[Population-based diagnostic study to compare the DSM-IV and the Questionnaire for screening Latin American schoolchildren and adolescents for attention deficit hyperactivity disorder]. / Estudio poblacional de diagnóstico comparativo entre el DSM-IV y el cuestionario para escolares y adolescentes latinoamericanos para la detección del trastorno por déficit de atención/hiperactividad.

AIM: To detect attention deficit hyperactivity disorder (ADHD) in children between 4 and 14 years of age by means of the Questionnaire for screening Latin American schoolchildren and adolescents for ADHD (QLSA-ADHD) and the criteria of the Diagnostic and statistical manual of mental disorders, fourth edition, ADHD version (DSM-IV ADHD). PATIENTS AND METHODS: A prospective, cross-sectional, analytical study was conducted to detect ADHD in the child population that visited the outpatient department at the Rodolfo Nieto Padron Children's Hospital. These children were administered two surveys: the DSM-IV ADHD and the QLSA-ADHD. The results were analysed using graphs and test statistics from the SPSS package, such as the correlation coefficient and chi squared. RESULTS: The questionnaires were analysed by finding the overall sum of the criteria of the 200 children included in the DSM-IV ADHD and the average score values were found to be 64 'yes' (32%) and 137 'no' (68%). The QLSA-ADHD was evaluated in the same way and the average was 50 'yes' (25%) and 149 'no' (75%). The chi squared test was then performed for the two, the result being 1.762, with 1 degree of freedom and p > 0.05; that is to say, there was no significant difference between the scores obtained in both surveys. With the QLSA-ADHD, 25% of children with ADHD were detected, whereas the figure rose slightly to 25.5% (51 patients) with the DSM-IV. The chi squared test was conducted between the results from the two surveys, the value being 3.405, with 1 degree of freedom and p > 0.05. CONCLUSIONS: Our findings show that, in our population, there is no difference between the QLSA-ADHD and the DSM-IV for detecting ADHD.

[Infantile autism and mirror neurons]. / Autismo infantil y neuronas en espejo.

INTRODUCTION: Infantile autism is a disorder that is characterised by alterations affecting reciprocal social interactions, abnormal verbal and non-verbal communication, poor imaginative activity and a restricted repertoire of activities and interests. The causes of autism remain unknown, but there are a number of different approaches that attempt to explain the neurobiological causes of the syndrome. A recent theory that has been considered is that of a dysfunction in the mirror neuron system (MNS). DEVELOPMENT: The MNS is a neuronal complex, originally described in monkeys and also found in humans, that is related with our movements and which offers specific responses to the movements and intended movements of other subjects. This system is believed to underlie processes of imitation and our capacity to learn by imitation. It is also thought to play a role in language acquisition, in expressing the emotions, in understanding what is happening to others and in empathy. Because these functions are altered in children with autism, it has been suggested that there is some dysfunction present in the MNS of those with autism. CONCLUSIONS: Dysfunction of the MNS could account for the symptoms that are observed in children with autism.

Autismo infantil y neuronas en espejo / Infantile autism and mirror neurons

Introducción. El autismo infantil es un trastorno caracterizado por una alteración en las interacciones sociales recíprocas, anomalías de la comunicación verbal y no verbal, pobre actividad imaginativa y un repertorio de actividades e intereses restringidos. Las causas del autismo se desconocen, pero existen diferentes abordajes que tratan de explicar las causas neurobiológicas de este síndrome. Recientemente se ha estudiado la teoría de una disfunción del sistema de neuronas en espejo (SNE). Desarrollo. El SNE es un complejo neuronal, descrito originalmente en monos y también hallado en humanos, que se relaciona con nuestros movimientos y que responde de forma especifica a los movimientos e intenciones de movimiento de otros sujetos. Asimismo se cree que este sistema se encuentra en la base de los procesos de imitación y en la realización de formas de aprendizaje por imitación. Se piensa también que participa en la adquisición del lenguaje, en la expresión emocional, en la comprensión de lo que les sucede a los demás y en la empatía. Debido a que estas funciones están alteradas en los niños con autismo, se cree que existe una disfunción del SNE en los autistas. Conclusión. Una disfunción del SNE podría explicar la sintomatología que se observa en los niños con autismo (AU)

