Reiss M, Reiss G. [The problem of anosmia]. Z Arztl Fortbild
Qualitatssich 2000;94:149-53. Review. German.
Olfactory problems have deleterious consequences to systemic health, nutritional
status and quality of life. Olfactory disorders are not as rare as generally
assumed. Chemosensory dysfunction is most often secondary to one of only a
few causes: nasal/sinus disease, viral infection, toxic chemical exposure,
head trauma, as well as medication-related and idiopathic conditions. Many
olfactory disorders are secondary to a wide variety of diseases, e.g. Alzheimer’s
disease. The patient’s history may provide clues to these and other problems
(e.g. toxin exposure, congenital dysosmia). Therapy should not begin until
a standardized test has been established the impairment of the sense of smell.
Treatment of the underlying diseases may restore chemosensory function. The
only truly reversible cause is inflammation, which is confirmed when smell
returns after administration of corticosteroids. Reference is made to the
need for adequate psychologic guidance of patients with chemosensorial problems.
If restoration of their sense of smell is unlikely, patients should be educated
to ensure safety in regard to such dangers as gas leaks, smoke, and spoiled
foods.
Bromley SM. Smell and taste disorders: a primary care approach.
Am Fam Physician 2000 15;61:427-36, 438.
Smell and taste disorders are common in the general population, with loss
of smell occurring more frequently. Although these disorders can have a substantial
impact on quality of life and may represent significant underlying disease,
they are often overlooked by the medical community. Patients may have difficulty
recognizing smell versus taste dysfunction and frequently confuse the concepts
of “flavor” and “taste.” While the most common causes of smell disturbance
are nasal and sinus disease, upper respiratory infection and head trauma,
frequent causes of taste disturbance include oral infections, oral appliances
(e.g., dentures), dental procedures and Bell’s palsy. Medications can interfere
with smell and taste, and should be reviewed in all patients with reported
dysfunction. In addition, advancing age has been associated with a natural
impairment of smell and taste ability. A focused history and a physical examination
of the nose and mouth are usually sufficient to screen for underlying pathology.
Computed tomographic scanning or magnetic resonance imaging of affected areas,
as well as commercially available standardized tests, may be useful in selected
patients. The causes of olfactory dysfunction that are most amenable to treatment
include obstructing polyps or other masses (treated by excision) and inflammation
(treated with steroids). Enhancement of food flavor and appearance can improve
quality of life in patients with irreversible dysfunction.
Beraud F, Friard D. [“I cannot smell her anymore”] Soins Psychiatr 2000;(206):30-2. [Article in French.] No abstract available.
Turetsky BI, Moberg PJ, Yousem DM, et al. Reduced olfactory
bulb volume in patients with schizophrenia. Am J Psychiatry 2000;157:828-30.
OBJECTIVE: The authors’ goal in this study was to compare the size of olfactory
bulbs of patients with schizophrenia and those of healthy subjects. METHOD:
Magnetic resonance imaging scans of olfactory bulbs were obtained from 26
patients with schizophrenia and 22 healthy comparison subjects. A reliable
region of interest procedure was used to measure olfactory bulb volume. RESULTS:
Patients exhibited 23% smaller bilateral bulb volume than comparison subjects,
independent of acute clinical, demographic, or treatment measures. Bulb volume
correlated with odor detection sensitivity in healthy subjects but not in
patients with schizophrenia. CONCLUSIONS: Patients with schizophrenia exhibit
structural olfactory deficits as well as functional olfactory deficits. The
olfactory system may be a model system in which to study the neurobiology
of the disorder.
Mori J, Aiba T, Sugiura M, et al. Clinical study of olfactory
disturbance. Acta Otolaryngol Suppl 1998;538:197-201.
The clinical records of 889 patients with olfactory disturbance who had been
examined at the Olfaction Clinic, Osaka City University Hospital, Japan from
January 1982 to December 1996 were studied in order to investigate the relationship
between the patients’ characteristics and their prognoses. Aetiologically
the characteristic variables of “head trauma” and “congenital” had the greatest
influence on prognosis, representing poor recovery. The patients with “rhinitis”
and “head trauma” showed faster improvement of olfactory disturbance in “females,”
“those with short duration of olfactory disorder” and “those with high olfactory
acuity before treatment.” None of the characteristic variables influenced
prognosis in the patients with “viral infection.” Age did not significantly
influence prognosis. Improvement was recognized in most patients within 6
months. Hence, we should treat patients with olfactory disturbance for at
least this length of time.
