A DEMENTIA /
PSEUDODEMENTIA CASE,
WITH INTOLERANCE TO
BENZODIAZEPINES,
TREATED WITH ANTISTRESS
AND ANTIDEPRESSANT DRUGS.
Renato COCCHI, a neurologist and a medical
psychologist.
Summary.
It is reported the
case of a 74-years-old man, who already showed symptoms of intellectual
deterioration, where a kidney colic with elevated fever elicited a collapse of
the cognitive performances. Besides it, he had clear depressive aspects, and,
discovered by chance, intolerance to benzodiazepines. A more targeted drug
therapy for these variables lasting 10 months, allowed, besides the sleep
normalization, a discreet improvement of the intellectual performances.
A pseudodemential
share, of various extent, is always adherent even in the surely demential
forms, as creditable to some neuronal dysfunctionality. This is the only one on
which we can operate with a therapy, even with a drug therapy.
Key words: SDAT, pseudodementia, stress,
hypersensitivity, benzodiazepines, depression, drug therapy.
Drug modulation of stress reactions
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In 1997, in my paper "possibilities and limits of drug therapies
of dementias" I wrote:
"If we want to propose even drug therapy in dementias, we should
clarify some basic ideas. In the same time we have immediately to reduce any
excessive trust in a drug able to act alone, like somebody should assert.
We need starting from a trivial but
often forgotten statement: We cannot revive dead neurons. So, to find a target
in our therapeutic action, we have to reconsider the idea of pseudodementia.
The elaboration of the term
"pseudodementia" as opposed to "dementia" comes out by the
crossing of two conceptual axes. The first axis relates to depression in a
broad sense as the causal factor, and the second derives from reversibility, as
a clinical-therapeutic result (Savoldi, Zerbi, Cocchi 1986; Zerbi and Cocchi,
1986).
Clinical forms of pure pseudodementia,
so defined because fully reversed by suitable drug therapy, first did not show
any specific symptoms driving to a functional origin (Cocchi, 1996).
No doubts that to find frank depressive
aspects can direct both diagnosis and therapy, but these are not always so
evident. Eventually indeed, is the ex juvantibus criterion what until
now remains as the surer way to differentiate these two frames.
Only by that we can distinguish dementia
as organic irreversible disease, from pseudodementia as functional reversible
disease (Fisman, 1985; Bulbena and Berrios, 1986; Savoldi, Zerbi and Cocchi,
1986).
To distinguish dementia from pseudodementia,
the reversibility of the latter opposes non reversibility of the first one
(Reifler and Sherril, 1990). But we can value this reversibility as distinctive
criterion, only after therapy. If cognitive impairment comes back after
suitable therapy, we have faced a form of pseudodementia.
We propose to go over this entanglement
of contradictions by using functional inhibition instead of depression.
Functional inhibition does not imply any specific causal factor. Depression is
a term too strictly defined in psychiatry and only one possible causal factor
(Savoldi, Zerbi and Cocchi, 1986).
It is well known that CNS can show
reversible situations of reduced or abolished functionality.
From this we can infer that not all the
cells of an ictal brain area are, for example, or damaged or healthy. Between a
share surely damaged and a share surely healthy there are even cells that ware
less hit by the vascular trauma, but now they are ill functioning.
We maintain the same should happen in
dementias where a share of pseudodementia is constantly present, and able to
make worse the whole cognitive performance elicited by neuropsychological
tests. It does that throughout the impairment of cognitive mechanisms such as
attention, concentration, memory, thinking mobility, ability to use second and
third order integrative mechanisms, etc.
This pseudodementia that escorts the
dementia will be the target of any partly successful drug therapy because only
pseudodementia is reversible. "
I quoted what I wrote then, because the case
I shall report fits well to exemplify this double aspect of contemporary
dementia and pseudodementia. I think it the nomal happening. What can varies is
the share of the pseudodementia, and in that patient it had a large extent.
The case history.
06 February 2003.
Male, 74 years-old at first examination. He
is under a midium dosing regimen with zuclopentixol, biperidene hydrochloride,
and citalopram. In the last December he has got a diagnosis of Alzheimer's
dementia, on the base of the following symptoms: Confusion and lack of
orientation, memory loss, behavioural troubles, very reduced sleep, bilateral
visual and auditory deficits. In 2001 he had checked a right frontal
meningioma, without any need of brain surgery.
In January 2003 a neurologist confirmed the
dementia on degenerative basis (Alzheimer's disease) and prescribed olanzapine
5mg daily.
