* Conductive defects
o Inflammatory processes cause a large portion of olfactory defects. These may include rhinitis of various types, including allergic, acute, or toxic (eg, cocaine use). Chronic sinus disease causes progressive mucosal disease and often leads to decreased olfactory function despite aggressive allergic, medical, and surgical intervention.
o Masses may block the nasal cavity, preventing the flow of odorants to the olfactory epithelium. These include nasal polyps (most common), inverting papilloma, and any malignancy.
o Developmental abnormalities (eg, encephaloceles, dermoid cysts) also may cause obstruction.
o Patients with laryngectomies or tracheotomies experience hyposmia because of a reduced or absent nasal airflow. Children with tracheotomies who are cannulated very young and for a long period may have a continued problem with olfaction even after decannulation because of a lack of early stimulation of the olfactory system.
* Central/sensorineural defects
o Infectious and Inflammatory processes contribute to central defects in olfaction and in transmission. These include viral infections (which may damage the neuroepithelium), sarcoidosis (affecting neural structures), Wegener granulomatosis, and multiple sclerosis.
o Congenital causes may be associated with neural losses. Kallman syndrome includes anosmia due to failed olfactory structure ontogenesis and hypogonadotropic hypogonadism. One study found the VNO to be absent in patients with Kallman syndrome.
o Endocrine disturbances (eg, hypothyroidism, hypoadrenalism, diabetes mellitus) affect olfactory function.
o Head trauma, brain surgery, or subarachnoid hemorrhage may stretch, damage, or transect the delicate fila olfactoria and result in anosmia.
o Toxicity of systemic or inhaled drugs (eg, aminoglycosides, formaldehyde) can contribute to olfactory dysfunction. Many other medications and compounds may alter smell sensitivity, including alcohol, nicotine, organic solvents, and direct application of zinc salts.
o Nutritional deficiencies (eg, vitamin A, thiamine, zinc) have been found to affect olfaction.
o The number of fibers in the olfactory bulb decreases at an approximate rate of 1% per year throughout one's lifetime. These olfactory bulb losses may be secondary to sensory cell loss in the olfactory mucosa and a general decline in the CNS cognitive processing functions.
o Degenerative processes of the central nervous system (eg, Parkinson disease, Alzheimer disease, normal aging) have been found to cause hyposmia. In the case of Alzheimer disease, olfactory loss can be the first symptom of the disease process. The sense of smell, more than taste, is impaired with aging, with a noticeable average decline in function during the seventh decade of life.
http://www.anosmia.net/
http://www.emedicine.com/ent/topic333.htm