Assouline S, Shevell MI, Zatorre RJ, et al. Children who
can’t smell the coffee: isolated congenital anosmia. J Child Neurol 1998;13:168-72.
Two children with isolated congenital anosmia, a rare syndrome of deficient
restricted neuronal migration, are presented with early diagnosis confirmed
by standardized smell testing and detailed neuroimaging studies. Recognition
of this disorder and its spectrum of presentations provides important insights
into the molecular mechanisms underlying the development of the olfactory
system.
Moberg PJ, Doty RL, Turetsky BI, et al. Olfactory identification
deficits in schizophrenia: correlation with duration of illness. Am J Psychiatry
1997;154:1016-8. Comment in: Am J Psychiatry 1998;155:1463-4.
OBJECTIVE: The authors examined the relationship between deficits in olfactory
identification and duration of illness in young and elderly patients with
schizophrenia. METHOD: Olfactory identification performance of 38 patients
with schizophrenia and 40 normal subjects was compared by using the University
of Pennsylvania Smell Identification Test. RESULTS: The schizophrenic patients
demonstrated olfactory deficits relative to the comparison group, and the
elderly schizophrenic patients displayed a greater magnitude of olfactory
deficit than the younger patients. Independent of normal aging effects and
cognitive deficit, patients with schizophrenia showed a strong relationship
between olfactory identification scores and duration of illness, which suggests
that olfactory abilities decline progressively over the course of the disorder.
CONCLUSIONS: In contrast to other neuropsychological measures that have been
reported to be stable over the course of illness, olfactory identification
abilities deteriorate steadily in patients with schizophrenia, even for those
with relatively recent onset.
Laska M, Distel H, Hudson R. Trigeminal perception of odorant
quality in congenitally anosmic subjects. Chem Senses 1997;22:447-56.
Twenty congenitally anosmic subjects and 50 normosmic controls were tested
for their ability (i) to assign verbal labels from a list of trigeminal-type
descriptors to six odorants believed to have a strong trigeminal component;
and (ii) to discriminate between intensity-matched pairs of these odorants
in an odd-ball paradigm. The following was found: normosmic controls judged
menthol and cineole as distinctly cool and fresh, acetic acid as pungent and
sour, and acetone as pungent, but showed no clear descriptive profile for
ethanol and propanol. The descriptive profiles given by the anosmic subjects
correlated significantly with those given by the controls for three of the
six odorants (menthol, cineol and ethanol), confirming that the sensations
described may indeed be mediated by the trigeminal system. In the odd-ball
test, the control subjects correctly identified an average of eight out of
the nine items presented, with most mistakes occurring in response to pairs
with a similar trigeminal profile. With an average of 7.2 of nine items correct,
the performance of the anosmic subjects was not significantly different to
that of the normosmics, except in discriminating between acetic acid and menthol.
Although additional tests are necessary to decide finally whether differences
in stimulus intensity may have contributed to this good discriminatory performance,
the present results suggest that the nasal trigeminal system may contribute
significantly to the perception of odor quality.
Cui L, Evans WJ. Olfactory event-related potentials to amyl
acetate in congenital anosmia. Electroencephalogr Clin Neurophysiol 1997;102:303-6.
Olfactory function was evaluated by olfactory event-related potentials and
standardized psychophysical measures including the Smell Identification Test
and odor detection threshold tests for 3 chemosensory stimulants in 9 subjects
with isolated congenital anosmia and 9 age- and gender-matched normosmic controls.
There was a significant difference in Smell Identification Test scores (P
< 0.001) and odor detection thresholds for phenylethyl alcohol (P < 0.001)
and isoamyl acetate (P < 0.001) between the anosmic and normosmic subjects.
