The original purpose of this study was to determine if Tegretol has an effect on the impulsive behavior exhibited by people with mental retardation. This was to be accomplished through a replication of the self-control choice procedures used by Ragotzy, Blakely, and Poling (1988). The procedure involved three stages. First, subjects chose between stimuli that provided either one or three edibles. Then the stimuli associated with the smaller and larger edibles were reversed. Following this, the procedure required the implementation of successively longer delays to the larger reinforcer. However, none of the subjects who participated was able to make the discriminations necessary to proceed, i.e., the subjects did not systematically select the stimulus associated with the larger magnitude edible choice. The identification and rectification of these errors in discrimination became the focus of this study. Various procedures were used to enhance discrimination, including fading, adjusting the magnitude of the edibles, and stimulus changes. None of these changes was successful in teaching the subjects the necessary discriminations.

The primary purpose was to determine the relative effects of drive level, degree of mental retardation, and nature of reinforcer on effectiveness of operant conditioning of mentally retarded children. Embodied in the general purpose were the following sub-purposes: 1. To determine if mentally retarded subjects of differing induced drive levels (defined as satiated, nondeprived, and deprived) learn a simple discrimination problem at different rates. 2. To determine if the nature of the reinforcer (social versus material) produces different effects on performance of the task. 3. To determine the extent to which retardates of differing levels of intelligence learn the task. 4. To determine the degree of interaction among the three main treatment variables (drive level, degree of retardation, and nature of reinforcer) simultaneously.

The present sbudy is an effort to seek information from a type of organization rarely studied along the lines of employee satisfaction's correlation to job performance—a state institution for the mentally retarded—which will shed significant light on the dynamics of this question. It is unique in that it focuses closely on the specific job duties of both managerial and non-managerial employees as a basis for understanding the relationship between employee satisfaction and performance.

The comparability of PPVT and PPVT-R scores among retarded adults were examined. The sample consisted of 96 clients, who had been previously diagnosed as mildly, moderately, or severely retarded. The PPVT (Form A) and PPVT-R (Form L) were administered to all participants in counter balanced order. Significant correlations were found between the two tests for the total sample as well as for females and males. Additionally, the PPVT-R was found to be capable of discriminating differing levels or retardation. However, with the exception of the severely retarded group, mean PPVT-R Standard Score Equivalent (SSE) scores tended to be approximately 20 points lower than PPVT IQ scores. Some clinical implications of these results were discussed.

Estudamos uma família com cinco homens (dois falecidos) afetados por deficiência mental (DM) não-sindrômica em duas gerações, num padrão de herança ligada ao cromossomo X. A análise do padrão de inativação do cromossomo X, com base na metilação do gene AR, evidenciou que a mulher portadora obrigatória tinha desvio completo de inativação nos leucócitos, uma característica freqüente em portadoras de mutações do cromossomo X relacionadas com DM. Para o mapeamento da DM, genotipamos 28 locos de microssatélites ao longo do cromossomo X e delimitamos um segmento de cerca de 32 Mb, entre os marcadores DXS986 e DXS8067, compartilhado pelos afetados e pela portadora obrigatória, mas não pelo homem normal ou pelas possíveis portadoras que não tinham desvio do padrão de inativação do cromossomo X. Na busca do gene mutado, analisamos, por seqüenciamento direto, genes mapeados no intervalo compartilhado e já relacionados a DM ou que tivessem expressão em cérebro e leucócitos. Nos afetados e na portadora obrigatória, encontramos a mutação c.845C→T no gene ACSL4, que resulta na substituição do aminoácido histidina, conservado na família de sintetases de acil-CoA humanas e em diversos outros organismos, por tirosina (p.H323Y da isoforma cérebro-específica). Tratando-se de mutação que altera um aminoácido evolutivamente conservado em gene já relacionado com DM, que segregava com a DM na família, não tendo sido encontrada em amostra controle de 160 indivíduos do sexo masculino, concluímos que era a causa da DM na família. Mutações de ponto no gene ACSL4 foram relacionadas com a DM não sindrômica em três famílias descritas na literatura. O gene ACSL4 codifica a acil-coA sintetase 4 da família das sintetases de cadeia longa, que catalisa a formação de ésteres acil-coA a partir