Anosmia and parosmia

Transcription

How to Treat
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INSIDE
Anatomy and
genetics
Pathophysiology
Assessment
Treatment
Prognosis
The future
the authors
Associate Professor
Richard Harvey
program head and conjoint
associate professor, rhinology and
skull base surgery, University of
NSW and St Vincent’s Hospitals;
clinical associate professor,
Macquarie University, North Ryde,
NSW.
Dr Pascal Bou-Haider
neuroradiologist, St Vincent’s
Hospital, Darlinghurst, NSW.
Anosmia and parosmia
Introduction
SMELL, or chemosensation, is a
major function of the nose. Although
humans are less reliant on olfaction
compared with other mammals it
remains a significant evolutionary
contribution to our physiology.1
Smell has many functions including the basic surveillance of our environment through both our olfactory
and trigeminal nerve systems. The
sense of smell plays an intimate
role in influencing mood, cognition
and behaviour. These behavioural
changes modify pleasure, sexuality
and even nutrition. Recent evidence
suggests that olfaction has a broader
role in mother–infant bonding,
pheromone detection, recognition
of kin and mates and longevity.2-6
Olfactory dysfunction can be categorised by the subjective experience. This may be a difficulty with
odour identification (dysosmia, which
encompasses hyposmia and anosmia),
sensation of an odour different from
the typical odour for that substance
(parosmia); and perception of an
odour where none is present (phantosmia). From a diagnostic perspective, olfactory dysfunction is more
commonly classified as conductive
(odorant delivery) or receptive (chemosensation).
The common risk factors are
age, male sex, viral infections, head
trauma, metal ion exposure and pes-
ticide exposure.7 Exposure to certain
occupational hazards, such as paint
solvents and hydrogen sulfide, have
been well characterised in patients
with olfactory disturbances.8,9 Perhaps the best-characterised study,
that of 2491 subjects from Wisconsin, showed that current smoking,
stroke, epilepsy and sinonasal disease
were associated with decreased olfaction.10
Our understanding of the mechanisms of smell has greatly evolved in
the past 25 years. However, there are
many unanswered questions about
how the human brain is able to interpret odorant complexity — from the
smell of grass after rain, baking of
food, to smoke from a barbecue. Even
less well understood is the subsequent
invoked emotional response from this
primitive sense. Over the past three
decades, an enormous contribution
has been made by pioneers such as
Richard Axel at Columbia University
and Linda Buck at the Fred Hutchinson Cancer Research Center in Seattle,
who shared the 2004 Nobel Prize in
Physiology or Medicine “for their discoveries of odorant receptors and the
organisation of the olfactory system”.
Their discoveries provide a detailed
picture of how odorants are detected
by sensory neurons in the olfactory
epithelium of the nose.
cont’d next page
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18 October 2013 | Australian Doctor |
27
How To Treat – Anosmia and parosmia
Anatomy and genetics
The olfactory apparatus
THE human body contains 10-20
million olfactory neurons. These
bipolar cells lie in a vast region
of mucosa almost 22cm2 in area
within the sinonasal cavity. Their
distribution is much greater than
previously thought with extension beyond the olfactory cleft
to include both the septum and
middle turbinate. These bipolar
cells have a single dendrite with
a thickened ending (the olfactory
knob) extending to the mucosal
surface where olfactory receptors
have access to the mucus (figure
1). When odorants are delivered to
this area they combine with odorant-binding proteins that facilitate
movement through mucus and
then subsequent rapid clearing
after recognition. Thus mucus rheology plays an important part of
odour detection. Odorants gain
access to the olfactory epithelium
via two important mechanisms.
The sniff produces turbulent air
flow that distributes odorants
away from the usual direct pathway to the posterior choana and
throughout the nasal cavity. This
is orthonasal smell. The retronasal delivery occurs when we
chew and is the main component
of the perception of flavour, which
is 70% smell and 30% taste.
Supporting cells in the olfactory
epithelium, including pluri-potential basal cells, are thought to
provide neuromodulation as well
as regenerative power to the olfactory neurons. The axonal arm of
Figure 1:
Structure
of olfactory
apparatus,
showing
odorants in the
mucus layer
transmitted
through
receptor
cells in the
supporting
cells layer to
the olfactory
bulb.
Neuron
Olfactory
bulb
Axonal arms
of olfactory
neuronal cells
Genetics
Receptor cell
Odorants
the olfactory neuronal cells transmits signals to the brain. These
axons group together to form
nasal to the cranial cavity (figure
2). From here, the axons synapse
in the olfactory bulb, which projects neurons along the olfactory
tracts to distribute the cortical
centres. The ‘primary olfactory
region’ (piriform cortex, olfactory
nucleus and tubercle, amygdala,
entorhinal cortex) and secondary
olfactory areas (hippocampus,
hypothalamus, thalamus, orbitofrontal cortex and the cerebellum)
have many links in the limbic and
primitive cortical areas and may
account for the role of olfaction in
mood, emotion, pleasure, sexual
behaviour and memory.
