Well, a most interesting reading.
Phantosmia
[Phantosmia (phantom smell), also called an olfactory hallucination,
is smelling an odor that is not actually there.]
https://www.ncbi.nlm...pubmed/24122320
Olfactory cocainization is not an effective long-term treatment for phantosmia.
Phantosmia, the perception of an odor when there are no odorants in the environment, can be a very debilitating symptom. In the 1960s, Zilstorff reported olfactory distortions could be treated by the topical application of a cocaine solution to the olfactory epithelium. In evaluating this treatment, we observed no long-term benefit using cocaine on 6 patients with phantosmia. Based on our observations, the patient's olfactory ability was not a determining factor in the initiation or quality of their phantosmia. Following topical cocainization, we observed a remarkable delay of hours to days in the return of olfactory ability, and when cocaine was applied to only 1 nostril, there was a decreased olfactory ability on the noncocainized side. These results may suggest the possibility that phantosmia is related to a central processing problem.
https://www.ncbi.nlm...pubmed/23883685
http://search.proque...igsite=gscholar
Enhanced parosmia and phantosmia in patients with severe depression.
Note - Parosmia, 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."
https://www.ncbi.nlm...pubmed/23456373
Phantosmia as a meteorological forecaster.
In normosmics, olfactory ability has been found to vary with ambient humidity, barometric pressure, and season. While hallucinated sensations of phantom pain associated with changes in weather have been described, a linkage to chemosensory hallucinations has heretofore not been reported. A 64-year-old white male with Parkinson's disease presents with 5 years of phantosmia of a smoky burnt wood which changed to onion-gas and then to a noxious skunk-onion excrement odor. Absent upon waking it increases over the day and persists for hours. When severe, there appears a phantom taste with the same qualities as the odor. It is exacerbated by factors that manipulate intranasal pressure, such as coughing. When eating or sniffing, the actual flavors replace the phantosmia. Since onset, he noted the intensity and frequency of the phantosmia forecasted the weather. Two to 3 h before a storm, the phantosmia intensifies from a level 0 to a 7-10, which persists through the entire thunderstorm. Twenty years prior, he reported the ability to forecast the weather, based on pain in a torn meniscus, which vanished after surgical repair. Extensive olfactory testing demonstrates underlying hyposmia. Possible mechanisms for such chemosensory-meteorological linkage includes: air pressure induced synesthesia, disinhibition of spontaneous olfactory discharge, exacerbation of ectopic discharge, affect mediated somatic sensory amplification, and misattribution error with expectation and recall bias. This is the first reported case of weather-induced exacerbation of phantosmia. Further investigation of the connection between chemosensory complaints and ambient weather is warranted.
https://www.ncbi.nlm...les/PMC4061890/
Olfactory Hallucinations without Clinical Motor Activity: A Comparison of Unirhinal with Birhinal Phantosmia
Olfactory hallucinations without subsequent myoclonic activity have not been well characterized or understood. Herein we describe, in a retrospective study, two major forms of olfactory hallucinations labeled phantosmias: one, unirhinal, the other, birhinal. To describe these disorders we performed several procedures to elucidate similarities and differences between these processes. From 1272, patients evaluated for taste and smell dysfunction at The Taste and Smell Clinic, Washington, DC with clinical history, neurological and otolaryngological examinations, evaluations of taste and smell function, EEG and neuroradiological studies 40 exhibited cyclic unirhinal phantosmia (CUP) usually without hyposmia whereas 88 exhibited non-cyclic birhinal phantosmia with associated symptomology (BPAS) with hyposmia. Patients with CUP developed phantosmia spontaneously or after laughing, coughing or shouting initially with spontaneous inhibition and subsequently with Valsalva maneuvers, sleep or nasal water inhalation; they had frequent EEG changes usually ipsilateral sharp waves. Patients with BPAS developed phantosmia secondary to several clinical events usually after hyposmia onset with few EEG changes; their phantosmia could not be initiated or inhibited by any physiological maneuver. CUP is uncommonly encountered and represents a newly defined clinical syndrome. BPAS is commonly encountered, has been observed previously but has not been clearly defined. Mechanisms responsible for phantosmia in each group were related to decreased gamma-aminobutyric acid (GABA) activity in specific brain regions. Treatment which activated brain GABA inhibited phantosmia in both groups.
