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ATTENTION-DEFICIET / HYPERACTIVITY DISORDER (AD/HD) A VAGUE DIAGNOSTIC FORMULATION WITH SERIOUS CONSEQUENCES

Autor: Ştefan Milea
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ABSTRACT: 

Firstly, the paper makes a short presentation of the history of the diagnostic formulations meant to describe what today is called AD/HD. We have underlined their great number, their inadequacy, the imposture of the clinical status assigned to the phrase “hyperkinetic disorder” and the merit of today’s American orientation in the field. The latter identifies, brings to the surface and places attention disorder to the centre of the basic psychopathological disorders; it offers a new „coat” for the basic clinical picture and a new term (AD/HD); it also places the field explicitly, within psychical pathology; as well as this , it directs the attention toward the neuropsychobiologic substrate of attention disorders. Secondly, the paper points out the negative aspects of the new concept and their unfortunate consequences. Among the drawbacks, the following are mentioned: • the use of the attention deficit concept. It ignores the fact that attention is a complex psychical function, involving both voluntary and involuntary attention which are in an antagonistic relationship. In the case of authentic forms of AD/HD, we are not dealing with an attention deficit but with an excess of involuntary attention (involuntary hyperprosexia). Only this involuntary attention is capable of generating and explaining the association between psychomotor hyperactivity, impulsivity and the diminishing of the capacity for voluntary attention • the lack of a clear option regarding the connection between the deficit of attention and hyperactivity. As for the negative consequences, mention should be made to the increasing possibility of diagnostic and treatment error.

In conclusion, the paper proposes, a simpler and more explicit term instead of AD/HD; one that is more direct and adequate: INSTABILITY OF ATTENTION.

 


 

1. Introduction

Approximate formulation characterized all the names which, over the years, covered psychopathological manifestations, which are now grouped under the diagnosis of AD / HD. That has never been ignored. It stands witness for the large number of names which and tried, without complete success, their luck in this domain. Some early approaches have failed the field such as the published classifications or treatises of: Henderson şi Gilepsie-1932; Kanner-1935; Miller-1936; Gerard- 1947; Tramer-1949; Heuyer-1952; Jensen- 1959; Ross-1964; Heuyer-1952; şi Lutz-1968. As it may be seen, among them there are, names of reference for the child and adolescent psychiatry and the first to be mentioned here should be Kanner, Tramer, Heuyer and Lutz. The explanation is simple: usually, the disorders falling into the present diagnosis formulation of AD/HD have been widely covered within the larger frame of behaviour disorders, an option which, as Thorley stresses (1984), has been dominant in Great Britain for many years.

At the same time, many points of view have been, and they still are subordinated to the myth of the hyperactive child. Other approaches, with more claims, become customized, preferring diagnostics based either on cardinal symptoms considered or on criteria considered etio-pathogenic.

In this context, the focus has been for a long time on one of the following landmarks, assessed as defining in the field, namely deficit of the moral control, instability, impulsiveness, irascibility, excitability of the child, lack of attention. On the level of etio-pathogenic factors , the lesion or the minor dysfunction caused by stroke. They were parts that were brought to the fore as diagnostic formulations (Table 1).

 

2. Th ree considerations on the history of the concept of AD/HD

It is not the place here to go into historical details, since we are not concerned with the evolution of the AD/HD concept. Nevertheless, we will comment on three issues subordinated to the statement concerning the permanent desire and difficulty experienced by the experts in approaching the reality; on the other hand it is also true that, very often, the specialists use to select diagnostic formulations which seem to be very far from the reality.

2.1. The first issue concerns the names given first to the lesion and secondly to the minimal brain dysfunction. They were imposed by the cool advantage conferred by the nomination of the etio-pathogenic support and by the numerous data attesting either the presence of disorders similar to AD / HD (in the case of psycho-organic brain syndromes) or the high incidence of pathological antecedents capable to affect the central nervous system of children with such disorders or the effectiveness of certain chemical psychoactive substances able to adjust certain dysfunctions in the structures of the brain.

Thus, during the years 1940-1960, these names had many supporters who believed that the issue of the causes and of the morphological substrate of these functional brain disorders was clarified.

In parallel, however, more data have accumulated which questioned the consistency, specificity and validity of those names today, which, for these reasons, have remained just history.

2.2. The second issue is considering our view that among the names used before the 80’s for the disorders covered today by AD /HD, the most appropriate one was psychomotor instability. This is because: • it strongly stresses the presence of two important facets of the phenomenon, the mental and the motor ones; • it highlights and focuses on the mental component • and it highlights what is essential and stable, namely the instability and, respectively, the excessive mobility of the mental processes.