Introduction. Infantile autism is a disorder that is characterised by alterations affecting reciprocal social interactions, abnormal verbal and non-verbal communication, poor imaginative activity and a restricted repertoire of activities and interests. The causes of autism remain unknown, but there are a number of different approaches that attempt to explain the neurobiological causes of the syndrome. A recent theory that has been considered is that of a dysfunction in the mirror neuron system (MNS). Development. The MNS is a neuronal complex, originally described in monkeys and also found in humans, that is related with our movements and which offers specific responses to the movements and intended movements of other subjects. This system is believed to underlie processes of imitation and our capacity to learn by imitation. It is also thought to play a role in language acquisition, in expressing the emotions, in understanding what is happening to others and in empathy. Because these functions are altered in children with autism, it has been suggested that there is some dysfunction present in the MNS of those with autism. Conclusions. Dysfunction of the MNS could account for the symptoms that are observed in children with autism (AU)

[The neurobiology of Tourette syndrome]. / Neurobiología del síndrome de Tourette.

INTRODUCTION: Tourette syndrome is a hereditary neuropsychiatric disorder that manifests as multiple chronic motor tics and verbal tics. The neurobiological disorders that seem to account for the symptoms that generate tics in these patients include alterations at three levels. DEVELOPMENT: These levels are as follows: alterations in the thalamocortical corticostriatal pathway; dopaminergic dysfunction that leads to hyperactivity of this neurotransmitter, which generates tics; and probably an immunological alteration triggered by infection by group A beta-haemolytic streptococcus that creates autoantibodies to combat specific neuronal systems; nevertheless, further study is required in this area. CONCLUSIONS: The aim of this paper was to review the pathophysiological mechanisms underlying the neurobiology of Tourette syndrome.

[The effects of protein-energy malnutrition on the central nervous system in children]. / Efectos de la desnutrición proteicocalórica en el sistema nervioso central del niño.

INTRODUCTION: Protein-energy malnutrition continues to affect millions of human beings in developing countries. Children suffer most from the shortage of nutrients because at early ages malnutrition has an important impact on the central nervous system. The changes that malnutrition triggers in the brains of these children will have severe consequences on their development and learning abilities. DEVELOPMENT: Reports of important alterations in the head circumference and brain growth of malnourished children have been published in the literature, together with accounts of changes in both the dendritic arborisation and the morphology of the dendritic spines, as well as in myelination. Computerised tomography brain scans and magnetic resonance imaging in children suffering from malnutrition show images that are compatible with cerebral atrophy. The lack of environmental stimulation associated with malnutrition worsens the damage to the central nervous system. All the alterations that are observed in such cases give rise to important compromise of the child's higher brain functions, which may well lead to permanent neuropsychological damage. CONCLUSIONS: Protein-energy malnutrition produces notable morphological changes in the brains of children in the developing world. These changes damage the intellectual potential of those who survive and limit their capacity to become part of the competitive world. Paediatric neurologists working in these areas of the world must make greater efforts to disseminate this problem and to make public institutions aware of the issue so that they do not desist in the fight against child malnutrition.

Efectos de la desnutrición proteicocalórica en el sistema nervioso central del niño / The effects of protein-energy malnutrition on the central nervous system in children

Introducción. La desnutrición proteicocalórica continúa afectando a millones de seres humanos en los países en desarrollo. Los niños son los que sufren más por la falta de nutrientes, ya que a edades tempranas la desnutrición tiene un impacto importante sobre el sistema nervioso central. Los cambios que la desnutrición produce en el cerebro de los niños, tendrán serias consecuencias en el desarrollo y el aprendizaje. Desarrollo. En los niños desnutridos se han descrito alteraciones importantes en el perímetro cefálico y en el crecimiento del encéfalo; asimismo, cambios en la arborización dendrítica y en la morfología de las espinas dendríticas, y también en la mielinización. Los estudios de tomografía computarizada de cráneo y de imagen de resonancia magnética en niños con desnutrición muestran imágenes compatibles con atrofias cerebrales. La falta de estimulación ambiental asociada a la desnutrición agrava más el daño al sistema nervioso central. Todas las alteraciones observadas originan afección importante en las funciones cerebrales superiores del niño, lo que condiciona daño neuropsicológico permanente. Conclusiones. La desnutrición proteicocalórica produce cambios morfológicos importantes en el cerebro de los niños del mundo en desarrollo. Estos cambios ocasionan daño al potencial intelectual de los supervivientes y limitan su integración al mundo competitivo. Los neurólogos pediatras que trabajamos en estas regiones del mundo debemos involucrarnos más en la difusión de este problema y desde nuestros lugares sensibilizar a los organismos públicos para que se continúen los esfuerzos contra la desnutrición infantil