Note - Hyposmia is a reduced ability to smell and to detect odors.
No wonderthat phantosmia has been linked to withdrawalconsidering the association with changes in GABA (neurotransmitter) activity.
https://www.ncbi.nlm...pubmed/21942993
Long lasting phantosmia treated with venlafaxine. (Effexor)
Qualitative olfactory disorders such as parosmia and phantosmia are not well investigated. In particular, the causes and treatment options for phantosmia are largely unknown. We report a case of long lasting phantosmia that disappeared under anti-depressive treatment, raising the question to what extent certain forms of qualitative olfactory disorders are an early symptom of depression.
Note - Venlafaxine does have a stabilizing effect on Gaba. See...
https://www.ncbi.nlm...pubmed/16075286
https://www.ncbi.nlm...pubmed/9453456/
https://www.ncbi.nlm...ubmed/12488792/
Et al.
https://www.ncbi.nlm...pubmed/20714205
Idiopathic phantosmia: outcome and clinical significance.
RESULTS:
None of the patients had developed any severe health condition or Parkinson's disease. More than 5 years after the occurrence of phantosmia, more than 50% of the patients experienced disappearance (31.8%) or improvement (25%). In the remaining cases, phantosmia did not change (38.7%) or became worse (<5%).
CONCLUSION:
The main findings of the present study were that idiopathic phantosmia improves or disappears in almost two thirds of the patients after more than 5 years, and that idiopathic phantosmia seems to be more likely a harmless symptom rather than a reliable predictor of early Parkinson's disease or other severe diseases.
Note - idiopathic - The cause may not be readily apparent or characterized. In these cases, the origin of the condition is said to be idiopathic.
https://www.ncbi.nlm...pubmed/18779429
Phantosmias and Parkinson disease.
We propose phantosmia as a new premotor manifestation of PD (Parkenson's Desease) and suggest that qualitative abnormalities of olfaction, rather than the typical smell loss demonstrated in this condition, should be more carefully examined in the prodromal phase of PD.
https://www.ncbi.nlm...pubmed/17006637
A study on the prognostic significance of qualitative olfactory dysfunction.
We investigated the frequency and prognostic significance of qualitative olfactory dysfunction (parosmia, phantosmia) in a retrospective patient based study. A total of 392 patients with impairment of olfaction were tested at least two times for their olfactory function using the "Sniffin' Sticks". The mean interval between the first and the last test was 11 months. At the first visit 34% of all patients reported parosmia. Parosmia was most frequent in patients with postinfectious olfactory loss (56%), and less frequent in idiopathic, posttraumatic, sinunasal disease with frequencies of 10, 14, and 28%, respectively. In contrast, only 12% of all patients had phantosmias, with no significant differences between the patient groups. Improvement of olfactory function was found in 23% of all patients (n = 90). Pre-existing parosmia or phantosmia had no significant effect on recovery rate. Regarding qualitative olfactory dysfunction, 29% of those patients reporting parosmia reported relief of this symptom after an average of 12 months, whereas 53% of phantosmic patients lost phantosmia during the observation period. Although it has been suggested that olfactory distortion s could be regarded as an indicator of early recovery of decreased olfactory sensitivity, the current data indicate that occurrence of parosmia or phantosmia has little prognostic value. Phantosmia disappears at a faster rate than parosmia. These insights into qualitative olfactory dysfunction are regarded to be significant in the counseling of patients with olfactory loss.
https://www.ncbi.nlm...pubmed/16308262
Euosmia: a rare form of parosmia.
The nature of qualitative olfactory disorders such as phantosmia and parosmia is a matter of debate. Parosmia and phantosmia mainly occur in combination with post-traumatic or post-infectious olfactory loss. Rare causes of these disorders such as brain tumors, side-effects of drugs, paraneoplastic syndromes, psychiatric disorders or intracerebral haemorrhage have been reported. Parosmias are distorted sensations of smell elicited by an odor, whereas phantosmias persist permanently or occur without the presence of an odor source. Phantosmias differ widely in terms of their nature. In contrast, parosmias always seem to be unpleasant. We report the case of a female with post-infectious hyposmia who reported a pleasant parosmia to selected odorants. We have called this rare clinical presentation euosmia.
https://www.ncbi.nlm...pubmed/12049557
Long-term follow-up of surgically treated phantosmia.
