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Introduction: Estimates of the prevalence of autism and pervasive developmental disorders (PDD) are discordant and are moving towards an apparent increase in rates., Literature Review: The studies carried out since 1966 illustrate the variability of the protocols used and explanatory hypotheses put forward. These investigations are difficult, sparse, but still growing at the same time that a debate develops on the possible increase in actual prevalence. Indeed, the rate initially admitted for classic autism was 5/10,000, then 1/1000 with an expanded definition to the forms, but the current figures are very different (almost 0.7% for all PDD), and this increase raises questions. The arguments in favour of an apparent increase are primarily methodological. Several biases are encountered when one compares the recent publications with those of previous years. First, autism is better known and recognized than 30 or 40 years ago. Then, the diagnostic criteria used over time are changing variables, and comparisons difficult. Recent studies using the criteria of a broader definition of autism, polyhandicap with severe retardation and autism signs of lighter forms. The fact that children with autism are diagnosed more frequently in the younger age could also occasionally lead to an artificial increase in the number of cases identified in new surveys in populations of young children. Other factors are cited to explain the current increase. There could be higher rates of autism (and mental retardation) among children of migrants from distant countries, with the aetiological hypothesis of maternal infections, more frequent due to immune deficiency against infectious agents depending on the environment, metabolic decompensations also related to changes in surroundings, or more births from unions among migrant mothers and men with Asperger syndrome (with increased risk of paternity of a child with autism). Other theories relate to pollution, vaccinations, a growing number of premature babies; all assumptions that appear, for the time being, insufficiently explored and documented. The issue is also one of the motivations underlying these steps, and setting a parallel prevalence actually increased with this or that factor has presently been scientifically validated. Finally, if a careful reading of recent publications indicates that autism has become more frequent; assumptions that describe an increase in "artificial", based on methodological arguments, seem to be more consistent. EFFECTS OF EXTENSION OF DIAGNOSTIC CRITERIA AND NOSOGRAPHY FOR PDD: Today, the recruitment of individuals with autism in a population far exceeds the initial criteria of Kanner in the 1970's. It includes clinical forms with associated pathologies, or lighter and probably more frequent clinical forms. Other assumptions arouse interest, but also controversy regarding their relevance. The enumeration of cases of PDD in a population is actually at its beginning. In the 1970's, "childhood psychoses" (the term then used) seemed rare. The identification of cases was probably the main reason. Long available figures remain scarce, and their rate increases gradually from the 1990s, but is, in fact, a problem of inflation. What is the part played in this flight of changing diagnostic criteria and substitutions, or other methodological effects? Or even opportunistic effects, if we speak of an epidemic to undermine a variety of factors. The evidence provided so far is the improved identification of cases, enlargement of the concept, and better shared diagnostic criteria. However, the validity and limitations of clinical forms are still vague and unresolved., Discussion: How to study epidemiology in the future - to move forward, studies should be designed with partners' medical history and medicosocial studies, based on a better consensual methodology, epidemiology, statistics and diagnosis, with a definition of the thresholds for inclusion, and arbitration procedures. On this basis, a study must also be coordinated with those concerning mental retardation, learning disorders, etc, otherwise the same topics will be counted twice or even three times. As for the addition of syndromic forms of PDD (those with known aetiology), their number is still below a proportion sufficient to be an appeal. Moreover, another problem exists: the degree of membership of each of these syndromes, or individual cases, or autistic spectrum disorders (internal variability phenotypes). For the moment, we could design two studies included better: developmental disorders and associated pathologies. Regarding the "ethic" dimension, a more regular diagnosis of PDD (preferred to that of mental retardation or learning disorder) will lead to shared practices and set limits for greater recognition.

