Table 1.

Types of olfactory dysfunction, pathology, and natural history

Type of olfactory dysfunction	Pathophysiology	Typical history
Sinonasal–e.g. chronic rhinosinusitis with polyps	Mechanical obstruction of the olfactory cleft, temporary interference with olfactory receptor binding due to inflammation, eventual neuroepithelial remodelling/CNS changes	Gradual onset fluctuates over time. Typically improves with adequate treatment (nasal/systemic steroids). Not commonly associated with parosmia. Most of these patients present to GP and are managed in the community or by otolaryngologists
Post-infectious olfactory dysfunction (PIOD)	Viral common pathogens include RSV, parvovirus and HIV Long-term inflammation causes neuroepithelial remodelling to respiratory type epithelium	Sudden onset often associated with parosmia, little fluctuation 1 in 3 recovery of psychosensory scores over 14 months. Viral common pathogens include common cold, influenza, and HIV [68]
Post-traumatic olfactory dysfunction (PTOD)	Severing of olfactory nerve filament or damage due to primary or secondary CNS injury	Sudden onset or delayed (may be related to noticing OD when back in normal environment) Fluctuation uncommon, phantosmia and parosmia are common Recovery, although less common than post-infectious, can be up to 30% depending on severity
Neurodegenerative causes–e.g. Alzheimer’s (AD) and Parkinson’s disease (PD)	Neurofibrile changes in the OB and higher olfactory network Lewy bodies deposit in the olfactory tract, OB, and anterior olfactory nucleus [69]	Insidious onset, unlikely to see improvement
Age-related	Loss of and replacement of olfactory neurons with respiratory epithelium. Decreased basal cell proliferation Decrease of interneurons in OB with reduced activity in olfactory cortex	Insidious onset, unlikely to see improvement. Impairment in 62% in people over 80. NSHAP study showed OD as a 5-year mortality predictor [49]
Other medication/toxin exposure/iatrogenic	Altered receptor function by binding G-protein coupling or affecting calcium or sodium channel activity	Sudden onset that is mostly alleviated by ceasing medication or exposure. Can persist in some cases requiring treatment. Can have medico-legal implications [70]