Surgical excision of olfactory epithelium is an effective and safe method to relieve phantosmia while potentially preserving olfactory ability. The abnormal histological features of the excised olfactory tissue suggest at least some pathological condition in the peripheral olfactory system. This nasal surgery requires intensive olfactory evaluation and follow-up. It is also extremely difficult with significant risks, and therefore should be limited to specialized centers.
https://www.ncbi.nlm...pubmed/10966179
Physiologically initiated and inhibited phantosmia: cyclic unirhinal, episodic, recurrent phantosmia revealed by brain fMRI.
1) Unirhinal phantosmia can be demonstrated by brain fMRI as can birhinal phantosmia; 2) unirhinal phantosmia can be initiated and inhibited by physiological maneuvers reflected by changes in fMRI brain activation; 3) fMRI brain activation of unirhinal phantosmia is bihemispheric and independent of peripheral side of phantosmia or patient handedness; 4) anterior frontal brain region plays a significant role in both phantosmia initiation and inhibition as, to some extent, do temporal brain regions; 5) activation of brain GABAergic systems appears to play a role in inhibition of unirhinal phantosmia; and 6) unirhinal phantosmia, similar to birhinal phantosmia, may reflect a type of maladaptive brain plasticity similar to that hypothesized to be responsible for phantom limb pain.
https://www.ncbi.nlm...pubmed/10667670
Taste and smell phantoms revealed by brain functional MRI (fMRI).
These results demonstrate that (a) phantom taste and smell can be revealed by fMRI brain activation, ( 
brain activation in response to taste and smell phantoms is localized in sensory-specific brain regions for taste and smell, respectively, © brain activation in response to memory of each phantom initiated the greatest degree of activation we had previously measured, and (d) treatment with thioridazine or haloperidol inhibited both the presence of each phantom and its associated fMRI brain activation. This is the first study in which phantom tastes and smells have been demonstrated by an objective technique and treatment that inhibited the phantoms was characterized by objective inhibition of fMRI activation. These two patients represent a relatively common group that may be classified as having primary phantageusia and phantosmia distinct from those with phantoms or auras secondary to neurological, migrainous, psychiatric, or other causes.
https://www.ncbi.nlm.../pubmed/1845270
Successful treatment of phantosmia with preservation of olfaction.
A 26-year-old woman had an 8-year history of phantosmia in her left nostril. The phantosmia could be eliminated by nostril occlusion or cocainization of the olfactory epithelium on the involved side. Because her symptoms and testing suggested a peripheral problem, a full-thickness "plug" of olfactory epithelium from under the cribriform plate (including all the fila olfactoria) was excised. At 5 weeks postoperatively, the phantosmia was completely gone, and her olfactory ability had returned to preoperative levels. Either the removal of abnormal peripheral olfactory neurons from the nose or the interruption of incoming signals to the olfactory bulb eliminated the phantosmia. This form of therapy for phantosmia offers an alternative to more radical procedures such as olfactory bulbectomy and may offer a significant sparing of olfactory ability.
https://www.ncbi.nlm...les/PMC3201003/
Re-establishment of olfactory and taste functions
Treatments -
Topical Steroids - Two open studies documented a significant improvement of olfactory performance after betamethasone drops [52] or flunisolide drops [53] administered by the so-called "head down forward technique" (see Figure 3 (Fig. 3)). However, Heilmann et al. did not find any significant improvement after administration of topical steroids [54].
Oral steroids are often effective in cases that do not respond to topical steroids. Their specific mechanism of action on olfactory performance remains unclear, but effects via glucocorticoid receptors in the olfactory mucosa [69], [70] or via regulation of adenosine triphosphate (ATP) activity in the olfactory mucosa [71] are being discussed. So far, no placebo-controlled, double-blind studies have been performed.
