Initiation of olfactory memory in patients after successful treatment of patients with congenital hyposmia – the role of neuroplasticity

Abstract

Congenital hyposmia is a genetic disorder associated with adenylyl cyclase deficiencies. These deficiencies cause smell loss (hyposmia) in these patients. These deficiencies are manifested by lower than normal levels of cAMP and cGMP in nasal mucus which cause olfactory receptor failure. Treatment with phosphodiesterase inhibitors (e.g., theophylline) increases nasal mucus cAMP and cGMP, corrects olfactory failure and initiates detection of olfactory sensory signals. While they can then detect odors they have difficulty in recognizing character of these odors since they have no past experience or memory of these odors. These signals were not previously integrated by limbic and other brain memory systems. However, over time patients learn to associate novel odors with specific objects and learn to recognize the appropriate character of various environmental olfactory stimuli. This usually begins with sweet odors since the largest receptor number in the olfactory epithelium deals with sweet detection. This is the first report of recovery of olfactory recognition with repair of congenital hyposmia. While the olfactory system is hard wired into brain in utero correction of receptor defects is only the first step in the complex process of regaining normal smell function. The second step is activation of central nervous system neuroplasticity by which olfactory recognition occurs. These results were confirmed by functional magnetic resonance imaging studies in which both detection and brain integration of olfactory stimuli were measured.