2.3. The third issue concerns the name of hyperkinetic disorder (including its synonyms: hyperkinetic syndrome and hyperkinetic response) This name occupied a privileged place for a long time and unfortunately it is still quite widespread.

 

To support the latter claim, it is sufficient to mention that it is still preferred by the DCI 10 and it is still common in specialized literature. We say “unfortunately” because the name of the hyperkinetic disorder is totally inadequate.

It is inappropriate because, as it is defined in DEX (1984), hyperkinesia is an “exaggerated activity performed by the skeletal muscles or the smooth muscles of a hollow organ”, and therefore it is a name limited exclusively to neurological semiology scope and is designed to focus primarily on myoclonus, choreic, cerebellar and extra-pyramidal involuntary movements as well as organic tics. Even if one is willing to expand the area of hyperkinesia so as to include certain acts, the situation does not become clearer because, to the above mentioned disorders, one should add those belonging to psychiatry: such as stereotypes of movement, compulsions, our organic tics, rituals, and even the behavior determined by our emotional states, agitation, or the manic ones. Consequently, we must recognize that, for the disorders it proposes to represent with priority, hyperkinesia is too large being neither functional, nor specific enough.

It ignores the fact that we are considering a mental disorder and not a mere excess movement.

Certainly, I am not the first to notes the imposture of status of psychopathological entity conferred to name of hyperkinetic disorder. The above considerations were obvious to those who have chosen the name of the hyperactive disorder. This has the advantage that, on the one hand, it restricts the motor scope of the disorders only to those in which there is a psychological involvement, and, on the other hand, it is worth noting that the new name leaves room for abnormal manifestations that take place at mental level.

It is right that, at least on the surface, these manifestations are not perceptible, though they are very important, and, if one uses the name of hyperkinetic disorder they remain totally ignored. Using the phrase hyperactive disorder we underline indirectly that it is a psychomotor hyperactivity.

According to Thorley’s statement (1984) hyperactivity was considered the preferred term in America for a while. But, perhaps the biggest objection to the two names mentioned above, the hyperkinetic disorder and the that overactive disorder, is the fact that both relate to clinical events that are neither representative nor that specific to the area which they propose to define, because what we call AD / HD is primarily a mental disorder and not simply an excess of movement. The excess of movement and activity are in fact the most visible and easily noticed clinical manifestations the ones that “steal the show” and it is sure that they are the most unpleasant for the child’s entourage.

They do not represent what we consider the core disorder, respectively, the instability of the mental processes and of the attention in the first place. In fact, when the primary or basic disorders of a clinical entity are dissimulated, covered, or at least overshadowed by others either following the first or belonging to a condition which is only associated to it, the disorder is characteristic to the psychiatric clinic and beyond.

We give as an example only the attempt to suicide, a symptom with many faces. Thus, it may be the most representative manifestation of self-aggression, or an act that is intended to be hetero-aggressive in case it is intended to punish others, or demonstrative or simple blackmail or meant to free the unbearable pressure of the present. And the one who gives alms to a beggar thinking that in the next world they will receive tenfold can easily be mistaken as being charitable.

That is why, most of the times, we are required to work hard, without being always successful, in order to identify what is behind what we are offered at the clinic. As is the case with AD / HD where hyperkinesia, an exclusively motor manifestation, and hyperactivity are only surface secondary psychopathological phenomena, covering in the primary, deeper ones. It is what made the American authors in 1980, to proceed to a substantial restructuring of the field.

 

3. DSM III (1980) a new approach and a new nam e

With the DSM III, American authors operate two fundamental changes in the approach to what is now called AD / HD.

3.1. The first change consisted in the identification and highlighting of the area of attention disorder. In addition, by putting it in tandem with hyperactivity in what was called AD/DH (attention deficit with or without hyperactivity) the attention deficit disorder was confirmed as the basic constituent of what today we call AD / HD.

3.2. The second change is equally important. It gives maximum importance to the attention deficit by placing it in central position, before the hyperacti vity symptoms, so that the latter might be absent altogether Thus, new clinical forms appear which focus on the attention deficit with or without hyperactivity.

It is true that later versions (DSM-III-R and DSMIV with subsequent revisions) take impulsiveness also into account and now we speak about AD / HD and three clinical forms: the combined type, attention deficit with hyperactivity; the type with the prevalence of attention deficit; and the type where hyperactivity and impulsiveness predominate.

