On Tyminsky's (2005) long-term group psychotherapy for children with pervasive developmental disorder.
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A young teenage male presenting for a routine check-up reported no health problems. Initial clinical examination revealed some enamel loss on the palatal surfaces of the maxillary incisors. Erosion lesions were suspected. Similar lesions, however, were not found throughout the mixed dentition and radiographic findings were inconclusive. To confirm the diagnosis of these lesions and, more importantly, to disclose the etiology, a thorough and detailed clinical examination of these lesions was conducted. Study models were made, mounted in centric occluding position, and closely screened. In addition, the health history was revisited, by interviewing the patient and his legal guardian. The information gathered led to the conclusion that the lesions in question were erosion lesions with concomitant wear facets that resulted from attrition of the softened enamel surface. An ample light on the possible etiological factors was shed, which assisted in the planning phase for the course of management. It is not uncommon that dental health care providers encounter in daily practice cases of early erosion lesions similar to those reported here. In most of these instances, minor changes in tooth morphology that represent a slight departure from the norm could be overlooked and often ignored. If such lesions go undetected, the underlying causes may escape diagnosis. However, if action is taken to pursue investigation of the causative factor, the result could assist in understanding the overall complexity of the health condition of the patient. This would enable planning the proper course of management for the total well being of the patient.
Autism is a disorder characterised by abnormalities in language and social development, and repetitive behaviours. Antipsychotics, including haloperidol and risperidone, are the most widely studied drugs for reducing symptoms in children and adolescents with autism. When administered at relatively low dosages, antipsychotics have been shown to reduce repetitive behaviours (stereotypies) and social withdrawal, as well as a number of related symptoms, such as hyperactivity, aggression, self-abusive behaviour, temper tantrums, lability of mood and irritability. Adverse effects of antipsychotics include sedation, dizziness, increased appetite, weight gain, changes in the electrocardiogram parameters, drooling, hyperprolactinemia and a risk of drug-related dyskinesias. Other agents have been less well studied for the treatment of autism, but there are suggestive data regarding their safety and efficacy. Of these agents, a number have been investigated, based on theories about the aetiology of autism, including SSRIs and naltrexone, although the efficacy of these agents has been limited. Stimulant drugs have been shown to reduce hyperactivity and improve focus, but they may cause behavioural worsening, weight loss and stereotypies de novo. Secretin is a treatment that has received much media attention after reports of efficacy from small open studies, but all controlled studies have failed to show any benefit. In autism, alternative treatments have also been used, but none have shown benefit in well-designed studies.
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A 5-year-old boy presented with very deviant phonological production, as well as some delay in acquisition of vocabulary for comprehension. Investigations showed that, in contrast to his very limited phonological system in word production and naming, he was able to repeat a variety of non-words with reasonable accuracy using a variety of syllable structures. A period of therapy aimed at improving his phonological segmentation skills resulted in dramatic improvement in real word production to the same level that he showed with non-words. This improvement was specific to the domain of treatment--real word phonology--demonstrating that the effects were a result of the therapy regimen. The reasons for this dissociation between the phonology of real words and non-words are discussed. It is concluded that the child's pattern of performance is incompatible with theories which assume that a single phonological representation is used both for word recognition and for output. His deficit appears to lie in a failure to update the underlying phonological representations used to drive spoken output as his phonological abilities develop--his lexical phonology was 'frozen'.
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A number of arboviruses have been associated with congenital defects in domestic aminals and man. In this review comparison is made of the temporal association between epidemics of arboviruses affecting man and animals in which there is an obvious relationship between the infection and the fetal defects, and arboviruses which cause no overt clinical symptoms in the vertebrate host but result in deformities of the fetus. The danger to the fetus following the use of live attenuated virus vaccines against several important arbovirus diseases is also examined. It is concluded that arboviruses which are capable of infecting humans or animals without producing overt clinical signs, and attenuated vaccine viruses pose the greatest threat to the fetus.
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INTRODUCTION: We believe that it is of great interest, in neuropediatric clinic, to value the molar behavior disorders and to accomplish the corresponding molecular alterations in the central nervous system. PATIENTS AND METHODS: We studied 26 patients diagnosed of serious disorders of the development, that were presenting a typical clinic with manual stereotypes. We choose at random 5 children to practice them a study of metabolic neuroimaging through the Positron Emission Tomography with 18Fluoro-Deoxi-Glucose (PET-FDG). RESULTS AND CONCLUSIONS: The conclusion, more meaningful, is that the children with serious disorders of the development present a mature failure in the neuro-function circuits of the thalamus, as well as the cortical connection and association areas. This clinical situation is reinforced by the results of the PET-FDG, that presents a characteristic metabolic image of the autism children, with a bilateral decrease of the capitation of FDG, mainly in regions as thalamus, frontal and temporary lobes.
INTRODUCTION: In this article we present a review of the aetiology and treatment of self-injury and self-stimulation in infantile autism and in generalized development disorders. We summarize 20 years of study and investigation in the treatment of these serious behaviour disorders, in a pioneer institution in Spain: the centre for rehabilitation 'El Cau' in Castellon. DEVELOPMENT: We describe the most frequent behaviour disorders, with particular reference to self-injury and self-stimulatory behaviour. Models explaining the aetiology and treatment are described in a brief general review of the subject, and we consider explicative models which integrate different treatments (in family and institutional contexts) by means of family therapy, psychoeducational models and social support networks.
The mammalian neocortex is a highly ordered structure with different classes of neurons aligning in an organized radial array of six cellular layers ranging from the pial surface to the white matter. Positioning of a particular neuron at the particular cortical layer is an essential step in forming an elaborate neuronal network in the neocortex. It is important to study the molecular mechanism how neuroblasts produced reach to a particular position in the laminated structure of the brain. We took advantage of reeler mutant mouse in which the position of the neurons is abnormal. We obtained an antibody against reeler gene product which we named CR-50, by immunizing wild type embryonic brains to reeler mice. CR50 blocked neuronal positioning in the cerebellum, hippocampus and cerebral cortex. CR-50 reacted with the product of the reelin gene, which was cloned as the responsible gene for the reeler mutant. Cajal-Retzius neurons secrete CR-50 antigen/Reelin and play an important role for neuroblasts to settle to their proper position in the brain. The mutant mouse missing "disabled 1", called yotari mouse, shows similar phenotypes in both morphology and behavior to those of reeler. The information of CR-50 antigen/Reelin is considered to be transmitted inside the neuroblasts to the "disabled 1", which is an adaptor protein to Src, Fyn, Abl tyrosine kinase.
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