe. During a temporal lobe seizure the patient rarely faints, but usually blacks out and cannot remember anything that happened during the seizure. Several people who have had these seizures did, however, recollect having phantosmia just prior to blacking out. Epilepsy is a disease characterized by seizures. In the case of phantosmia, if smelling and something else become so strongly linked, the action of "something else" occurring can induce activation of the olfactory bulb even though there was no stimulus for the bulb present. This is an example of plasticity gone awry. Those with lesions on the temporal lobe, often brought about by a stroke but also from trauma to the head, also experience these olfactory hallucinations.

Other leading causes of phantosmia include neurological disorders such as schizophrenia and Alzheimer's disease. Both of these disorders have well documented cases of hallucinations, most commonly visual and auditory. Both also, however, have instances of phantosmia too, although not as frequently. In both cases, incidences[ spelling? ] of olfactory delusions are more common, especially in Alzheimer's, where it is exceedingly difficult to convince the patient that these are in fact hallucinations and not real. Specifically in Alzheimer's disease, atrophy in the temporal lobe has been known to occur. As evidenced in trauma and seizures, phantosmia is strongly associated with this area; leading to its appearance in some Alzheimer's patients. Parkinson's disease patients can also experience phantosmia, as well as parosmia, however their appearance is less common than the muscle tremors the patients experience. [16]

Neuroblastoma

Neuroblastoma is a rare form of a malignant cancer which can start in the olfactory nerve, which is responsible for smell sensation. This cancer can become aggressive and progress into the ethmoid sinuses, brain cavity, surrounds the cribriform plate. The tumor can be tested for by performing a surgical biopsy and the possible treatment options include surgical removal of the tumor, radiation therapy and chemotherapy, which can cause damage to the olfactory system and possibly result in phantosmia, in turn. [17]

Development

The complaints of phantosmia involving the perception of unpleasant odors most commonly include "burnt", "foul", "rotten", "sewage", "metallic" or "chemical". Sometimes the odor is described as exhaust fumes. These odors may be triggered by strong odorants, changes in nasal airflow, or even loud sounds. Sometimes they occur spontaneously. Patients having complaints of phantosmia might self-admit a poor quality of life, with each meal having the unpleasant odor as well. The disorder's first onset, usually spontaneous, may last only a few minutes. Recurrences may gradually increase from monthly, then weekly, and then daily over a period of six months to a year. The duration of the perceived odor may also increase over the same time, often lasting most of a day after one year. [18] Some patients also state that the odor they smell is different from any known odor.

Diagnosis

The most challenging task for the examiner is to determine and obtain the correct symptoms and associate them with one of the olfactory disorders, as there are several of them and they are related to each other.

The first step the examiner usually takes is to investigate if the problem is olfactory or gustatory related. As it may be that the patient releases certain bodily odors that are causing them to have this perception. [19]

If the examiner is able to confirm that the problem is olfactory related, the next step is to determine which olfactory disorder the patient has. The following is a list of possible olfactory disorders:

The second step is difficult for both the examiner and the patient as the patient has some difficulty describing their perception of the phantom odor. Furthermore, the patient is in a position of stress and anxiety thus it is crucial that the examiner be patient.

After determining the nature of the disorder, and confirming phantosmia, the examiner must then have the patient describe their perception of the phantom odor. In many cases, patients have described the odor to be that of something burning and rotten and have described it to be unpleasant and foul.

The third step for the examiner is to determine the health history of the patient to take note of head trauma, accidents, upper respiratory infections, allergic rhinitis or chronic rhinitis. [14] Although these may be events that have resulted in the phantom odor, studies conducted by Zilstrof have found that the majority of phantosmia patients have no previous history of head trauma and upper respiratory infections. [20]

Treatment

Due to the rareness of the disorder there is no well-defined treatment. Sometimes the patients are just told to live with the disorder or the patients end up performing "stereotypical methods" that might help in reducing the severity of the odor. This might include forced crying, bending over holding knees while holding breath, rinsing the nose with saline water and gagging. All these behaviours at the end fail to resolve the hallucination. Various treatments like prophylaxis have been suggested but more research is needed for its confirmation. Also, due to being a poorly understood disorder, and having analogies to some psychiatric conditions, some patients are told that they have a mental illness.