With these two options alone, we speak of a substantial basic restructuring of the field because: • they bring to the fore a totally new “coat” for the semiology of field, namely for its essential disorders; • they reconsider the biological basis of the field placing it firstly within the sphere of the neurophysiological and neuropsychological mechanisms underlying the disorders of attention. This offers a new, more valid target for the therapeutic approach. We state this because we know that: the more efficient the treatment, the better it targets the basic disorders, and not only the background ones. That is to say: the more pathogenic, the less symptomatic; • finally, this restructuring places the targeted field explicitly among the mental disorders, on the one hand, delimiting them clearly from the neurological ones and on the other hand, putting a definite end to the use of the name “hyperkinetic disorder” in this clinical context. Considering the above, two more observations must be made, namely: although over 30 years have passed since the term “hyperkinetic disorder” was recognized as being inadequate to be use in this area, it is still used with disengagement.

All the more troublesome is the fact that this wrong term is the source of regrettable diagnostic errors, where different hyperkinetic manifestations are assimilated with AD /HD and therefore, treated incorrectly. the second observation refers to the long period of time which was needed to decipher what is essential in the disorder that today is called AD/HD. In fact, in our view, even this term is not flawless, a fact which has consequences that can not be ignored. I propose to consider two of these consequences.

 

4. Th e nam e of AD/HD and its imperfections

The DSM option concerning the diagnostic criteria of AD/HD and of its clinical forms has raised well known and founded criticism.

This is pointed out, among many others, by Weiss and Trokenberg Hechtman (1987), Safer (2000) and Dobrescu (2004). We will not refer to the criticism, but to the nosology of this clinical reality.

4.1. The first observation focuses on the formulation “lack of attention” which we consider inappropriate. This is because:

  • referring only to the concentrating capacity of voluntary attention, it ignores the fact that, psychologically speaking:

attention is a complex function, interacting with all the other mental processes and, in particular, with thinking and affectivity; in its case one identifies • an involuntary attention,

  • a voluntary attention • and a third post voluntary attention , each with its own biological substrate (morpho- neuro- chemo- physiological) and one speaks of features like: mobility, ability to focus attention and resistance to disruptive stimuli, stability and volume; it has an external target “object” represented by stimuli in the surrounding world and a second, internal target offered both by intero and by proprioceptors as well as by the subjective space made up of images, ideas, memories, representations, thoughts, feelings, etc. which populate and even besiege, the individual’s mind every moment; between the involuntary and voluntary attention, there is a conflicting interrelation in that an increase in the first one reduces the second, and vice versa, an aspect that is particularly important in this case; in the young child, involuntary attention prevails on the voluntary one, a relation that changes continuously through the process of maturation of involuntary attention, resulting in increased resistance to irrelevant stimuli, in parallel with the development of the capacity to concentrate the voluntary attention; the relationship between voluntary and involuntary attention is amended: • gradually, under the influence of training and of favorable environmental conditions; • at every step, as a result of the interaction of various internal and external factors, influencing either the involuntary attention, or the voluntary one or both forms of attention.
  • The term ignores the AD / HD polymorphism: • etiological, •pathogenic, • genetic and • especially clinical. The AD/HD polymorphism is supported by numerous studies: (Taylor 2004), since there is the possibility that what we are offered at the clinic are more secondary manifestations concealing others, more significant ones, taking place in the background.
  • It is dependent, we consider, on the direct, exclusive and facile link, between the benefic response to the psycho stimulant medication and its explanation as being just a simple, direct activation of a deficit. Thus, we overlook the fact that, in the neuro- and psychophysiology, each functional balance is achieved by the antagonistic action of at least two instances: one activating and the other inhibitory. In this way, the functional excess can be achieved either by stimulating surplus or by decreasing the inhibitory control mechanisms, or by both mechanisms.

The reverse formula is equally valid, the deficit in the activity of a morfo-functional structure is achieved by an exaggerated suppressive action, by an excessive reduction of the facilitating action or by the convergent combination of the two mechanisms. These common features of the whole bio-regulating system make it very difficult to interpret the experimental data, even the most modern ones .

This is all the more true because today we know that the response of the same type of receptor to the action of a particular mediator varies, depending on its location in the central nervous system. For example, the effect of the narcoleptic medication, which acts upon D2 receptors, differs according to its preference for one location or another of the latter. In this context, we believe that what we call today the AD/HD, in a major sub-group, namely the most representative cases (where the child is like “quicksilver”) we notice first, that the involuntary attention is excessively alive and mobile, unable to select and stop too much where it is solicited moment by moment. We mean those lively and tireless children whose attention is too easily scattered and who pass too fast, without a prior selection, from one stimulus to another and from one activity to another, without completing whicheve takes a longer period of time. Such a clinical picture is the expression of what is called the involuntary hyperprosexia, a primary disorder, excess, or deficiency, to use a too general word, but in any case, it is not a lack of attention. On a secondary level, involuntary hyperprosexia determines both the deficit of concentrating the voluntary attention, which is emphasized by the term AD / HD, and the motor and psychic hyperactivity and impulsiveness. It is true that involuntary hyperprosexia is well disguised by the deficit of concentrating the voluntary attention which, for many various reasons is centre stage for those who are disturbed by the child’s inability to perform his tasks, even if he is well-meaning.