16-20 olfactory fascicles (olfactory fila) that perforate the cribriform plate of the ethmoid bone.
The cribriform plate is known for
its appearance because of these
fascicles transgressing from the
The aetiology of such a wide
variability of reception is a fundamentally unanswered question
of olfactory biology. Humans
have an enormous part of their
genome dedicated to the olfactory genes with almost 900 genes
identified (half non-functional).
These genes represent 3% of the
estimated 30,000 genes in the
human genome and are underutilised compared with other mammals, such as the mouse that has
three times the amount of activated olfactory genes.11 However,
only one olfactory receptor gene
is expressed in each neuron. The
neurons come together in multiple
cross-linking connections within
the bulb and cortex to produce the
enormously diverse olfactory map
that represents the smells that we
can distinguish.
Figure 2: Olfactory area
and cribriform plate. A:
The superior view of the
cribriform plate and olfactory
groove in the floor of the
anterior cranial fossa. This
site is prone to fracture
extension as a result of
the thin bone. B and C: The
endoscopic view of the
cribriform plate and olfactory
cleft. The position is posterior
to the middle turbinate.
Pathophysiology
OLFACTORY disturbance is usually clinically categorised into
conductive (odorant delivery) and
receptive (chemosensation) to associate better the presenting complaint
with the appropriate investigation
and treatment. Common conductive and receptive aetiologies are
listed in table 1. Some associations
are from low levels of evidence but
many have large epidemiological
studies and biological plausibility to
support the association.
Age is a common cause of olfactory decline.10,12 Up to 25% of all
patients older than 55 have evidence
of olfactory changes and 62.5%
of octogenarians have objective
impairment, although a lesser proportion will complain of it.13 Additionally, urban living, male sex,
smoking, stroke, and epilepsy are
more commonly associated with
earlier olfactory decline.14 It is unusual, however, for patients younger
than 60 to have environmental or
age-related decline.
28
| Australian Doctor | 18 October 2013
Sinonasal disease, primarily
rhinitis and rhinosinusitis, are
common causes of olfactory loss.
There is a component of conductive disturbance (ie, affecting
the delivery of an odorant) with
oedema and sometimes frank
nasal polyps. However, it is well
recognised that the inflammation
associated with these conditions
also produces an abnormality of
the olfactory neurons and chemosensation.
Olfactory decline has been
associated with several neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s
disease, which is believed to be a
result of disordered central or cortical olfactory processing. While it
is possible that olfactory decline
may precede the more severe
manifestations of these diseases,
its role as a predictor or marker of
disease onset has not been clearly
established.7
cont’d page 30
Table 1: Common causes of olfactory disturbance
Conductive (odorant delivery)
Receptive (chemosensation)
Mucosal oedema (figure 3)
Postviral
Chronic rhinosinusitis with nasal polyps (figure 4)
Neurodegenerative disease (figure 6)
Sinonasal tumours (figure 5)
Age-related decline
Local infective conditions (odontogenic sinusitis)
producing cacosmia
Smoking
Sjogren’s disease
Occupational exposure (benzene, menthol, sulfur dioxide, carbon
disulfide, heavy metals, and dust)
Trauma (cribriform fractures)
Tumours of the olfactory apparatus (figure 8)
Liver disease and alcohol abuse
Renal disease
Menopause, menstrual cycle, pregnancy
Drugs (cancer chemotherapy, antibiotics (aminoglycosides,
macrolides, tetracycline), anti-thyroid medication, opiates,
sympathomimetics, antacids, and L-dopa)
Vitamin A, B and thiamine deficiency
Diabetes
from page 28
Figure 3: A: The
endoscopic appearance
of the right olfactory cleft
in a patient with wellcontrolled inflammatory
sinus disease, but with
oedema and polypoid
changes to the olfactory
cleft mucosa (arrow).
B: This area (*) lies
between the septum and
middle turbinate and
can be challenging to
examine.
Figure 5: Olfactory
neuroblastoma is a
classic tumour that
presents with smell loss
(A) seen here between
the left middle turbinate
(*) and septum (#). The
MRI demonstrates the
left olfactory cleft mass
and relationship to the
olfactory bulbs, which
appear normal in this
study (B).
