Anosmia is defined as the general inability to perceive olfaction and represents the most profound olfactory dysfunction (OD). OD can be due to different pathophysiological mechanisms; it can either be a primary dysfunction and developed embryologically (e.g., due to telencephalic maldevelopment or from peripheral lesions involving the olfactory fibers at the level of the cribriform plate) or it can be due to impairment of any of the intracranial relay stations. In the latter scenarios, it may involve any of the central pathways such as the olfactory bulb (OB) and olfactory tract (OT), as well as the orbitofrontal cortex, the frontal lobe, and the antero-inferior part of the temporal lobe, the piriform cortex, the periamygdaloid cortex, the amygdala proper as well as the entorhinal cortex and the entorhinal tubercle 1).
Anosmia is due to a number of factors, including an inflammation of the nasal mucosa, blockage of nasal passages or a destruction of one temporal lobe. Inflammation is due to chronic mucosa changes in the paranasal sinus lining and the middle and superior turbinates. Since anosmia causes inflammatory changes in the nasal passageways, it is treated by simply reducing the presence of inflammation.
It can be caused by chronic meningitis and neurosyphilis that would increase intracranial pressure over a long period of time, and in some cases by ciliopathy including ciliopathy due to primary ciliary dyskinesia (Kartagener syndrome, Afzelius' syndrome or Siewert's syndrome).
A related term, hyposmia, refers to a decreased ability to smell, while hyperosmia refers to an increased ability to smell. Some people may be anosmic for one particular odor. This is known as “specific anosmia”. The absence of the sense of smell from birth is called congenital anosmia.