THE FALSE MOTOR DEBILITY IN CHILDREN WITH
MENTAL RETARDATION.
Renato COCCHI, a neurologist and a medical
psychologist. Summary.
Summary.
This text started from the observation of
a false motor debility in Downs where it exists mental retardation not referable
to previous risk factors outside the chromosomal anomaly.
Such motor debility always improves, in a
short time (within 3-6 months), following a drug therapy that acts on
modulation of stress reactions. Excluding the hypothesis of a vicarious
substitution by other brain areas, the only possible explanation is that we are
dealing with a dysfunctionality of the cells of the brain motor areas, with the
result of a false debility by reduced functionality. Such false motor debility
does not necessarily justify the whole motor trouble, to which can contribute
other components (vestibular, cerebellar, visual and other ones) but it seems
the motor equivalent of the false mental debility. As such, it may be suspected
in all people with mental retardation and motor debility without any evident
motor lesions.
Word keys: False motor debility, mental
retardation, Down syndrome, motor rehabilitation, Vojta, Bobath, Doman, cell
dysfunction, cell function restoring.
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In the introduction to the investigation on the
anticipation of walking in Down children treated by drug therapy (Cocchi, 1989)
I wrote:
"One effect most frequently observed in
Down children to whom I have applied drug therapy has been an improvement in
their motor abilities.
This improvement is evident in both gross
motor activity (demodulation, running, going up and down stairs, kicking a
ball, biking), and fine movement (the handling of cutlery; cutting with
scissors; buttoning and unbuttoning clothes; tying up shoelaces; pretension,
direction and control in handwriting).
This improvement has been observed and
commented on, from a clinical point of view, by parents, teachers and
professionals involved in motor and psychomotor rehabilitation.
During nine-year practice I have seen that
drugs can affect various components of the Down child motor activity.
In particular I have noted:
- An increased strength;
- A reduction in joints' laxity;
- An improved sense of balance;
- Coordination and movement precision;
- The acquisition of complex motor
sequences;
- A reduction of clumsiness."
After other three years experience, I can
only reinstate what I reported above, and I started to investigate better these
aspects of the motility in Down children. In a preliminary paper on the
balance, I suggested them to be referred to a prevailing vestibular and
cerebellar dysfunction (Cocchi, 1991).
Then one of us suggested that some aspects
of this motor disturb are common to other mental retardation forms, while the
intolerance to the oscillating platforms, is specific (Cocchi, 1991).
We already wanted to investigate the
hypotonia presence, as considered a symptom of cerebellar dysfunction (Favuto
and Cocchi, 1992 ).
Waiting to investigate all the symptoms of
the motor trouble in Downs, and their mitigation or disappear following drug
therapies, we shall try the clarification of a greatly relevant problem, not
exclusive of the Down, so stated:
Here I shall try the clarification of a
problem of great relevance, not exclusive of the Down. It may be so questioned:
How can we justify of the positive results
in disabled motility, with or without any brain lesion, mainly when we can
reach positive results on it in a short time?
To the moment, the reasoning will develop as
the more probable suggestion, as the more economic one at least in energy
wasting terms. I shall use exclusively the support of known data and reported
phenomena, even if not inserted into a general frame of reference.
Does exist a therapy for
motor troubles?
After nearly half a century neur.-motor
rehabilitation (the various methods after Vojta, Bobath, Doman, Perfetti and
eclectic ones) we have to ask still the question: Exists there a therapy for
the motor troubles? It is hard to answer in an exhaustive way, independently
from the anecdotal affirmations and the dogmas of the rehabilitation
professionals. Today we do not surely know if these methods, even if early
applied and in a right way, are advantageous or their application obeys more to
emotional reasons, being said as the only available and able to reach results.
As for forms of sure damage as the cerebral
palsies (CPs), it seems acquired that they can improve or even entirely cure
with physiotherapy treatments (Koeng, 1966; Nelson and Ellemberg, 1982; Taudor,
Hansen, Melchior and Pedersen, 1986); Nelson and Ellemberg, 1982; Taudor,
Hansen, Melchior and Pedersen, 1986) or even without any treatment (Brandt,
1966; Illingsworth, 1970; Tizard 1980 as quoted by Nelson and Ellemberg, 1982).
This rises the doubt if the rehabilitation is really effective or it is an
appropriation of the results of spontaneous evolution.