Moreover, in our opinion, the deficit of concentrating the voluntary attention in such cases, is more an expression of excessive mobility than of weakness and insufficient energy. Here, the voluntary attention can not handle its tasks, especially because, in the absence of the support of censorship from a rigorous filter, in the form of involuntary hyperprosexia, it is overwhelmed by the flood of random signals coming from the external and internal environment, which prevent it from fulfilling its tasks once they have started.

The above remarks make us say that, at the basis of what is is called the AD / HD, there is exaggerated mobility of involuntary and voluntary attention and not attention deficit, both being excesses not deficiencies. These are disorders which, given the interaction between attention and the whole psyche, externalize themselves by instability and impulsivity, too, both mental and motor.

Thus, in AD / HD, at least in the most representative cases, the idea of attention deficit is incorrect because ignoring the basic disorder, the excess of mobility in voluntary and involuntary attention is limited to stating only the secondary part of the reality, namely the decreased attention span of voluntary attention.

In fact, it is not the deficit of voluntary concentration of attention which is essential at the child with AD /HD but the fact that, due to excessive involuntary attention, he is constantly hindered by the many stimuli around him and even by those which inhabit his mind at any time, highly mobile association of images, memories or ideas. First of all, due to involuntary hyperprosexia the child with AD / HD can not focus his voluntary attention and neither can he to accede to the status of post voluntary attention. As such, it is not inattenţion which is mentioned the most often in the forefront of major symptoms but distractibility, exaggerated mental and motor mobility expressions superficiality and impulsiveness, which are direct expressions of involuntary hyperprosexia, respectively, of exaggerated mobility of attention to represent the main features of children with AD / HD.

4.2 The second objection related to the term of AD / HD that we intend to address is the ambiguity with which the relationship between attention disorder on the one hand, and hyperactivity and impulsivity, on the other, is treated The line separating AD from HD seems to say that we are faced with clinical situations with equal status, be they associated or not. It is true that, later in the text, their obligatory combination in varying proportions is mentioned; depending on these varying proportions of combination, distinct clinical forms are described, but the separation of the two abbreviations remained unchanged.

We believe that the mere recognition of involuntary hyperprosexia as background disorder is able to provide the domain with unity, boundaries and identity. This is because involuntary hyperprosexia can generate, explain and accept as natural the joint presence of both the decrease of the capacity of voluntary attention and of hyperactivity and impulsivity.

The phenomenon is an expression of the interaction between involuntary hyperprosexia and the whole psyche, interaction which, as it was already mentioned, is expressed as excessive mobility of impulsivity and instability, both mental and motor. If I were not so, the child with AD / HD would look like the one with primary deficit of the attention concentration of whatever cause (boredom, he does not like what he does, lack of training, interest or motivation, different somatic, neurological, psychiatric or organic diseases, etc.) to which voluntary hypoprosexia is not flanked by liveliness or motor and psychic hyperactivity, but, at best , by hyperkinesy.

We stress again that it is important to distinguish between hyperkinesy and hyperactivity since the latter involves intent and a mental component which is not only very active in AD / HD but, especially with age, as a rule, it can come to dominate the hyperkinesia, the motor expression of hyperactivity.

 

