PSEUDO-DEBILITY IN
MENTAL RETARDATION:
A FRAME OF REFERENCE
Summary
Mental retardation
is defining a functional phenomenon,
i.e. the reduced performance in
intellectual tasks. This impairment
can be
produced by two different
pathological conditions: 1. a
true mental deficiency originated by lesion and death of brain neurons; 2. a
false deficiency (pseudodebility) mostly due to functional inhibition of brain
areas, structures or pathways involved
in intelligent behaviour.
These two conditions
differ because pseudodebility is fully
reversible when correctly treated.
In other
terms, besides lesional debility
there always exists a share
of treatable pseudodebility of
primary origin (the same factors that produced
the lesion produced also
functional impairments in the surrounding neurons) and of secondary
origin (the consciousness of own debility produced more intellectual inhibition of psychological and
relational origin).
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This fact asks for a reflection. Having
seen over than 500 Down subjects, at the moment I will refer to
these patients
Patients’ parents,
teachers and professionals
have clearly seen
and reported such progress. This progress
coming out in Down children treated with drugs give rise to a
very important problem.
What is the
neuropathological basis of such positive results in brain damaged mentally retarded,
mainly when, after a comparative short
period of drug therapy, we can see evident
improvements? For the moment my argument should only be viewed as a very
probable explanation since it is the easiest to be developed.
If we consider damage as not going to go
backwards, Bax’s inference
(1988) which deny the chance of
treatment or therapy can be accepted as correct, even written for CP.
Therefore we are no treating these children, nor do we
provide a therapy - we are providing care and management and we want it to be
as effective as possible".
As for mental deficiency, I wrote some years ago
(Cocchi 1985) that beside the brain lesion,
in the same subject had to be
suspected a component
of cell dysfunction, to which a share of the overall deficit
should be due. We must get
rid of the concept of full opposition (a neuronal cell may be either dead, or alive and healthy). I think that the three-party scheme
(a neuron may be either dead,
or alive but sick, or alive and healthy) is more useful
(see Fig. 3).
Then it
is easy to understand
that a treatment or a
proper therapy on alive but
impaired cells (because they
are "sick") might exist. In such a way these
cells may be improved.
For
the present, education or behaviour therapies, though
with poor results, seem to be satisfactory, failing
all else.
Moreover
it is fully compatible with education or rehabilitation programs. The definition
itself of mental retardation is hereby specified.
- caused by pure
dysfunction (full mental pseudo-debility);
Both
of them coexist in the same subject.
Dysfunction
of brain cells: myth or reality?
Do we have any evidence of the existence of
alive neurons, which are "sick" and then with a dysfunction? The answer is: yes we do. By now the fact
that an epileptic focus
is made by alive cells but sick, often around the lesion,
is well known fact. Under the
effect of special stimuli, which are
all stressors (physical,
chemical, biological or psychological stressors) these cells start up an
anomalous discharge. This is the starting-point of an epileptic fit.
Although
these cells can be also part of a brain area such as the temporal region, whose links with intelligence certainly exist
but are not well defined, one can object that mental retardation and epilepsy
are different and not comparable phenomena.
It
is however urgent to point out another
fact. In the forms of depression so-called
"inhibited" a cognitive
slowing down is often put
into light. In childhood
depression this happens in 2 out of 3 cases (Nissen,
1973). This process concerns
the greater number of mental pseudo-deficiency forms
in children (Cocchi, 1985; Cordella 1988). On the other hand psychodrug
therapy is to be seen, or at least it
should be, a therapy of the neuronal dysfunction. It is therefore easier to relate the partial
recover of cognitive impairment to cell dysfunction, reversible as such.