As childhood autism is usually considered as a developmental disorder, complete assessment of each patient requires non only clinical examination but various biological investigations: EEG and evoked potentials recordings, biochemical dosages and sometimes, cerebral blood flow measures, molecular biologic explorations.... These investigations help to understand neurophysiological dysfunctionings which underly different autistic syndromes. It therefore seems necessary to develop quantified clinical tools which could allow closer matching between clinical evaluations and biological numerical data. These complementary evaluations must be both simple and quick to perform in medical practice, as they are added to an already heavy clinical examination. The main tools used in our bioclinical Department are described here. For each child, psychiatric, pediatric and neurological examination was performed. Different scales were progressively elaborated and validated to complete and precise behavioral parameters. Attention and perception were evaluated by a Behavior Summarized Evaluation (BSE) scale, association and imitation by appropriate scales, language by the Pre-Verbal Behavior Summarized Evaluation (PV-BSE) scale, early symptoms by the Infant Behavior Summarized Evaluation (t-BSE) scale. The main neurophysiological dysfunctionings were grouped in a Behavioral Functional Inventory (BFI). Clinical genetic data were scored in a summarized assessment carrying both on the antecedents and on the somatic abnormalities. The completed clinical data were gathered in a Quantified Multidimensional Assessment (QMA), with four axes: socialization, communication, cognition and neurological observation. These clinical evaluations provide behavioral details that can be integrated into a bioclinical database and give an objective approach to the heterogeneity of autism. They invite both clinicians and biologists to deepen the description of individual profiles which allow better understanding of physiopathological mechanisms in autistic children.

Rett's syndrome progresses in 4 stages: the first signs of the disorder appear after a period of 6 to 7 months, during which development is considered to be normal. This asymptomatic period is apparently an essential criterion of the diagnosis, but some parents have reported some prodromes. In stage II of the disease (before 3 years), signs common with autism dominate the clinical picture and the diagnosis of the latter was often formulated. Our working hypothesis is that the pedopsychiatric analysis of home movies of young girls with Rett's syndrome, taken by the parents before the age of 2, may be able to show early clinical signs. The present study involved examining home movies of children subsequently diagnosed as having Rett's syndrome (n = 9) in comparison to those of autistic (n = 9) and normal (n = 9) children, using semiological evaluation tools (IBSE, BFE). The persons scoring were not advised of the diagnosis. The observations were thus situated before the disorders and/or at the time of their appearance. The study confirms the asymptomatic interval between birth and the first signs of the disease, it defines the mode of onset and shows the disturbance of certain functions such as intent and imitation, more pronounced in Rett's syndrome children between 12 and 18 months. At this age, it also enables Rett's and autistic children to be differentiated on the basis of the different involvement of the "cognition" function and unusual posture, more pronounced in these girls. It does not, however, differentiate Rett's from autism between 6 and 12 months and it is thus not surprising that at this stage the diagnosis of rett's syndrome or autism may be a source of confusion.

Natural history of infantile autism goes from its first description to current classifications. Most authors agree upon the perfect character of Kanner's description in 1943. But its situation in the nosography has much developed. The parution of 4th edition of Diagnostic and Statistical Manual of mental disorders (DSM IV) bring us to analyse this evolution and the place of autistic disorders in the pervasive developmental disorders, with this of associated pathologies. The comparison of current classifications (DSM IV, ICD 10, CFTMEA) allows us to do correspondence between each diagnostic category in psychosis or developmental disorders of these classifications. It exists a real concordance between DSM IV and ICD 10. The french classification of child and adolescent mental disorders (CFTMEA) proposes original categories.

Childhood autism is not usually considered as a neurological disease although frequent antecedents of ante, peri and postnatal injuries are found in its antecedents. Several symptoms of autism particularly in the early development, resemble the signs observed in frontal, temporal, striatal and brainstem dysfunctioning. These cerebral structures are connected with the central dopaminergic system which may be disturbed in autistic children. Such hypotheses suggest the necessary elaboration of an infant and child "behavioral neurology".

The term "inhibition" is not usually employed in the psychopathology of schizophrenia. However, in defining some neuroleptics' action, the work "desinhibition" is currently used and Pavlov explained the main features of the schizofrenic syndrome through a transmarginal inhibition mechanism. The purpose of this study is to investigate if an inhibition process underlies some phenomena shown up by the evoked potentials (EPs) method. Usually, a lower EPs' amplitude is seen in schizophrenic patients than in normals. This phenomenon is displayed by: -- simple stimuli EPs: they show weak amplitude and high variability; -- double-shock EPs: they have a long recovery-cycle; -- conditioned EPs: their amplitude is minimally augmented by coupling the conditioned and the unconditioned stimulus; -- EPs in experiments with increasing-intensity stimuli: their amplitude decreases as stimulation intensity increases. Some of these concurrent data could indicate a transmarginal inhibition, particularly the lengthening of the recovery cycle and the amplitude-reduction phenomenon. Although these are preliminary results, nevertheless some relationships emerge between clemical, electrophysiological and biochemical data.