Most cases of phantosmia are related to nasal or respiratory infections. These usually respond well to antibiotic treatment.
Olfactory Cleft Surgery - In certain cases with pathological findings confined to the olfactory cleft, lateralization of the middle turbinate may be of benefit, although conclusive data are still missing.
Postviral Olfactory Disorders - Every acute infection of the upper respiratory tract may potentially lead to an olfactory disorder, but the exact pathogenesis remains unclear [104]. Elderly subjects and women are affected more often [17], [46], and parosmia as well as dysosmia are common [105], [106]. Akerlund et al. [107] observed an elevated olfactory threshold correlating with nasal congestion in 9 volunteers experimentally infected with coronavirus with subsequent development of a common cold. In 36 volunteers suffering from a common cold, reduced amplitudes of the initial components in olfactory potentials were seen in addition to elevated thresholds, even after use of the nasal decongestant oxymetazoline [108]. This finding indicates that olfactory impairment may, in part, be independent of nasal congestion, thus explaining the failure of oxymetazoline to improve olfaction [109].
Biopsies usually reveal a patchwork pattern, i.e., olfactory and respiratory epithelia alternate, and the number of olfactory receptor neurons is reduced. It remains controversial whether the extent of damage observed correlates with olfactory dysfunction [110], [111]. Dendrites of the olfactory receptor neurons often have cytoplasmic inclusions whose function is not yet understood [98].
Treatment of Postviral Olfactory Disorders
Treatment with alpha-lipoid acid seems promising. In an open, prospective study, patients [n=23, 19 hyposmic patients, 4 functionally anosmic patients, based on "Sniffin' Sticks" test results [29], [30], received alpha-lipoid acid (600 mg/day) for 4.5 months on average [114]. Six patients experienced mild improvement and 8 patients clear improvement of olfactory performance. However, the authors stated that confirmation of these findings warrants a double-blind study because spontaneous recovery and regeneration are common in postviral olfactory disorders and may occur up to 2 years after viral exposure [105].
Treatment of Parosmia / Phantosmia
Apart from various drugs, e.g., antiepileptics, antidepressants, and local anesthetics [115], surgical removal of the olfactory epithelium, reported for the first time in 1991 by Leopold et al. [116], may be of use. Long-term follow-up (for 5 years after surgery) revealed that 7 of 8 patients were completely free of complaints, with only 2 patients showing reduced olfactory performance [117]. Bulbectomy may also be of use in specific cases [118].
Toxic Olfactory Disorders
Many substances, such as metals (e.g., lead or cadmium), organic substances (e.g., solvents or formaldehyde), inorganic substances (e.g., chlorine, CO, ammonium chloride), and other substances (e.g., cement dust) may be olfactotoxic [144], [145], [146]. Although the olfactory epithelium is located away from the main airway, 10% to 15% of the inhaled air reaches the olfactory epithelium even without sniffing, thus causing exposure to potentially toxic substances [147]. Chronic exposure is more likely to induce lasting damage than acute exposure [148].
Treatment of Toxic Olfactory Disorders
No treatments with proven success exist, and larger studies documenting a clear relationship between exposure and olfactory loss are missing. Nevertheless, careful assessment of the work-place history is essential for all olfactory disorders.
Experimental Drugs and Other Treatments
Hormonal Therapy
Studies by Deems et al. showing that only a small percentage of postmenopausal women with olfactory disorders receive hormonal therapy triggered speculation about a protective effect of hormones [17]. The smaller bulb volume in men suffering from post-traumatic olfactory disorders, relative to that in women [121], as well as olfactory performance in schizophrenic women shown to differ in relation to their menopausal status was interpreted along the same lines [157]. In animal experiments, ovarectomized mice exposed to olfactotoxic substances recovered more quickly if they received hormonal replacement than did those not receiving any hormones [158]. However, a longitudinal study in 62 women failed to confirm these findings; the only finding was a correlation between loss of olfaction and age progression [159].
