|Classification and external resources|
Parosmia (from the Greek ???? pará and ???? osm?), also known as troposmia (Gk.) or cacosmia (Gk.), is an olfactory dysfunction that is characterized by the inability of the brain to properly identify an odor's "natural" smell. What happens instead, is that the natural odor is transcribed into what is most often described as an unpleasant aroma, typically a "'burned,' 'rotting,' 'fecal,' or 'chemical' smell". There are instances, however, of pleasant odors; this is more specifically called euosmia (Greek).
One method used to establish parosmia is the University of Pennsylvania Smell Identification Test, or UPSIT. "Sniffin' Sticks" are another method that can be used to properly diagnose parosmia. These different techniques can also help deduce whether a specific case of parosmia can be attributed to just one stimulating odor or if there is a group of stimulating odors that will generate the displaced smell. One case study performed by Frasnelli et al. offers a situation where certain smells, specifically coffees, cigarettes, onions, and perfumes, induced a "nauseating" odor for the patient, one which was artificial but unable to be aptly related to another known smell. In another case study cited in the same paper, one woman had parosmia in one nostril but not the other. Medical examinations and MRIs did not reveal any abnormalities; however the parosmia in this case was degenerative and only got worse with time. The authors do comment, however, that cases of parosmia can predict regeneration of olfactory senses.
There are numerous diseases that parosmia is associated with. In the case study cited above, Frasnelli et al. examined five patients that endured parosmia or phantosmia, most as a result of upper respiratory tract infections (URTIs). It is hypothesized that URTIs can result in parosmia because of damage to olfactory receptor neurons (ORNs). Exposure to harmful solvents has also been linked to parosmia and more specifically damaging ORNs. Damage to these neurons could end in the inability to correctly encode a signal representing a particular odor, which would send an erroneous signal to the odor processing center, the olfactory bulb. This, in turn, leads to the signal activating a different trigger, i.e. a different smell, than the stimulating odor, and thus the patient cannot sync the input and output odors. Damage to ORNs describes a peripheral defect in the pathway, but there are also instances where damage to the processing center in the brain can lead to distorted odors as well.
Different types of head traumas could obviously lead to dysfunctions that relate to what the afflicted brain area controls. In humans, the olfactory bulb is located on the inferior side of the brain. Physical damage to this area would alter how the area processes information in a variety of ways, but there are also other types of diseases that can alter how this area works. If the part of the brain that interprets these input signals is damaged, then a distorted output is possible. This would also lead to parosmia. Temporal lobe epilepsy has also led to cases of parosmia, but these were only temporary; the onset of parosmia was a seizure and it typically lasted a week or two after. Parosmia is also a known symptom for Parkinson's disease, though not ubiquitous for patients with it, and although the specific pathway is undetermined, the lack of dopamine has resulted in documented cases of parosmia and phantosmia.
Fortunately for patients afflicted with parosmia, symptoms usually decrease with time. Although there are instances of parosmia affecting patients for years at a time, this is certainly not the majority of cases. There have been experiments done to treat parosmia with L-Dopa, but besides that there are no current treatments other than inducing anosmia or hyposmia to the point where the odors are negligible.