5. THE ABOVE ISSUES ARE NOT NEW

This is because they overlap, reinforce each other and aquire older views and data. Thus, speaking of neurophysiology of attention and of the state of alert, the description of the diffuse ascending projection system activation and its possible hyperfuncţion. is classic. Laufer (1957) Freibergs şi Douglas (1969) şi Buckley (1972) think that at the hyperactive child there is a high level of autonomous activity and that this has a high alert state as a result of excess excitatory processes through their own hyperfuncţion or , after Wender (1971) and Dyckman (1972) it is seen as a secondary consequence of the weakness of the inhibitory processes. In his turn, Oettinger and col. (1974) speak of the immaturity of the system which regulates the state ofalert, an idea suggested by data showing the presence in two thirds of cases of the bone age being inferior to the calendar age. There are a lot of data (Verry 1970, Satterfield and col. 1971, Wender 1973, Zentall 1978) which turned attention to the low level of cortical alert status which does not enable the selection of cortical stimuli. There are ideas issued and documented many years ago which we find reactivated in recent decades with the help of data provided by modern techniques of investigation of the background components placed at the base of neuro-physiological and neuropsychological processes of attention. In this respect it is stated that: • distractibility is part of the characteristic symptoms of children with AD / HD (Rutter şi col.-1975, Douglas -1983, Weiss şi Trokenberg Hechtman -1987) to which the recent authors (page 9) ??, explicitly added, the inability to ignore external stimuli when trying to perform a task; • it is not rigorously demonstrated that subjects with AD / HD are less attentive than children with other forms of psychologicaldisorder (Schaffer 1980); • or that a decrease in the inhibition of orientation attention takes place (Banasschevici and col. 2004 cited by Sergeant 2004) and this means involuntary hiperprosexia.

Also, in children with AD / HD, data of Moll and col. (2003) confirmed the presence of diminished intra- cortical inhibition. The hypothesis of the involvement of immaturity is suggested by the findings of various authors cited by Weiss and Trokenberg Hechtman (1987) and Lie (1992) who made retrospective studies according to which, with age, at more than 50% of cases there is a significant spontaneous decrease of the intensity of disorders. And the fact that the morphophysiological differences between children with AD / HD and normal ones in terms of caudate nucleus (Castilian and col. – 2002), or the amplitude of response of the evoked visual electric potentials and of the EEG aspects (Rothenberger (1995) plead in favour of this hypothesis. Moreover, dealing with issues underlying psychophysical processes of involuntary attention, Barkley (quoted by Trifan 2007) speaks of the damaging of the mechanisms of delayed answer. The author refers to the disorders of the capacity of inhibition respectively, for AD / HD, to facilitate a response to stimuli which brings to the fore the impulsiveness that DSM places on the background, in our view, without reason.

Entering into more detail, Jacob Bronowski (quoted Trifan 2007) speaking about the in the mechanisms that ensure the individual’s ability to respond to stimuli finds out four complimentary fenomena namely: separation of stimuli from affects; timing the response, internalization and processing significance of the stimulus, and finally, reconstruction according to which the organism reacts. In that way the stimuli are selected. In AD / HD this complex is functionally impaired, respectively, the involuntary attention becomes discretionary.

Certainly, the scientific literature abounds in data which do not support the above. This should not come as a surprise, given the heterogeneous nature of the field and, as a result of cases investigated and of the possibility of interpretation of the data which take no account of particular complexity outlined above, of the processes concerning the bio psycho physiological basis of attention.

 6. U nwanted consequences of imperfect nam ing

The fact that the name of AD / HD is inadequate has at least three major negative consequences.

6.1 The first negative consequence relates to the Higher difficulties of differential diagnosis and increased risk of wrong diagnoses. In fact, the emphasis on the idea of deficit of voluntary attention greatly complicates the differential diagnosis. This is because we are obliged to take into account the full range of disorders in which the child has such difficulties, whether primary or secondary, without specifying where and to what level they belong to the same diagnostic framework. Thus, the status of attention deficit is accordingly unclear: immaturity, lack of motivation, fatigue, the fact that the patient is not interested or does not like what he does, is bored because he already knows what it is all about or he does not understand the explanation, the notions being exposed too quickly or being too difficult for him and the lack of exercise and training. Here we should add the cases with obvious cerebral organic substrate. For example, it is well known the fact that usually, children grown up in rural areas, in terms of full freedom, until school age adapt themselves with difficulty to the rules imposed by the discipline of school and to the life in apartment blocks. Due to the too alert pace of deployment of action even the children exposed too much to cartoon programs may face the risk to present the immature attention suggested by ADHD. The idea of the presence of attention deficit disorder as main disorder, in practice and some weaknesses of attention present in children with clear organic brain lesions, with slight delays in language or mentald evelopment and even with autistic disorders create diagnostic difficulties even when the underlying disease is correctly identified.

Typically, in these cases, taking advantage of the etiologic nature of current classifications of psychiatric disorders, the idea of the presence of a comorbidity is the most readily available diagnostic option but not the most accurate,at least when it comes to treatment.

To give an example, this time the situation of a serious autistic disorder in which the presence of attention deficit, in reality a voluntary hyperprosexia this time, and of the stereotypes of motion interpreted as hyperactivity or hyperkinesy facilitate diagnostic confusion often the idea of a comorbid AD / HD.