One of the surgical treatments proposed has included olfactory bulb ablation through a bifrontal craniotomy approach. [21] [22] But a counter-argument by Leopold, Loehrl and Schwob (2002) has stated that this ablation process results in a bilateral permanent anosmia and includes risks associated with a craniotomy. According to them, the use of transnasal endoscopic exhibition of olfactory epithelium is a safe and effective treatment for patients with unremitting phantosmia with the olfactory function being potentially spared. It is also cautioned that the surgery is challenging one and is associated with major risks, and that it should be restricted to expertise centres. [18]

On the other hand, many cases have also reported that the strength of their symptoms have decreased with time. (Duncan and Seidan, 1995) A case involving long term phantosmia has been treated with the use of an anti depressive medication by the common name Venlafaxine (Effexor). The relation between mood disorders and phantosmia is unknown, and is a widely researched area. In many cases, the symptoms of phantosmia have been reduced by the use of anticonvulsants and antidepressants that act on the central and peripheral neurons.

The most commonly used treatment method is the removal of the olfactory epithelium or the bulb by means of surgery to alleviate the patient from the symptoms. Other traditional methods include the use of topical anesthetics (Zilstorff-Pederson, 1995) and use of sedatives. [3]

Nasal spray

Many patients seeking a quick form of relief achieved it by rinsing the nose with a saline solution. This treatment option is easily available and can be repeated several times throughout the day to obtain relief. An example of a nasal spray that can be used to alleviate symptoms is Oxymetazoline HCl, which seems to provide relief for a longer time period. The relief achieved by the use of nasal sprays seems to be because it results in the blockage of the nostril that does not allow any air to enter the olfactory cleft. [3]

Topical solutions

Another treatment option is the topical solution of cocaine HCl which also provides relief for a short time period by acting as an anesthetic and desensitizing the nasal neurons. The topical solution is applied on the nostril. This topical solution can have several side effects as it has been found that some patients with troposmia started to show symptoms of phantosmia after its use. Other patients have lost complete function of the nostril where the drug was applied. [3]

Venlafaxine

Structure of Venlafaxine Venlafaxine.svg
Structure of Venlafaxine

This antidepressant medication is a serotonin norepinephrine reuptake inhibitor (SNRI). In the case study of a 52-year-old female with phantosmia for 27 years, a dose of 75 mg a day relieved and eliminated her symptoms. The drug was prescribed initially in order to treat her depression. [5]

Occurrence

Phantosmia is most likely to occur in women between the ages of 15 and 30 years. The duration of the first hallucination(s) is likely to be from five to twenty minutes. It has also been found that the second hallucination is likely to occur approximately a month later in the same manner as the first. Over time, the length of the hallucination(s) may begin to increase. [15]

Pregnancy

A longitudinal study on pregnant women found that 76% of pregnant women experienced significant changes in gustation and olfaction perception. This was found to be caused and linked to their pregnancy. The study concluded that 67% of the pregnant women had reported a higher level of sensitivity to smell, 17% had an olfactory distortion and 14% had phantosmia; these distortions were very minimal towards the last stages of pregnancy and in the majority were not present post partum. Furthermore, 26% of these participants also claimed that they also experienced an increased sensitivity to foods that were bitter and a decreased sensitivity to salt. These findings suggest that pregnant women experience distorted smell and taste perception during pregnancy. [23] It has also been found that 75% of women alter their diets during pregnancy. Further research is being conducted to determine the mechanism behind food cravings during pregnancy. [24]

