HYPEROSMIA, AND
HEADACHE'S FITS FROM HEAVY, OLFACTORY STIMULI IN A 35-YEARS-OLD MAN OF 35
YEARS. AN APPROACH WITH ANTIEPILECTIC AND ANTISTRESS DRUGS.
Renato COCCHI, a neurologist and a medical
psychologist.
(Ten other articles on this topic)
Summary.
A man of 35 years suffering, since his 12
years, of headache fits at the nose's root, elicited by heavy smell stimuli,
started an antistress drug therapy. Following the results, we thought that we
were in presence of what a time we called "an epileptic equivalent".
The headache could be the post fit's symptom of it. The therapy had reinforced
doses either as its antistress and as antiepileptic action.
Key words: Hyperosmia, headache,
epilepsy, stress, depression, drug therapy.
Drug modulazione of stress reactions
A man of 35 years came to my outpatients'
clinic, because suffering from an unusual trouble of the smell, which started
23 years ago. A headache always more resistant to painkillers drugs immediately
accompanies it.
Following the first checkup after a drug
therapy attempt, having glimpsed a possible causal mechanism, I decided to
start this report. I want to update it, if I can do it.
End June 2004.
The patient got in touch with me through the
following letter sent by electronic mail.
"... I am writing it after I read on
Internet your four studies on anosmia-hyperosmia cases.
I am 35 and since I was about 12 I am cohabiting
with a trouble that has conditioned all my life. This trouble is a particular
migraine [it is not a pure migraine,
but several physicians called it so] with very frequent episodes. It related
to an aspect that, I think, can be called "hyperosmia". Some times I
had the diagnosis of a cacosmia.
The characteristic of this headache and
of linked troubles is exactly the fact that it is elicited in presence of
odours and particularly of perfumes that I perceive amplified and intolerable.
Many odours that for the other persons are just perceptible, result for me
varying in graduation [intensity] and tolerance.
During these years I got many
specialists' examinations: In the headache centre of Rome, they diagnosed a migraine
without any aura; In the Mondino institute of Pavia, I had same diagnosis; In
the polyclinic Gemelli of Rome a specialized doctor has excluded the multiple
chemical sensibility ( or "the illness of the building" ) and he
suggested a cacosmia.
Different laboratory examinations, among
which the NMR, excluded any serious pathology. Various treatments prescribed
did nor reach the hoped results. It is not hard to imagine how much suffering
and how many difficulties in social relationships all that caused me. So, often
the depression could take the
upper hand. With this letter I wish to ask your attention for my case, [etc.]."
End July 2004, first consultation. M, of 35
years, with a diploma of a higher school, married, with two sons. He is working
in a factory with a continuous cycle, for which he is forced in do even night
shifts. He has hyperosmia, but not cacosmia, with a headache that follows
immediately the episode of the troubled sense of smell. It is a long lasting
pain.
The case history.
He is born after a prolonged delivery with
fetal suffering and perinatal cyanosis. In the first year of life he fell
banging his head, but he did not lose his conscience. Moreover, he did not know
if they were anomalous neurovegetative symptoms in the first year of life.
This trouble first occurred when he was 12
years old.
Following intense olfactory stimulation, he
goes into a very short lasting delirium. Immediately after it he feels a
headache, front sided at the root of the nose, with sometimes left orbital diffusion.
The headache can last many hours, even till the following day. He tries to stop
it with analgesic drugs, which by now work a few (nimesulide) or badly ( a
compound of indometacine, caffeine, prochlorperazine). This last gave him a
kind of impatient, not euphoric excitement.
This morbid phenomenon may happen either in
the morning either in the afternoon. He says that it doesn't depend on stress (
or at least on what he considers such) and it doesn't necessarily follow a flu
episode. He never observed any seasonal difference, and affirmed to feel the
causing perfumes when goes to the cafeteria, but not when he works with an only
co-worker.
In the holiday time this trouble does not
change. His wife does not use perfumes. The odour of the just made coffee
induces this bother. Other smells of cooking do not disturb him, but of burnt.
He does not bear even the gasoline odour and cars exhaustion gas. He is
indifferent to the faeces' odour. When he suffers from a headache is more pale,
with eye sockets and more irritable.
