xRead - Olfactory Disorders (September 2023)

S.-C. Hong et al.

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Abnormalities in axonal targeting from regenera ting axons after injury may also explain olfactory distortions. In animal experiments, alterations in sensory perception after recovery from nerve transec tion are observed, and restoration of odor quality discrimination requires that the animal must again learn to associate individual odor sensations with a behavioral response [10]. This suggests that the origi nal olfactory map changes after signi fi cant injury, which then needs to be relearned in these animals. Support for this theory is observed using a mono clonal antibody to OCAM/mamFas (olfactory cell adhesion molecules/mammalian homolog of fasciclin II) that demonstrates a speci fi c reproducible pattern of staining of the olfactory neurons within the epithelium as well as their projections to the olfactory bulb. The terminal projections in the bulb after tran section contrasted with the restoration of the normal zonal patterning of the projection after recovery from methyl bromide lesion, but were consistent with reports of mistargeting by a receptor-de fi ned subset of neurons after transection [11]. While obtaining a clinical history from someone with a complaint of olfactory distortion it is important to be sympathetic, since many of these individuals are anxi ous about their symptoms. The fi rst determination should be whether the distortion is real or a product of the environment. Questions relating to time and place of phantosmia occurrence revealing a repetitive pattern can help recognize an environmental source for the abnormal smell. A medical history pointing to recent acute or chronic rhinosinusitis can identify infection as a possible cause. Next, the clinician should attempt to establish the distortion as centrally or peripherally related. A history of seizure disorder, migraine symptoms, psychiatric/neurologic disorders, or cognitive dysfunction favors a central cause. Peripheral causes of distortions are commonly expe rienced with a perception of hyposmia and/or dimini shed fl avor. According to the analysis of a series of 56 patients with parosmia, all patients noted quantitative olfactory dysfunction. Hyposmia was found in 40 patients (71.4%) and 16 patients (28.6%) were con fi rmed to have anosmia [2]. These patients can sometimes identify one side for the distortion and may report alleviating the abnormal smell with unilateral occlusion. They often report the lack of distortion on awakening in the middle of the night or fi rst thing in the morning. Forced crying is often reported to temporarily alleviate symptoms [12]. Clinical evaluation History

Central causes can be related to an area of hyper-functioning brain cells generating this odor perception [4]. It is known that an olfactory aura can sometimes accompany seizures. This typically lasts only a few seconds. Some individuals with phantosmias have commented that they can feel a phantom odor coming before it actually arrives. Psychiatric etiologies for olfactory distortion can exist with schizophrenia, depression, alcoholic psychosis, and olfactory reference syndrome [5]. Olfactory distortions have also been observed with epilepsy and migraine. Are there different types of parosmias? Most parosmias appear in relation with olfactory loss, often after upper respiratory tract infection (URTI); the majority of them disappear within 1 year. A small minority of parosmias is idiopathic, associated with normosmia, and can often vary with head movements, Valsalva maneuver, etc. This second form has a poor prognosis, and may even become worse over time. A peripheral etiology for distorted smells is sug gested by the fi nding that many of the individuals without a central cause have hyposmia or anosmia associated with the distortion and often the degree of loss is asymmetric. Phantosmia is almost always worse in the nostril with the least olfactory ability and those phantosmias that occur in only one nostril can be eliminated by occluding the air fl ow or anesthetizing the olfactory mucosa in that nostril. Patients thought to have a peripheral cause for distortions will also say that the abnormality was worse while the loss was occurring, suchasthe fi rst few hours after head trauma or an URTI loss. Support for peripheral causes also comes from imaging studies performed after treatment. Brain imaging using PET scans of individuals with phantos mia has revealed increased activity in the contralateral frontal, insular, and temporal regions, which decreased after excision of the olfactory epithelium from the nasal cavity involved [4]. In addition, structural MRI indi cates that hyposmic patients with parosmia exhibit smaller olfactory bulb volumes compared with hypos mic patients without parosmia [6,7]. Here it has been hypothesized that a decreased number of interneurons in the olfactory bulb might result in a decrease of neuronal inhibition that might be the cause for ‘ aberrant ’ odorous sensations. One common hypothesis to explain peripheral causes for distortions is that ‘ rogue ’ neurons that emit abnormal signals to the brain or loss of inhibitory cells to normally functioning olfactory neurons could be playing a role [8,9]. The olfactory histopathology of individuals with phantosmia shows a decreased number of neurons, a greater ratio of immature to mature neurons, and distorted growth of olfactory axons with intraepithelial and submucosal neuromas [8,9].