A SECOND CASE OF
RECURRENT ATYPICAL DEPRESSION WITH AN ALTERED EEG (EPILEPTIC DEPRESSION?) IN A
27-YEARS OLD MAN.
Renato Cocchi, a neurologist and a medical
psychologist.
(Five other similar case histories)
Summary.
A young adult of 27 years at the first
consultation, after an episode that could be interpreted as "an epileptic
flight" with depressive traits, started a drug therapy of amitriptyline,
carbamazepine, and oxazepam then replaced by lorazepam. Subsequently fit
episodes rested with a depressive mood variation, reduction of the sociability
and of the speech use. Six years later, a second EEG control had a report of
normalcy like the first one. In 2004 this EEG was revised, and theta waves
sequences laid upon a slowed alpha rhythm, prevailing in the right side of
parietal-temporal areas, were observed. The increasing of the antistress-antiepleptic
drug therapy had progressively reduced the frequency of the fit episodes. Their
intensity narrowed down after further increasing of the daily doses, following
this reexamining of the EEG.
This recurrent trouble of an atypical
depression seems a further case of partial epilepsy, whose only manifestation
is of psychic type as possible epileptic depression.
Key words: Atypical depression, stress,
epilepsy, EEG, theta waves, epileptic depression, perinatal risk factor, drug
therapy, amitriptyline, carbamazepine, lorazepam.
Drug modulation of stress reactions.
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I recently published a first case of
possible epileptic depression with the following features:
1. Poor response to the serototoninergic
drugs, tricyclics and SSRIs;
2. Recurrent fit changes of the mood that
may be such for a long time;
3. Lack of any relationship with external clearly
identifiable causes;
4. An altered EEG but not meaningful for
epilepsy;
5. A good response to the antiepileptic and
antistress drugs;
6. Positive personality variations following
the therapy (Cocchi, 2004).
Checking the clinical cards of preceding
similar cases where an EEG examination was acted, I found at once some others.
In one of them the EEG had a referral as normal ( that is to say: not epileptic
). Since the case had some peculiar interesting symptoms, I wanted to report it
as the second one of a series.
The case hystory.
M, 27-years old at the first examination,
with diploma of technical high school, not marry. He works as mechanical
fitter. He doesn't remember to have heard about troubles during the pregnancy.
He had birth on the 41st week of pregnancy, by a dry delivery lasting at least
24 hours and then accelerated in the expulsive phase. The birthweight was 2800
grams. There is not any report on cyanosis, respiratory distress or
pathological neonatal jaundice.
In his first year of life, he started upper
respiratory tract infections, treated by antibiotics, for which on about three
years he was given the tonsillectomy. During the first year of life, there is
not any remember of other visible signs of previous possible brain suffering. Subsequently
he showed behaviour similar to the ADHD (a trouble of the attention with
hyperactivity), but with no impulsive traits. The hyperactivity lasted till his
pubertal years.
At school he had always difficulties either
for attention and memory, but to the Professional Technical High School he
succeeded in practical matters. To the end he held his diploma.
February 1998. He felt himself as bewilder,
confused, and he had to go away from his work and he wandered pointlessly and
without any destination (nearly an epileptic flight?). Anything seemed him as
negative. So, he worried much for what was occurring, which perhaps happened
once in past, but not in so intense way. He was standing badly the noise
produced in his working place. His head had fullness of fluctuating thoughts,
but this occurred already in past because he could not remember what he was
reading (a trouble of the concentration). Since some time he has a continuous
production of furuncles of middle-little greatness, pustulous, in his face and
in his back.
By suspecting some anomaly in the temporal
brain areas, I asked an EEG, which was referred as normal.
In spite of that, I prescribed a drug
therapy (daily doses by the oral via) with oxazepam 15mg; amitriptyline 10mg;
carbamazepine 200mg.
June 1998. He had an other episode, featured
primarily by depression, and difficulty to stay together other persons and to
speak with them. He inclines to find the cause of his discomfort in other
people, so creating at least a debatable relationship of cause and effect.
Since he does take the drug regimen I prescribed on last February, he can read
better and can remember much more. The oxazepam stopped and lorazepam 1mg took
its place (daily dose by the oral via).
May 1999. He resigned his job as mechanical
fitter because required him to wake up very early in the morning. Now he works
in a factory where they package the sugar, not far from his house. The working
time is more favourable, but the noise of the machinery disturbs it much. So he
has had to put the corks in the ears. As an average, at least once in a month
he has sudden depressive episodes, with interpretative thinking, social
closing, evident reduction of the verbal language. This is limited to sentences
of fewer words, only in reply to others' questions. Then he started to study
CAD programs. I prescribed the lorazepam 2mg daily.