Figure 4: Endoscopic
view of chronic
rhinosinusitis with nasal
polyps on the right (A)
and left (B). The polyps
(*) are clearly different
from normal mucosa
of the septum (#) or
turbinate.
Figure 6: Degenerative
brain disease can
account for central
olfactory loss. The
subcortical high signal
changes (arrow) seen
in Alzheimer’s disease
is one example of
central pathology that
is investigated with this
axial MRI scan.
Assessment
History
IDENTIFYING patients who progress to hyposmia or anosmia outside of normal olfactory decline is
the main focus of clinical history
and examination. The majority
(75% of patients) will complain of
both loss of smell and diminished
flavour of food. This is due to the
loss of both orthonasal and retronasal mechanisms of odorant delivery
to the olfactory apparatus. It is less
common to have orthonasal-only
olfactory dysfunction, where the
flavour of foods is intact but smell
is reduced. This occurs in 24% of
patients. Only 1% of patients have
retronasal loss, where there is loss
of flavour but retention of smell via
sniffing.15 Both of these groups that
only have either orthonasal or retronasal loss should be investigated
early for local sinonasal pathology.
Urban living and a history of
smoking, stroke and epilepsy
are all potential risk factors that
should all be sought on history.
There is also an increased risk with
age and being male.
Early symptoms and signs of
Parkinson’s disease, Alzheimer’s,
other dementias and diabetesassociated polyneuropathy should
be sought. Another clue may be
recent changes to the patient’s
drug regimen.
While the presence of sinonasal
symptoms of nasal obstruction,
discharge and pressure is important, it is the loss of smell during
exacerbations of these symptoms
and the concomitant improvement
with treatment that is most telling.
A response to treatment may highlight the pathophysiology of the
olfactory loss.
Anterior rhinoscopy and
endoscopy
Figure 7: Smell
identification
testing is the
simplest form
of objective
assessment.
The Smell
Identification Test
is a collection of
40 ‘scratch and
sniff’ panels that
is easy to selfadminister.
oxymetazoline will greatly assist
the examination.
Objective smell tests
Smell tests are divided into
odour identification tests, odour
threshold assessment and odour
discrimination tests. The most
commonly used is the odour identification test, which assesses how
well patients can identify specific
odours. We use the Smell Identification Test, which is a commercial version of the University of
Pennsylvania Smell Identification
Test, a 40-item scratch-and-sniff
smell test that has been validated
in cross-cultural populations with
age and sex norms provided. It
has a high test–retest reliability,
is easy to administer and is inexpensive (figure 7).16 Many other
smell tests have been developed
over the past three decades but
the Smell Identification Test and
the ‘Sniffin’ Sticks’ tests are the
most widely accepted.17 The ‘Sniffin’ Sticks’ tests are a group of 12
pens with a volatile odour that is
released from the nib when the
Figure 8:
Olfactory groove
meningioma
(arrow) is an
example of
‘peripheral’
olfactory loss due
to involvement of
the olfactory bulbs
and tracts seen on
this coronal MRI
scan.
Simple assessment of the nose is
critical, even when performed with
the simple otoscope. The presence
of polyps (figure 4) or an intranasal mass (figure 5) are easy diagnoses to exclude. Subtle mucosal
oedema (figure 3) will require a
formal endoscopy. Spraying the
nose with a decongestant such as
30
cap is removed. They are widely
used in Europe but have also been
validated in the Australian population.12,18 Both tests force the user
to choose a response. There are no
options to leave responses blank
or empty and thus these tests have
mechanisms to detect malingering
when intentional avoidance or the
correct response occurs.
Radiological assessment
If there is clinical suspicion of
sinonasal disease, then a non-contrast CT scan may be warranted.
CT imaging is performed merely
to define mucosal inflammatory
changes and adding IV contrast
does not enhance diagnostic ability. CT should be considered when
defining the extent of mucosal
changes, confirming the diagnosis
of chronic rhinosinusitis when in
doubt and when surgery is being
considered.
However, in all other circumstances, MRI is the mainstay
of imaging. MRI has greatly
improved the value of medical
imaging in olfactory disorders by
allowing precise depiction of the
olfactory bulb, olfactory tract and
even very early damage to the CNS.
It excludes intracranial pathology
of the olfactory apparatus (figure
8) and highlights subtle changes
not seen on endoscopy (figure 9).
It may also detect grey and white
matter features of neurodegenerative disease that may account for
‘cortical’ olfactory loss (figure 6).
The normal volume of the
olfactory bulb depends on age
and is 40-60mm3 when measured
on high-resolution MRI.19,20 In
cases of congenital anosmia, MRI
examination usually demonstrates
severely hypoplastic or absent
olfactory bulbs along with flattening or even absence of the olfaccont’d page 32
Figure 9. Subtle
inflammatory
changes within
the olfactory
cleft bilaterally
on patient with
previously treated
inflammatory
airway disease.