Detection thresholds for chloracetyl phenone, a trigeminal stimulant, did
not differ between the 2 groups. Olfactory evoked potentials were recorded
in response to amyl acetate and air control stimuli presented at volume flow
rate of 5 l/min, stimulus duration of 40 ms, and randomized interstimulus
intervals of 6-30 s. In the control subjects, evoked potentials to amyl acetate
were characterized by 4 reproducible components (P1, N1, P2, and N2). In the
subjects with congenital anosmia, no reproducible evoked potential components
were identified in response to amyl acetate. No reproducible evoked potential
components were seen in response to the air control stimulus in either the
anosmic or normosmic groups. These data suggest that olfactory evoked potentials
provide a specific measure of olfactory function.
Jimenez DF, Sundrani S, Barone CM. Posttraumatic anosmia
in craniofacial trauma. J Craniomaxillofac Trauma 1997;3:8-15.
Although the clinical implications of anosmia can be significant, posttraumatic
anosmia is generally given relatively little attention in the clinical setting.
Patients who sustain craniofacial trauma are most at risk. The incidence of
posttraumatic anosmia varies according to the severity of injury and has an
overall estimated incidence of 7%. Factors that increase the risk of developing
anosmia include anterior skull base fractures, bilateral subfrontal lobe injury,
dural lacerations, and cerebrospinal fluid leakage. Recovery of function has
been estimated to be approximately 10%. Time of recovery, if it occurs, varies
between 8 weeks and 2 years. Presented herein are the clinical, radiographic,
pathophysiologic, and anatomic substrata of posttraumatic anosmia.
Vowles RH, Bleach NR, Rowe-Jones JM. Congenital anosmia.
Int J Pediatr Otorhinolaryngol 1997;41:207-14. Review.
Congenital anosmia is well described in conjunction with various sexual and
other developmental abnormalities and has been reported to run in families.
Congenital anosmia occurring as an isolated defect in a single family member
is extremely rare, and tends to present late. We describe a case of a five
year old girl with congenital anosmia and we outline the investigations which
should be undertaken in such cases.
Yousem DM, Geckle RJ, Bilker W, et al. MR evaluation of patients
with congenital hyposmia or anosmia. Am J Roentgenol 1996;166:439-43.
OBJECTIVE: The purpose of this study was to evaluate patients with reduced
or no sense of smell since birth for sites of abnormality by MR imaging. MATERIALS
AND METHODS: Twenty-five patients who reported no olfactory function since
birth were evaluated by olfactory testing, sinonasal endoscopy, and MR imaging.
Surface coil and head coil images of the olfactory bulbs, olfactory tracts,
subfrontal cortex, and temporal lobes in contiguous 3-mm sections were obtained.
Two reviewers determined unilateral olfactory bulb and tract volumes and temporal
lobe volumes in two separate sessions. Qualitative grading for olfactory bulb,
olfactory tract, olfactory sulcus, subfrontal region, hippocampus, and temporal
lobe damage also was performed. RESULTS: The absence of olfactory bulbs and
tracts (68-84%) or the presence of hypoplasia (16-32%) was noted in all cases.
Eight individuals had Kallmann’s syndrome (hypogonadotropic hypogonadism with
anosmia). Temporal and/or frontal lobe volume loss was noted in five individuals
and was mild in all but one individual. CONCLUSION: Congenital anosmia or
hyposmia appears to be an olfactory bulb-olfactory tract phenomenon rather
than a cerebral process.
Crawford DZ, Souder E. Smell disorders = danger. RN 1995;58:40-3. No abstract available.
Murphy C, Jalowayski AA. Smell impairment. Can it be reversed?
Postgrad Med 1995;98:107-9, 112-8. Review.
Patients who have lost the sense of smell usually come to a doctor on their
own, reporting loss of the sense of taste. Inflammation (often due to allergy),
viral infection, and head trauma are common causes of olfactory disturbance.
History taking may provide clues to these and other problems (eg, toxin exposure,
congenital dysosmia). Workup should not begin until a standardized test has
been given that established impairment of the sense of smell. The only truly
reversible cause is inflammation, which is confirmed when smell returns after
a course of corticosteroid. Sinus computed tomography is necessary to view
the olfactory cleft; lack of obstruction indicates that smell impairment is
nonreversible. Patients deserve an explanation for their disorder and a prognosis.
If restoration of their sense of smell is unlikely, patients should be cautioned
to take steps to ensure safety in regard to such dangers as gas leaks, smoke,
and spoiled foods.