Case studies

Surgical treatment with the preservation of olfactory ability

A 26-year-old woman was diagnosed with mononucleosis at the age of 18. After this diagnosis she began to experience headaches on the right side of her head, and phantosmia in her left nostril that would often occur together. The olfactory hallucination reported by the woman was an unpleasant mixture of vinegar, fecal material, and rotten eggs. This would happen every day beginning in the morning, and the symptoms would worsen during the few days before her menstrual period. If the symptoms did not occur in the morning, they would be triggered by strong olfactory stimuli or by loud noises. Occasionally she could avoid the phantosmia symptoms by forcing herself to sneeze.[ citation needed ]

The woman consulted many medical practitioners but could not receive a reliable diagnosis. She was prescribed medications including nasal steroid sprays and other drugs, but they would not relieve her of her headaches and phantosmia symptoms. Through chemosensory evaluation, it was found that her senses of smell and taste were working normally. Due to some phantosmias believed to be caused by a blockage causing the odor molecules to not reach the olfactory receptors, doctors surgically widened the olfactory cleft. Unfortunately, the phantosmia symptoms remained. Further unsuccessful treatment included a long-term disruption of the axonal projections from the primary olfactory sensory neurons onto the olfactory bulb. This was accomplished by intranasal irrigation with zinc sulfate.[ citation needed ]

The patient was successfully treated with a surgical procedure involving permanent disruption of the olfactory epithelium. This was accomplished with the surgical excision of a "plug" of olfactory epithelium from the area of the cribriform plate. This excision was meant to sever all the fila olfactoria entering the central nervous system from her left nostril. Five weeks after surgery, the woman reported a complete absence of her phantosmia symptoms, and her olfactory ability was maintained (Hornung et al. 1991). [3]

Drug treatment

For a 52-year-old woman, phantosmia occurring as fluctuating episodes occurred for a period of 27 years, and there was no discernible reason for the onset of symptoms. She could weaken the symptoms by rinsing her nose with a saline solution, and by going to sleep. The smells she would encounter often were very unpleasant, resembling a burnt and rotten fruity odor. When her family doctor prescribed her the antidepressant venlafaxine, she noticed that the drug resulted in the complete elimination of her phantosmia symptoms. This discovery has caused scientists and doctors to research if a link between phantosmia and mild depressive disorders exists, and this idea is supported by the reported improvement of phantosmia after repeated transcranial stimulation used to treat depression. [25]

Co-morbidity with Parkinson's disease

In the case of a 57-year-old woman, strong olfactory sensations were reported, ranging from odors of perfume to slightly unpleasant odors of "wet dog". The episodes experienced would last between seconds and hours and would occur multiple times per day. The patient would report phantosmia symptoms, but would correctly identify known odors and would claim to have no symptoms of smell loss. She had no history of epilepsy, and her electroencephalographic results were normal. Later on, while the symptoms of phantosmia were decreasing, she developed severe symptoms of Parkinson disease. While the patient was treated for her tremors with pramipexole, amantadine hydrochloride, levodopa, carbidopa and entacapone, the phantosmia symptoms disappeared completely.

In the case of a 52-year-old woman, the first symptoms of phantosmia reported appeared to the woman as an increased sense of smell. She believed to have the ability to detect odors before other people, and with better accuracy. She later began to experience the typical symptoms of phantosmia and would smell things that she could recognize in the absence of any odor producing molecules. The reported smells were of perfumes, candles, and fruits, however the woman could not accurately identify what type of perfume or fruit she was smelling. Her phantosmia episodes would occur abruptly and would last from minutes to half an hour. A rhinologic examination came back with normal results. When her phantosmia symptoms began to dissipate, she began to complain of clumsiness, slowness, and problems with her left hand that would alternate between tremors and rigidity. A neurologic examination revealed symptoms of Parkinson's disease. [6]

See also

Other

Related Research Articles

<span class="mw-page-title-main">Hallucination</span> Perception in the absence of external stimulation that has the qualities of real perception

A hallucination is a perception in the absence of an external stimulus that has the qualities of a real perception. Hallucinations are vivid, substantial, and are perceived to be located in external objective space. Hallucination is a combination of two conscious states of brain wakefulness and REM sleep. They are distinguishable from several related phenomena, such as dreaming, which does not involve wakefulness; pseudohallucination, which does not mimic real perception, and is accurately perceived as unreal; illusion, which involves distorted or misinterpreted real perception; and mental imagery, which does not mimic real perception, and is under voluntary control. Hallucinations also differ from "delusional perceptions", in which a correctly sensed and interpreted stimulus is given some additional significance. Many hallucinations happen also during sleep paralysis.