The confusion is serious as some diligent observations Sporn and Pincser (1981) Schmidt (1982), Aman and Langworthy (2000) remark both the occurrence of adverse events and the amplification of stereotypes and hyperactivity.

6.2 The second negative consequence is the misleading of the therapeutic approach. Of course, I appreciated the American option which directed the chemo treatment from the chemical-neural- biological base of the hypekinesy and hyperactivity disorders to that of attention d isorders. But not to then attention deficit. This is because, in practice, the target of the treatment remains outlined vaguely, if not incorrect for many cases while the absence of markers to guide the optimal choice of the best medicine makes it possible the administration of a test treatment. Yet we know, this time, recommendations insist that we should overcome some drawbacks considered transitory and wait for several weeks longer It means not only unnecessary costs but also suffering induced to the child by the side effects , even if they are transient but also the erosion of the doctor’s prestige if the treatment failed.

6.3 The emphasis on attention deficit is also a factor that determines the contradictory character of the data of the studies meant to identify the neurobio- psycho-physiological basis in AD / HD. It is undisputed that the investigation of groups of children with a diagnosis that covers a clinical reality known for its heterogeneous character and etiologic and pathogenic polymorphism and thus the mechanisms at the origin of the psychopathological manifestations of AD / HD will not be able to give only results that will differ from study to study.

 

7. Advantages of recognizing the presence of involuntary hyperprosexia, respectively of, the excessive mobility of the prosexy activity as central disorder in AD / HD

We believe that recognition and placement of involuntary hyperprosexia, respectively of excessive prosexy mobility as central disorder within the clinical picture of children diagnosed with AD / HD has real advantages namely:

7.1 First, in the context of the interaction between attention and the whole psyche that generates excessive mobility and difficulty in concentrating voluntary attention and hyperactivity and impulsivity, the following can be easily explained: coexistence of hyperactivity, impulsivity and deficit of concentration of attention, their interdependence, their belonging to a common morpho-functional subsubstrate; the answer of all the disorders to the same medication, and why the clinic form described in DSM – III (1980) need to be eliminated as being unrealistic and characterized only by the deficit of attention.

We also mention the fact that hyperactivity is not only motor but also mental, the latter being often overshadowed by the motor one. In fact, it is known, the children with AD / HD talk a lot, a fact that externalizes part of what is going on in their minds. I make these provisions because, most often in a wrong way, the defined clinical forms delimitated depending on the prevalence of hyperactivity or of attention disorders have been usually take into account especially what is seen, namely the motor manifestation, the hyperkinetic expression.

In addition it should be remembered: not the fact that the clinical forms of attention disorder is evident are the majority, or that motor hyperactivity decreases spontaneously with age leaving the psychological activity in view; or that the AD / HD motor sphere, at least in intent, contains the idea of conducting a task even if, often, the intention is not completed.

7.2 Secondly, the new sense of AD / HD semiology allows centering the concerns related neuro chemo psycho physiology voluntary attention deficit to deepen the knowledge and the endorsement of that that underlying involuntary hyperprosexia and excessive mobility of attention in general. Thus it could be identified the potential of clinical markers, (morphological, neurochemical, neuro or psychophysical) able to differentiate on this basis any clinical forms, and provide benchmarks needed to guide preventive and curative therapeutic approach.

It is not just chemotherapy. We are convinced that if the psychologycal approach should be concerned not only with the deficit of voluntary attention but also with involuntary hyperprosexia and its unintended consequences, the child will benefit a lot. Moreover, we will understand and stress the need for adequate education of preschool children in which the training of the capacity to concentrate voluntary attention and to mature the involuntary attention should occupy a well defined place. In addition we should pay more attention to the negative consequences of watching cartoons in excess, even if they are quality ones and age-appropriate, on the process of attention development in the child. I used to emphasize in 2006 in Volume I “Primary prophylaxis in child and adolescent mental disorders” that by the their alert pace, cartoons defy reality and spare the child’s psychological immaturity, a reason why it is so much enjoyed by the child. They are not asked to be patient, to wait, to notice and analyze the details, to deepen the information and give answers, in a word, they did not seek nor entail voluntary ability to concentrate attention or thinking.

7.3 In the third place we consider it possible the individualization of the clinical polymorphism recognized as AD / HD has a significant group of cases with representative diagnostic symptoms that to which involuntary hyperprosexia constitutes the background disorder, an excess and not deficit of attention.

 

8. I nstab ility of attention a more direct nam e simpler, more explicit and appropriate for some children diagnosed as AD / HD

As noted above, in children with involuntary hyperprosexyia and excessive mobility of the prosexy function the idea of attention deficit does not seem satisfactory. We believe that it is not functional the step back that can be made if one speaks about disorder or attention deficiency because the wording becomes impractically universal. Nor explicit targeting involuntary hyperprosexia, although valuable, as it highlights the primary disorder, is not practical.