Residual smell
loss was the
only outstanding
symptom after
initial treatment.
from page 30
tory sulci (figure 10). Trauma is
a leading cause of olfactory dysfunction. In cases where the usual
work-up fails to reveal gross cerebral damage or fractures, reduced
olfactory bulb volume may be
the only sign. This is likely to be
due to a tearing or shearing of
the olfactory fila on their way
through the cribriform plate of
the ethmoid bone.
Finally, the assessment of the
state of the olfactory bulb has prognostic implications. The size of the
Figure 10: Olfactory
bulb and tract
agenesis (A) and
atrophy (B) are
important findings to
identify that allow for
accurate diagnosis of
anosmia or prognosis
for olfactory return.
Compare with
anatomy in figure 5.
olfactory bulb closely correlates
to function, and its measurements
have demonstrated high diagnostic
and even prognostic value in the
evaluation of olfactory disturbances
(figure 10).19,21,22 Smell loss can be
an early sign of a neurodegenerative disorders such as Alzheimer’s
(figure 6). In patients who have Alzheimer’s disease, a correlation has
been demonstrated between olfactory bulb volume and the severity
of cognitive decline as evaluated by
the Mini-Mental State Examination score.23
Treatment
AN enormous variety of therapies
have been trialled for the loss of
smell, including steroids, zinc, theophylline, lipoic acid, caroverine,
strychnine, vitamin B and various
topical agents. When an obvious
cause exists, then this should be
addressed. However, when no obvious cause exists (ie, idiopathic), or
the loss of smell is suspected to be
postviral, from environmental exposure, post trauma or from minor
rhinitis or rhinosinusitis, it is still
possible to be systematic and sensible in the approach. General advice
to patients should always include a
caution on their reduced ability to
identify spoiled food, smoke and
gas.
Steroid therapy
Initial therapy should include systemic corticosteroids.24 Intranasal
steroid sprays are not effective in
olfactory loss in chronic rhinosinusitis patients and are not delivered
effectively to the olfactory epithelium.25,26 A three-week course of systemic corticosteroid (prednisone) is
used with a weaning regime starting
at a dose of 25mg for seven days,
then 12.5mg for seven days, then
5mg for seven days, based on a 70kg
male. This dosing regime is practical,
represents the equivalent potency
dose from studies performed using
betamethasone and is recommended
for 14-21 days as this best equates
to the lifespan of a tissue eosinophil.15,27 A cumulative dose of less
than 300-1000mg is recommended,
with a maximum of 30-40mg daily,
as this is the range in which significant complications and medicolegal
complaints occurred.28 Twenty-five
percent of patients will improve on
systemic steroids during the treatment period. A further 12% will
improve on 12 weeks of direct topical steroid (with drops as opposed to
simple sprays) delivered in a ‘supine
head-back’ or ‘head to floor’ position. The remaining 63% will not
recover and will need further assessment and consideration for alternative treatments discussed below (see
figure 11).
Topical delivery is less effective in cases of loss of smell due to
trauma and chronic rhinosinusitis.15
Fluticasone 400µg nasule drops are
available in Australia and come in
28-capsule packets for this purpose.
Other forms of local steroid delivery
are creams, irrigations or injections
prescribed off-label. It is important
to emphasise that only oral corticosteroid is effective and the addition of
simple nasal sprays (as opposed to
nasal drops) does not offer any further benefit.29 However, direct appli-
32
Figure 11: Management algorithm for
anosmia and parosmia.
Step 1
Screen for metabolic disorders, EUC, LFT, zinc, vitamin B (serum
pyridoxal phosphate), vitamin A (serum retinol), HbA1c, BSL
CT if sinonasal disease
Prednisone (three weeks)
Minocycline 100mg/d (three weeks for acute losses)
Vitamin A, B and zinc replacement
Step 2
Hormonal/inflammatory screen – TFT, FSH, LH, beta hCG, FBC,
ESR, CRP, ANCA, rheumatoid factor, anti-dsDNA, anti-SSA/SSB
MRI
Topical budesonide/fluticasone
(12 weeks)
Step 3
Novel topical agents
Olfactory stimulants (theoyphylline)
neurodegenerative conditions. The
neuroprotective potential of this drug
has been suggested by several studies
on various neurological disorders,
including neurodegenerative conditions, cerebral ischemia, trauma and
the degeneration of retinal cells.30-34
We currently recommend that newonset olfactory loss patients use
minocycline 100mg a day for three
weeks during their corticosteroid
therapy although we acknowledge
that its benefit is theoretical rather
than clinically proven. There is evidence that its use in all patients with
olfactory loss is not warranted.35
However, like sensorineural hearing
loss or Bell’s facial palsy, the potential to reverse the decline early in
the process outweighs the risk of the
medication in most cases.
