1. Abnormalities of smell
The ability to detect environment chemicals is a primary function of nose. A proper functioning
sense of smell allows a person to discriminate between thousands of largely organic, low molecular
mass , volatile compounds & provides information regarding 1) the safety of substance or
environment for example spoiled food, leaking gas 2)the aesthetic properities of every day objects
for example rose, dirty laundry.3) element of basic communication for example mother/infant
interaction.
The olfactory neuroepithelium exists within a small region of nasal cavity (approximately 2cm2) in
the upper recesses of nasal chambers lining the cribriform plate& sectors of the superior turbinate,
middle turbinate & septum. This specialised epithelium is situated behind approximately 1mm wide
olfactory cleft, making it difficult to observe even with modern endoscopic devices.
Four neural systems within the nose:
1. The main olfactory system(cranial nerve I mediates common odour sensation
,vanilla,rose chocolate)
2. The accessory olfactory system( vomeronasal system)
3. The trigeminal somatosensory system( CN V , mediates in the form of somatosensory
sensations, irritation, burning, cooling, tickling & touch).
4. Terminal nerve (CN O); may be vestige of an ancient nerve.
Olfactory pathways:
Olfactory area contains million of olfactory receptors cells. The mucosal surface of olfactory receptor
cell expanded into a ventricle with several cillia on it, this receive odorous substances.
Central process of olfactory cells grouped into olfactory nerves which pass through the cribriform
plate& synapse with mitral cell of the olfactory bulb.
Axon of mitral cells form olfactory tract synapse to prepiriform cortex &amydaloid nucleus where it
reaches consciousness.
Olfactory system is also associated with autonomic system at the hypothalamus level.
Olfactory disorder classification
Anosmia : absence of olfactory sensation.
Partial anosmia: an ability to perceive some but not all odours.
Hyposmia or microsmia: decrease sensation to odours.
Hyperosmia :increase sensivity to common odours.
Dysosmia (sometimes term cacosmia or parosmia) is distorted or perverted smell perception.

2. Phantosmia : is a dysosmic sensation perceived in the absence of an odours(olfactory hallucination).
Olfactory agnosia: inability to recognise an odour sensation.
Presbyosmia :a decline in sense of smell with age.
Osmophobia : dislike or fear of certain smells.
Olfactory dysfunction can be unilateral or bilateral.
Clinical evaluation of smell function
Proper assessment of a patient olfaction function requires 1) a detailed clinical history 2)
quantitative olfactory testing 3) a through physical examination emphasing head & neck with brain
& rhinosinus imaging.
Sudden loss –possible trauma, ischaemia, or psychiatric.
Gradual loss – nasosinal disease,inflammatory process.
Comorbidities that can smell disorder ; renal failure,liver failure, hypothyroidism, DM, dementia.
Physical examination; nasal cavity for polyps , sinusitis, congestion, deviation of septum. Presence of
mucopus above ET orifice suggest posterior ethmoidal cell or sphenoid sinus infection. However ,
mucopus below the ET orifice implies involvement of the ostiomatal complex.
A pale mucosa suggest allergy.
Exposure to environmental or industrial pollutants can result in metaplasia in addition to swelling,
inflammation , exudates, erosion, ulceration.
The neurological evaluation should focus on cranial nerve with particular attention to optic nerve
visual acuity & visual field( intracranial mass lesion > intracranial raised
pressure>papilloedema>optic atrophy).
Trigeminal nerve & facial nerve should be examined.
Quantitive olfactory testing
1. Smell identification test or UPSIT(university of Pennsylvania smell identification test);ranging
from three-items pocket smell test to 40-items. Test result are in terms of a percentile score of a
patient’s performance relative to age & sex-match controls. Olfactory function basis into one of
one to six categories: normosmia, mild microsmia, moderate microsmia,severe microsmia,
anosmia, & probable microsmia.
2. Olfactory event-related potentials(OREP) to assessing the integrity of the olfactory system.
Causes of smell disturbance
Loss of olfactory function can be subdivided into two classes

