The most difficult task for the examiner is to determine and maintain the right symptoms and associate them with one of the olfactory disorders because they are several and they are related to each other. In the case of a 57-year-old woman, strong olfactory sensations were reported, ranging from perfume smells to slightly unpleasant „wet dog” odors. The episodes would last between a few seconds and a few hours and would occur several times a day. The patient would report symptoms of phantosmia, but correctly identify known odors and claim to have no symptoms of odor loss. She had no history of epilepsy and her electroencephalographic results were normal. Later, as the symptoms of phantosmia decreased, she developed severe symptoms of Parkinson`s disease. While the patient was being treated for her tremors with pramipexole, amantadine hydrochloride, levodopa, carbidopa and entacapone, the symptoms of phantosmia completely disappeared. Bydgoszcz W, Schilder P (1934) Olfactory fantasy and olfactory hallucinations. Arch Neurol Psychiatry 32:467-492 The woman consulted many doctors, but could not get a reliable diagnosis. She was prescribed medication, including steroid nasal sprays and other medications, but they did not relieve her headaches and phantosmia symptoms. Through chemosensory examination, it was found that his senses of smell and taste were functioning normally.
Due to certain phantosmias that are believed to be caused by a blockage that prevents odorous molecules from reaching olfactory receptors, doctors have surgically dilated the olfactory cleft. Unfortunately, the symptoms of phantosmia persisted. Another unsuccessful treatment involved long-term disruption of axonal projections of primary olfactory sensory neurons onto the olfactory bulb. This was achieved by intranasal irrigation with zinc sulfate. [ref. needed] Olfactory disorders are reported in multiple psychiatric disorders, including schizophrenia. Olfactory distortion patterns in schizophrenia include impaired olfactory cognition, olfactory discrimination, olfactory memory, and sensitivity to the perceptual olfactory threshold. Olfactory dysfunction is considered a warning sign of schizophrenia and an important endophenotypic marker. We highlight a case of late acute and transient psychotic disorder with olfactory hallucination. Various implications of olfactory hallucinations in a psychotic patient are discussed with a literature review.
Olfactory performance was assessed using Sniffin` Sticks, a standardized 16-point odor identification test. The Sniffin` Sticks test battery is a well-validated, standards-based test set with high test-retest reliability (Hummel et al. 1997; Croy et al., 2015). The test procedure has been described in detail elsewhere (Larsson et al. 2016). In short, the smells were presented with felts containing the following odors: apple, banana, cinnamon, cloves, coffee, fish, garlic, leather, lemon, licorice, mushroom, peppermint, essence, pineapple, rose and turpentine. Participants were first asked to freely identify the smells. If they could not correctly identify an odor, they were asked to choose 1 of the 4 written response solutions, 1 of which was correct. The score of interest here was the proportion of correctly identified odors with free or cooked identification.
Participants with a score of 10 points or less were classified as olfactory dysfunctional based on established clinical practice (Hummel et al. 2001). Olfactory hallucinations in schizophrenia: is it important? Sujita Kumar Kar, Kabir Garg, Adarsh Tripathi Department of Psychiatry, King George`s Medical University, Lucknow, Uttar Pradesh, India Leopold D (2002) Olfactory Perceptual Distortion: Diagnosis and Treatment. Shem Senses 27:611-615 The cause of phantosmia can be peripheral or central, or a combination of both. The peripheral explanation for this disorder is that rogue neurons do not function and transmit false signals to the brain, or it may be due to the dysfunction of olfactory neurons.  The central explanation is that active or defective brain cells cause the perception of disturbing odor. Another central cause is that the perception of ghost odor usually follows the occurrence of seizures. The period of symptoms usually lasts a few seconds.  Overall, the prevalence of phantosmia is consistent with previous reports in healthy individuals where phantosmia was reported by 6.0-8.5% of the sample (Ohayon, 2000; Rawal et al., 2016). Studies with 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) examined phantosmia in relatively healthy ambulatory patients with ear, nose and throat and found that only 0.8% of patients without loss of smell had phantom odors. An explanation for the discrepancy could be attributed to differences in how phantosmia was operationalized and described to participants. Another explanation could be that previous work has focused on different groups of patients with mixed pathogenesis. There are a few causes of phantosmia, but one of the most common and well-documented are brain damage or seizures in the temporal lobe. During a temporal lobe attack, the patient rarely faints, but usually turns black and does not remember anything that happened during the attack. However, several people who have had these seizures have remembered having phantosmia just before darkening the darkening. Epilepsy is a disease characterized by seizures. In the case of phantosmia, when smell and something else are so strongly associated, the effect of „something else” can induce activation of the olfactory bulb, although there was no stimulus for the bulb. This is an example of plasticity gone wrong.
Those who have lesions on the temporal lobe, often caused by a stroke, but also by trauma to the head, also experience these olfactory hallucinations. In addition, the present study showed a significant association between the number of vascular risk factors and phantosmia. One possible explanation for this finding could be that some drugs alter olfactory functions and alter olfactory perception (Doty and Bromley 2004). No association was observed between other clinical variables and phantosmia, suggesting that phantosmia is specifically linked to vascular disease. Several reports report transmodal effects of olfactory dysfunctions, mainly on other chemosensory systems. There is a proven harmful effect of olfactory dysfunction on trigeminal perception. Compared to controls, individuals with impaired olfactory function can perceive trigeminal stimuli only at higher concentrations (Frasnelli et al., 2010; Gudziol et al., 2001) and perceive superthreshold stimuli as less intense (Frasnelli et al., 2007a). However, this reduced sensitivity to trigeminal is limited to trigeminal chemosensory fibres (Frasnelli et al., 2006). A specific method for testing trigeminal sensitivity is the olfactory lateralization task.
In this test, subjects must determine which of their two nostrils was stimulated by an odorant in a monorhinal stimulation paradigm. We can only do this if the odorant also stimulates the trigeminal system (Kobal et al., 1989). Anomamic individuals have been shown to perform worse than healthy controls in odour localization (Hummel et al., 2003). Leopold et al. (1991) took a different approach to surgical treatment of long-term phantosmia and reported a woman whose 8-year-old phantosmia germinated in the left side of the nose. Phantosmia was eliminated by cutting out a section of the left olfactory epithelium. Before the operation, these researchers confirmed that phantosmia disappeared after occlusion of the left nostril, as well as after cocaine of the left olfactory epithelium.