Vitamins and trace elements
Olfactory training is a
valid tool to stimulate
patients who are keen
on being involved in
their recovery when
there is no steroid
response in the initial
treatment.
cation with nasal drops will benefit a
further 12%.15
Neuroprotection
The basis of neuronal decline is
thought to be increased apoptosis in
a system that has been exposed to a
significant insult or ongoing inflammation ensuring apoptosis occurs
faster than regeneration from the
basal cells.
Minocycline exerts a neuroprotective effect by reducing apoptosis
in neurons and may be used to treat
olfactory disturbance associated with
A trial of vitamins and zinc has a
low risk for causing harm and may
be considered. Vitamin A has been
shown to improve olfaction and
there are plausible mechanisms for
its effects as it is involved in olfaction.36,37 However, a randomised
controlled trial on olfactory loss
due to many varied causes did not
show a benefit.38 When trauma and
chronic rhinosinusitis are not present, the use of vitamin A 10,000
IU daily (maximum dose during
pregnancy is 2500 IU/day) may be
considered for three weeks. Vitamin B and pyridoxal phosphatedependent enzymes play a role in
the biosynthesis of five important
neurotransmitters: serotonin, dopamine, adrenaline, noradrenaline
and gamma-aminobutyric acid
(GABA). Vitamin B therapy in
olfactory loss showed a benefit in
a multi-arm randomised controlled
trial.39 A vitamin A, B and zinc supplement would need to be taken
at the rate of four tablets a day in
order to reach investigated doses.
Olfactory training
Olfactory training is a valid tool
to stimulate patients who are keen
on being involved in their recovery
when there is no steroid response
in the initial treatment. Patients can
purchase four intense odours in the
form of essential oils: phenylethyl
alcohol (rose), eucalyptol (eucalyptus), citronella (lemon), and eugenol
(cloves). A twice-daily exposure has
been shown to improve objective
olfactory testing in patients compared with controls over a 12-week
period.40
Methylxanthines
Finally, when there is no steroid
response, topical therapy has failed,
secondary causes excluded and
patient is between three months
and 12 months post olfactory loss,
methylxanthines in the form of oral
theophylline have both laboratory
and clinical data to support use as a
stimulant of hyposmia.41,42
Anti-epileptics
When phantosmia or dysosmia
persist in the absence of other aetiologies, they are treated as inappropriate local neural activity, as seen
in epilepsy, and medications such as
gabapentin may be useful.
Surgery
Surgery is beneficial when chronic
rhinosinusitis is present.43 Removal
of polyps and other factors that
influence the conduction of odorants
is likely to account for the benefit
seen with sinus surgery.44 However,
control of the inflammatory process in chronic rhinosinusitis is the
goal and poorly controlled mucosal
inflammation on endoscopy is highly
correlated with poor olfaction postsurgery.45,46
Prognosis
SPONTANEOUS recovery occurs
in a large proportion of patients —
20-35% of patients have improvement in the first 12 months.12,35,47
Recovery is best in postviral cases,
females, non-smokers and parosmia. Low anosmic scores on smell
identification correspond to a
lower chance for complete recovery but do not take into account
the rate of improvement. Duration of olfactory loss is negatively
correlated with recovery.48 Traumatic causes are most likely to
lead to complete and permanent
anosmia.
Recovery of some olfactory function within one year of traumatic
or postviral loss is a positive prog-
The future
VERY active research is ongoing
in the area of olfactory disturbance, with much of it funded by
the flavour and fragrance industry.
Commercial interests exist not just
in food and perfume but in medicines that can alter obesity, diabetes and the delivery of agents to
the CNS via the olfactory system.
Some of the early reports on
vitamin A therapy involved very
high doses and future topical
therapy with high local concentrations is being investigated. Nonhuman applications include the
insect repellent industry looking to
develop pest controls with odorant
molecules such as carbon dioxide
to mimic substances that insects
avoid.
Very active research
is ongoing in the
area of olfactory
disturbance, with
much of it funded
by the flavour and
fragrance industry.