de ácidos graxos de cadeia longa. Sua expressão já foi documentada em vários tecidos, incluindo o cérebro e dados recentes mostraram que a proteína é essencial para a formação normal de espinhos dendríticos. A nova mutação do gene ACSL4 que descrevemos como causa de DM vem reforçar a relação alterações desse gene e a DM de herança ligada ao X. O padrão de inativação do X totalmente desviado foi mais uma vez observado em mulher portadora da mutação, indicando a importância da expressão desse gene em leucócitos. A presença de dificuldades de aprendizado na portadora da mutação concorda com o observado nas três famílias da literatura em que o estudo das portadoras foi relatado, indicando o efeito de mutações do gene ACSL4 sobre a função intelectual mesmo em heterozigose. A ausência de correlação entre o padrão de inativação do cromossomo X em células do sangue periférico e o comprometimento intelectual foi confirmada. Na família estudada, a identificação da mutação permitiu o aconselhamento genético. / We studied a family with five men (two of them deceased) affected by nonsyndromic mental retardation in two generations, in a pattern of X-linked inheritance (MRX). The study aimed at identifying the causative mutation. The obligate female carrier showed completely skewed inactivation of the X chromosome, based on the methylation status of the AR gene in peripheral blood in leukocytes, a common feature in carriers of X-linked mutations that cause mental retardation. We genotyped 28 microsatellite loci mapped throughout the X chromosome and delimited a 32 Mb segment, between markers DXS986 and DXS8067, that was shared by the affected males and obligate carrier, but was not present in a normal man or in two women who did not show skewed X-inactivation. We searched for the causative mutation by sequencing genes mapped to this candidate interval that had been associated with MR and/or were expressed in brain and leukocytes. In the affected men and obligate carrier, we found a c.845C→T mutation in the ACSL4 gene, resulting in the amino acid tyrosine substituting for a histidine (p.H323Y in brain isoform), which is conserved in the acyl-CoA synthetase family in humans and others organisms. This mutation was not found in a control sample of 160 men. Previously, point mutations in the ACSL4 gene had been identified as the cause of MRX in three families. ACSL4 encodes the acyl-CoA synthetase long-chain family member 4, which catalyzes the formation of acyl-CoA esters from long-chain fatty acids. It is expressed in several tissues, and in brain it is essential for the normal formation of dendritic spines. The novel mutation here described confirmed the causal association of ACSL4 mutations with non-syndromic mental retardation. The completely skewed Xinactivation, also observed in the previously described carriers, supported a functional role for this gene in peripheral blood leukocytes. The intellectual impairment present in the carrier in the family here reported is in accordance with previous findings pointing to the effect on intellectual abilities of ACSL4 mutations in heterozygosis. The absence of correlation between the pattern of X-inactivation in leukocytes and mental status was confirmed.

Em estudos etiológicos sobre a deficiência mental (DM), as anomalias cromossômicas, tanto numéricas quanto estruturais, são fatores que apresentam frequência relativa significante. O objetivo deste trabalho foi estudar as frequências e os tipos de anomalias cromossômicas em afetados por DM nas APAEs (Associação de Pais e Amigos dos Deficientes) de Batatais, Altinópolis e Serrana, objetivando conhecer melhor a contribuição destas anomalias na DM nessa região, caracterizando os tipos e as freqüências das aberrações cromossômicas observadas e compará-las entre as APAEs. Pacientes com suspeita de anomalias cromossômicas foram selecionados para o estudo. O critério usado para a seleção da amostra foi a realização do cariótipo em todos os afetados por DM com anomalias estruturais maiores e/ou menores. A análise citogenética foi feita através de cultura de linfócitos do sangue periférico e a coloração utilizada foi banda G, sendo analisadas 20 metáfases por paciente. Dos 505 indivíduos avaliados nas três APAES, 265 realizaram estudo citogenético, sendo encontradas 61 alterações cromossômicas (12,1% do total e 23,0% dos selecionados para cariótipo). Na APAE de Batatais, dos 305 indivíduos avaliados, 174 realizaram cariótipo, sendo encontradas 33 (10,8% do total) anomalias cromossômicas. Em Altinópolis, dos 107 indivíduos avaliados, 54 realizaram cariótipo, sendo observados 16 cariótipos anômalos (14,9% do total). Na APAE de Serrana, dos 93 indivíduos avaliados, 37 realizaram cariótipo, sendo encontradas 12 (12,9% do total) anomalias cromossômicas. Esses resultados demonstram que anomalias cromossômicas contribuem significativamente para a etiologia da DM e que a citogenética clássica possui importantes implicações na prática médica para o diagnóstico