Stress symptoms: He is not easy to fall asleep, for the rhythm
sleep-alertness altered from his work shifts. During the sleep, he wakes up. In
past he used to leave his bed for some time. Drooling during the sleep rarely
occurs. During night he does not breathe normally and so he uses the bandaids
to dilate the nostrils. Rarely he has bad dreams, never nighttime muscular
cramps. Often he gets out of bed tired. He bears badly both the light and
confusion. Nighttime bruxism, or daily dental shut do not occur. Rarely he
speaks during his sleep.
Any need to count uselessly, any dyslalias
were reported as well as disbandment or faint feelings, mediastinal oppression,
but gastritis.
He alternates constipation to diarrhea.
Oversweating does not run, nor the need to have frequent sexual intercourse.
His hair is fat. He doesn't feel the sudden need to curse or scream. Liking
sweet things, or meat and cube broth is normal. He suffers from the cold.
Other symptoms: His diet is limited, perhaps with too much fat
food. He tries to avoid milk and cheese, because they stimulate the gastritis
he suffers, but it may eat yogurt.
Depression: His mood shows some depressive moments, not
contingent upon these headache attacks, and he does not believe in a possibility
of control of his trouble. "It is not hard to imagine how much suffering
and how many difficulties in social relationships all that caused me. So, often
the depression could take the upper hand".
Symptoms of the troubled half-brain
dominance: To the test: Which is the
opposite of the colour Red? He answers: Yellow. His head is full of thoughts
with intrusive thought. There is an emergency of bad thoughts against beloved
persons. He was a Contrary Mary character.
Test therapy (daily doses, by the oral via):
Glutamine 125mg; Pyridoxine 75mg; Carbamazepine 100mg; Amitriptyline 10mg;
Bromazepam 1mg.
October 2004, the first checkup after 70
days of drug therapy.
The hyperosmia feeling did not change. After
20 days since the starting of the therapy he had an improvement. The headaches
were less frequent, less intense, and less lasting. The heavier episodes
persisted, but they were however better tractable with the painkiller
(nimesulide) which had recovered to work. The more intense headaches incline to
diffuse towards the left orbit. The inductive factor is always a strong
fragrant feeling.
From September beginning there was a
regression that still resists.
An EEG (never before performed): It had a
report of normalcy, but it shows delta sequences that are superimposed to the
basic alpha rhythm, presumably in C4-T6 according to Jaspers' standards (the
technician did not point out the electrodes disposition scheme). There were
also, in the same areas, scattered sharp waves, and two short sequences of
peaks and peak-and-waves with the tendency to the forward diffusion.
Stress symptoms: Perhaps he bears a little better the light and the
confusion.
The sleep improved as for quality and
length, and at the awakening the patient is less tired. The gastric troubles reduced
and the diarrheas disappeared.
Other symptoms: Appetite and sexual activity did not change.
Depression: The mood did not vary.
Symptoms of the troubled half-brain
dominance: The feeling of heavy head
with overcrowding thoughts did non improve. It rests always the emergency of
bad thought against beloved persons.
Therapeutic variation (daily doses, by the
oral via): Glutamine 250mg; Carbamazepine 200mg.
Discussion.
Even if it could not do another follow-up of
this case, we deal however with an extremely interesting history, which type
now can be the only one reported.
First the patient wrongly refers two
symptoms, which is his reporting of what he heard from other experts. He
doesn't absolutely have cacosmia, and the same for a migraine.
In the second place, nobody ever required,
in past, an EEG, in spite of the typical fit features of the headache trouble.
This EEG is not clean, and it is not "normal" as reported by the
first examiner.
Lastly, the response course of the drug
therapy is curious, with slow starting, an improvement after about twenty days,
and then regression, since September beginning.
This last temporal period corresponds to
seasonal variation negatively felt by at least about thirty patients with
various psychiatric pathologies. This addresses to an exact direction. There is
a low stress threshold that interferes with a partial non convulsive
epileptogenic activity.
The "switching" element (as it was
termed a time ago) of the epileptic attack is exactly the stress. It may even
be suitable as a variation of the balance between glutamate and GABA, both
brain neurotransmitters mainly involved in epilepsy.
Here the main internal stress could be done
to an excessive glutamate turnover (being the glutamate as the primary
neurotransmitter of the sensory afferent pathways) in a brain specific
structure (the amygdala? See Victor and Adams, 1989) following intense
olfactory stimuli.
The onset seems an other meaningful element.