Change in diet
nostic sign.49
An olfactory bulb volume of
40mm3 or less on MRI has been
associated with no recovery regardless of the duration of anosmia.50
tary regimes are more frequent.51
Many patients have a change in
their usual diet — 30% eat less,
almost half eat or drink less sweet
foods and fluids, 47% eat out less
and most favour savoury, more
spicy and salty foods.51 Weight
gain is harder to predict as congenital anosmics tend to be more
likely to have a healthy weight
compared with the average population. However, younger, overweight patients (BMI >30kg/
m2) with acquired olfactory loss
and a long duration of gradually
developing anosmia tend to gain
weight. Nutritional deficiency is
potential sequelae in patients with
acquired olfactory loss as poor die-
Psychosocial impact
Depression is a frequent association
in anosmia and lower quality of
life has been recorded.52 Particular
attention should be paid to patients
with dual sensory loss (olfactory
loss with either hearing or visual
loss that may be more common
with age) as this is a proven risk
for depression.53 Adjustment does
occur for the majority of patients
with anosmia. It is thought to take
up to 12 months for patients to
abandon behaviour meaningful
only to normosmics although 13%
continue to have adjustment issues
beyond 12 months.54
Case studies
RACHEL is a 45-year-old female
who presents with a 20-year history
of worsening nasal congestion with
cycling blockage between sides. The
nasal obstruction is worse at night
when she is lying flat. She has little in
the form of nasal itch, sneeze or discharge. Rachel says that smell loss or
“poor” smell has been a significant
feature. There are no accompanying
conjunctival, asthma or dermatitis
symptoms or signs.
Her nasal peak inspiratory flow
is 90L/minute. Endoscopy demonstrates severe turbinate hypertrophy and a deviation of her
septum (figure 12A, B). There are
no inflammatory changes (polyps, oedema, and secretions) in
her nose. CT scan demonstrates
normal sinus mucosa. Allergy
screening is negative for inhalant
antigens.
Initial treatment was with a trial
of steroid drops/irrigation to better
target the olfactory cleft and with
vitamin A, B and zinc replacement.
There was no response to the corticosteroid. These findings are out of
keeping with olfactory disturbance
from rhinitis alone. Objective testing
demonstrates total anosmia (figure
13). A diagnosis of non-allergic rhinitis and potentially unrelated anosmia is made.
She proceeds with surgery to correct her nasal airway but the cause
of the olfactory loss requires further
investigation as it is unlikely to be
conductive or related to persistent rhinitis alone. An excellent airway result
is obtained at three months (figure
12C, D — the changes reflect remodelling the nasal airway anatomy to
allow nasal function despite the condition, rather than a treatment for the
condition). However, smell remains
unchanged. An MRI is organised and
demonstrates dysgenesis of the olfactory apparatus (figure 10).
Rachel’s loss of smell has been
present for many years and she has
adapted well. She does not perceive
herself as anosmic, although testing
suggests total anosmia. Her other
senses, including taste, have adapted
accordingly. A discussion of longterm awareness of difficulty with
smoke and gas detection and the need
to ensure good alarm systems at home
is made. Improvements in smell are
not anticipated and the patient stops
attempting to treat the condition.
cont’d next page
Figure 12: The
endoscopic
appearance of the
nasal airway of
the patient with
persistent nonallergic rhinitis on
the right (A) and left
(B). The postoperative
view of the right (C)
and left (D) show the
changes to the nasal
airway with a midline
septum and uniformly
reduced inferior
turbinates.
NOSE LAB
354 Victoria Street, Darlinghurst NS
tel: 02 9360 4811 • fax: 02 936
web: http://sydneyentclin
@ Sydney Ear Nose and Throat Clinic
NOSE LAB
NOSE
@ Sydney EarLAB
Nose and Throat Clinic
354 Victoria Street, Darlinghurst NSW 2010
tel: 02 Street,
9360 4811
• fax: 02 NSW
9360 2010
9919
354 Victoria
Darlinghurst
http://sydneyentclinic.com
tel:web:
02 9360
4811 • fax: 02 9360 9919
web: http://sydneyentclinic.com
@ Sydney Ear Nose and Throat Clinic
Date:
13/09/2013
Date:
UPSIT 40
Date:
UPSIT 40
UPSIT 40
Test Score
13/09/2013
Score13/09/2013
18
Score
Score
18
18
Males
Olfactory Diagnosis
00-05
Test Score
06-18
Males malingering
Probable
Olfactory Diagnosis
Males
Total
anosmia
00-05
Test
Score
19-25
06-18
00-05
26-29
19-25
06-18
30-33
26-29
19-25
34-40
Probable
malingering
Olfactory
Diagnosis
Severe
microsmia
Total anosmia
Probable
malingering
Moderate
microsmia
Severe
microsmia
Total
anosmia
Mild
microsmia
Moderate
microsmia
Severe
microsmia
Normosmia
30-33
26-29
34-40
30-33
34-40
Mild microsmia
Moderate
microsmia
Normosmia
Mild
microsmia
Normosmia
Diagnosis (see below for definitions)
anosmia
Diagnosis (seeTotal
below
for definitions)
Diagnosis (see below for definitions)
Total anosmia
Total Females
anosmia
Test Score
00-05
Test06-18
Score
00-05
Test
Score
19-25
06-18
00-05
26-30
19-25
06-18
31-34
26-30
19-25
35-40
31-34
26-30
35-40
31-34
35-40
Olfactory Diagnosis
Females
Probable malingering
Olfactory
Diagnosis
Females
Total
anosmia
Probable
malingering
Olfactory
Diagnosis
Severe
microsmia
Total
anosmia
Probable
malingering
Moderate
microsmia
Severe
microsmia
Total
anosmia
Mild
microsmia
Moderate
microsmia
Severe
microsmia
Normosmia
Mild microsmia
Moderate
microsmia
Normosmia
Mild
microsmia
Normosmia
Interpretation of
scores
Interpretation
of scores
In general,
the following
In general, the following has
hasInterpretation
been developed
of scores for establi
been developed
for Interpretation
establishing
In
general,
the
followingolfactory
has
ofpatient's
scores
an adult
an In
adult
patient’s
been
developed
forclassification
established
general,
the following
has
diagnosis.