dos indivíduos afetados, assim como, para o aconselhamento genético das famílias. Além disso, observa-se que a APAE de Batatais, por apresentar uma porcentagem menor de indivíduos afetados por DM grave, 60,7%, possui uma menor incidência de anomalias cromossômicas quando comparada as APAEs de Altinópolis e Serrana que apresentam uma frequência de 87,8% e 83,9% de indivíduos com DM grave, respectivamente, indicando que alterações cromossômicas são mais frequentes em indivíduos afetados por DM grave. / In etiological studies on mental retardation (MR), the chromosomal abnormalities, both numerical and structural, are factors that have significant relative frequencies. The objective was to study the frequencies and types of chromosomal abnormalities in patients affected by MR in APAEs (Associação de Pais e Amigos dos Deficientes) of Batatais, Altinópolis and Serrana. This aims to better understand the contribution of these abnormalities to MR in these regions, and thus characterizing the types and frequencies of chromosomal aberrations observed in order to compare them between APAEs. Patients suspected of chromosomal abnormalities were selected for the study. The criterion used for sample selection was the achievement of the karyotype of all patients affected by MR with major and/or minor structural abnormalities. Cytogenetic analysis was performed on cultures of peripheral blood lymphocytes, where the band G was used for staining. Twenty metaphases were analyzed per patient. Of the 505 individuals evaluated in three APAEs, a cytogenetic study was performed on 265 patients, and 61 chromosomal abnormalities were found (12.1% of the total and 23.0% of the selected karyotypes). In APAE of Batatais, karyotypes were performed on 174 of the 305 subjects studied, and we found 33 chromosomal abnormalities (10.8% of total). In Altinópolis, 54 karyotypes were performed out of the 107 subjects studied, and we observed 16 abnormal karyotypes (14.9% of total). In APAE Serrana, 37 karyotypes were performed out of the 93 subjects studied, and 12 chromosomal abnormalities (12.9% of total) were found. These results show that chromosomal abnormalities contribute significantly to the etiology of MR and that classical cytogenetics have important implications in medical practice for diagnosis of affected individuals as well as for genetic counseling of the families. Moreover, it is noted that in the APAE of Batatais, because of the smaller percentage of individuals affected by severe MR, 60.7% have a lower incidence of chromosomal abnormalities when compared to the APAEs of Altinópolis and Serrana which have frequencies of 87.8% and 83.9% of individuals with severe MR, respectively. This indicates that chromosomal abnormalities are more frequent in individuals affected by severe MR.

[pt] Esta tese tem por objetivo principal analisar os processos de produção da longa permanência de crianças e adolescentes com deficiência na rede assistencial de abrigamento. Partindo da descrição da própria experiência profissional, impulsionada pelas contribuições de Erving Goffman e Franco Basaglia, a autora introduz o conceito de hibridismo assistencial para analisar o problema da deficiência institucionalizada nas interfaces entre os campos da Psiquiatria e da Assistência Social. Tendo como campo de estudo a rede de abrigos específicos para a deficiência no estado do Rio de Janeiro, a autora utiliza metodologias quantitativas e qualitativas para analisar o quadro atual da assistência asilar para crianças e adolescentes com deficiência, definindo-se o seguinte corpus de análise: (1) elementos da historiografia da psiquiatria infantil brasileira, tendo por referência as contribuições de Michel Foucault. Nesta perspectiva, discute-se a figura histórica do Pavilhão-Escola Bourneville - dispositivo vinculado ao Hospício Nacional de Alienados e marco inaugural da psiquiatria infantil brasileira para a internação de crianças anormais; (2) dados do Datasus referentes às internações de crianças e adolescentes com deficiência, no período de 1998 a 2010, em território nacional, ressaltando-se a dimensão quantitativa do problema, e (3) entrevistas realizadas junto a agentes sociais do Sistema de Garantia dos Direitos da Criança e do Adolescente do estado do Rio de Janeiro, tendo por referência de análise o conceito de campo de Pierre Bourdieu, e de Complexo Tutelar, de Jacques Donzelot. O estudo conclui que (1) existe uma correlação entre os abrigos específicos e a história da institucionalização da deficiência mental, mantendo-se a figura híbrida do abrigo-hospital, (2) as atuais políticas de desinstitucionalização não vêm incluindo crianças e adolescentes com deficiência, sendo necessário rever o conceito de crônicos para crianças e adolescentes no regime de internação hospitalar e, (3) a presença da deficiência é um fator de maximização das práticas tutelares, o que é verificado a partir dos discursos dos agentes sociais. A autora articula o tema em uma agenda de interesse