The early application of the Vojta's method
in forms of spastic diplegia is reported as given increased results of its late
application (Kanda, Yuge, Yamori, Susuki and Fucase, 1984). The application of
the Bobath's method, compared with not specific game sessions, did meaningful
lesser results in four infants with different forms of CP. The physical
therapy, applied for 12 months, did not have better results than the learning
games treatment in 48 children with spastic diplegia (Palmer, Shapiro, Wachtel
et al., 1988). A search on the recovering the intellectual development with the
Doman-Delacato method drew not meaningful results, in this field (MacKay,
Gollogly and McDonald, 1986).
The controversy on the stimulation programs
had, from both sides of the barricade, own undecided defenders (Ferry, 1986;
Russman 1986; Hachinski, 1986), nobody of them did successfully in getting rid
of the straitjacket "brain lesion means neuronal death, for which no
possibility of any therapy ".
The never verified hypothesis of the
entrance in operation of so-called "vicarious motor areas"
cannot fully be proposed because it would require the put of too many
intermediary passages. Nevertheless, the neurologists and mainly all the child
neur.-psychiatrists thought differently, hoping that it corresponded to the
truth. They always tried to deny the permanent and inflexible nature of the
greatest part of brain damages in the pediatric age, by upsetting it. (Ferry,
1986).
The hypotheses of "the advantage of
the child age" in the recovery of early brain lesions, the "save
up" of function in little children, the supposed brain plasticity, the
neurons "sprouting", the increased DNA content in the brain DNA of
rats raised in fields rich of stimuli, all those are the face of the same
effort. This last denies the reality of a little child who grows with motor
disability of brain origin.
Given the premise of the irreversibility of
the damages, then the conclusion of Bax (1988) that denies any treatment or
therapy possibility, is correct. The child has a fixed encephalopathy and the
basic neurologic abnormalities do not will repair anymore. Therefore we do not
act a treatment to these children, nor we lead them in therapy; we give them
assistance and management, and we want that they are the more effective as
possible.
From a two-sided
conception to a three-sided one.
As stated in these terms, we need to bring
to the extreme consequence the affirmation of Bax (1988) just quoted. If we do not
apply therapies or treatments, but only assistance and management, all the
rehabilitative methods are the deceptive ideological presupposition of a
worldwide colossal fraud, stubbornly pursued since nearly half a century, by
the professionals of the neuromotory rehabilitation.
Assistance and management, beyond the
parents training to more suitable relationships with their disabled children,
can be reached with decidedly reduced costs in every sense, and not only in
economic one.
Personally I, do not have much sympathy for
the Italian professionals of the neur.-motor rehabilitation with whom I argued
often (Cocchi, 1986). I always found them with an attitude of uncritical
omnipotence, as they used to say that "only the physiotherapy can do
something". In Italy, but I believe even abroad, This assertion has
the favour of full entrusted reliance they had from pediatricians and child
neur.-psychiatrists (Cocchi, 1992).
To believe however that i. All these
professionals and the parents are self-deceiving and that the problem is only
the improvement of the parents-child relationship; ii. The relief of the
ability of communication, of feeding, of the posture, of walking and statics of
the child, and the reduction of the developmental future troubles, cannot be accepted.
All they frankly seem an incapability of observing the problem under an other
point of view.
Much more because the datum does not go with
the results I had in Downs by using drug therapy, as the anticipation of
walking (Cocchi, 1989) and the short-term motor improvement, documented even
with films, one of which shown during the conference. [See even added
references].
As already affirmed for dementia (Savoldi,
Zerbi and Cocchi, 1986) and for mental retardation (Cocchi, 1985) close to the
damaged share, in the same individual, there exists a share of cell dysfunction
responsible for a quota of the general deficit.
If we succeed to go out conceptually from
the state of absolute opposition (a cell or it is dead, or it is living and
healthy), we may enter a tripartite scheme (a cell is dead, or it is
living but sick, or it is living and healthy). Then it is easy to
understand that it may be a treatment or a therapy acting on the living but
dysfunctional cells (because they are "sick"), which can be driven to
improved functionality.
If the neuromotor rehabilitation therapies
need long times to get a result that has always even a biological
correspondent, an appropriated drug therapy may gain it shorter times. It can
be experimentally verified without any difficulty, as compared with any of the
rehabilitation therapies, or with of the learning games or with an any other
approach used to improve the motility of the disabled child.
Dysfunctionality of
brain motor cells: A myth or reality?
I said that a part of motor neurons, as
living but with reduced functionality, could be the key to resolve positively
the contradiction between the datum of recovering of a motor function and the
usual theoretical frame of reference. This last is: 1. A dead neuron cannot be
resuscitated; 2. The sprouting of new neurons, if possible, will never be the
fruit of the physiotherapy.