<span class="mw-page-title-main">Anosmia</span> Inability to smell

Anosmia, also known as smell blindness, is the loss of the ability to detect one or more smells. Anosmia may be temporary or permanent. It differs from hyposmia, which is a decreased sensitivity to some or all smells.

<span class="mw-page-title-main">Olfactory nerve</span> Cranial nerve I, for smelling

The olfactory nerve, also known as the first cranial nerve, cranial nerve I, or simply CN I, is a cranial nerve that contains sensory nerve fibers relating to the sense of smell.

<span class="mw-page-title-main">Olfactory bulb</span> Neural structure

The olfactory bulb is a neural structure of the vertebrate forebrain involved in olfaction, the sense of smell. It sends olfactory information to be further processed in the amygdala, the orbitofrontal cortex (OFC) and the hippocampus where it plays a role in emotion, memory and learning. The bulb is divided into two distinct structures: the main olfactory bulb and the accessory olfactory bulb. The main olfactory bulb connects to the amygdala via the piriform cortex of the primary olfactory cortex and directly projects from the main olfactory bulb to specific amygdala areas. The accessory olfactory bulb resides on the dorsal-posterior region of the main olfactory bulb and forms a parallel pathway. Destruction of the olfactory bulb results in ipsilateral anosmia, while irritative lesions of the uncus can result in olfactory and gustatory hallucinations.

<span class="mw-page-title-main">Olfactory system</span> Sensory system used for smelling

The olfactory system, or sense of smell, is the sensory system used for smelling (olfaction). Olfaction is one of the special senses, that have directly associated specific organs. Most mammals and reptiles have a main olfactory system and an accessory olfactory system. The main olfactory system detects airborne substances, while the accessory system senses fluid-phase stimuli.

Parosmia is a dysfunctional smell detection characterized by the inability of the brain to correctly identify an odor's "natural" smell. Instead, the natural odor is usually transformed into an unpleasant aroma, typically a "burned", "rotting", "fecal", or "chemical" smell. There can also be rare instances of a pleasant odor called euosmia. The condition was rare and little-researched until it became relatively more widespread since 2020 as a side effect of COVID-19.

Patulous Eustachian tube (PET) is the name of a physical disorder where the Eustachian tube, which is normally closed, instead stays intermittently open. When this occurs, the person experiences autophony, the hearing of self-generated sounds. These sounds, such as one's own breathing, voice, and heartbeat, vibrate directly onto the ear drum and can create a "bucket on the head" effect. PET is a form of eustachian tube dysfunction (ETD), which is said to be present in about 1 percent of the general population.

<span class="mw-page-title-main">Aura (symptom)</span> Symptom of epilepsy and migraine

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is a seizure.

Chronic atrophic rhinitis, or simply atrophic rhinitis, is a chronic inflammation of the nose characterised by atrophy of nasal mucosa, including the glands, turbinate bones and the nerve elements supplying the nose. Chronic atrophic rhinitis may be primary and secondary. Special forms of chronic atrophic rhinitis are rhinitis sicca anterior and ozaena. It can also be described as the empty nose syndrome.

Olfactory reference syndrome (ORS) is a psychiatric condition in which there is a persistent false belief and preoccupation with the idea of emitting abnormal body odors which the patient thinks are foul and offensive to other individuals. People with this condition often misinterpret others' behaviors, e.g. sniffing, touching their nose or opening a window, as being referential to an unpleasant body odor which in reality is non-existent and cannot be detected by other people.

