Bernard Biacabe

OBJECTIVES: Olfactory cleft disease was defined as (1) an olfactory disability related with a clinical and/or radiologic abnormality of the olfactory cleft and (2) a pathologic process limited to or predominating in the olfactory cleft. The objectives of this study were to describe the clinical and radiologic findings of this entity and to report the effect of medical therapy on the sense of smell.STUDY DESIGN AND SETTING: Thirteen patients with the criteria of olfactory cleft disease were included in this retrospective study. All patients had bilateral olfactory cleft abnormalities. A complete ENT examination with endoscopic evaluation and a computed tomography scan were performed in all cases. An olfactory threshold test was available in 12 cases before and after medical therapy, which included oral and topically administered steroid therapy.RESULTS: Olfactory disability was the major symptom of olfactory cleft disease. Other symptoms of chronic rhinosinus dysfunction was present in 75% of cases. Three pathologic processes were identified in patients with olfactory cleft disease: malformative, inflammatory, and inflammatory associated with anatomical deformities of olfactory cleft boundaries. Medical therapy was effective in lowering olfactory thresholds in 25% of the cases.CONCLUSIONS AND SIGNIFICANCE: Olfactory cleft disease involves various pathophysiologic processes. Computed tomography scanning provides the most information for diagnosis. Indications of functional endoscopic surgery remain to be defined after failure of medical therapy.

Systematic administration of corticosteroids was attempted in the treatment of olfactory loss in 41 patients with post-upper respiratory infection and 21 patients with idiopathic anosmia. In our study, anosmia failed to respond to this treatment, as no patient noted any improvement of olfaction.

AN IMPORTANT PROBLEM: Occupational exposure to chemical products can have toxic effects on the olfactory system. An important number of patients have experienced olfactory disorders subsequent to the development of the chemical industry and atmospheric pollution. EPIDEMIOLOGY DATA: Straightforward data are difficult to collect because several cofactors other than the toxic product are involved. Two lists of toxic products can be made. The first list includes products for which scientific data is available and the second products for which data is lacking. Olfactory tests also differ between authors and countries. TWO TYPES OF TOXICITY: Acute, accidental toxicity is evidenced by the lesions caused by inhalation of high-doses of strongly toxic agents. Chronic intoxication caused by lower concentrations of these inhaled agents does not produce a trigeminal reflex leading to a modified respiratory rate reducing the airborne aggression. APPROXIMATIONS: Clinical data describing the olfactory toxicity of certain industrial and chemical compounds are very significant but often cannot prove a cause and effect relationship. Data obtained with experimental models in rodents are difficult to extrapolate to humans.

Olfactory disorders subsequent to head trauma can raise medicolegal problems when the olfactory deficit occurs after a work accident or a traffic accident and also raises the problem of psychological and functional tolerance when the patient consults late for a therapeutic solution. We studied the epidemiology of olfactory disorders after head trauma. Such disorders have been recognized since the XIX(th) century. Several studies have attempted to determine the prevalence of olfactory sequelae after head trauma. We then describe the pathophysiology of these lesions and emphasize that the degree of severity is related with the gravity of the head trauma and that the prevalence of these disorders varies considerably depending on the site of the trauma. Mechanisms which can lead to lesions of the olfactory system include, damage to the olfactory nerve bundles, naso-sinus lesions, or lesions of the cerebral olfactory centers. Brain MRI in anosmic patients after head trauma allows a visualization of intracranial lesions. The degree of reversibility of olfactory disorders after head trauma is imperfectly evaluated and discordant results have been reported. Some authors consider loss of olfaction is definitive. Others suggest an improvement in olfaction the year following head trauma. We reviewed the literature on these different elements. Expert opinions concerning patients complaining of olfactory disorders should relate this disorder to the initial trauma and determine the personal and occupational impact of the deficit. Attribution of cause must take into account all the clinical, radiological and psycho-olfactory factors.

Olfactory disorders in Alzheimer's disease and Parkinson's disease have been the topic of a large body of work over the last decades. Work devoted to olfactory disorders in Alzheimer's disease includes over 300 papers providing clinical and fundamental data. Anatomy studies in Alzheimer's disease have demonstrated a specific concentration of lesions in peripheral and central olfactory structures (senile plaques, neurofibrillary degeneration) as well as lesions in layers II and III of the entorhinal cortex. These neuropathological findings led to the development of the hypothesis that olfactory disorders in Alzheimer's disease would result from a toxic process. Observed olfactory deficits involve both identification and recognition of odors and detection thresholds. Nevertheless, patients with Alzheimer's disease rarely consult for sensorial deficits as the other signs of the disease predominate. Neuropathology data on the olfactory system are much more sparse in Parkinson's disease. Lewy bodies suggestive of Parkinson's disease have been observed in the olfactory bulb and pathways, but, unlike Alzheimer's disease, the olfactory disorders appear to be stable, changing little over time, as opposed to the evolution of neurological symptoms and cognition impairment. Clinicians should be aware that olfactory disorders are an integral part of Alzheimer's disease and Parkinson's disease. Screening for sensorial impairment however is a secondary objective in the context of these neurodegenerative diseases.

We report here a series of 118 patients (79% women) who developed dysomia after acute rhinitis. Mean age was 59 years. Mean follow-up after the initial rhinal episode was 36 months. The dominant olfactory disorder was anosmia (71% of the patients) and dysgeusia in 71%. The prognosis of anosmia was poor as it persisted in 50% of the patients. Six patients (5%) recovered normal olfaction after a delay of 11 months. Partial recovery was observed in 45% of the patients with a mean 14-month delay. Recovery of olfaction was thus observed within the first year. Parosmia was also frequent (59% of the patients). In two out of three cases, parosmia persisted. Improvement generally occurred during the first 18 months. These olfactory disorders have an impact on the patients' psychic equilibrim since a depressive syndrome was observed in 60% of the cases.

AGING EFFECT: The effect of aging on the olfactory system is generally observed in subjects over the age of 65 and is the number one cause of olfactory disorders. Several studies taking into account the state of the naso-sinus system and possible early stage of developing dementia have examined the precise effects of aging on olfaction. AGE-RELATED CHANGES: Aging affects olfactory thresholds, estimation of the intensity of an olfactory stimulation, and identification and memorization of odors. The elderly subject identifies food and other odors less easily than the young subject although elderly subjects can learn to improve their performance. Changes in the nasal cavity, particularly an alteration of the processes involved in neuron distribution in the olfactory neuroepithelium, may be involved. IMPACT OF OLFACTORY DEFICIENCY: There is much morphological and experimental evidence showing the effect of aging on both peripheral and central olfactory pathways allowing a better understanding of the functional impact of the sensorial deficit. Olfactory deficiency can explain in part the eating problems encountered in elderly patients.