This brief bibliographical review analyzes the genetic basis of violence. The definition of Antisocial Psychopathic Personality includes criminal behavior; however, not all crimes are the result of a dysfunctional personality. Since the transgression of a law is a legal construct, the idea of its being a psychiatric category is rejected. We review studies of monozygotic and dizygotic twins, and analyze the influence of adoption and the role of the family in the twins' behavior. All these studies indicate that heredity is a significant factor in violent behavior. Some important scientific investigators propose a clear differentiation between offenders whose violent behavior begins during adolescence and can be rehabilitated, and recidivists whose aggressiveness first manifests itself in early childhood. We also discuss the defects found in several genes that have been found to be associated with aggressive behavior in research with both humans and animals. Finally, we emphasize that there is not a specific violence gene, but that aggressive behavior is always the result of the interplay between heredity and the social environment

Esta breve revisión bibliográfica pretende analizar las bases genéticas de la violencia. Se recuerda el concepto de Personalidad Psicopática Antisocial, que implica en su definición actos delictuales, sin pretender que todos los crímenes obedecen a una Personalidad Disfuncional. Siendo el delito un constructo legal se rechaza la idea de que exista una categoría psiquiátrica aplicable a los transgresores de las normas sociales aunque sean recidivantes. Se revisan los estudios entre gemelosmonozigosotos y dizigotos criados juntos o aparte. Se analizaron las investigaciones en gemelos que habían sido adoptados, haciendo énfasis en la influencia del ambiente familiar. Todos estos estudios indican una importante influencia de la herencia en las conductas violentas. Una contribución relevante la hacen los investigadores que postulan una tesis dual, diferenciando, la delincuencia juvenil, que ocurre en la adolescencia y susceptible de rehabilitación, de la delincuencia reincidente cuya conducta agresiva comienza en los primeros años de la vida. Se describen los genes que se han descubierto en familias con conductas violentas y las alteraciones neuroquímicas, que explicarían la agresión observada en un grupo de enfermos esquizofrénicos. Se insiste en que no puede haber un gen de la violencia, que probablemente son múltiples y que la violencia siempre es el resultado de la interacción de las disposiciones hereditarias y de la influencia del ambiente

There is increasing investigation and scientific publications related to stem cells. In our literature review, we describe what a stem cell is, what are it’s properties, some of the strategies to isolate and proliferate neural stem cells and the molecular mechanisms involved in the functional integration of these cells in the receptor cells. Finally, the possible steps in future investigations are described: better identification of the signals from the receptor to the donor cells; how to decipher in more depth the neurogenic capacity at a cellular level in the adult brain

Las investigaciones sobre células troncales han concitado creciente actividad en el campo de la investigación y publicaciones científicas. Nuestra revisión de la literatura expone qué es una célula troncal, sus propiedades, algunas de las estrategias para aislar y hacer proliferar células troncales neurales y los mecanismos moleculares involucrados en la integración funcional de estas células al cerebro receptor. Finalmente se comentan los posibles pasos de las futuras investigaciones, las que deberán identificar mejor las señales del receptor a las células donantes, así como descifrar con mayor profundidad la capacidad neurogénica del ambiente celular del cerebro adulto

Listeria monocytogenes infections can involve the central nervous system in the form of a rhomboencephalitis. Three possible cases of rhomboencephalitis by Listeria monocytogenes are reported (2 females, aged 44 and 49 and a man of 36 years old). The three cases were preceded by an unspecific prodrome of headache, vertigo and fever in absence of a meningeal syndrome. The neurological stage was defined by the unilateral involvement of cranial nerves and the cerebellum and a clear inflammatory cerebrospinal fluid (CSF) with the presence of polymorphonuclear leukocytes, and normal glucose and protein levels. A magnetic nuclear resonance (MRI) showed the appearance of characteristic images, present in the bulboprotuberancial region. These images are one of the most constant features of this disease, reported in the literature. The early diagnosis of rhomboencephalitis was based on the clinical picture, the study of the CSF and the MRI, allowing the use of antimicrobials, prior to microbiological identification. Therefore, the risk of brain stem and cardiac complications of the disease is reduced (Rev Méd Chile 2003; 131: 921-8)

We report a previously healthy 44 years old female, that presented with mild clouding of consciousness, a left cerebellar syndrome, involvement of V, X and XII left cranial nerves and an alteration of epicritic sensitivity in the left half of the body. Cerebrospinal fluid had inflammatory features. Cerebrospinal fluid and blood cultures were positive for Listeria monocytogenes. Magnetic resonance imaging disclosed a rhomboencephalitis. Antibiotics were started and the clinical condition of the patient improved progressively. After three months of follow up, the patient is notably recovered and there is a regression of hyperintense lesions of the brainstem in the magnetic resonance imaging. The diagnosis of Listeria monocytogenes infection must be born in mind in the presence of a rhomboencephalitis.

Two syndromatic forms of Creutzfeldt-Jakob disease are illustrated with data from two cases confirmed by necropsy and studied by means of electroencephalogram, evoked potential recording and neuropathological techniques. One of the cases presented the typical hypersynchronous periodic discharges thougth to be characteristic of this disease. The other did not exhibit epileptiform diischarges, showing an evolution in which progressive diffuse slowing was the prominent feature. Cortical spongyosis, gliosis, and neuronal lose were intense in the case showing spikes, and moderate in the one without spikes. Subcortical involvement was similar in both cases. This different topography of pathological involvement might explain, in addition to electroencephalographic findings, the different behavior of somatosensory evoked potentials, which were of larger amplitude in the case showing epileptiform discharges, although in both cases deterioration of clinical state was accompanied by a progressive amplitude decrement in the evoked potential. Sleep induced by barbiturates was disrupted in the case with spikes, its pattern being closer to normal in the case with less severe cortical involvement. A Wada test demostrated that discharges in the hemispheres were independent. Spike periodicity is discussed. It is postulated that the heavier involvement of cortical layers II to IV deprive the remaining pyramidal cells of inhibitory influences, a condition which might explain the generation of periodic spike discharges.

Se estudian dos casos de enfermedad de Creutzfeldt-Jakob comprobados por examen necrópsico. Uno de ellos presentaba típicas descargas hipersincrónicas, periódicas en el electroencefalograma; el otro caso no mostraba estas descargas epileptiformes y evolucionó con una lentitud difusa progresiva. La espongiosis, gliosis y pérdida neuronal fué intensa en la corteza del caso con espigas y muy moderada en el caso sin espigas. El compromiso subcortical era similar en ambos casos. Se postula que la diferente expresión topográfica de su histopatología explicaria tambien la diferencia en el comportamiento de los potenciales evocados somatosensoriales y el diferente modelo electroencefalográfico del sueno penthotálico. La independencia de las descargas epileptiformes en cada hemisferio se prueba con el test de Wada. Se discute el origen de las espigas y su periodicidad. Se postula teóricamente que el predominio de las lesiones de las capas II a IV privaria a las células piramidales remanentes, de influencias inhibitorias, lo que explicaria la génesis de las espigas.