ABSTRACT
El modelo cognitivo de la depresión que fuera formulado por Beck hace más de 40 años se fundamentaba en procesamientos sesgados de la atención, memoria y el pensamiento, con rumiación y desvíos hacia los llamados pensamientos negativos repetitivos, como jugando roles primarios en el desarrollo y mantenimiento de la depresión. En 2011, el propio Beck y sus colaboradores hacen un resumen de los hallazgos referentes a los mecanismos neurales que subyacen a los aspectos cognitivos de la depresión. Sin embargo, sólo se consideran aquellos aspectos referentes al procesamiento cognitivo sin hacer lo mismo con el procesamiento emocional que es el endofenotipo nuclear del trastorno depresivo y se refleja en la lectura de las emociones por el cerebro emocional y la corteza de la ínsula según el esquema de Damasio actualizado por Craig (14), que deberá tenerse en cuenta como la base fundamental de las terapias cognitivo/conductuales y las cognitivo/emocionales junto al necesario tratamiento farmacológico, adecuadamente complementados en tiempo y forma
The cognitive model of depression, which was formulated by Beck more than 40 years ago, was grounded on biased processings of attention, memory and thought, with rumination and deviations towards the so-called "negative repetitive thoughts", as playing primry roles in the development and maintenance of depression. In 2011, Beck himself, as well as his collaborators, summarized the findings concerning the neural mechanisms underlying the cognitive aspects of depression. However, only those aspects relating to the cognitive processing are considered and not the emotional processing that is the nuclear endophenotype of depressive disorder and is reflected in the reading of emotions by the brain and the insular cortex, according to Damasio's scheme updated by Craig (14), which should be considered the fundamental basis of cognitive/behavioral therapies and cognitive/emotional therapies together with the necessary pharmacological treatment, adequately complimented in due time and forma
Subject(s)
Humans , Cognition , Depression/diagnosis , Depression/pathology , Depression/psychology , Stress, Psychological/pathology , Imprinting, Psychological , Memory/physiology , Nerve Net/pathology , Anxiety Disorders/pathologyABSTRACT
The relationship between depression and epilepsy has been known since ancient times, however, to date, it is not fully understood. The prevalence of psychiatric disorders in persons with epilepsy is high compared to general population. It is assumed that the rate of depression ranges from 20 to 55% in patients with refractory epilepsy, especially considering those with temporal lobe epilepsy caused by mesial temporal sclerosis. Temporal lobe epilepsy is a good biological model to understand the common structural basis between depression and epilepsy. Interestingly, mesial temporal lobe epilepsy and depression share a similar neurocircuitry involving: temporal lobes with hippocampus, amygdala and entorhinal and neocortical cortex; the frontal lobes with cingulate gyrus; subcortical structures, such as basal ganglia and thalamus; and the connecting pathways. We provide clinical and brain structural evidences that depression and epilepsy represent an epiphenomenon sharing similar neural networks.
A relação entre depressão e epilepsia é conhecida desde a antiguidade; entretanto, até o momento, não é completamente compreendida. A prevalência de transtornos psiquiátricos nas pessoas com epilepsia é elevada quando comparada à população em geral. A taxa de depressão varia de 20 a 55% nos pacientes com epilepsia refratária, especialmente considerando-se aqueles com epilepsia do lobo temporal causada por esclerose mesial temporal. A epilepsia do lobo temporal é um bom modelo biológico para compreender as bases estruturais comuns entre a epilepsia e a depressão. É relevante ressaltar que a epilepsia do lobo mesial e a depressão apresentam circuitos similares envolvendo: os lobos temporais com o hipocampo, a amigdala, o córtex entorrinal e o neocortex; os lobos frontais com o giro cíngulo; estruturas subcorticais, como os núcleos da base e o tálamo, e suas vias de conexão. Postulamos por meio de evidências clínicas e estruturais que a depressão e a epilepsia representam um epifenômeno com redes neuronais similares.