Dopamine
Although it is established that the neurotransmitter dopamine is present in the olfactory bulb, existence of D2 receptors in the olfactory epithelium has only recently been described [160]. Dopamine triggers neuronal differentiation and maturation in the epithelium in vitro, while on stimulation of the lamina propria, dopamine induces the liberation of substances that block neuronal differentiation [160]. Dopamine led to a significantly reduced rate of apoptosis in olfactory biopsies of schizophrenic patients but clearly accelerated apoptosis in the olfactory epithelium of control subjects [161]. In Parkinson's patients, Huisman et al. determined a doubling of dopaminergic cells in the olfactory bulb and interpreted this as a possible cause of the olfactory disorders seen in Parkinson's disease [162].
Acupuncture
Data confirming the benefit of acupuncture are missing. In an open study, auricular acupuncture improved olfactory threshold in 23 healthy volunteers [163]. In addition, a case report documented restored olfaction after acupuncture in a female patient who had been suffering from anosmia for 2 years [164].
Theophylline
Levy et al. [165] used theophylline (250 to 500 mg, given for 4 to 6 months) in 4 hyposmic patients (allergic rhinitis, n=3; post-traumatic hyposmia, n=1) and reported normal post-treatment olfaction in 2 patients, improved olfaction in 1 patient, and unchanged olfaction in the remaining patient. Functional MRI in 3 patients indicated enhanced central activation after treatment. No additional data are available.
Growth Factors (Transforming Growth Factor)
Olfactory receptor neurons are continuously replaced during the course of life, with the rate highest at younger age [9]. Because the rate of neurogenesis can be manipulated by external factors (e.g., doubling after ablation of one olfactory bulb [166], decrease after unilateral nostril occlusion [167]), acceleration by using growth hormones appears feasible. Intraperitoneal administration of transforming growth factor-alpha (TGA-alpha) resulted in enhanced cell proliferation not only in fetal but also in adult mice [168]. So far, no studies in humans have been performed.
Vitamin A
Vitamin A has been reported to normalize olfactory performance in malabsorption conditions or A-β-lipoproteinemia [169]. Moreover, Garrett-Laster et al. [170] reported a significant improvement of olfactory threshold for pyridine and taste threshold for bitter and salty substances in 37 patients with vitamin A deficiency due to alcoholic liver cirrhosis undergoing a 4-week therapy with oral vitamin A (10 mg/day). No additional data are available.
Zinc
Zinc sulfate (100 mg) did not have any significant effects in 106 patients participating in a double-blind study reported by Henkin et al. [171] (see also Quint et al. [134]). High doses of local intranasal zinc may even be olfactotoxic [172].
https://www.ncbi.nlm...les/PMC3450842/
Olfaction — Quantification and management
Neuroimaging: Presently, high resolution CT appears to be the most useful and cost-effective screening tool for the assessment of sinunasal tract inflammatory,disorders. The nasal cavity, paranasal sinuses, hard palate, anterior skull base, orbits and nasopharynx should be scanned and if central causes of olfactory dysfunction are suspected, the brain as well.
MRI is the modality of choice for evaluation of the olfactory bulbs, olfactory tracts and intracranial causes of olfactory dysfunction because they can be visualized rather clearly on the coronal slices. Moreover MRI is the procedure of choice for evaluation if skull base invasion by sinunasal tumors is suspected. Gadolinium enhancement is particularly valuable for leptomeningeal involvement at the skull base. Its utility isin distinguishing solid enhancing tumors from rimenhancing inflammatory processes
Fluid and Tissue analysis: A complete blood count isessential to rule out infective, nutritional or hemopoetic processes if involved in smell dysfunction. A nonspecific
indication of autoimmune or inflammatory processes can be obtained from erythrocyte sedimentation rate. Since vitamin B 1 deficiency is clearly implicated in Wernicke-
Korsakoff syndrome, determination of erythrocyte thiamine level is indicated in patients with a significant history of suspected or documented chronic alcohol abuse.