público e acadêmico, buscando contribuir para a superação do modelo assistencial centrado na longa permanência, na rede asilar, de crianças e adolescentes com deficiência. / [en] This thesis aims at examining the processes that produces long-term placement of children and adolescents with mental disabilities in the shelter care facility network. The author begins hers analysis with the description of her own professional experience, driven by the contributions of Erving Goffman and Franco Basaglia. She introduces the concept of hibridismo assistencial (the idea of social assistance as an entangled reality) to analyze the problem of institutional disability looking at the interconnection between the areas of psychiatry and social work. Taking as her field of study the network of special purpose shelters (intended exclusively for children and youth with disabilities) in the State of Rio de Janeiro, the author combines quantitative and qualitative methodologies to analyze the current situation of the shelter care system for children and adolescents with disabilities, with the following corpus of analysis: (1) elements of the Brazilian historiography of child psychiatry, with reference to an analysis of the concept of power based on Michel Foucault. Under this perspective, the author discusses the historical figure of the Bourneville School - an institution linked to the National Asylum for the Insane and the founding landmark of the Brazilian child psychiatric for the hospitalization of the so called abnormal children, (2) Datasus data on hospitalization of children and adolescents with mental disabilities, highlighting the numerical dimensions of the problem, and (3) interviews with social agents connected to the System of Guarantee of the Rights of Children and Adolescents in the State of Rio de Janeiro, using as reference analysis the concepts of field by Pierre Bourdieu, and guardianship complex by Jacques Donzelot. Based on her study, the author concludes that: (1) there is a correlation between the existing shelters and the history of the institutionalization of children with mental disabilities as well as the presence of the ‘hybrid’ institution – the ‘shelter-hospital’, (2) the current policies aiming at closing down residential institutions have not included children and adolescents with disabilities, therefore it is necessary to critically review the concept of crônicos (chronically impaired) as referred to the young population that is hospitalized, and (3) based on testimonies of the social agents interviewed, it is possible to conclude that the presence of a disability becomes a factor of maximizing paternalistic practices. The author concludes her analysis linking some of the main issues to an agenda of academic and public interest, in an attempt to contribute to overcome old models centered on the long-term placement of children and adolescents with disabilities in institutions.

Submitted by admin tede (tede@pucgoias.edu.br) on 2016-08-18T13:16:28Z No. of bitstreams: 1 Roberto Carlos Gomes da Silva.pdf: 3176847 bytes, checksum: b508a4a3eb30a62abd86ea9330f277e4 (MD5) / Made available in DSpace on 2016-08-18T13:16:28Z (GMT). No. of bitstreams: 1 Roberto Carlos Gomes da Silva.pdf: 3176847 bytes, checksum: b508a4a3eb30a62abd86ea9330f277e4 (MD5) Previous issue date: 2008-04-09 / Since DNA structure was described, several studies have been carried out in genetics that promoted a revolution in the practice of medicine. Human syndromes that were practically undiagnosed became easily diagnosed with molecular tools. However, most of the genetic diseases remain under diagnostic obscurity, increasing health concerns for affected people and public demand for preventive health care such as the case of Fragile-X Syndrome, the most common heritable form of mental retardation in humans. FXS is caused by an expansion of CGG repeat sequence in the promoter region of FMR1 gene, located in Xq27.3. Both men and women are affected by FXS and pre-mutation can expand to a full mutation in the next generation. Under full mutation status ( 200 repeats) the gene is silenced and FMRP protein is not produced causing mental retardation, speech delay, and behavior problems, the most frequent symptoms in FXS. Prevalence of FXS is estimated in 1:4000 and 1:8000 and of carriers in the general population as 1:813 and 1:259 for men and women, respectively. Because of FXS potential to affect subsequent generations it is crucial to properly diagnose the syndrome. Laboratory analysis of DNA from FXS, using PCR or Southern Blotting, allows reaching the diagnosis in 99% of cases carrying mutated genes. However, to date the Brazilian Public Health System does not recognize the molecular methods to reach complete diagnostic in FXS. Early diagnose would allow fore more appropriate and efficient therapy approaches, favoring satisfactory development of all affected people, minimizing their suffering and the burden on their families, increasing, on the