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The False Motor Debility in Children with Mental Retardation
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Renato Cocchi M.D., Ph.D. (Sociology)
English translation posted on the Internet on February 3, 2005
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
Copyright by Renato Cocchi, © 2005
Reprinted with the permission of Renato Cocchi|
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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.
Key words: False motor debility, mental retardation, Down syndrome, motor rehabilitation, Vojta, Bobath, Doman, cell dysfunction, cell function restoring.
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.
After nearly half a century neuromotor 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.
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 neuromotor 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 neuromotor 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 neuro-psychiatrists (Cocchi, 1992).
To believe however that
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.
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.
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.
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.
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.
Cocchi R.: Birth – The second breakpoint in the Down Subject's biological balance: Confirmation and implications. It. J. Intellect. Impair. 1990, 3: 179-183.
Cocchi R.: Cerebral palsy in Down children: Three cases. It. J. Intellect. Impair. 1990, 3: 327-330.
Cocchi R.: Does S-adenosil-l-methionine (SAMe) decrease articular laxity in Down children? Preliminary report. It. J. Intellect. Impair. 1990, 3: 141-143.
Cocchi R.: On difficulties of equilibrium control in Down children (A preliminary note). It. J. Intellect. Impair. 1991, 4: 267-270.
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 useful? 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.
Cocchi R.: Evaluation of balance in Down persons. An epidemiological and clinical investigation on 383 subjects. 2003.
Cocchi R.: The balance in 230 Down subjects. An evaluation after one-year antistress drug therapies. 2003.
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.
Cocchi R.: Study on bike riding in Downs aged 10 or more. It. J. Intellect. Impair. 1994, 7: 159-162.
Cocchi R.: Ligamentous laxity and hypotonicity in Downs. An epidemiological investigation on 510 subjects. 2003.
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.
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.
Cocchi R.: Tongue protrusion in Downs. An epidemiological survey on 510 subjects. 2004.
Cocchi R. Which relationship between tongue protrusion and joint laxity/hypotonia in Downs? An epidemiological investigation on 452 subjects. 2004.
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.
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.
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.
Crivelli C., Donati A., Cocchi R.: Cerebral palsy in Down's syndrome children: Another two cases. It. J. Intellect Impair. 1998, 11: 31-37.
Tassani G., Cocchi R., Pagani P.A.: Atlanto-axial instability in Down persons. neurologic risks in the sport practice, mainly in the judo. It. J. Intellect Impair. 1992, 5: 239-244.