Mainly during the Eighty years, he suffered
of sudden fevers till 40 degrees which lasted 3-4 hours, and then they got off
to 35 C degrees. They did not give him any confusion. In the hospital to find
the cause was never successful. The relatives admit that in the last years
there were elements of intellectual difficulty, mainly for the short-term
memory and some praxias. However they were not particularly worrisome, as
attributed to the age.
In the latest two weeks he had elevated
fever following renal colic, treated in the hospital by antibiotics. Since then
there was a cognitive collapse.
Currently he is much inhibited and confused,
with an intellectual deficit, which however, to the first sight, could be less
serious than what appears. The spoken language is poor, scarcely fluent, but
altogether correct. There are evident depressive and anxious aspects.
The mental confusion is particularly present
at night, when he is always waking up after 1-2 hours sleeping, and he doesn't
want to more staying in the bed. He used walking along the house, pointlessly
and for no reason, and so he forces the elderly wife to be close to him, to
avoid he can leave his home. Moreover he does confusion with spaces of the
house, uses incorrectly the bath, at night he doesn't recognize the wife.
Therapy: Citalopram and biperidene
hydrochloride stopped.
I prescribed (daily doses, by the oral via):
Glutamine 250mg, vit. B1+B6+B1, 75mg + 75mg + 250mcg, carbamazepine 100mg,
zuclopentixol 4mg, amitriptyline 8 --> 14 mg, oxazepam 15mg.
20 February 2003. There are positive and
negative symptoms. At night he has many difficulties to maintain the sleep. He
inclines to have no rest. Walking did not change. In the afternoon he is worse.
The recent memory is always poor and he has visual and auditory hallucinations.
He doesn't find the way to go to the bath or other rooms of his home.
His bowel function is constipated, atonic or
spastic.
Now he has less pain in his legs, and he
does his rehabilitation program with more diligence. His appetite is discreet.
Sometimes he speaks in more coherent way and longer. He has more attention and
he remembers better past things.
Therapeutic variation (daily doses, by the
oral via): Zuclopentixol, amitriptyline and oxazepam stopped; I prescribed:
carbamazepine 200mg, lorazepam 0.5 mg, amitriptyline + perphenazine 25mg + 2mg,
glutamine 62.5mg, s-adenosil-l-methionine 100mg.
20 March 2003. Depressed with collapse
ideas, he succeeds to sleep 2-3 hours, then only for short periods. When awake
he is much confused. Now, he does not mourn during the sleep. He doesn't
remember the topography of his house, and so he does not find again the rooms.
He doesn't always recognize his wife. Now, he remains seated when he is eating.
For about two months I tried to improve the
sleep, adding and removing, niaprazine 30mg, 5-hydroxy-tryptophan 50mg,
clotiapine 3.3-6.6mg, barbituric acid 25mg, mianserine 20mg, clonidine 0.075mg,
valpromide 300mg, bromazepan 1.5mg, delorazepam 1mg without appreciable
results. It comes the doubt that he has hypersensitivity to the
benzodiazepines, so the delorazepam stopped and trazodone 1.3mg substituted it.
From the night following the trazodone
intake he started sleeping much more even if with some awakening, but without
burden confusional aspects.
On half May the drug therapy gets therefore
stabilized (daily doses, by the oral via): Niaprazine 30mg, trazodone 1.3mg,
carbamazepine 200mg, amitriptyline 14mg, 5-hydroxy-tryptophan 50mg,
dihydroergotoxin mesilate 3mg, glutamine 125mg, vit. B1+B6+B12, 75mg + 75mg +
250mcg.
27.11.2003: This is the last checkup. He
always took the drug therapy.
Positive results: For his son he has much attention, he recognizes the
relatives, he restarted to watch television. At night he normally sleeps. Since
the last May he improved, and now he does not have hallucinations. Usually he
wakes about the six of the mornings for going to the toilet. His anxiety
disappeared. He did eye cataract surgery, with local anaesthesia. A feverish
rise with mental confusion followed, but he recovered in a short time.
Now he has an anorthography with difficulty
at dictation. His signature became more readable. He uses eating without help
and he remains seated all the time of eating. He uses well the fork, but not
the knife, and not dirties himself with the foods. If he is asked for a little
help in the house, he does not refuse. His language is enough fluent, and has
restarted to say some jocular sentence. Normally, he attends the rehabilitative
centre three times for every week.