other hand, their quality of life which should go beyond survival. / A partir da descrição da estrutura do DNA, várias pesquisas foram desenvolvidas na área da Genética, promovendo uma revolução na prática da medicina. Síndromes, antes difíceis ou até impossíveis de serem detectadas, com tecnologia e ferramentas moleculares, tornaram-se facilmente diagnosticadas. Entretanto, diversas doenças ainda persistem na obscuridade de diagnóstico e geram problemas de saúde pública como é o caso da Síndrome do X-Frágil (SXF), que é a causa mais comum de retardo mental masculino herdado, e que consiste na expansão do número de cópias de uma seqüência de bases CGG do DNA no gene FMR1, localizado no cromossomo Xq27.3. A SXF afeta tanto homens quanto mulheres e a pré-mutação poderá expandir-se à mutação completa nas próximas gerações. Os portadores da pré-mutação continuam produzindo a proteína FMRP e os portadores da mutação completa são afetados pela SXF, pois o gene FMR1 é silenciado, e a proteína não é produzida, causando retardo mental, problemas de linguagem e de comportamento. A prevalência da SXF é estimada em 1:4000 e 1:8000, e para portadores na população em geral é 1:813 e 1:259 para homens e mulheres respectivamente. A importância do reconhecimento clínico e diagnóstico da SXF vem do fato de que as gerações futuras poderão estar comprometidas. O estudo do DNA para X-frágil pela PCR e Southern blotting permite determinar com segurança superior a 99% quem é portador da pré-mutação do gene FMR1 e quem possui a mutação completa. Entretanto, o SUS não reconhece os métodos moleculares, apesar do diagnóstico permitir intervenções terapêuticas, com respostas bastante eficientes, favorecendo o desenvolvimento de modo integral das pessoas afetadas, minimizando seu sofrimento e de seus familiares, uma vez que a qualidade de vida deve ir além da sobrevivência.

5 mutations responsables de retard mental ont été identifiées dans le gène p21-activated kinase 3 (pak3). Nous avons récemment identifiés dans pak3 deux exons alternatifs très conservés appelés b et c. Ainsi, en plus du variants PAK3a (dépourvu des inserts b ou c), le gène pak3 code pour 3 nouveaux variants d’épissage PAK3b, PAK3c et PAK3cb qui sont constitutivement actifs et insensibles aux GTPases. De plus, contrairement à PAK1 et PAK3a, leur domaine d’auto-inhibition est incapable d’inhiber un domaine kinase. Ainsi, le but de ce projet était de comprendre le mécanisme de régulation de la kinase PAK3. Un modèle de régulation a récemment été proposé dans lequel PAK1 forme des homodimères pouvant être dissociés par les GTPases, permettant ainsi l’activation de la kinase. En se basant sur ces observations j’ai cherché à identifier les dimères PAK3 et j’ai montré que les kinases PAK3a, b, c et cb forment préférentiellement des hétérodimères avec PAK1. J’ai démontré l’existence de ces dimères dans le cerveau et j’ai mis en évidence que ces hétérodimères permettent à chaque monomère de réguler l’activité kinase de son partenaire in vitro. Ce travail permet de proposer un modèle de régulation symétrique pour PAK3a qui forme des hétérodimères avec PAK1 et un nouveau modèle de régulation asymétrique pour les variants d’épissage, également basé sur leur hétérodimérisation avec PAK1. Mes résultats montrant une corégulation des kinases PAK neuronales suggèrent d'une part que leur activation puisse être synchronisée et d'autre part que dans certaines situations physiopathologiques (Cancer et maladies neurologiques) leur dérèglement puissent interférer. / 5 mutations responsible for mental retardation have been identified in p21-activated kinase 3 (pak3) gene. We recently identified in pak3, two highly conserved alternative exons called b and c. In addition to the classical PAK3a variant (without any alternative exon), the pak3 gene encodes 3 new splice variants PAK3b, PAK3c and PAK3cb which are constitutively active and insensitive to GTPase activation. Moreover, unlike PAK1 or PAK3a, their autoinhibitory domain is unable to inhibit a kinase domain. The aim of this project was to understand how PAK3 regulation occurs. A model of regulation was recently proposed in which PAK1 forms homodimers that can be dissociated through GTPase binding, leading to kinase activation. Given these observations, I searched to identify PAK3 dimers and I showed that PAK3a, b, c and cb preferentially form heterodimers with PAK1. I demonstrated the existence of such dimers in the brain and that the different heterodimers allow each monomer to regulate the kinase activity of its partner. Through this study, I propose a symmetric regulation model for PAK3a which heterodimerizes with PAK1 and a new asymmetric regulation model for splice variants, also based on heterodimerization with PAK1. My results showing a co-regulation of neuronal PAK kinases suggest that their activation may be synchronized but also that, in some physiopathological situations (cancers and neurologic diseases), their misregulation may interfere.