Exists there any demonstration of living
nervous cells, but "sick" then dysfunctional? The answer is yes. We
have now acquired the datum that an epileptic focus is made up by cells, often
around the lesion, which are living but "sick". Under particular
stimuli, which we can summarize as stress conditions (a physical, chemical,
biological or psychological stress) they give beginning to a synchronized, anomalous
electrical discharge, which is the starting point of the epileptic fit.
Although these cells can also have a part of
a brain motor area, one may object that motor troubles and epilepsy are
different phenomena and not each other comparable.
To stay in the field of the epilepsy, the
temporary postictal paralyses, said also Todd's paralyses, can already be the
demonstration of a temporary dysfunctionality, such to elicit an imposing motor
trouble, which however resolve in short time.
To this example too, one may object that is
not at all convincing since its cause is not linked to coming out of a brain
lesion. Moreover, the times of resolution are decidedly short ( hours, or a
day, as the maximum).
The brain haemorrhages and ictus, causing
hypoxic-ischaemic lesions in the adult, often give origin to motor deficits,
which can partially or entirely regress in much longer times. I do not believe
that people can express doubts about it. I think that it is difficult to affirm
that the posthaemorrhagic or postictal recovers, is an illusion, or that the
physiotherapy, in this cases, is without an exact function.
If one wants to play the contrary Mary, he
may oppose to this example, the daily bread and butter of all the neurologists,
that the adult brain and the childish brain are not the same. In this way he
threatens however to say that the brain of the child has reduced possibilities
of recover. Or, in other words, that hypoxic-ischaemic brain lesions that cause
CPs in the child are different, and more burden, of that hypoxic-ischaemic
brain lesions that cause motor paralysis in adults.
There is however a further datum that I need
to remember. In the so-called "inhibited" depression, in children,
adults or elderly persons, we find usually a motor deceleration that disappears
with the resolution of the depressive state (Wolff, Putman and Post, 1985 ).
It is the motor parallelism, similar for
causes and effects, of the cognitive deceleration that accompanies it. In
children it sustains the overwhelming majority of false mental retardation
(Cocchi, 1985; Cordella, 1986).
Therefore, it is more simple to bring back
the whole or partial reversibility of the motor trouble to the cellular
dysfunctionality, reversible as such. What does consist this cellular dysfunctionality
is a matter of hypotheses. The more probable, in the chronic forms is dendritic
and then synaptic reduction that follows the neurotoxic action of the
glycocorticoids and glutamate (Cordella 1988, 1989a and 1989b ), kept so from
the state of stress that every illness ( CPs inclusive) imposes to the body.
In the acute forms, as in the depressive
motor deceleration, the dysfunction is provoked only from the stress state,
possibly without any dendritic and synaptic decrease.
In this way it is possible to find a unique
explanation for the phenomena of the false mental retardation, of the false
dementia and of the false motor debility.
On the contrary, there is the risk to
multiply the explanatory hypotheses, going against to William Ockam principle (Frustra
fit per plura quod per pauciora fieri potest). The paraphrase of it is:
Among explanations having the same probability, we have to choose what is
sustained by fewer hypotheses. To well see, it is then the exact logical
equivalent of the principle of economy applied to the biological level.
Motor troubles in the
mentally retarded without evident brain damages.
The preceding reasoning may be considered as
a great deal probable explanation of the reached improvements in persons with
motor troubles from evident brain lesions. Moreover, the same may apply to the
therapy of motor troubles in subjects with mental retardation, when they cannot
point up as having a peculiar and detailed lesion of the motor brain areas, or
of other areas.
For convenience, over than for my long
professional experience, I shall refer on the children with Down syndrome.
We could term the motor trouble in these
persons as general clumsiness. In it, the various brain components, as necessary
to realize the motor action, participate every one by its share of the trouble,
because of a presumed diffused micro-lesions.
On the other hand, based on an investigation
of mine, these children seem own some protection against the anoxic-ischaemic
damages coming out from pre-, peri- and neonatal risk factors (Cocchi 1987;
Cocchi, 1988).
The increased CP prevalence in postnatal age
(Cocchi, 1990 ), seems related to the beginning of a diffused deterioration
that clearly accelerates after the birth (Cocchi, 1990).
Proposed various rehabilitation methods get
good results even if in a long time (Felicioli and Moretti, 1984) and the drug
therapy significantly gets it in a short time (Cocchi, 1989; Cocchi 1990). In
both results this happens following a share decrease of the false motor
debility by dysfunctionality of various brain motor areas neurons.
As I already wrote previously (Cocchi, 1991)
this neuronal dysfunctionality in the mentally retarded, generally may be kept
by the biopsychological stress that the same illness imposes.