At
the moment we do not exactly know what such a neuronal dysfunction is. The most
probable hypothesis refers to
reduction of dendrites and then
synaptic decrease, as a result of neurotoxic effect of glucocorticoids and
glutamate (Cordella 1988, 1989a
and 1989b). Such a reduction is preserved by
the stress condition
that every chronic disease (mental retardation included) imposes
on the organism. In acute forms, such as in cognitive slowing down in
cases of pure depression, the dysfunction would be fully caused by stress
condition, probably without any
dendrites or synapses reduction but with decrease of receptor sites.
In
such a way it is possible to find out a single explanation to mental pseudo-debility, pseudo-dementia and also to
motor pseudo-debility. Otherwise we may run the risk of needing of more
explicative hypothesis. This would violates Occam’s razor principle, the exact logical counterpart of the
principle of economy at biological level.
Previous
argumentation might be accepted in order to explain any improvement which could be obtained
in mentally retarded children with evident brain
lesions. All the more reason, the
same argument may be considered valid
for the reduction of mental retardation in those subjects where is not possible to
determine a specialised lesion. This is odd to the cognitive or
other brain areas.
The cognitive
disease of these
subjects may be
defined as a
general retardation.
In any case, if the drug therapy gets evident
results in a short time, it can only act
through the reduction of part of the
mental pseudo-debility caused by
neuronal dysfunction. This
portion is connected to the true mental deficiency and it is jointly
responsible for the overall
mental retardation. As it has been
said before (Cocchi, 1991)
this neuronal dysfunction in
mentally retarded can generally be preserved by the
bio-psycho-social stress which the disease
itself implies. Yet a metabolic
endogenous stress, induced by the acceleration of all metabolisms which
are controlled by genes placed on the
chromosome 21, also persists in Down children.
This metabolic stress was the principal cause of a
negative influence on the brain
cognitive areas since their differentiation, because it starts from
the conception, or little after, in mosaic forms.
The
treatment of this part of mental pseudo-debility with drugs in such subjects
has obtained positive results in short time.
This fact opens the way
to further practical and
theoretical prospects in the field of cognitive diseases and their treatment.
References.
Cocchi R.: La pseudoinsufficienza mentale. In: Strutture e
dinamiche neuropsi-copatologiche in eta’
evolutiva. Montefeltro, Urbino 1985.
Cocchi R.: Presenza di scavengers e incidenza di
paralisi cerebrali infantili da prematurita’
e basso peso alla nascita in 381
soggetti Down allevati
in famiglia. Giorn. Neuropsich.
Eta’ Evol. 1987, 7: 317-323.
Cocchi
R.: The birth as a second breakpoint in the biological balance of Down’ syndrome subjects: Confirmation and implications. It. J. Intellect. Impair.
1990, 3: 179-183.
Cocchi R.: Paralisi cerebrali infantili in bambini
Down; 3 casi. Riv. It. Disturbo Intellet. 1990, 3: 327-330.
Cordella
L.: Mental pseudo-debility: An expanding concept. It. J. Intellect. Impair. 1988, 1: 3-8.
Cordella L.: Stress, glucocorticoidi e
handicap. II. Le influenze post-natali. Riv. It. Disturbo Intellet. 1989, 2:
93-101.
Gillberg
C., Schaumann H.: Epilepsy presenting as Infantile Autism? Two
case studies. Neuropediatrics
1983, 14: 206-212.
Nissen
G.: La depression masquee chez l'enfant et l'adolescent. In:
Kielholz P. (ed) La depression masquee, Huber, Berne 1973: 135-151.
Savoldi F.,
Zerbi F., Cocchi R.: Sull'entita' clinica di pseudodemenza. In: L'invecchiamento tra paura e desiderio.
Vol. I. Idelson, Napoli 1986: 251-256.
Paper presented
during the IX World Congress of the IASSMD. Brisbane / Broadbench, 1992.
Printed on It. J. Intellect. Impair. 1992, 5: 137-142
Author's
address : dr Renato COCCHI, via Rabbeno, 3
42100 Reggio
Emilia (Italy)
renatococchi@libero.it
Testo in italiano
Mental retardation
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