Esta dissertação tem o objetivo de questionar o diagnóstico de debilidade mental, a partir das contribuições da psicanálise, segundo Freud e Lacan. Partindo de uma análise histórica da construção de um discurso social e científico do termo, discutimos se este diagnóstico, e os fenômenos a ele associados, indicam alguma particularidade que pode fornecer uma orientação para a direção do tratamento, ou para a clínica. Apontamos que nem Freud nem Lacan possuem uma teoria específica da debilidade mental. Por outro lado, Lacan sustentava que Freud errou em contraindicar a análise aos débeis, dizendo que essa análise é sim, possível. Além disso, Lacan utilizou o termo debilidade mental em diferentes sentidos e em diversos momentos de sua obra, para fazer ironia ou para destacar aspectos estruturais da relação do homem com o saber. Este trabalho foca-se nos comentários de Lacan, quando o autor se debruça de forma mais enfática ao diagnóstico da debilidade mental. Posteriormente, analisamos três eixos de análise de autores lacanianos que, a partir da mesma referência (da obra de Lacan), indicaram diferentes estatutos da debilidade mental. O primeiro eixo refere-se à diferenciação entre a psicose e à debilidade mental. O segundo eixo considera a debilidade mental enquanto um fenômeno, ou uma defesa, articulada a uma estratégia de imaginarização, que poderia estar presente nas três estruturas clínicas (neurose, psicose, perversão). O terceiro eixo relaciona a debilidade mental à inibição. A partir dessa discussão e da análise de casos clínicos, apontamos que o que se nomeia de debilidade mental pode ser associada a certos fenômenos, relacionados a uma inflação imaginária. De um lado, este caminho mostra-se interessante, pois possibilita nos distanciarmos do caráter de déficit articulado à concepção de debilidade mental, bem como considerarmos a inclusão de um sujeito neste campo. Por outro lado, quanto à clínica propriamente dita, concluiremos que ela terá seu valor mais acentuado ao não se reduzir a esta análise. Para isso, devemos considerar: o desafio, já indicado por Mannoni (1985), de que médicos e psicanalistas não estão isentos de preconceitos; a consideração de Bruno (1986) de que a clínica com os ditos débeis não revela nenhuma clínica específica; e a fala de Lacan, quando ele indica que sempre falamos mais do que queremos dizer e que o homem sabe mais do que ele crê saber / Drawing heavily on Freud and Lacans contributions psychoanalysis, this dissertation aims to explore the diagnosis of mental retardation. Therefore, beginning with an historical analysis of the construction of a social and scientific discourse of the very expression mental retardation1 we discuss whether such a diagnosis and its associated phenomena can point to some particularity that might furnish a guideline either to treatment or to some clinical direction. While we point out that neither Freud nor Lacan espoused a specific theory about mental retardation, Lacan for his part believed not only that psychoanalysis could be effective in treating the retarded but also that Freud had erred in contraindicated such treatment. However, Lacan in his oeuvre never settles on one fixed meaning for the term mental retardation but rather uses this turn of phrase in several manners and contexts, often in order to underscore some irony or to highlight certain structural aspects of mans relationship to knowledge. Therefore, this work focuses on the commentaries of Lacan, in which he carefully examines the diagnosis of mental retardation. Later, we examine three distinct analytical modes, whose authors, drawing upon the same source material (i.e., Lacans work), proposed three different definitions of this mental handicap. The first mode refers to the distinction between psychosis and mental retardation. The second mode reflects on mental retardation as a phenomenon, or defense, linked to a strategy of imaginarization this strategy in fact could be present in all three clinical structures (neurosis, psychosis, and perversion). The third mode relates mental retardation to inhibition. From this discussion and from the analysis of clinical cases, we indicate that so-called mental retardation can be a function of certain phenomena related to an imaginary inflation. On one hand, this treatment path seems interesting, because it allows us both to go beyond the concept of a deficit related to mental retardation and to consider the inclusion of a subject in this field. On the other hand, the real value of clinical treatment becomes apparent when such treatment is not reduced to a mere analysis of certain phenomena. In this sense, we must take into account: Mannonis challenge (1985), that doctors and psychoanalysts are not free from prejudice; Bruno´s consideration (1986), that the psychoanalytical treatment of the so-called mentally retarded in fact follows the guidelines of standard treatment; and Lacans speech, that we always say more than we want to say and know more than we believe we know