Kopala LC, Good K, Goldner EM, Birmingham CL. Olfactory
identification ability in anorexia nervosa. J Psychiatry Neurosci 1995;20:283-6.
OBJECTIVE: The hypothesis tested was that patients with severe eating disorders
would demonstrate olfactory identification deficits as a result of zinc deficiency
or malnutrition. METHOD: The University of Pennsylvania Smell Identification
Test (UPSIT) was administered to 27 hospitalized female patients with anorexia
nervosa and 50 normal control female subjects. For a subgroup of patients,
serum zinc levels and body mass indices were obtained at pre- and post-nutritional
repletion phases. RESULTS: UPSIT scores for patients with eating disorders
were equivalent to normal control subjects in spite of the fact that the patients
were nutritionally compromised as determined by body mass index. Serum zinc
levels were not significantly different at pre- and post-nutritional repletion.
CONCLUSIONS: In contrast to patients with schizophrenia, patients with severe
eating disorders have intact olfactory function. This finding suggests that
transient metabolic or nutritional disturbances alone cannot account for previously
reported olfactory deficits.
Moran DT, Jafek BW, Eller PM, Rowley JC 3rd. Ultrastructural
histopathology of human olfactory dysfunction. Microsc Res Tech 1992;23:103-10.
This paper presents electron-microscopic observations on biopsies of the olfactory
mucosae of several classes of patients with smell disorders: 1) patients with
loss of smell function following head injury (post-traumatic anosmics or hyposmics);
2) patients with loss of smell function following severe head colds and/or
sinus infections (post-viral olfactory dysfunction, or PVOD); and 3) patients
that have lacked smell function since birth (congenital anosmics). Of these,
the traumatic anosmics’ olfactory epithelia were quite disorganized; the orderly
arrangement of supporting cells, ciliated olfactory receptor neurons, microvillar
cells, and basal cells was disrupted. Although many somata of ciliated olfactory
receptors were present, few of their dendrites reached the epithelial surface.
The few olfactory vesicles present usually lacked olfactory cilia. The post-viral
anosmics, too, had a greatly reduced number of intact ciliated olfactory receptor
neurons, and most of those present were aciliate. The post-viral hyposmics
had a larger population of intact, ciliated olfactory receptor cells. In the
seven cases of congenital anosmia studied, no biopsies of olfactory epithelium
were obtained, indicating the olfactory epithelium is either absent—or greatly
reduced in area—in these individuals.
Leopold DA, Hornung DE, Schwob JE. Congenital lack of olfactory
ability. Ann Otol Rhinol Laryngol 1992;101:229-36.
Twenty-two patients, all of whom reported never having been able to smell
anything, were studied to determine the particular features that distinguish
individuals with congenital anosmia. The clinical evaluation on these patients
included a thorough medical and chemosensory history, physical examination,
nasal endoscopy, chemosensory testing, olfactory biopsies, and imaging studies.
There was no evidence to indicate that these patients ever had a sense of
smell. The results of olfactory testing suggested that these patients had
an inability to detect both olfactory and trigeminal odorants; however, many
of the patients in the group seemed to have a slight ability to perceive at
least some component of trigeminal odorants. The olfactory epithelium, if
it was present at all on biopsy, was abnormal in appearance.
Jafek BW, Gordon AS, Moran DT, Eller PM. Congenital anosmia.
Ear Nose Throat J 1990;69:331-7.
Seven patients with congenital anosmia underwent detailed chemosensory evaluation,
followed by the performance of biopsies of the olfactory region. Olfactory
epithelium was not found in any of the biopsy specimens. It appears therefore
that patients with congenital anosmia lack any olfactory epithelium. Several
possible explanations for this finding are discussed. The most attractive
hypothesis is that the olfactory placode forms either normally or abnormally
during development but later degenerates and is replaced with respiratory
epithelium. Only one patient in our series had congenital anosmia in association
with a syndrome (Kallmann’s syndrome), indicating that congenital anosmia
is found more often as an isolated symptom.
Yamagishi M, Hasegawa S, Nakano Y. Examination and classification
of human olfactory mucosa in patients with clinical olfactory disturbances.
Arch Otorhinolaryngol 1988;245:316-20.