Unchanged symptoms: He has derangement with the toilet accessories, both
at night and at the day. He doesn't succeed to dress by himself, and ha some
difficulty in using the toilet. He cannot drive in a nail, neither to use the
key of the door. Because the lack of orientation, he does not go out. There are
difficulties to turn on and extinguish the lights. His recent memory does not
work well. Now he is unable play cards, although he was a good player
Therapy unchanged.
Discussion.
The subject is surely suffering from
dementia, but, according to the case history, the more probable diagnosis is
"senile dementia of Alzheimer type " (SDAT). The true Alzheimer's
dementia has an earlier onset.
His family was aware of some memory trouble
and of some praxical difficulty, but this all did not first arouse a particular
alarm.
Here a rather wide pseudodemetia was
present, as retrospectively diagnosed on the base of reversibility. The doubt
of a pseuodemential component however arose since the first consultation after
the parental report of the catastrophic worsening following the renal colic and
the elevated fever. The presence of depression seems more the norm than an
occasional fact, and it may be considered a reaction of stress elicited by the
illness itself.
Eventually, and this fact was a chance
discovery, there was also hypersensitivity to benzodiazepines leading to late
insomnia and mental confusion. This last was however present even when the
patient took two drugs regimens without benzodiazepines, before my first
meeting with him.
The depressive aspect, which then was at
once evident to me, had therapy with citalopram, but, previously, ignored.
From the case history even other information
arises. The hypothalamic centre of the thermoregulation was fragile, and this
brought to sudden high fevers which lasted fewer hours, and this centre
re-balanced throughout a phase of hypothermia (overcompensation?). The
hypothalamus is a brain structure very rich of GABAergic receptors, and the
GABA receptor is the first that modifies following stress of any external or
internal origin.
Till a certain age the body of that patient
seems had find compensation this situation lasted many years. Lately, and we
have two reports about it, the mental confusion followed the fever, which, I
need to remember it, is even a reaction from a severe stress.
The idea that dementia and pseudodementia
can coexist, each in various extent, in the same subject, too being the more
logical, has a poor audience. The result is a scarcely functional diagnosis and
sometimes, as here, an error in the therapeutic formulation. That one drives to
consider as poorly or not modifiable, a condition that could have, as it had,
notable margins of recover.
Is this an exceptional case? The other three
cases I reported (Cocchi, 1996) drive to think to a condition rather than
infrequent, with all the consequences that come out, for subjects the same and
for their families.
Conclusions.
A pseudodemential share, of various extent,
is always adherent even in the sure demential forms, and it is the only one on
which we can operate with a therapy.
To exemplify it, I reported the case of a
man of 74 years, who had already symptoms of intellectual deterioration, where
a renal colic with elevated fever elicited a collapse of the cognitive
performances. Besides it, he had clear depressive aspects, and, discovered by
chance, intolerance to benzodiazepines. A more targeted drug therapy for these
variables lasting 10 months, besides the sleep normalization, allowed a
discreet improvement of intellectual performances, considered by then lost.
References.
Bulbena A., Berrios G.E.: Pseudodementia: Facts
and figures. Br. J. Psychiatry
Cocchi R.: Drug therapy of pseudodementia as
modulation of stress reactions: Three cases. It. J. Intellect. Impair. 1996, 9:
173-180.
Cocchi R. Possibilities and limits of drug
therapies in dementias. It. J. Intellect. Impair. 1997, 10: 29-33.
Fisman M.: Pseudodementia. Prog.
Neuro-Psychopharmacol. & Biol. Psychiat. 1985, 9: 482-484.
Reifler B., Sherril K.: Dementias:
Reversible and irreversible. In. Tasman A., Goldfinger S.M., Kaufman C.A.
(eds): Review of psychiatry, Vol. 9. American Psychiatric Press, Washington DC
1990: 220-231
Savoldi F., Zerbi F., Cocchi R.:
Sull'entita' clinica di pseudodemenza. In: Atti del 1^ Congresso SIPG, Vol. I.
Idelson, Napoli 1986: 251-256.
Savoldi F., Zerbi F., Cocchi R.:
Possibilita' teoriche e pratiche di una prevenzione delle demenze. Minerva
Psichiatrica 1988, 29/2: 61-65
Zerbi F., Cocchi R.: La pseudodemenza
depressiva. Minerva Psicogeriatrica 1986, 1/2: 77-79.
Posted on Internet on December 2003.
Copyright by Renato Cocchi, 2003.
Author's address: dr Renato COCCHI, via
Rabbeno, 3
42100 Reggio Emilia
renatococchi@libero.it
Drug modulation of stress reactions
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