Treatment of Olfactory Disorders

Surgical

The effect of surgery on quantitative olfactory disorders has already been mentioned above. Beside the routine surgery indicated in advanced and medication resistant nasal polyposis, ESS has also been proposed in very particular cases of qualitative olfactory disorders [221, 222]. Leopold was the first to describe the selective excision of the olfactory epithelium in patients suffering from very handicapping phantosmias. These cases, less than two dozen so far, have been carefully selected, and ESS in phantosmia is far from being routinely indicated. Interestingly, the histological analysis of these epithelia revealed numerous neuromas within the olfactory epithelium. Whether these neuromas are the substrate of the phantosmia is not clear. One report also treated parosmia with selective resection of the olfactory bulb [223] and a recent paper rediscovered the technique used by Leopold to treat parosmia [224]. These latter authors were unable to analyze the excised tissue and apparently ignored the existence of Leopold's work. This underlines the fact that this procedure should be reserved to experienced surgeons and is far from being a routine operation.

Conservative/Medication

Conservative Therapy of SND Related Olfactory Loss

Antibiotics: Putrid acute sinusitis is most frequently the result of infection by streptococcus pneumoniae, haemophilus influenzae, and moraxella catarrhalis which are relatively sensitive to antibiotic therapy. However, in the chronic form of putrid sinusitis, staphylococcus aureus and pseudomonas aeruginosa are much more important. Whenever possible, antibiotic therapy should only be started after the bacteria have been identified and tested for resistance to antibiotics. It is important to note that in chronic putrid sinusitis antibiotic treatment is not always successful.

Steroids: Among many other effects corticosteroids act as anti-inflammatory drugs, the anti-inflammatory effects being produced via a number of different pathways including inhibition of phospholipase A2 through induction of lipocortin [225]. They reduce submucosal edema and mucosal hypersecretion and thereby increase nasal patency. Systemically administered steroids are of help in many sinu-nasal disease (SND) patients [129, 226-228]. For example, Stevens reported that systemic administration of steroids was effective in 12 of 24 patients with SND-related olfactory loss [229]. In addition to the anti-inflammatory activity it has been postulated that corticosteroids directly improve olfactory function [230, 231] by modulating the function of ORN through effects on olfactory Na, K-ATPase [225]. In fact, also based on our own experience, systemic ste roids are often helpful even in patients without nasal obstruction due to polyps or obvious inflammatory changes (compare [229, 232]).

Steroids may be administered systemically or topically. With regard to idiopathic olfactory dysfunction, systemic administration is often applied for diagnostic purposes [233]. If systemic steroids improve olfactory function, treatment is typically continued with locally administered steroids. Although systemic steroids are usually more effective than locally administered steroids [230, 234], prescription of systemic steroids over an extended period of time is rarely warranted due to their side effects [150, 232]. While there are no exact recommendations, it is possible, however, to repeatedly administer short courses of systemic steroids with an interval of 6-12 months between courses.

A number of studies indicate the usefulness of topical steroids [153, 226, 228, 235]; however, the role of topical steroids in the treatment of SND related olfactory loss has been questioned [230, 233, 234, 236-239]. So far, no factors predicting a favorable response to topical steroids have been identified. It is not entirely clear why systemic steroids have a higher therapeutic efficacy compared to topical steroids [129, 234]. One reason may relate to the deposition of the spray in the nasal cavity. In fact, it has been shown that only a small amount of nasally applied drugs reaches the olfactory epithelium which is situated in an effectively protected area of the nasal cavity [240-242]. This situation can be slightly improved by the application of sprays in ''head-down-forward position'' [230, 239].

Other treatments: In addition to the use of steroids there are other therapeutic approaches to restoration of olfactory loss. They include the use of anti-leukotrienes [243], saline lavages [244], or approaches which have received less vigorous scientific investigation, e.g., dietary changes [245], acupuncture [246], anti-allergy immunotherapy [247] and herbal treatments.

Conservative Therapy of Post-URTI/Posttraumatic Olfactory Loss

Post-URTI smell dysfunction seems to be due to an impairment of ORN, both in function and in numbers [248, 249]. While numerous treatments have been tried in post-URTI anosmia (e.g., zinc, vitamin A; see below), no pharmacological therapy has been established so far (see [250-252]). The situation is similar for posttraumatic olfactory loss where therapeutic options are lacking. The absence of conservative treatment for certain forms of olfactory dysfunction is underlined by the fact that, when ''parosmia'' is present [253, 254], in some patients surgical removal of the olfactory epithelium may be considered as a cure [255].

Having said this, there are still numerous candidates for the pharmacological treatment of olfactory dysfunction, one being alpha-lipoic acid (aLA) which is used in the treatment of diabetic neuropathy [256]. The ef fect of aLA is well described both in experimental animals and in humans (for review see [257]). It is known to stimulate the expression of nerve growth factor, substance P, and neuropeptide Y [258-260]. It enhances motor nerve conduction velocity as well as microcirculation [261, 262]. Further, due to its potent anti-oxidative effects, aLA also has neuropro-tective capabilities indicating that aLA is suited to treat neural damage involving free radicals [263]. Preliminary work has already indicated that it may be useful in post-URTI olfactory loss when administered at a dose of 600 mg/d over a period of 4-7 months [136]. Other encouraging pilot studies have been performed with the NMDA-antagonist caroverine [135] administered at a dose of 120 mg/d for 4 weeks. Potential mechanisms for the hypothesized effect included reduced feedback inhibition in the olfactory bulb as a consequence of NMDA-antagonistic actions, or antagonism of an excitotoxic action of glutamate.

Although frequently mentioned as a therapeutic option, studies on zinc treatment for olfactory dysfunction have produced negative results [135, 250] (see also [264]). It may, however, be of therapeutic value in patients with severe zinc deficiency, e.g., in hemodialysis. In studies in postmenopausal women estrogens have been reported to provide a certain protection against olfactory disturbances [130]. However, as mentioned above, recent studies [138] indicate that estrogens are probably ineffective in the treatment of olfactory loss. Finally, although discussed frequently, the potential therapeutic use of orally administered vitamin A [251, 265] is questionable unless appropriate double-blinded studies become available.

A different approach to the treatment of olfactory disorders is the detection and treatment of underlying causes. This approach may also involve the replacement of drugs suspected of affecting the sense of smell [172, 266, 267]. Other possible treatments may include, for example, acupuncture [246].

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