3. 1) Conductive impairments from obstruction of the nasal passages(chronic nasal
inflammation,polyposis)
2) Sensorneural impairment from damage to the olfactory neuroepithelum, central tract &
connection i.e. viruses, airborne,tumours,seizures, toxin.
3) In addition diffcult to classify, mixed type, these above two affected, receptor damage or
blockage.
Upper respiratory infection
Upper respiratory viruses such as those associated with the common cold & influenza are
considered the most common aetiology of parmanant olfactory loss in man. Others infectious
that have been reported include hepatitis, herpes simplex encephalitis, pneumonia, & variant of
Creutzfeldt-Jacob disease. HIV-infected patients are said to show an early impairment in odour
thresholds & later decline in odour identification.
Head trauma
Head trauma oftern results in smell loss, particularly where rapid acceleration/deceleration of
the brain occurs (i.e. coup/contracoup injury). Blunt injury in the occiput has been found to
produce greater olfactory loss than trauma to the front of the head.
1)Common mechanisms include disturption from shearing forces of the olfactory fila through the
cribriform plate.
2) direct contusion & ischaemia to the olfactory bulb & frontal & temporal poles.
Fracturing of cribriform plate is not prerequiste for smell loss.
MRI may reveal damage to the olfactory bulbs, tracts & area of of the temporal & frontal poles.
Nasal & sinus disease
Upper respiratory infection & head trauma can be classified as sensorineural, the dysfunction that
result from nasal & sinus disease is usually considered conductive- in orther words there is impaired
airflow to the olfactory receptors. Common examples being allergic rhinitis, rhinosinusitis, nasal
polyposis, intranasal tumours, previous nasal surgery.
There is a significant correlation between olfactory thresholds(smell impairment) & levels of
eosinophils in the blood & nasal secrection. Treatment in the form of surgery(excision of polyps) or
medication(local or systemic steroids) may improve the olfactory function. Systemic steroid more
effective.
Excessive dryness of the nasal mucosa as seen in atrophic rhinitis, Sjogren,s syndrome & repeated
nasal surgery can cause olfactory dysfunction, since a moist receptor environment aids
chemoreception & transduction.

4. Tumours & mass lesions
A number of tumours in & around the olfactory bulbs or tracts can cause olfactory disturbance,
example olfactory groove meningioma, frontal lobe gliomas, suprasellar ridge meningioma from the
dura of the cribriform plate
Also olfactory tumours may extend into frontal lobes resulting in symptoms of dementia & possibly
the release of primitive reflexes( for example grasping, snout, glabellar).
Lymphoma may also infiltrate in this area cause dysfunction. Similarly granulomatous such as
syphilis, sarcoidosis, SLE, wegener’s granulomatosis can often result in anosmia.
Neurodegerative diseases
Olfactory dysfunction may be the first clinical sign of Alzheimer’s disease or idiopathic parkinson’s
disease. Smell testing is useful in identifying person (alzheimer’s & idiopathic parkinson’s disease). In
parkinson’s disease, bilateral olfactory deficits occur before onset of the classical neurological
signs/symptoms. Given a male suspect of Parkinson’s disease who is less than 60, an UPSIT score of
31 carries a 91% sensitivity. In a woman suspected of Parkinson’s disease who is less than 60years
old, UPSET score of 33 carries a 79% sensitivity.
The olfactory loss associated with multiple sclerosis is directly proportional to the number of MS-related
demyelinating lesions in olfactory processing region (perorbital & inferior middle temporal
lobe.) Therefore, knowledge of a patient’s UPSIT score can be predictive of the plaque load in the
olfaction-related regions.
Schizophrenia is associated with significant deficits in odour identification & threshold sensitivity.
Epilepsy & migraine
Olfactory aura also describe as hallucination are rare. In epilepsy mesial temporal lobe structures
such as amygdale & hippocampus have been implicated as the generators of ictal olfactory
sensations that often evolve as generalized seizures.
Treatment of smell disorders
After diagnosis is confirmed using tools such as nasal endoscopy & CT scanning of the sinuses, next
appropriate course of action may include topical or systemic steroids.
Conductive & sensorineural olfactory losses are often distinguishable using a brief course of systemic
steroid, since patients with conductive impairment frequently responds to systemic steroid. Topical
steroid are often ineffectual in returning smell function because local steroid fail to reach the
affected region in the upper nasal passages. Increase efficacy occurs when nasal drops or spray are
administered in the head down position.
Proper allergy management is essential & may require use of antihistamine.
When a bacterial infection is suspected, a course of antibiotic should be used.