Hyperosmia is an increased olfactory acuity, usually caused by a lower threshold for odor. This perceptual disorder arises when there is an abnormally increased signal at any point between the olfactory receptors and the olfactory cortex. The causes of hyperosmia may be genetic, hormonal, environmental or the result of benzodiazepine withdrawal syndrome.

Dysosmia is a disorder described as any qualitative alteration or distortion of the perception of smell. Qualitative alterations differ from quantitative alterations, which include anosmia and hyposmia. Dysosmia can be classified as either parosmia or phantosmia. Parosmia is a distortion in the perception of an odorant. Odorants smell different from what one remembers. Phantosmia is the perception of an odor when no odorant is present. The cause of dysosmia still remains a theory. It is typically considered a neurological disorder and clinical associations with the disorder have been made. Most cases are described as idiopathic and the main antecedents related to parosmia are URTIs, head trauma, and nasal and paranasal sinus disease. Dysosmia tends to go away on its own but there are options for treatment for patients that want immediate relief.

<span class="mw-page-title-main">Sense of smell</span> Sense that detects smells

The sense of smell, or olfaction, is the special sense through which smells are perceived. The sense of smell has many functions, including detecting desirable foods, hazards, and pheromones, and plays a role in taste.

Olfactory memory refers to the recollection of odors. Studies have found various characteristics of common memories of odor memory including persistence and high resistance to interference. Explicit memory is typically the form focused on in the studies of olfactory memory, though implicit forms of memory certainly supply distinct contributions to the understanding of odors and memories of them. Research has demonstrated that the changes to the olfactory bulb and main olfactory system following birth are extremely important and influential for maternal behavior. Mammalian olfactory cues play an important role in the coordination of the mother infant bond, and the following normal development of the offspring. Maternal breast odors are individually distinctive, and provide a basis for recognition of the mother by her offspring.

Many types of sense loss occur due to a dysfunctional sensation process, whether it be ineffective receptors, nerve damage, or cerebral impairment. Unlike agnosia, these impairments are due to damages prior to the perception process.

Sniffing is a perceptually-relevant behavior, defined as the active sampling of odors through the nasal cavity for the purpose of information acquisition. This behavior, displayed by all terrestrial vertebrates, is typically identified based upon changes in respiratory frequency and/or amplitude, and is often studied in the context of odor guided behaviors and olfactory perceptual tasks. Sniffing is quantified by measuring intra-nasal pressure or flow or air or, while less accurate, through a strain gauge on the chest to measure total respiratory volume. Strategies for sniffing behavior vary depending upon the animal, with small animals displaying sniffing frequencies ranging from 4 to 12 Hz but larger animals (humans) sniffing at much lower frequencies, usually less than 2 Hz. Subserving sniffing behaviors, evidence for an "olfactomotor" circuit in the brain exists, wherein perception or expectation of an odor can trigger brain respiratory center to allow for the modulation of sniffing frequency and amplitude and thus acquisition of odor information. Sniffing is analogous to other stimulus sampling behaviors, including visual saccades, active touch, and whisker movements in small animals. Atypical sniffing has been reported in cases of neurological disorders, especially those disorders characterized by impaired motor function and olfactory perception.

<span class="mw-page-title-main">Tactile hallucination</span>

Tactile hallucination is the false perception of tactile sensory input that creates a hallucinatory sensation of physical contact with an imaginary object. It is caused by the faulty integration of the tactile sensory neural signals generated in the spinal cord and the thalamus and sent to the primary somatosensory cortex (SI) and secondary somatosensory cortex (SII). Tactile hallucinations are recurrent symptoms of neurological diseases such as schizophrenia, Parkinson's disease, Ekbom's syndrome and delerium tremens. Patients who experience phantom limb pains also experience a type of tactile hallucination. Tactile hallucinations are also caused by drugs such as cocaine and alcohol.