This is because it externalizes involving voluntary attention, motor activity, mental and even emotional, all of them marked by an excess of mobility, respectively, of instability.

This is the argument that makes us prefer the name of instability of attention.

This specificies which is the background or primary disorder, it recognizes its status as the central disorder connecting it with the past, represented by the name of psychomotor instability.

 

Bibliography

  1. Ajuriaguerra J. (1974) Manuel de Psychiatrie de L`Enfant. Masson, Paris.
  2. Ajuriaguerra J, Marcelli D (1989) Psychopathologie de l`Enfant. Masson Paris.
  3. Aman M, Langworthy K. (2000) Pharmacotherapy for Hyperactivity in children with Autism and Other Pervasive Developmental Disorders. Journal of Autism and Developmental Disorders 30, 5: 461-462
  4. Banaschevici T,Brandeis D, Heinrich H, Albrecht B, Brauner E, Rothenberger A (2004) Questioning inhibitory control as the specific deficit of ADHD –evidence forebrain electrical activity. J Neural Transm. 111: 841-864
  5. Brown S. Pollock H, Potter HW. Cohen DW (1937) Outline for Psychiatric Classification of Problem children. Rev. Ed State Hospital Press, Utica, New York
  6. Cameron K (1955). Diagnostic Categories in Child Psychiatry. British Journal of Medicine and Psychology, Vol. 28 (Part 1); 67-71
  7. Castellanos FX, Lee PP, Sharp W, Jeffries NO, Greenstein DK, Clasen LS, Blumenthal DJ, James RS, Ebens CL, Walter JM, Zijdenbos A, Giedd JN, Rappaport JL (2002). Developmental trajectories of brain volume abnormalities in children and adolescent with attentional-deficit/hyperactivity disorder. J. Am. Medical Assoc. 288: 1740-1748.
  8. Chess S (1959). An introduction to Child psychiatry, Grune and Stratton Inc. New York
  9. Chess S (1960). Diagnosis and treatment of the hyperactive child. New York State J Med.: 1379-1385
  10. CIM-8 (Clasificarea Internaţională a Maladiilor (1965) Editura Medicală
  11. CIM-9 (Clasificarea Internaţională a Maladiilor (1975) Editura Medicală
  12. CIM -10 (1993) Clasificarea Internaţională a Maladiilor . Revizia a 10- a OMS. Bucureşti. Editura Medicală.
  13. Classification Francaise des Troubles Mentaux de l`Enfant et de l`Adolescent (1990) PUF, Paris
  14. Clements SD Peters JE, (1962) Minimal brain dysfunction in the school age children.
  15. DEX – Dicţionar Explicativ al Limbii Române (1984) Editura Academiei Republicii Socialiste România
  16. Dobrescu I (2005) Copilul neascultător, agitat şi neatent. Ed. Medica, Bucureşti
  17. DSM-III (1980) Diagnostic and Statistical Manual of Mental Disorders (Third Edition) American Psychiatric Association
  18. DSM-III -R (1987) Diagnostic and Statistical Manual of Mental Disorders (Third Edition Revised) American Psychiatric Association
  19. DSM IV–TM (1994) Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) American Psychiatric Association
  20. DSM- IV-TM -1994 (2000) Manual de Diagnostic şi Statistică Medicală a Tulburărilor Psihice (Ediţia a patra). Asociaţia Psihiatrilor Liberi din România.
  21. DSM- IV-TR 2000, (2003) Manual de Diagnostic şi Statistică Medicală a Tulburărilor Psihice (Ediţia a patra revizuită). Asociaţia Psihiatrilor Liberi din România.
  22. Eck M Novicoff MC, Bonnet D (1973) Neuropsyhiatrie Infantile, Paris, English GS, Pearson GHJ (1937) Common Neuroses of Children and Adult WW Norton and Co, Inc. New York.
  23. Gerard M (1947). Psychological Disorders in Childhood. In E Harms Ed., Handbook of Child Guidance. Child Care Publications, New York.
  24. Henderson DK, Gillepsie RD (1932) A Textbook of Psychiatry 3-ed Oxford University Press Ltd. London.
  25. Heuyer G (1952) Introduction à la psychiatrie infantile. PUF, Paris.
  26. Jensen RA (1959). Child Psychiatry. In: I McQuarrie and VC Kelly ed. Brennenman`s Practice of Pediatrics WF Prior Inc Hagerstown Md.