In Down children, to this contributes the
endogenous metabolic stress induced by the acceleration of all the metabolisms
controlled by the genes allocated on the chromosome 21, which increased of the
50%, (the so-called "dosage effect", experimentally verified). It
occurs so, because these metabolisms are controlling not more by two genes
(100%) as normal but by three genes (150%) following the third chromosome 21.
Conclusions.
A motor debility partly or fully reversing,
has its more probable explanation in the presence of a share of false motor
debility, from dysfunctionality of the neuronal cells, caused by an active
stress. In the motor troubles of the mentally retarded without evident
neurologic damages, as for example, in the Down syndrome, the false motor
debility, ex juvantibus, seems to sustain the most part of the reduced motor
performance.
This type of explanation could open new
theoretical and practical perspectives in the field of motor troubles of any
origin.
References.
Bax M.: Controlled trial of physical therapy
at John Hopkins. Develop. Med. Child Heurol. 1988, 30: 285-286.
Cocchi R.: La pseudoinsufficienza mentale.
In: Strutture e dinamiche neuropsicopatologiche in età' evolutiva. Montefeltro,
Urbino 1985.
Cocchi R.: La farmacoterapia come ulteriore
ausilio nel trattamento del cerebropatico gravissimo. Atti del primo
aggiornamento regionale "II cerebropatico gravissimo". AIAS
Castelfranco Veneto 1987: 15-21.
Cocchi R.: Presenza di scavengers e
incidenza di paralisi cerebrali infantili da prematurità e basso peso alla
nascita in 381 soggetti Down allevati in famiglia. Giorn. Neuropsich. Età Evol.
1987, 7: 317-323.
Cocchi R.: The
anticipation of walking in drug treated Down infants: A controlled study. It. J. Intellect. Impair. 1989, 2: 15-19. <www.stress-cocchi.net/Down9.htm>
Cocchi R.:
Cocchi R.: Cerebral palsy in Down children: Three cases. First
printed in Italian on Riv. It. Disturbo Intellet, 1990, 3: 327-330.
Translated into English <www.stress-cocchi.net/Down21.htm>
Cocchi R. Does S-adenosil-l-methionine (SAMe) decrease articular laxity
in Down children? Preliminary report. In Italian on Riv. It. Disturbo Intellet.
1990, 3: 141-143, translated in English on 2001, <www.stress-cocchi.net/Down18.htm>
Cocchi R.: On difficulties of equilibrium control in Down
children (A preliminary note). Printed in Italian on Riv. It. Disturbo
Intellet. 1991, 4: 267-270. Translated into English
<www.stress-cocchi.net/Down30.htm>
Cocchi R.: Mental handicap today in Italy. It. J. Intellect. Impair.
1992, 5: 13-20.
Cordella L.: Mental pseudodebility: An expanding concept. It. J.
Intellect. Impair. 1988, 1: 3-8.
Cordella L.: Stress, glucocorticoidi e handicap: il danno pre- e
perinatale. Riv. It. Disturbo Intellet. 1989, 2: 75-83.
Cordella L.: Stress, glucocorticoidi e handicap. II. Le influenze postnatali.
Riv. It. Disturbo Intellet. 1989, 2: 93-101.
DeGangi G., Hurley L., Linscheid T.R.: Toward a methodology of
short-terni effects of Neurodevelopmental Treatment. Am. J. Occup. Ther. 1983,
37: 479-484.
Felicioli F., Moretti A.: Sviluppo motorio, comunicazionale e
linguistico ed evoluzioni dei livelli di apprendimento. In: Ce.Pi.M.: Aspetti
epidemiologic!, genetici, clinici, riabilitativi e sociali della Sindrome di
Down. Ce.Pi.M., Genova 1984: 307-342.
Ferry P.C.: Infant stimulation programs. A neurological shell game?
Arch. Neurol. 1986, 43: 281-282.
Hachinski V. : Infant stimulation programs. Arch. Neurol. 1986, 43: 283.
Kanda T., Yuge M., Yamori Y., Suzuki J., Fukase H.: Early physiotherapy in
the treatment of spastic diplegia. Develop. Med. Child Neurol. 1984, 26:
438-444.
MacKay D.N., Gollogly J., McDonaId G.: The Doman-Delacato treatment
methods. II. Follow-up study. Br. J. Ment. Subnormal. 1986, 32: 13-19.
Nelson K.B,, Ellenberg J.H.: Children who "outgrew" cerebral
palsy. Pediatrics 1982, 69: 529-536.
Russman B.S.: Are infant stimulation programs usefui? Arch. Neurol.
1986, 43: 282-283.