Mucosat biopsies: For documentation of cellular changes at neuroepithelium, biopsies are, on rare occasion, performed by an experienced surgeon. In such cases a small piece of olfactory mucosa is stripped along the nasal septum by an endoscopic approach (Lovell et al 1982, Lanza et al 1993). The surgeon should perform multiple biopsies to obtain a reasonable accurate assessment of epithelial changes, given the considerable metaplasia of respiratory like epithelium in the region of olfactory neuroepithelium.
http://archotol.jama...rticleid=620253
Successful Treatment of Phantosmia With Preservation of Olfaction
A 26-year-old woman had an 8-year history of phantosmia in her left nostril. The phantosmia could be eliminated by nostril occlusion or cocainization of the olfactory epithelium on the involved side. Because her symptoms and testing suggested a peripheral problem, a full-thickness "plug" of olfactory epithelium from under the cribriform plate (including all the fila olfactoria) was excised. At 5 weeks postoperatively, the phantosmia was completely gone, and her olfactory ability had returned to preoperative levels. Either the removal of abnormal peripheral olfactory neurons from the nose or the interruption of incoming signals to the olfactory bulb eliminated the phantosmia. This form of therapy for phantosmia offers an alternative to more radical procedures such as olfactory bulbectomy and may offer a significant sparing of olfactory ability.
http://www.academia...._Cell_Carcinoma
A Rare Cause of Phantosmia: Metastatic Small Cell Carcinoma
Olfactory hallucinations, known as phantosmias, are a poorly understood phenom-enon. It has been associated with a wide rage of differential diagnosis. However, most cases are idiopathic. The author’s presents a 70-year-old man with olfactory hallucinations as the predominant symptom of the brain metastatic small cell carcinoma in order to clarify the causal relationship. Little is known about the origin and clinical significance of phantosmias. It can even be the predominant symptom of an underlying small cell metastatic brain tumor as presented in our case. Therefore a detailed history of the symptoms along with a neurological and physical examination and routine laboratory and screening tests should be provided in order to exclude any organic causes.
http://microship.com...ation-syndrome/
Phantosmia and SSRI Discontinuation Syndrome A frustrating change of perception
My friend approached the problem with care, sticking to a schedule of tapering (Effexor) over four weeks, then at last took her final fraction of the prescribed dose. A nightmare immediately ensued, with intense anxiety, pain, and the classic “flu-like symptoms,” but she persevered and managed to keep her dosage level at zero. (It should be noted that some people take as much as 2 years to taper off this drug, so that may have been dangerously rapid.
Her acute discontinuation symptoms subsided after a few days… with one exception. Her sense of smell was broken.
In addition, she began to experience a disturbing phenomenon known as phantosmia, or the sensation of strong smells that don’t exist… usually smoke or “burning electrical cucumber.” At the same time, a prized fragrant rose smelled like cardboard.
Researching this, I began to find an unexpected connection… Effexor is often used to treat phantosmia. It is suspected that there is a link between mild depression and the detection of non-existent odors, a theory that has gained additional traction from the improvement of phantosmia after repeated transcranial stimulation used to treat depression. If this is indeed the case, we may be seeing a rebound effect similar to what happens when you stop taking a medication, with the original problem returning in stronger form. (When repeated, this is known as the kindling effect, where each withdrawal leads to an increasingly severe return of symptoms.)
GABA and Olfactory Attention
But why would our patient be experiencing this in the first place? What is the connection, if any, between the SNRI discontinuation and a mix of phantosmia and partial anosmia?
The conclusion of this paper is a provocative link that may be our culprit.
There has been research linking phantosmia with a depressed level of the inhibitory GABA in the CNS. In addition, there have been unrelated research
projects linking SSRI/SNRI discontinuation with disinhibition of the excitatory glutamatergic system. Discussion of this can get lost in double-negatives, but in essence, from the perspective of many parts of the brain, GABA is a brake and glutamine is an accelerator (a grotesque simplification, but instructive).
In one test, patients with phantosmia were seen to have reduced CNS GABA levels in the
cingulate, right and left insula, and left amygdala. This is particularly interesting, as a retrograde projection from the anterior cingulate cortex to the anterior olfactory nucleus appears to have a role in attention to olfaction… which reinforces our “automatic gain control”theory.