  27. Kanner L. (1935) Child Psychiatry. Charles C Thomas, Springfild.
  28. Laufer MW, Denhoff E, Solomons S (1957) Hyperkinetic Impulse Disorders in: Children`s Behaviour Problems. Psychosomatic Medicine 19, 38-49.
  29. Lebovici S, Diatkine R, Soule M (1997) Nouveau Traite de Psychiatrie de l`Enfant et de l`Adolescent PUF
  30. Lie N (1992) Follow-up of children with attention deficit hyperactivity disorder. (ADHD) Acta Psihiatr. Scand. Supplementum 386. vol. 85: 1-40.
  31. Leeuwen th, Steinhausen Hc, Overtoom CCE, Pasqual- Marqui Rd, Rothenberger A, Sergent Ja, Brandeis D (1988) The continuous performance test revisited with neuroelectric mapping.
  32. Lutz J (1968) Psychiatrie Infantile Delachaux et Niestlé Neuchâtel.
  33. Mazet Ph, Houzel D (1979) Psychiatrie de L`enfant et de L`adolescent Vol 1 şi 2 Maloine S A Editeur.
  34. Michaux L (1967) Psychiatrie Infantile, PUF, Paris.
  35. Milea St. (1988). Principalele sindroame psihopatologice. Un Tratat de Pediatrie vol. 6, Meilă, Milea, Editura Medicală, Bucureşti.
  36. Miller E. (1936) Classification of the Disorders of Children. In: Sir Humphrey Rolleston ed. British Encyclopedia of Medical Practice Butterworth and Co, Ltd, London.
  37. Moll GH, Heinrich H, Rothenberger A (2003) Methilphenidate and intracortical excitability: opposite effects in healthy subjects and attention- hyperactivity disorder. Acta Psychiatr. Scand. 107 69.
  38. Rothenberger A (1995) Electrical brain activity in children with hyperkinetic syndrome: evidence of frontal cortical dysfunction. In: Sergent J (Ed) Eunethidis – European Approaches to Hyperkinetic Disorder. Trumpi, Zurich: 255-270.
  39. Ross DC (1964) A Classification in Child psychiatry. Privately printed at 4951 Philadelphia.
  40. Rutter M, Shaffer D, Sturge C (1975) A Guide to a Multiaxial Classification Scheme for Psychiatric Disorders in Childhood and Adolescence Institute of Psychiatry London.
  41. Afer DJ (2000) Are stimulants overprescribed for youth with ADHD? Ann. Clin. Psychitry 12: 55-61.
  42. Sergent J. (2004) EUNETHIDIS –Searching for valid aetiological candidates Attention-Deficit Hyperkinetic Disorder. Eur. Child and Adolesc. Psychiatry Vol. 13 Supl. 1:143-149.
  43. Schmidt K (1982). The effect of stimulant medication in childhood onset pervasive developmental disorders: a case report. Journal of Developmental and Behavioural Pediatrics 3: 244-246.
  44. Sporn A, Pinsker H (1981) Use of stimulant medication in treating pervasive developmental disorders. Journal of Psychiatry 138: 997-1003.
  45. Still GF. (1902) Coulstonian lectures on some abnormal physical condition in children. Lancet: 1:1o77-1082.
  46. Strauss AA, Lehtinen I (1947) Psychopathology and education of the brain-injured child. New York, Grune and Stratton.
  47. Suhareva G E (1955-1969) Kliniceskie Lecţii po Psihatrii Detscogo Vozrosta Vol 1-2 şi 3.
  48. Taylor E (1990). Syndromes of overactivity and attention deficit. In: Child and Adolescent Psychiatry Second edition Ed. Rutter and Hersov Blackwel Scientific Publications. Oxford London Edinburg.
  49. Taylor E (2004) European clinical guideline for hyperkinetic disorder – first upgrade. Eur. Child and Adolesc. Psychiatry Vol 13 Supl. 1:7-30.
  50. Thorley G. (1984) Hyperkinetic syndrome of childhood: Clinical characteristics. Brit. J Psyhiatry- 144: 16-24.
  51. Tramer M. (1949) Manuel de Psychiatrie Infantile. PUF. Paris.
  52. Trifan A, (2007) Redefinirea sindromului deficitului de atenţie cu hiperkinezie. Viaţa Medicală Nr. 15 pg. 6.
  53. Weiss G, Trokenberg Hechtman L. (1987) Hyperactive Children Grown Up The Guilford Press, New York, London.
  54. Wender PH. (1971) Minimal brain dysfunction in children. Wiley-Interscience. New York, London, Sydney, Toronto.