The University of Pennsylvania Smell Identification Test (UPSIT) is a test that is commercially available for smell identification to test the function of an individual's olfactory system.

<span class="mw-page-title-main">Impact of the COVID-19 pandemic on neurological, psychological and other mental health outcomes</span> Effects of the COVID-19 pandemic and associated lockdowns on mental health

There is increasing evidence suggesting that COVID-19 causes both acute and chronic neurologicalor psychological symptoms. Caregivers of COVID-19 patients also show a higher than average prevalence of mental health concerns. These symptoms result from multiple different factors.

Smell training or olfactory training is the act of regularly sniffing or exposing oneself to robust aromas with the intention of regaining a sense of smell. The stimulating smells used are often selected from major smell categories, such as aromatic, flowery, fruity, and resinous. Using strong scents, the patient is asked to sniff each different smell for a minimum of 20 seconds, no less than two times per day, for three to six months or more. It is used as a rehabilitative therapy to help people who have anosmia or post-viral olfactory dysfunction, a symptom of COVID-19. It was considered a promising experimental treatment in a 2017 meta-analysis.

References

  1. ↑ "That stinks! 1 in 15 Americans smell odors that aren't there". National Institutes of Health (NIH). National Institute on Deafness and Other Communication Disorders. National Institute on Deafness and Other Communication Disorders. August 16, 2018. Retrieved 23 August 2018.
    PD-icon.svg This article incorporates public domain material from websites or documents of the National Institutes of Health.
  2. 1 2 3 4 Hong SC, Holbrook EH, Leopold DA, Hummel T (2012), "Distorted Olfactory Perception: A Systematic Review", Acta Oto-Laryngologica Supplementum, 132 (S1): S27–31, doi:10.3109/00016489.2012.659759, PMID   22582778, S2CID   207416134
  3. 1 2 3 4 5 6 7 8 9 10 Leopold DA (2002a), "Distortion of Olfactory Perception: Diagnosis and Treatment", Chemical Senses, 27 (7): 611–615, doi: 10.1093/chemse/27.7.611 , PMID   12200340
  4. 1 2 3 4 HealthUnlocked (2014), "Phantosmia (Smelling Odours That Aren't There)", NHS Choices, retrieved 6 August 2016
  5. 1 2 Landis BN, Croy I, Haehner A (2012). "Long lasting phantosmia treated withvenlafaxine". Neurocase. 18 (2): 112–114. doi:10.1080/13554794.2011.568497. PMID   21942993. S2CID   205774933.
  6. 1 2 Landis BN, Burkhard PR (2008). "Phantosmias and parkinson disease". Archives of Neurology. 65 (9): 1237–1239. doi: 10.1001/archneur.65.9.1237 . PMID   18779429.
  7. ↑ Nye E, Arendts G (2002). "Intracerebral haemorrhage presenting as olfactory hallucinations". Emergency Medicine. 14 (4): 447–449. doi:10.1046/j.1442-2026.2002.00385.x. PMID   12534490.
  8. ↑ Paskind HA (1935). "Parosmia in tumorous involvement of olfactory bulbs and nerves". Archives of Neurology and Psychiatry. 33 (4): 835–838. doi:10.1001/archneurpsyc.1935.02250160150012.
  9. ↑ Muffatti R, Scarone S, Gambini O (2008). "An olfactory reference syndrome successfully treated by aripiprazole augmentation of antidepressant therapy". Cognitive and Behavioral Neurology. 21 (4): 258–260. doi:10.1097/wnn.0b013e318185e6bd. PMID   19057178. S2CID   206127878.