5. In rheumatological granulomatous disease is suspected such as Wegener’s granulomatosis or
sarcoidosis , immunomodulation using agents as cyclophosphomide or methrotrexate may be
necessary.
Sensorineural impairment of olfaction is typically more difficult & prognosis for the patients
suffering from upper respiratory infection or head trauma is poor.
Majority of patients who recover smell function subsequent to trauma do so within 12weeks of
head-injury.
When epilepsy or migraine is suspected , a course of antiepileptic or antimigigraine may be
beneficial.
In patient with Multiple sclerosis, immunomodulatory therapies, including interferon-beta &
occasional steroid is the main stay of treatment.
When depression or psychosis is suspected , a course of antidepressant may be necessary.
Best clinical practice
1.A clear distinction between a complaint of taste loss secondary to lack of flavour due to olfactory
loss & true taste loss(i.e. sweet, sour, bitter, salty sensation) must be ascertain.
2. Quantitative assessment of dysfunction is critical to determine validity of the patient’s
complaint,degree of dysfunction,establishing the treatment efficacy & determining prognosis.
3. Antibiotic should not be given unless indication of bacterial involvement, as some adverse
influence smell function.
4. Zinc , vitamin A & α-lipoic acid are not effective unless frank deficiencies are present.
5. A short course of systemic steroids can be given to determined whether conductive or
sensorineural.
6. Routine MRI rarely provide adequate visualization of the olfactory bulbs, tracts,( multiple cuts are
often needed to ascertain).
7. Decrease smell function can be a early sign of neurodegerative diseases (Alzheimer’s disease,
Parkinson’s disease, Multiple sclerosis).

6. In rheumatological granulomatous disease is suspected such as Wegener’s granulomatosis or
sarcoidosis , immunomodulation using agents as cyclophosphomide or methrotrexate may be
necessary.
Sensorineural impairment of olfaction is typically more difficult & prognosis for the patients
suffering from upper respiratory infection or head trauma is poor.
Majority of patients who recover smell function subsequent to trauma do so within 12weeks of
head-injury.
When epilepsy or migraine is suspected , a course of antiepileptic or antimigigraine may be
beneficial.
In patient with Multiple sclerosis, immunomodulatory therapies, including interferon-beta &
occasional steroid is the main stay of treatment.
When depression or psychosis is suspected , a course of antidepressant may be necessary.
Best clinical practice
1.A clear distinction between a complaint of taste loss secondary to lack of flavour due to olfactory
loss & true taste loss(i.e. sweet, sour, bitter, salty sensation) must be ascertain.
2. Quantitative assessment of dysfunction is critical to determine validity of the patient’s
complaint,degree of dysfunction,establishing the treatment efficacy & determining prognosis.
3. Antibiotic should not be given unless indication of bacterial involvement, as some adverse
influence smell function.
4. Zinc , vitamin A & α-lipoic acid are not effective unless frank deficiencies are present.
5. A short course of systemic steroids can be given to determined whether conductive or
sensorineural.
6. Routine MRI rarely provide adequate visualization of the olfactory bulbs, tracts,( multiple cuts are
often needed to ascertain).
7. Decrease smell function can be a early sign of neurodegerative diseases (Alzheimer’s disease,
Parkinson’s disease, Multiple sclerosis).