People often think of the antidepressant withdrawal syndrome as just being a matter of getting neurotransmitters back in balance, but it is more complex than that. The drugs damage an autonomic system, downregulating receptors (reducing their number), and thus removing some of the tools used to maintain
homeostasis. Discontinuation of the drug introduces CNS instability that manifests itself throughout the system… hence the extremely wide range of reported effects that include intense “brain zaps” and my own long-term crosstalk between lateral eye movement and somatosensory perception in the hands caused by a whiff of Remeron many years ago (6 half-doses, prescribed off-label for sleep). There is an enduring mythology that it is just
simple imbalance, but instead we are dealing with a dynamic self-correcting system… and there is ample evidence that this class of drugs causes actual damage from which recovery can be excruciatingly slow.
It would be interesting to do a test with GABAergic drugs (or receptor agonists) and attempt to recreate a phantosmia episode… that may confirm part of our theory, though not necessarily point to a useful solution.
The hopeful note in our patient’s case is that she reports a gradual improvement as the years pass. I believe she is being analytical about this and not just expressing adaptation to a static condition.
http://europepmc.org...ct/med/20022663
Improvement in smell and taste dysfunction after repetitive transcranial magnetic stimulation.
These results suggest that rTMS is a potential future therapeutic option to treat patients with the relatively common problems of persistent phantosmia and phantageusia with accompanying loss of taste and smell acuity. Additional systematic studies are necessary to confirm these results.
http://health.uconn....rticle_mann.pdf
Management of smell and taste problems
Drugs that can cause impaired smell or taste
Antidepressants and anticonvulsants
Amitriptyline, carbamazepine, clomipramine, clozapine, desipramine, doxepin, fluoxetine, imipramine, lithium, phenytoin, trifluoperazine
Antihistamines and cold medications
Chlorpheniramine, loratadine, pseudoephedrine, terfenadine
Antihypertensives and cardiac medications
Acetazolamide, adenosine, amiloride, benazepril and hydrochlorothiazide, betaxolol, captopril, clonidine, diltiazem, enalapril, ethacrynic acid, nifedipine, propranolol, spironolactone
Anti-inflammatories
Auranofin, colchicine, dexamethasone, diclofenac, dimethyl sulfoxide, gold, hydrocortisone, d-penicillamine,penicillamine
Antimicrobials
Ampicillin, ciprofloxacin, clarithromycin, ofloxacin, streptomycin, tetracyclines
Antineoplastics
Cisplatin, doxorubicin, methotrexate, vincristine
Bronchodilators and other asthma medications
Albuterol, cromolyn sodium, flunisolide, metaproterenol, terbutaline
Lipid-lowering drugs
Cholestyramine, clofibrate, fluvastatin, gemfibrozil, lovastatin, pravastatin
Muscle relaxants and drugs for parkinsonism
Baclofen, dantrolene, levodopa
Radiation therapy
Radiation of the head
Vasodilators
Dipyridamole, nitroglycerin patch
TREATMENT OF IMPAIRED SMELL
Drugs
Topical corticosteroids. In patients with anosmia due to edema from rhinosinusitis or
polyps, topical corticosteroids can bring striking improvement. Their lack of significant
adverse effects with long-term use is impressive compared with systemic corticosteroids.
Antibiotics, decongestants, antihistamines.
In patients with loss of smell due to bacterial infection, antibiotics (a penicillin or
cephalosporin), decongestants, and antihistamines are useful.Desensitization with the aid of an allergist is sometimes indicated if the smell problem isdue to allergic rhinitis.
Surgery
When conservative approaches are not sufficient, endoscopic nasal and sinus surgery can
produce dramatic changes.
Reassuring the patient
In patients with loss of smell following an upper respiratory tract viral infection, no
effective therapy is available. However, since olfactory cells may regenerate with time, from
months to years,20,21 patients can be told that their condition may eventually resolve.
Although not all patients can be helped, they deeply appreciate the attention andinvestigation given to them, because their previous visits to other physicians may have been frustrating.
https://www.utmb.edu...y-2003-1126.pdf
Olfactory Dysfunction and Disorders
Studies have shown that olfactory dysfunction affects at least 1 % of the population
under the age of 65 years, and well over 50% of the population older than 65 years.
https://www.aan.com/...e and Smell.pdf
TASTE AND SMELL DISORDERS IN CLINICAL NEUROLOGY