This is happening in the puberty age when the brain is "poisoned" by
the quantitative blowup of the sexual hormones, then in a condition of
metabolic internal stress. We know that several epileptic forms begin in the
puberty. Moreover, in epileptic women, during the premenstrual period, with the
internal metabolic stress by the altered homeostasis of the balance between
estrogen hormones and progesterone, epileptic fits become more frequent
(Cocchi, 1998).
We don't forget the report of the perinatal
risk, with prolonged delivery and cyanosis, which could have elicited in a
stable way a greater sensitivity of some brain zones related to the olfactory
pathways.
The relationship between the sense of smell
and epilepsy has its even experimental literature (Bergamini and Mutani, 1967;
Devinsky, Khan and Alper, 1998; Chen at al., 2003; Ebert and Loscher, 2000;
Acharya, Acharya and Luders, 1998).
As more probable place of the epileptogenic
lesion was pointed out the mesial right temporal lobe (Lehrner and coll.,
1997).
A link between headache and troubles of the
sense of smell was discovered in 25 patients out of 50 investigated. Pleasant
or unpleasant odours could result in the attack of a headache in 11 of these
(Blau and Solomon, 1985). This is the only literature reference I found.
For what concerns the more intense odours,
just prepared coffee and exhausted gas of gasoline were reported from a patient
(Cocchi 2004) while "gasolinic" byproducts had unbearable smell for a
woman patient (Cocchi, 2002).
The place of the headache is even curious,
bein frontal but immediately over the root of the nose, with a poor tendency to
widen, and eventually only to the left side.
One could think that the headache is a
retroactive projection (going the structures of the cribriform lamina?) of
something that happens in a proximal brain area. The amygdala could be a
justifiable center for all that.
The initial therapy, by low dosing and
primarily as an antistress one) was prescribed when delivery troubles were not
known and the EEG was not performed. This maintained some positive results
among the stress symptoms (it improved the sleep, made the diarrhea disappeas,
reduced the gastritis) and this confirms the implication of the current stress.
The doubling of the carbamazepine is already
in the direction of a more suitable antiepileptic therapy. It is probable that
the dosing of this drug will should be increased.
References.
Acharya V, Acharya J, Luders H. Olfactory
epileptic auras. Neurology (United States),l 1998, 51: 56-61.
Adams RG, Victor M. Principles of Neurology.
McGraw-Hill, New York, 1989.
Bergamini L, Mutani R. Epilessia sensoriale
riflessa di tipo olfattorio nel gatto (lesione epilettogena amigdaloide causata
da cobalto). Boll Soc Ital Biol Sper (Italy), 1967, 43: 318-320.
Blau JN, Solomon F. Smell and other sensory
disturbances in migraine. J Neurol. 1985, 232: 275-276.
Chen C, Shih YH, Yen DJ, et al. Olfactory
auras in patients with temporal lobe epilepsy. Epilepsia (United States), 2003,
44: 257-260
Cocchi R. Pre-menstrual syndrome as the
paradigm of an internal biochemical stress. Melbourne, 1998. On internet, on
www.stress-cocchi.org/speculation3.htm
Cocchi R. An anosmia-hyperosmia case
with hypogeusia, from probable stress, Improved following an antistress drug therapy. June 2002
Cocchi R. A third case of anosmia-hyperosmia with ageusia,
following stress and possible viral infection, improved with an antistress drug
therapy. (Updated March 2004) <www.stress-cocchi.net/Other7.htm>
Devinsky O, Khan S, Alper K. Olfactory
reference syndrome in a patient with partial epilepsy. Neuropsychiatry
Neuropsychol Behav Neurol (United States), 1998, 11: 103-105.
Ebert U, Loscher W. Strong olfactory stimulation
reduces seizure susceptibility in amygdala-kindled rats. Neurosci Lett
(Ireland), 2000, 287: 199-202.
Lehrner J, Baumgartner C, Serles W, et al.
Olfactory prodromal symptoms and unilateral olfactory dysfunction are
associated in patients with right mesial temporal lobe epilepsy. Epilepsia
(United States), 1997, 38: 1042-1044.
Posted on Internet on 17 October 2004. Copyright by Renato Cocchi,
2004.
Author's address: dr. Renato COCCHI, via Rabbeno, 3
42100 Reggio Emilia
email: renatococchi@libero.it
Drug modulazione of stress reactions