This
an adult
patient's for
olfactory
been
developed
established
olfactory
diagnosis.
scheme
is based
on a
diagnosis.
This classification
an
adult patient's
olfactory
This
classification
characterisation of the test
scheme
is This
based
diagnosis.
classification
scheme
is based
onon a
that
is independent
of subje
characterisation
scheme
is based of
onthe
a test scores
a characterisation
of
age.
It
does
apply
that is independent
ofnot
subject
characterisation
of the
test
scoresin
thethat
test
scores
that
is
case
of
individuals
less
than
age.is independent
It does not apply
in the
of subject
of
. less
independent
of age
subject
caseyears
of individuals
than
age.
It does
not
apply
in 15
the
years
of individuals
age
case
of
age.
It does
not. applyless
in than 15
age
.
Inof
this
classification
scheme,
theyears
case
of
individuals
In this
classification
scheme,
anosmia
defined
as total
younger
than 15isyears
anosmia
is defined
as totalqualitat
In
thisinability
classification
scheme,
to
perceive
of age.
inability
to
qualitative
anosmia
is perceive
defined
as
total
odour
sensations,
whereas
odour
sensations,
inability
to perceive
qualitative
microsmia
is whereas
defined
as
In this
classification
microsmia
is defined
asability.
odour
sensations,
whereas
decreased
smell
scheme,
anosmia
isability.
decreased
microsmia
issmell
defined
as
decreased
smell
ability.
defined
as total
inability
to perceive qualitative
odour sensations,
whereas microsmia is
defined as decreased
smell ability.
Figure 13: Rachel’s olfactory identification test results. The score of 18 places her in the anosmic range for her age group.
18 October 2013 | Australian Doctor |
33
Conclusion
Summary
Olfactory dysfunction should not
be overlooked as a health issue as
it has a significant impact on quality
of life, mental health and may flag a
more significant condition.
OLFACTORY loss can be devastating to patients especially when
it occurs suddenly and in young
patients. It has a significant impact
on nutrition, wellbeing and mental
health. A comprehensive approach
should be taken to exclude underlying causes followed by the early
and aggressive implementation of
a structured stepwise plan.
Recovery of the sense of smell at
12 months is a positive sign. However, those patients with evidence
of olfactory bulb atrophy should
not pursue active treatments that
may carry both expense and risk.
Corticosteroids given orally are
the mainstay of treatment when
inflammatory aetiology is suspect
and should be given early in
postviral anosmia
MRI scan is essential in
patients who do not respond to
corticosteroids and have otherwise
normal examinations.
References
Available on request from
[email protected]
Instructions
How to Treat Quiz
Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points.
We no longer accept quizzes by post or fax.
The mark required to obtain points is 80%. Please note that some questions have more than one correct answer.
