AN
ANOSMIA-HYPEROSMIA CASE
IMPROVED
FOLLOWING AN ANTISTRESS DRUG THERAPY.
(Other five
articles on this topic)
An anosmia-hyperosmia case with partial loss of
the taste in a physician patient of 44 years, is reported. Suddenly come out and caused from the
hydrocarbon scent, an
antistress-antidepressant low dose drug therapy, acting on the GABA, on the
serotonin, on the dopamine and on the
glutamic acid, could face it.
Key
words: Anosmia, hyperosmia, ageusia, stress, GABA, drug therapy, glutamine,
carbamazepine.
It came to my attention an
anosmia-hyperosmia case with partial
ageusia (loss of taste), in a female physician, decidedly improved following an
antistress drug therapy. Since this rare event, their particular features, the own history made by the patient, I wanted to report it,
after a survey of the recent literature.
A short review of the literature.
The number of
medical expert opinions dealing with smell and taste disorders has continuously
increased in recent years. However, an overview of the specific problems and
results of those expert opinions has not been published until now. (Delank,
Nieschalk, Schmal and Stoll, 1999).
As for anosmia I
refer to each type of quantitative alteration in the sense of smell, and I am dealing with a
symptom induced by many causal factors. Because the classification is based on
the diagnosis of the different causes of anosmia, it implicitly includes
etiological and topographic considerations. We agree on three main groups by
the site of the causal lesion:
conduction, sensorineural, and mixed anosmias. In addition, within the
sensorineural anosmias, they distinguish between the epithelial, retroepithelial, and central
anosmias. (Gil-Carcedo, Gil-Carcedo, Vallejo and
Ortega, 1999).
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 many diseases, eg Alzheimer's disease. (Reiss
and Reiss, 2000).
As for allergic
rhinitis, there appears a continuum of
duration and severity of olfactory loss that parallels increasing severity of
nasal-sinus disease. Because of the increased frequency of respiratory
infection associated with allergic rhinitis, these patients are at risk for
damage to the olfactory epithelium. (Apter, Gent and Frank, 1999).
According to
Klimek, Muttray, Moll, Konietzko and Mann (1999), we underestimate olfactory disorders in occupational and environmental medicine.
We have to postulate relevance of olfactory-toxic substances for occupational
medicine in metal and chemical workers, in welding and disinfection.
About 66% and 24%
of all individuals, respectively, claimed about some anosmia or hyposmia.
(Delank, Nieschalk, Schmal and Stoll, 1999).
There is even
anosmia in the Kallmann's syndyome, a complex genetic hypogonadotropic
hypogonadism. (John and Schmid, 2000).
Among iatrogenic
factors of anosmia, several reports refer to it following alpha-interferon
treatment in C hepatitis patients. (Cocquyt and Van Belle, 1994; Fernandez Fernandez, Castiella Eguzkiza, Tejada Calabra and Garcia
Bengoechea, 2000; Kraus and Vitezic, 2000). In a patient, anosmia was still
present 13 months after the discontinuation of the alpha interferon. (Kraus and
Vitezic, 2000).
So, 50%
troublesome parosmias often accompany the loss of smell (Bonfils, Corre' and Biacabe, 1999). Then, the
first-episode-psychosis patients had significantly higher sensitivity to
isoamyl acetate and to androstenone, both as tested compounds (Sirota,
Davidson, Mosheva, Benhatov, Zohar, and
Gross-Isseroff, 1999).
About the
psychological approach there is even an issue of Koch-Gromus, and
Schmeling-Kludas, 2000, who suggest it besides any medical intervention.
The case history.
Female, of 44
years at first consultation. She has
always been a little hypersensitive to scents. What follows is a third-person
relationship written by herself.
"On 26
August of the 2000, she remembers that in the mornings she
inhaled accidentally dusts polluted by a petrol-derived solvent (naphtha).
In the afternoon
she had an accidental spray of an OTC analgesic product (Autan TM) on her face
and her nose.
On 2 September
following, she inhaled some smoke deriving from a bonfire, during a country
festival. From the following day it was impossible to bear the scents of
cleansers and detergents, which
stimulated the sense of smell in very strong manner. She doesn't succeed to bear the scent of freshly laundered
sheets, or also previously washed and stored into drawers.
The whole month of
September was therefore a month of panic. A consulted otorhinolaryngologist prescribed her some cortisone tablets'
regimen, but she has to interrupt it after 10 days because she was worsening.