To determine objectively the degree of olfactory disturbance, we biopsied
the olfactory mucosa from patients who complained of anosmia. The olfactory
disturbances in this study were caused by choanal atresia, chronic sinusitis,
viral inflammation, and head trauma, as well as by congenital and idiopathic
anosmia. The biopsy specimens were examined by light microscopy and the degree
of mucosal degeneration present was classified according to five grades. The
clinical courses of the patients studied paralleled the changes found in the
olfactory mucosa.
Myers LJ, Nash R, Elledge HS. Electro-olfactography: a technique
with potential for diagnosis of anosmia in the dog. Am J Vet Res 1984;45:2296-8.
Diagnosis of olfactory dysfunction in the dog has been rare. Few techniques
for this diagnosis are available. Electro-olfactography, an electrophysiologic
technique for evaluating the function of the olfactory mucosa, was developed
as a relatively noninvasive technique for diagnosis of functional abnormalities
of the olfactory mucosa in mesatocephalic canines. The technique was validated
by several experiments and normative values for the electro-olfactogram were
obtained.
Schellinger D, Henkin R, Smirniotopoulos JG. CT of the brain
in taste and smell dysfunction. Am J Neuroradiol 1983;4:752-4.
Three hundred fifty-four patients with taste and/or smell disorders were evaluated
with computed tomography (CT). The largest group was characterized by head
trauma (27%), followed by idiopathic causes (26%), postinfluenza-like hyposmia
and hypogeusia (15%), and congenital etiologies (14%). Hyposmia and hypogeusia
occurred concomitantly in 21%-45%, the percentage varying according to etiologic
subgroup. CT abnormalities were found in 108 (31%) of the 354 patients. The
most frequent pathologies were frontal encephalomalacia, subfrontal atrophy
in the region of the olfactory bulbs, and anterior temporal lobe atrophy.
These changes were found alone or in tandem. Some CT findings suggest common
cerebral taste and smell centers and common neural pathways and association
centers.
Schiffman SS. Taste and smell in disease (second of two
parts). N Engl J Med 1983;308:1337-43.
Disorders of taste and smell are common occurrences that can lead to modifications
of dietary habits that may in turn exacerbate disease states or nutritional
deficiencies. In addition, they are often nagging problems that diminish the
quality of life. Such disorders can result from a range of disease states,
pharmacologic and surgical intervention, aging, radiation, and environmental
exposure. A search for the pathogenetic mechanism should include the determination
of possible (1) local injury from physical or chemical causes, (2) damage
to neural projections, (3) disturbance of the cycle of regeneration of chemoreceptors
resulting from general malnutrition, disease agents, metabolic disturbances,
drugs, or radiation, and (4) alteration in the saliva or fluids bathing the
olfactory mucosa by drugs or metabolic agents. Viral infections, normal aging,
head injuries, and nasal obstructions are the most common causes of smell
disorders. Drugs are common offenders in taste dysfunction. Chemosensory disorders
frequently remit when concomitant medical conditions are treated or offending
drugs removed, although full recovery may take several months. Considerable
research is now under way in this area, and it is to be hoped that we will
soon have a better understanding of how to diagnose and treat these common
disorders.
Gordon CB. Practical approach to the loss of smell. Am Fam
Physician 1982;26:191-3.
Loss of the sense of smell can be easily confirmed in any physician’s office
by having the patient try to identify various odors. The etiology of anosmia
can be extremely varied, including nasopharyngeal disorders such as rhinitis
and tumors; neurologic conditions such as head trauma, neoplasms, vascular
lesions and infections of the central nervous system; viral infections; familial
and congenital disorders; drugs; industrial exposure; endocrine diseases,
and several other disorders. The prognosis of anosmia is guarded, and its
treatment depends on the etiology.
Houpt KA, Davis PP, Hintz HF. Effect of peripheral anosmia
in dogs trained as flavor validators. Am J Vet Res 1982;43:841-3.
The importance of olfaction in perception of flavor by flavor-validating
dogs was studied. The flavor-validation technique is widely used by pet food
manufacturers to determine if a given formula is perceived by dogs as having
the flavor of a specific meat. Five Beagles were trained as flavor validators;
2 dogs were trained to select beef and 3 to select lamb from a panel of 4
meats. When the dogs had been trained to select the correct meat on 100% of
the trials, they were made anosmic. Reversible peripheral anosmia was produced
in the dogs by inflating a cuff on a surgically implanted tracheostomy tube.