Anosmia and parosmia —
18 October 2013
1. Which TWO statements are correct
regarding the anatomy and genetics of
the olfactory apparatus?
a) There are 10-20 million olfactory neurons
b) The distribution of the olfactory neurons are
restricted to the cribriform plate
c) The olfactory axons form fascicles that
synapse in the olfactory bulb and then
distribute to the cortical centres
d) Only a small percentage (<0.1%) of the
human genome is associated with olfaction
regarding the pathophysiology of
olfactory disturbance?
a) Olfactory decline has been associated
with several neurodegenerative diseases,
including Alzheimer’s disease and
Parkinson’s disease
b) Studies have shown an association between
epilepsy and decreased olfaction
c) Age is usually not a factor in the loss of smell
d) Sinonasal disease causes loss of smell only
through conductive disturbance
3. Which THREE of the following pathoaetiologies may cause conductive
a) Sinusitis caused by an upper dental
abscess
b) Sjogren’s disease
c) Sinonasal tumours
d) Fracture of the cribriform plate
GO ONLINE TO COMPLETE THE QUIZ
www.australiandoctor.com.au/education/how-to-treat
regarding history and examination of
a) The Smell Identification Test has not been
validated in the Australian population
b) History-taking should include asking about
smoking, stroke and epilepsy
c) Otoscopes are not useful in assessing the
nose
d) Nasal examination may be aided by a
decongestant spray such as oxymetazoline
regarding imaging in olfactory
disturbance?
a) The addition of IV contrast improves the
diagnostic accuracy of CT in sinonasal
disease
b) The normal volume of the olfactory bulb is
40-60mm3 on high-resolution MRI
c) Trauma causing shearing of the olfactory fila
can be detected as a swelling in the volume
of the olfactory bulb
d) The severity of associated Alzheimer’s
disease correlates with the volume of the
olfactory bulb
6. W
hich TWO statements are correct
regarding steroid treatment for olfactory
disturbance?
a) The recommended duration of steroid
treatment is 14-21 days
b) The improvement from topical steroid sprays
is greater in cases of traumatic and chronic
rhinosinusitis than in other patho-aetiologies
c) A cumulative dose of less than 300-1000mg
is recommended, with a maximum of 3040mg daily
d) T
he addition of simple nasal sprays
improves the effectiveness of the oral steroid
treatment of chronic rhinosinusitis
7. W
regarding other potential treatments of
a) Minocycline may theoretically be useful in
treating olfactory disturbance associated
with neurodegenerative conditions
b) P
oorly controlled mucosal inflammation
on endoscopy will have a poor olfactory
outcome with surgery
c) Randomised trials have shown clear benefit
with vitamin A but not with vitamin B
supplementation
d) O
lfactory training involves stimulating the
nose daily with garlic, onion and other strong
provoking agents
8. W
regarding prognosis in olfactory
disturbance?
a) Recovery from olfactory disturbance is best
in postviral causes, females, non-smokers
and parosmia
b) L
ow anosmic scores on smell identification
signify a poor rate of improvement
c) Spontaneous recovery occurs in a very small
proportion of patients (<0.1%) in the first 12
months
d) N
utritional deficiency may accompany
acquired olfactory loss as poor dietary
regimes are more frequent
9. Norman is an 87-year-old man who had
a recent fall causing head trauma and
anosmia. Which TWO statements are
correct regarding his anosmia and acute
management?
a) Anosmia at his age has been clearly
shown to be a marker for the onset of
a neurodegenerative disease such as
Parkinson’s
b) Norman should be cautioned about his
reduced ability to identify spoiled food,
smoke and gas
c) Traumatic causes of anosmia have the best
chance for subsequent recovery
d) An olfactory bulb volume of 40mm or less
on MRI has been associated with minimal
recovery regardless of the duration of
anosmia
10. Norman returns for follow-up after
discharge from acute care for traumatic
anosmia. Which TWO statements are
correct regarding holistic management
and prognosis of his condition?
a) Depression is a rare association in anosmia
b) Patients who have signs of recovery from
traumatic anosmia at one year have a good
prognosis
c) It may take up to 12 months for patients
to abandon behaviour meaningful only to
normosmics
d) Duration of olfactory loss is not a prognostic
marker
CPD QUIZ UPDATE
The RACGP requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2011-13 triennium.
You can complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept
the quiz by post or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.
how to treat Editor: Dr Steve Liang
Email: [email protected]
Next week Tumour screening aims to decrease the morbidity and mortality of cancer by detecting cancers at an earlier stage. The next How to Treat examines the role of tumour markers in the context
of cancer screening, assessing their usefulness in the monitoring and surveillance of diagnosed cancers. The authors are Associate Professor Gavin Marx, associate professor, Sydney Medical School,
University of Sydney, and oncologist, Sydney Adventist Hospital, Wahroonga, and Cancer Institute, Frenchs Forest, NSW; and Dr David Chan, advanced trainee in oncology, Royal North Shore Hospital,
St Leonards, NSW; and Dr Adrian Lee, medical oncology advanced trainee, Royal North Shore Hospital, St Leonards, and clinical lecturer, Sydney Medical School, University of Sydney.
34

Anosmia and parosmia

Transcription

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