Palmer F.B., Shapiro B.K., Wachtel R.C., Allen M.C., Harryman 3.E.,
Mosher B.S., Meinert C.L., Capute A.J.: The effects of physical therapy on
cerebral palsy: A controlied trial in infants with spastic diplegia. New Eng.
J. Med. 1988, 318: 803-308.
Savoldi F., Zerbi F., Cocchi R.: Sull'entità clinica di pseudodemenza.
In: L'invecchiamento tra paura e desiderio. Vol. I. Idelson, Napoli 1986:
251-256.
Taudorf K., Hansen F.J., Melchior J.C., Pedersen H.: Spontaneous
remission of cerebral palsy. Neuropediatrics 1986, 17: 19-22.
Wolff E.A., Puttnan F.W., Post R.M.: Motor activity and affective
illness. Arch. Gerì. Psychiatry 1985, 42: 288-294.
This
text was first printed in Italian on Atti del III Convegno di aggiornamento: Il
disturbo cognitivo in età scolare: Disturbi motori e psicomotori e difficoltà
di apprendimento (a cura di R. Cocchi), GISSTIMMAI editore, S. Costanzo 1992:
63-68.
Between 1992 and 2005 the research on the motility in Downs was pushed
into various fields as reported below:
Cocchi R. Evaluation of balance in Down persons. An epidemiological and
clinical investigation on 383 subjects. 2003,<www.stress-cocchi.net/Down35.htm>
Cocchi R. The balance in 230 Down subjects. An evaluation after one-year
antistress drug therapies. 2003 <www.stress-cocchi.net/Down36.htm>
Cocchi R. Comparison on balance development in Downs aged from 13-24 to
61-72 months, not pretreated and pretreated with antistress drug therapy.
2003<www.stress-cocchi.net/Down37.htm>
Cocchi R.: Study on bike riding in Downs aged 10 or more. It. J.
Intellect. Impair. 1994, 7: 159-162.
<www.stress-cocchi.net/Down16.htm>
Cocchi R. Ligamentous laxity and hypotonicity in Downs. An
epidemiological investigation on 510 subjects.. 2003, <www.stress-cocchi.net/Down34.htm>
Cocchi R. Gestational age at delivery and laxity / hypotonia in Downs:
Is there a link? An epidemiological extension of two separate investigations on
a series of 510 subjects. 2004,
<www.stress-cocchi.net/Down45.htm>
Cocchi R. Low birth weight and joint laxity / hypotonia in Downs. Is
there some relationship? An other epidemiological development of two preceding
different investigations on a series of 510 subjects.. 2004
<www.stress-cocchi.net/Down46.htm>
Cocchi R. Tongue protrusion in Downs. An epidemiological survey on 510
subjects. 2004 <www.stress-cocchi.net/Down42.htm>
Cocchi R. Which relationship between tongue protrusion and joint laxity
/ hypotonia in Downs?
An epidemiological investigation on 452 subjects. 2004
<www.stress-cocchi.net/Down43.htm>
Cocchi R., Favuto M.: Hyperkinesis in Down's syndrome: A survey on 510
persons. It. J. Intellect. Impair, 1997, 10: 19-23. <www.stress-cocchi.net/symptoms4.htm>
Cocchi R., Favuto M.: Hyperkinesis in Down children aged up to 12
years: A survey on 442 cases.. It. J. Intellect. Impair. 1997, 10:
25-28. <www.stress-cocchi.net/symptoms5.htm>
Cocchi R., Favuto M.: Time course of hyperkinesis in
Down's syndrome: A survey on 498 persons. It. J.
Intellect Impair. 1998, 11: 141-146.
<www.stress-cocchi.net/symptoms7.htm>
Cocchi R., Favuto M.: Study on bike riding in Downs aged 10 or more and
treated by drug therapy It. J. Intellect. Impair. 1995, 8: 31-36
<www.stress-cocchi.net/Down17.htm>
Crivelli C., Donati A., Cocchi R.: Cerebral palsy in Down's syndrome
children: Another two cases It. J. Intellect Impair. 1998, 11:
31-37. www.stress-cocchi.net/Down3.htm>
Tassani G., Cocchi R., Pagani P.A.: Atlanto-axial instability in Down
persons. neurologic risks in the sport practice, mainly in the judo. First
printed in Italian on Riv. It. Disturbo Intellet. !992, 5: 239-244. Translated
into Englisg www.stress-cocchi.net/Sport2.htm>
Translated
in English and posted on internet on 3 February 2005. Copyright by Renato
Cocchi, 2005.
Author's address: dr Renato Cocchi, via Rabbeno,3
42100 Reggio Emilia
renatococchi@libero.it
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