  10. ↑ Prazeres AM, Fontenelle LF, Mendlowicz MV, de Mathis MA, Ferrao YA, de Brito NF, Diniz JB, Gonzalez CH, Quarantini LC, Marrocos RP, Miguel EC (2010). "Olfactory reference syndrome as a subtype of body dysmorphic disorder". Journal of Clinical Psychiatry. 71 (1): 87–89. doi: 10.4088/jcp.09l05040 . PMID   20129009.
  11. ↑ "Phantosmia". Prospect. Retrieved July 15, 2012.
  12. ↑ Coleman ER, Grosberg BM, Robbins MS (2011). "Olfactory hallucinations in primary headache disorders: Case series and literature review". Cephalalgia. 31 (14): 1477–1489. doi:10.1177/0333102411423315. PMID   21945891. S2CID   24994785.
  13. ↑ Schrieber AO, Calvert PC (1986). "Migrainous olfactory hallucinations". Headache: The Journal of Head and Face Pain. 26 (10): 513–514. doi:10.1111/j.1526-4610.1986.hed2610513.x. PMID   3818266. S2CID   26403632.
  14. 1 2 Leopold DA, Schwob JE, Youngentob SL, Hornung DE, Wright HN, Mozell MM (1991), "Successful treatment of phantosmia with preservation of olfaction", Archives of Otolaryngology–Head & Neck Surgery, 117 (12): 1402–1406, doi:10.1001/archotol.1991.01870240094016, PMID   1845270
  15. 1 2 3 Leopold DA, Myerrose G (1994), "Diagnosis and treatment of distorted olfactory perception", in Kuriha K, Suzuki N, Ogawa H (eds.), Olfaction and Taste XI, Tokyo, Japan: Springer-Verlag, pp. 618–622
  16. ↑ Hirsch AR (April 2009). "Parkinsonism: The Hyposmia and Phantosmia Connection". Archives of Neurology. 66 (4): 538–9. doi:10.1001/archneurol.2009.38. PMID   19364944.
  17. ↑ "Side effects of radiation for olfactory neuroblastoma". Livestrong.com. Retrieved July 3, 2012.
  18. 1 2 Leopold DA, Loehrl TA, Schwob JE (2002b), "Long-term follow-up of surgically treated phantosmia", Archives of Otolaryngology–Head & Neck Surgery, 128 (6): 642–647, doi: 10.1001/archotol.128.6.642 , PMID   12049557
  19. ↑ Leopold DA, Preti G, Mozell MM, Youngentob SL, Wright HN (1990), "Fish-odor syndrome presenting as dysosmia", Archives of Otolaryngology–Head & Neck Surgery, 116 (3): 345–355, doi:10.1001/archotol.1990.01870030118022, PMID   2306356
  20. ↑ Zilstorff K (1966). "Parosmia". The Journal of Laryngology & Otology. 80 (11): 1102–1104. doi:10.1017/s0022215100066457. PMID   5927746. S2CID   221921058.
  21. ↑ Kaufman MD, Lassiter KR, Shenoy BV (1988). "Paroxysmal unilateral dysosmia: a cured patient". Annals of Neurology. 24 (3): 450–451. doi:10.1002/ana.410240315. PMID   3228277. S2CID   36535652.
  22. ↑ Markert JM, Hartshorn DO, Farhat SM (1993). "Paroxysmal bilateral dysosmia treated by resection of the olfactory bulbs" (PDF). Surgical Neurology. 40 (2): 160–163. doi:10.1016/0090-3019(93)90129-o. hdl: 2027.42/30650 . PMID   8362355.
  23. ↑ Nordin S, et al. (2004). "A Longitudinal Descriptive Study of Self-reported Abnormal Smell and Taste Perception in Pregnant Women;". Chemical Senses. 29 (5): 391–402. doi: 10.1093/chemse/bjh040 . PMID   15201206.
  24. ↑ Cantoni P, Hudson R, Distel H, Laska M (1999). "Changes in olfactory perception and dietary habits in the course of pregnancy: a questionnaire study". Chemical Senses. 24: 58. doi: 10.1093/chemse/24.1.47 .
  25. ↑ Landis B, Croy I, Haehner A (2012). "Long lasting phantosmia treated with venlafaxine". Neurocase. 18 (2): 112–114. doi:10.1080/13554794.2011.568497. PMID   21942993. S2CID   205774933.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.