The second
prescribed low doses haloperidol, starting from 0.5mg, a never started regimen.
Meanwhile
a hypersensitive taste appeared which she related to everything
artificial in foods (stuff colours, preservative, etc.).
The following passed through a phase of
hyperosmia, first for wood, for which she could not sleep near to pieces of
furniture. A hyperosmia for the rubber succeeded, with intense rubber scent
into her car, and into the bus.
Still hyperosmia
came for the drawers of wardrobes, and
finally for any printed paper. For this, it became impossible for her to open a
magazine, or even to be near to a person that was skimming it through. To be
beside her child studying became a torture.
In November, during her last hyperosmic phase,
she resumed her work.
During the
Christmas holidays 2000 and New Year's Day 2001, as the relatives' guest, she
noticed a worsening of the situation. This happened for the scents of the
kitchenware, washed in the dishwasher with detergent-deodorant stuffs and a feeling of "an olfactory panic"
for scent deriving from the stoves. They arrived her too much scents, often
confused, and she was unable to distinguish some of them.
Since January 2001, to the time of the fourth
check, she noticed that from about 10 days had some vertigo, which she can
control when she does not change her head position in a too sudden way. It persisted
like a hypersensitivity to the detergents and to all perfumes used by the
people. The scents of the kitchen begin to be better distinguished."
From a week this
last, is diminishing. She bears badly the scent of the people. At night, she
sleeps well. Now, she remembers that in 1995 she had a similar problem, but
with less intensity, and less lasting. It came again from "the
petrol-derived scent" in the condominium where she was living. It seems that the sense of the taste, that
she had lost for many foods, is recovering.
To the trial
therapy with carbamazepine 100mg,
bromazepam 1.5mg and a compound of amitriptyline 10mg + perphenazine 2mg, I
added glutamine 125mg and pyridoxine 150mg, the all to daily doses.
11.12.2000: She
feels differently. Now, she believes that she is only as hyperosmic.
She paid less
attention to this last sense, because smell worried her much more.
08.01.2001. She has
still problems of hypersensitivity for some odours (garlic lightly fried in
oil). Then, she had nausea in concomitance with dizziness, successfully controlled with domperidon, and
bicarbonate + lemon juice (= sodium citrate).
She was given even
some applications of acupuncture. Dizziness went down, and it always related
with sudden breams of her head that interested always the centre of the balance
(labyrinth). She does not stand well both toilet soap and detergents' scents.
In the following times the patient and the
neurologist met in an informal way. Symptoms progressively improved and it was
agreeing that, anyhow, the drug therapy will last at least for 18 months.
25.03.2002: The
last checkup before the therapy stop. She has had a slow and gradual relief.
Now she is less disturbed from the use perfumes from third persons. The sense
of smell fully recovered
The scents of
drugs excreted with the sweat and urine still bother her. There was a
predisposition to smell almonds, melon and onion in urine and in the sweat. However, there is
some hypersensitivity to particular scents.
Referring to the
past, she says that at the beginning she had some myoclonies to the thigh and
to the eyelids lasted 3-4 months. She did a blood check that resulted negative,
but a light increasing of serum-albumins from the electrophoresis, with 68.1%
(normal range: 52.0-65.0). In such conditions, she found it hard to maintain
her job, but she never left it. Since six months she is rather stabilised, and
the taste troubles resolved for first. She has had some problems for seeing
from near.
The hyperosmia
increases in the premenstrual phase. She admits that she took drugs because she
did not have other choice. The results, and the small doses prescribed, changed
her mind.
Discussion.
It is not so easy
to classify the anosmia type here described, according with the criteria of
Gil-Carcedo, Gil-Carcedo, Vallejo and Ortega, 1999. If we remember its
debut, the lack of a defined peripheral cause and the
good result obtained following an
antistress drug therapy, it seems that it fit better the reference frame of the
sensorineural anosmia, central variety, idiopathic type.
Many
characteristics make this case deserving of note. The fact that it happened to
a physician, for example, has allowed a much detailed and effective
description.
Eventually, its treatment did not have any
psychotherapeutic support, in spite of that as an essential element of the
therapeutic regimen (Koch-Gromus, and Schmeling-Kludas, 2000).