2001. Since the new year he works as
mechanical planner in a firm to 20km distance from his house. In the preceding
workstation, he did not succeed to bear the continuous noise. It is possible
that the noise was stress causing which eased the fit. The new job gives him
much satisfaction. In spite of that, the depressive sudden episodes, for no
reason, of the same type of past, are going on. They are less frequent but they
not stopped. The supposed persecuting person is now a family member. During the
fit days he takes 3mg lorazepam every day, then he comes back to 2mg, since the
sudden depressive moment passed, about after 2-3 days. A ground secondary
depressive trait rests, as a link to not succeeding to stop these critical
episodes. He nearly missed the furuncles in his face, and reduced them in his
back.
2002. After having lost his job at the end
of July for closing of the firm, and having found a similar job in October, he
resigned even this one at the end of November. Then he started to work together
a team of technicians and engineers much considered in the field of the
mechanical planning. That was his objective in the long running. In this year
he could understand that his depressive relapses not have any relationship with
other persons, but it is something that happens within him, without external
causes.
2003. The fits continue almost with the same
rhythm, and even on his job some colleague is aware that in some moments he
becomes more silent, and darkened.
EEG examination (08.30.2003 ) with current
drug therapy (daily doses, by the oral via) by amitriptyline 10mg,
carbamazepine 200mg, lorazepam 2mg.
The EEG was referred as "the graphic
is without well identifiable anomalies".
In a further time I attempted to prescribe
the etosuximide, to replace the carbamazepine, but without appreciable results,
if not worsen.
In the meantime the lorazepam went to daily
2.5mg during the intercritical periods, to 3.75 in the days of fit.
2004. When he was 33, there was not any
noticeable variation as for the depressive fits, which happen always suddenly,
for no reason, temporarily modifying even the patient's personality. Between a fit
and the other they last from 30 to a maximum 45 days.
The same EEG graphic of August 2003 was
revised by me at the end of October 2004. So, after having asked the town
hospital laboratory that did it, to have the picking up the set out of the
electrodes, first not furnished and not written.
Revised report: Basic activity made by an
alpha rhythm of low-medium voltage, 8-9 Hz, more ample in the right half-brain,
irregular, reacting. On such rhythm in the temporal-parietal areas of the two
hemispheres, synchronous and asynchronous sequences of 5-6 Hz theta waves are
superimposed, with greater wideness to the right side, lasting 2-5 seconds. The
Intermittent Light Stimulation (ILS) and the Hyperpnea do not modify the
graphic.
Conclusion: The EEG shows temporal-parietal
non specific anomalies, with right-side prevalence, not sensitive to the
hyperpnea and to the ILS, from probable brain suffering in past.
I revised the drug therapy by prescribing
400mg carbamazepine, and 5mg lorazepam, and maintaining 10mg amitriptyline. It
seems to have a better result, being already passed nearly two months without
prolonged fit. Sometimes has a sadness moment, towards the end of the working
week, when he is more tired and under stress. He does not show it, and these
sad moments do not last more than 2-3 hours.
Discussion.
This second case of a possible epileptic
depression has aspects that make it similar to the first case I described
(Cocchi, 2004 ) and others that make it different.
As for the similar feature: 1. In the EEG,
referred as normal, has been found a theta waves presence in the
temporal-parietal areas, prevailing in the right side, with a basic alpha
rhythm slowed down. 2. The depressive episodes come out in form of a sudden
fit, even without any evident relationship with an express cause, a fact that
both patients eventually understood. 3. Both had a delivery suffering. 4. Still
common is the presence of intrusive thinking of fluctuating type. 5. During the
depressive period, the reality assumes a general negative tonality.
Elements of difference are: 1. The way by
which the depression show it that is much more atypical in this second case. 2.
The relationship between depression and work, negatively stressed in the first
case, nearly nonexistent in the second one. 3. The presence of weeping and of
symptoms like panic attacks in the first case, not existing in the second. 4.
Duration of the depressive episode, for weeks or months in the first case, 2-3
days in the second. 5. Clear symptoms of childhood depression in the first
case, but not evident depressive symptoms of this type in the second case,
perhaps because masked by symptoms of ADHD type. 6. Trouble of the
concentration, initially much heavy in the second case.
The present case has then peculiar features.
He had a delivery suffering even if he did not show it clearly with at least
two specific troubles in the first year of life. Surely he had a prolonged
perinatal stress, with trouble of non specific immunity, from which easiness to
URTI, since even the first year of life.
To this reduction of the not specific
immunity, the hyperactivity as a compensation producer of adrenaline and
cortisol, surely made its contribution. When I saw him for the first time, he
had even symptoms suggesting troubles of the half-brain dominance, as tendency
to the pessimism, and intrusive thinking with a severe trouble of the
concentration.
Well or badly, his body, with some
difficulty too, could go on till half the third decade of life. Then it could
not succeed more to sustain a discreet compensation and an evident
decompensation came out, as recurrent in a fit way, with depressive traits.