Introduction. Protein-energy malnutrition continues to affect millions of human beings in developing countries. Children suffer most from the shortage of nutrients because at early ages malnutrition has an important impact on the central nervous system. The changes that malnutrition triggers in the brains of these children will have severe consequences on their development and learning abilities. Development. Reports of important alterations in the head circumference and brain growth of malnourished children have been published in the literature, together with accounts of changes in both the dendritic arborisation and the morphology of the dendritic spines, as well as in myelination. Computerised tomography brain scans and magnetic resonance imaging in children suffering from malnutrition show images that are compatible with cerebral atrophy. The lack of environmental stimulation associated with malnutrition worsens the damage to the central nervous system. All the alterations that are observed in such cases give rise to important compromise of the child’s higher brain functions, which may well lead to permanent neuropsychological damage. Conclusions. Protein-energy malnutrition produces notable morphological changes in the brains of children in the developing world. These changes damage the intellectual potential of those who survive and limit their capacity to become part of the competitive world. Paediatric neurologists working in these areas of the world must make greater efforts to disseminate this problem and to make public institutions aware of the issue so that they do not desist in the fight against child malnutrition

[Septic thrombosis of cavernous sinuses. Report of 2 cases]. / Trombosis séptica de senos cavernosos. Informe de 2 casos.

We report two male adolescents who developed septic thrombosis of the cavernous sinuses after manipulation of a furuncle on the nasal dorsum. We noted in both patients, besides the clinical findings of a generalized infectious process, palpebral edema, proptosis, ptosis, altered pupillary reactivity and bilateral III, IV and VI nerve palsies, as well as dysfunction of the ophthalmic branch of the fifth cranial nerve. One of the patients also had bacterial meningitis. Their cerebral angiograms demonstrated narrowing of the intracavernous portion of both internal carotid arteries. They improved with the antimicrobial treatment, but were left with ptosis and ocular palsies as sequelae. The adequate management of facial furuncle to prevent such a serious complication is emphasized.

[Cerebral infarct secondary to an intraoral injury from a spoon. A case report]. / Infarto cerebral secundario a traumatismo intrabucal con una cuchara. Informe de un caso.

We report the case of a 4-year-old female who developed an extensive cerebral infarction after trauma to the right peritonsillar area with a spoon. Blunt injury to the intima of the interna carotid artery promotes thrombus formation or clot embolization which results in an ischemic cerebrovascular event. We emphasize the need to prevent this rare complication of intraoral trauma in childhood.

[Acute hemiplegia in childhood and alternating hemiconvulsions secondary to Moya-Moya disease. Report of a case associated with Down's syndrome]. / Hemiplejía aguda de la infancia y hemiconvulsiones alternantes secundarias a enfermedad de Moya-Moya. Reporte de un caso asociado a síndrome de Down.

Moya-Moya disease has been associated to a number of disease entities including Down syndrome. Initial clinical manifestations in our patient were alternating lateralizing seizures with sudden onset hemiparesis. Ct scan demonstrated several infarcts in different stages of evolution, in the territory of left middle cerebral artery. Single digital subtraction angiography showed bilateral occlusion, predominantly on the left side of the supraclinoid portion of the interna carotid arteries with formation of collateral circulation in the diencephalic territory. The association of Moya-Moya disease and Down syndrome is not fortuitous and it is probably due to a congenital vascular dysplasia. It should be suspected in children with trisomy 21 (with or without congenital heart disease) who presents with alternating hemiplegia and convulsions or acute hemiplegia.