Introduction

The olfactory bulb is responsible for processing information about odors detected by cells in the nasal cavity. It differentiates during adulthood and its growth is dependent on stimulation or sensory input. Lack of stimulation causes cell death and a decrease in its size and volume.

Rhinosinusitis is the most frequent cause of anosmia. It causes inflammation of the nasal sinuses which allows access of odors to the olfactory cleft and, disturbs the function of the olfactory epithelium which house cells in the nasal cavity that detect smell. This consequently leads to a decrease in the size of the olfactory bulb due to lack of stimulation (no sense of smell). Rhinosinusitis is treated using glucocorticoids and in case of presence of nasal polyps surgery is also indicated.

The aim of this study was to assess whether olfactory bulb volume increases after short term treatment in patients with a diagnosis of rhinosinisitis with polyps. A previous study done on rodents revealed it takes approximately 40 days for the olfactory bulb to regain its size after normalization of olfactory stimulation. The study participants were grouped into two; patients and healthy controls. Healthy controls were aged between 20 to 54 years while patients were aged between 36 to 73 years.  Olfactory function tests were done on both nostrils in both groups at the beginning of the study and 3 months later on follow up. Sniffin sticks tests was used to determine threshold odor (T), odor discrimination (D) and identification (I). Olfactory bulb volume was also measured using MRI scanners.

Anosmia is slowly becoming a major public health issue owning to its increase in prevalence.  No therapy has been proven to help alleviate olfactory dysfunction especially if attributed to post upper respiratory tract infections and post traumatic injuries.

Research shows that exposure to odors can restore olfactory function. This is due to the ability of olfactory receptor neurons to regenerate. This study1 aimed to determine if patients with olfactory loss could improve their sensitivity to smell through smell training.

Study participants were grouped in two. One group was exposed to four types of odors twice daily for 12 weeks (training group) while the other group was not (non-training group). Patient olfactory variables in terms of odor threshold, odor discrimination, and odor identification (TDI scores) were measured before and after the study period using the Sniffin Sticks battery test.

The prevalence of olfactory loss is estimated to be approximately 15% though many cases still go undiagnosed. Upper respiratory tract infections (URTI) and traumatic injuries to the head and face are the most reported cases of olfactory loss. The negative impact of these conditions on the quality of life of those affected has lead to research on treatment options aimed at restoring olfactory function. Such include use of repeated exposure to odors1.

This study2 aimed at evaluating the effect of repeated exposure of odors on patients with anosmia resulting from post URTI and craniofacial injuries at a smell and taste clinic.

Sense of smell was determined using the Sniffin’ Stick battery test. This is quantitative test used to assess the sense of smell. Odor identification, discrimination and threshold (TDI) scores were calculated.

Olfactory training was done for 16 weeks where patients were exposed to flowery, fruity, aromatic and resinous odors. This was done twice daily (morning and evening) for 5 minutes with each rotation of exposure lasting 10 seconds at intervals of 10 seconds between each odor. Past published literature indicates extended periods of exposure (over 16 weeks) do not show any additional benefits or improvement in sense of smell1.

There is evidence of the effect of repeated odor exposure in restoring olfactory function. This is due to the ability of the receptor and granular cells of the olfactory bulb to regenerate. This also applies to the central olfactory nerves. Smell training has also been shown to gradually aid in the improvement of smell memory.

Forty-six participants had suffered olfactory loss through sinonasal causes, post-upper respiratory tract infections (URTI), post-traumatic injuries and idiopathic grouped into two. The first group was exposed to odors only while the second group was exposed to both odors and topical corticosteroids. Smell training was done twice a day using 4 different types of odors for a period of 8 months. Olfaction was assessed at baseline and during flows up sessions at the 4th and 8th month.

Results were quantified using TDI scores, i.e. threshold, discrimination and identification of smell. A change in a mean score of 6 and above points was considered a significant improvement in olfaction.

Olfaction can be defined as the sense of smell. Asnomia is a chronic olfactory disorder characterized by partial or complete loss of the sense of smell. The prevalence of chronic olfactory disorders has risen over the past few years with current estimates being at 19%. Infections are the major causes of olfactory loss though sinusitis, drugs/toxins, traumatic head injuries and congenital anomalies have also been identified as possible etiologies.

In this study, voxel-based morphometry (VBM) in magnetic resonance imaging (MRI) was used to check for changes on the gray matter of the brain in participants suffering from asnomia. Voxel-based morphometry allows measurement of such changes over the whole brain as opposed to marginal segmentation techniques which restricts measurement to a region of the brain.

Test results revealed significant atrophy of olfactory parts of the brain. These included:

  • The medial prefrontal cortex (MPC) which consists of the subcallosal gyrus (SCG), nucleus accumbens (NAc) and the dorsolateral prefrontal cortex (dlPFC) and the nucleus accumbens (NAc). These are responsible for food cravings, appetite and memory of tastes of food.
  • The occipital gyrus and the precuneus (Prec) responsible for smell memory and taste matching.
  • The cerebellum, superior occipital gyrus (SOG), piriform cortex (PC), anterior insular cortex (IC), orbital frontal cortex (OFC), supramarginal gyrus (SMG), hippocampus and the parahippocampal which are also involved in olfaction.