As for that, I do
not wish that somebody should maintain that I believe the psychotherapeutic
support as useless. But in this patient it had no room, and here I stop myself.
We can straight
think that it concerns several cells specifically appointed to process the
aliphatic hydrocarbons stimuli.
Another element of
interest is the implication of the sense of the taste. This fact is not a
novelty. The association with the hyposmia forms an idiomatic syndrome
described by Henkin et al., 1971, or a side result of flu (Henkin et al.,
1975).
However we cannot
say that the subjective feeling corresponds to a true partial loss of the
taste. That sense depends, to a large extent, from foods and drinks deriving
volatile particles that reach the olfactory receptors through the
rhino-pharyngeal pathway. The perception of the taste comes from the
combination of the senses of smell and of taste (Adams and Victor, 1989).
In our patient the
reduced taste surely finds its cause in the anosmia or in the parosmia. Anyway,
we do not know if it is an exhaustive one, not having the patient performed
specific tests for the sense of the taste.
Another
symptomatic aspect that deserves to be noted is the hyperosmia presence, a
quantitative anomaly of the sense of smell.
There are even
discussions if exists such a phenomenon. It seems more probable that it exists,
as it happens for sounds, and lights. In migraine fits it has been found an
abnormal sensitivity to these three
senses (Adams and Victor, 1989). For anyone who has had contacts with
autistic children, in many of them the hypersensitivity to sounds seems an
indisputable element. The fact that the child stretches to limit the entry of sounds by closing the ears with his hands
confirms it. A reduced threshold for
noises, which become less tolerable, is nearly a constant of certain
depressive forms of adult persons.
Feelings of hypersensitivity of the taste for
the bitter or for the acid, had reports in some patients with cancer (Adams and
Victor, 1989 ).
A form of
intolerance for suits, always in the autistic or in the mental retarded, lead
to think that even the touch can be in this condition.
A sure link
between troubles of the sense of smell and stress, in this patient, comes from
the affirmation that the hyperosmic troubles increases in the premenstrual
phase. The symptoms of that syndrome are not specific, and I stated them as
stress symptoms (Cocchi, 1998).
Moreover it is
worthy to note that the restoration of the sense of smell went through a
hyperosmic phase, an intermediary step common to the period of its partial
loss. It is a great deal probable that this sensory chain - normality ->
hyperfunction -> hypofunction/loss and possible vice versa -is not an
individual fact of this patient, and not specific of the sense of smell. Drugs can even influence it, as it did here.
An anosmia-hyperosmia case with partial loss of the taste in a
physician patient of 44 years, suddenly came out, caused from the hydrocarbon
scent. An antistress-antidepressant low dose drug therapy, acting on the GABA,
on the serotonin, on the dopamine and on
the glutamic acid, could face it.
The restoration of
the taste and of the sense of smell, already started after one month, was
consolidated during 18 months of therapy, with residual episodic hyperosmic
feelings. It is not clear if such improvement is a steady state, or it is such
in relationship to a temporary balance, maintained for some time even after the drugs stopping.
(Other four articles on this topic)
References.
Adams
RG, Victor M. Principles of Neurology. McGraw-Hill, New York, 1989.
Apter
AJ; Gent JF; Frank ME. Fluctuating olfactory sensitivity and distorted odor
perception in allergic rhinitis. Arch Otolaryngol Head Neck Surg 1999, 125:
1005-1010.
Cocchi
R. Pre-menstrual syndrome as the paradigm of an internal biochemical stress.
Melbourne, 1998. In internet, on www.stress-cocchi.org/speculation3.htm
Davidson
TM; Freed C; Healy MP; Murphy C. Rapid clinical evaluation of anosmia in children:
the Alcohol Sniff Test. Ann N Y Acad Sci 1998, 855: 787-792.
Delank KW;
Nieschalk M; Schmal F; Stoll W. Besonderheiten in der Begutachtung von Riech-
und Schmeckstorungen. Laryngorhinootologie 1999, 78: 365-372.
John
H; Schmid C. Kallmann's syndrome: clues to clinical diagnosis. Int J Impot Res 2000,
12: 121-123
Klimek L;
Muttray A; Moll B; Konietzko J; Mann W. Riechstorungen durch nhalative
Schadstoffexposition. Bedeutung fur die gutachterliche Praxis. Laryngorhinootologie 1999, 78: 620-626.
42100 Reggio Emilia.
renatococchi@libero.it