When the cuff was inflated, air entered the trachea via the tracheostomy tube,
rather than via the nasal cavity, and the percentage of correct choices on
the flavor-validating test fell to 62 +/- 14%. When the tracheostomy tubes
were removed, performance returned to 100% correct. The nasal cavities of
3 dogs were infused with zinc sulfate to produce a more complete and longer-lasting
anosmia. The percentage of correct choice on the flavor-validation test fell
to 24 +/- 5%. These findings indicate that the flavor-validation test is based
primarily on one sensory modality, that of olfaction; therefore, formulas
selected by flavor-validating dogs may smell similar to the specific meat,
but do not necessarily taste similar to that meat.
Lushchekin VS. [Role of species-specific acoustic signals
in the “homing” orientation of intact and olfactory deprived kittens.] [Article
in Russian] Zh Vyssh Nerv Deiat Im I P Pavlova 1981;31:1171-8.
Vocal responses of lactating cats were recorded and used to investigate
home orientation in 1-30 days old kittens. Two types of species-specific acoustic
signals were chosen and used in acoustically-guided homing. Type 1 comprised
fricative signals below 1.5 kHz of low intensity and long duration. Type 2
comprised intense tonal calls with 2-4 resonant frequency components below
4 kHz. Presentation of tape-recorded signals 1 and 2 through the speaker placed
into the home site increased the ability of the kittens to return to the nest.
Zn-induced anosmia eliminated home orientation. Presenting of the signals
1 and 2 to anosmic kittens resulted in the recovery of homing. Acoustically-guided
behaviour first appears at 6-9 days of age and fully matures by 25-30 days.
Rosen SW, Gann P, Rogol AD. Congenital anosmia: detection
thresholds for seven odorant classes in hypogonadal and eugonadal patients.
Ann Otol Rhinol Laryngol 1979;88(2 Pt 1):288-92.
Detection thresholds for a representative from each of seven odorant
classes (putrid, pepperminty, ethereal, camphoraceous, pungent, musky, floral)
were determined by double-blind smell testing of seven normal males, six normal
females, 6 patients with uncomplicated congenital anosmia and 13 patients
with the syndrome of congenital anosmia and hypogonadotropic hypogonadism
(the Kallmann syndrome, olfactogenital dysplasia). The median detection thresholds
did not differ significantly between hypogonadal and eugonadal anosmics for
any of the odorants, suggesting that the endocrine deficit does not result
from inadequate rhinencephalic input to brain centers controlling gonadotropin
release. Phenylethylmethylethylcarbinol (PEMEC), a stable chemical of the
floral class, was detecred at very low concentrations (10(-6) to 10(-8) M
in water) by all normals tested. Since no patient with congenital anosmia
was able to distinguish even undiluted PEMEC from water, we suggest that this
compound is the material of choice for convenient, rapid and objective testing
of the sense of smell (cranial nerve I).
Doty RL. A review of olfactory dysfunctions in man. Am J
Otolaryngol 1979;1:57-79. Review.
Although a large number of individuals experience olfactory disorders
following accidents, disease states, medical interventions, aging, and exposure
to environmental chemicals and pollutants, few medical practitioners have
the expertise or staff to provide appropriate clinical evaluation, treatment,
counseling, or referral for such patients. The present review examines studies
associated with the diagnosis and treatment of olfactory disorders, as well
as ones noting olfactory signs as diagnostic markers for brain tumors and
other serious problems. A basic taxonomy of smell dysfunctions is presented,
along with a review of etiologic factors, including local diseases and mechanical
obstruction of the airways, viral infections, trauma, congenital anomalies,
endocrine disorders, tumors, psychiatric disorders, aging, drugs, environmental
and industrial pollutants, iatrogenic factors, and miscellaneous diseases.
A discussion of current disability compensation guidelines in the United States
and Britain is also presented.
Kitsera AE. [Case of congenital hereditary anosmia]. Zh Ushn Nos Gorl Bolezn 1975:102-3. Russian. No abstract available.
Hart BL, Haugen CM. Scent marking and sexual behavior maintained in anosmic male dogs. Commun Behav Biol 1971;6:131-5. No abstract available.