The therapy has always encompassed an
antidepressant drug(amitriptyline) and two antistress-antiepileptic drugs
(carbamazepine, and oxazepam then lorazepam).
This last two drugs had their doses
progressively increased. They in order reduced the intensity and the frequency
of the phenomenon, without being successful in controlling it definitely, at
least till now.
The EEG presence of theta waves, which
should not be more detected after the 25th year of life, suggested a
relationship between this atypical depression and the EEG trouble, as a nearly
surely residue of perinatal suffering.
Quoting here what I wrote to comment of the
first case I referred (Cocchi, 2004 ) "related specific brain areas, as
such, can go even by themselves to bioelectrical instability. So they can drive
to depression, without any apparent reason.
In other words, and excuse me for my coarse
definition, epileptic depressions can occur, which have as the only epileptic
symptom, the sudden variation (a fit) of the mood. They will be therefore a
form of partial epilepsy."
From that it follows, to well observe, that
these depressive disturbs, too originating from a bio-electrical trouble, can
be different, since 1. The origin of the trouble may have a different location
although in the same area; 2. They could have a different cortical diffusion in
the ictal moment; 3. In this last case, the suppressive mechanisms on such instability
can be different.
It is the ictal aspect that has to at once
induce some suspects.
A hyperosmia and an ictal headache
from intense olfactory stimuli are answering well to an
antiepileptic-antistress drug therapy (Cocchi, 2004). On the other hand, sudden
episodes of green colouration of the whole field of vision, as persisting after
six months from a skull trauma (Cocchi, 2004) may only have an explanation in
terms of "epileptic equivalent", if we use an old specification. In
both cases the EEG had not specific alterations.
Grecu and Kalman, in 1973, wrote about
"temporal episodic depressions", speaking of interictal forms. This
statement does think that those authors pointed out on episodes coming out in
subjects with other precise epileptic fits. I cannot be more exact to this
quotation because I was unable in finding the original text of their work,
besides written in Romanian.
According to Matarazzo, 1976, who
wrote about episodic or permanent depressions, the problem of the duration,
which badly fits the usual epilepsy, is known. Such depressions have epileptic
etiology, with localization to the brain temporal lobe. By basing on symptoms
found in four patients such an author presumed that the epileptic depression
has peculiar features. So, it should be possible to distinguish it clinically
from the other depressions. For the permanent forms he suggested the name of
"the temporal lobe depression." It does not result that the
Matarazzo's suggestion, 1976, did have much success.
A last problem remains. This forms, as it
seems, is an epileptic depression, and its disappearance, after the fit, occurs
after hours, currently, but initially after 2-3 days. In this it differs by the
normal epileptic forms that, except the continuous partial epilepsy of
Kojewnikow, and the epileptic status, do disappear their symptoms in a short
time.
Conclusions.
The seven-year course of this case of
atypical depression, after an episode interpreted as "an epileptic
flight" with depressive traits, drived to a possible diagnosis of
"epileptic depression."
The antidepressant and
antistress-antepileptic drug therapy on the fit episodes of depressive mood
variation, reduction of the sociability and of the speech use, has
progressively reduced the frequency of them.
Six years later, a second EEG control had a
report of normalcy like the first one. In 2004 this EEG was revised, and theta
waves sequences laid upon a slowed alpha rhythm, prevailing to the right side
of the parietal-temporal areas, were observed. The increasing of the
antistress-antiepleptic drug therapy had progressively induced further
improvement. This recurrent trouble of an atypical depression seems a further
case of partial epilepsy, whose only manifestation is of psychic type as
possible epileptic depression.
(Two other similar case histories)
References.
Cocchi R. 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. 2005
<www.stress-cocchi.net/Other14.htm>
Cocchi R. Short-lasting sudden episodes of
green colouration of the whole visual field, even persistent six months after a
cranial trauma. 2004 <www.reversebrain.net/Case10.htm>
Cocchi R. An atypical depression with an
altered EEG (epileptic depression?) and his evident improvement with
antiepileptic and antistress drug therapy. November
2004,<www.stress-cocchi.net/Depression6.htm>
Grecu G, Kalman C. [Clinical and
electroencephalographic observations made on 38 patients with "temporal
episodic depression"] Neurol Psihiatr Neurochir. 1973,18: 471-80. (In
Rumanian. No abstract available, quoted by Medline).
Matarazzo EB: [Chronic depression and
temporal lobe dysrhythmia] : Arq Neuropsiquiatr. 1976, 34: 173-187. (In
Portuguese, quoted by Medline).
Posted on internet on 2 January 2005. Copyright by Renato Cocchi, 2005.
Author's address: Dr
Renato COCCHI, via Rabbeno, 3
42100 Reggio Emilia