Phantosmia, or olfactory hallucinations, involves smelling odors that are not derived from any physical stimulus. These phantom odors can range from rotting flesh to a spring meadow, though most cases report unpleasant aromas.[1] In some cases phantosmia has even led to the afflicted individual to believe that both the odor and source in fact exist, a condition known as olfactory delusions.
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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 victim 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 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 more uncommon than the muscle tremors the patients experience.[2]
Phantosmia can also be attributed to overactive olfactory receptor neurons (ORNs) or the loss of inhibitory neurons brought on by a sinus infection or some other type of head cold. These overactive ORNs could be activated by some other input through a fluke in wiring where they would normally remain inactive or inhibited, so a signal is sent to the olfactory bulb when no stimulus is present. The inhibitory neurons are also a part of the pathway just described. If extraneous information that is normally stopped at these impasses is allowed to continue along the pathway, the brain will interpret a signal that has no intrinsic value. This will provide a sensation without a proper stimulus.
At the onset of these hallucinations, the odor will last only for a few minutes and then dissipate. It may start with incidents occurring once a month, but then progresses to weekly and daily episodes.
In one study, a long-term (average 5.4 years after surgery) follow-up on 8 patients that underwent transnasal excision of olfactory epithelium revealed that 7 of them had their phantosmia permanently resolved. Before the surgery all of the patients had tests to show there were no psychological or pathological evidence for the hallucinations.[3][4]
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