Teorías Etiológicas de la Depresión

Notas del editor

• #5: Mood is bleak, pessimistic, and despairing. A deep sense of futility(inutilidad) is often accompanied, if not preceded, by the belief that the ability to experience pleasures is permanently gone. There is a slowing or decrease in almost all aspects of emotion and behaviour: rate of thought and speech, energy, sexuality, and the ability to experience pleasure. Basic physical ‘neurovegetative' activities are affected, such as eating, sleeping, and grooming. Severity varies widely, ranging from mild physical and mental slowing to severe psychosis, with self-denigrating, profoundly negative delusions and hallucinations.
• #7: Argumentó que eran enfermedades de cuerpo, no de espíritu ni mágicas Melancolía: The Hippocratics described melancholia as a condition ‘associated with “aversion to food, despondency (desánimo), sleeplessness, irritability, restlessness”, aetiology of mood disorders in the brain. This Hippocratic insight was buried (enterrado) for two millennia under the humoral theory, solidified in medicine by Galen (second century AD), which held that melancholia resulted from excessive black bile, and mania from excessive yellow bile. The heart, rather than the brain, also was long thought to be the organ of mood disorders. Celsus, ‘believed that right treatment would frighten the patient out of mental illness'.
• #8: The Greek clinical–empirical tradition survived in the early Middle Ages among Arab Muslims (musulmanes) and European Christians, although it later succumbed to religious intolerance. Cassiodorus (490–585), upheld (mantuvieron, apoyaron) humane treatment and emphasized the Hippocratic empirical tradition. that tradition had given way to a more theological–non-empirical bent (inclinación). . From the fourteenth century onwards (hacia adelante), the Inquisition silenced empiricism as heresy, by intimidating or even killing its advocates. Avicenna (AD 980–1037) ‘undoubtedly the material which is the effective producer of mania is of the same nature as that which produces melancholia'. The first asylums for the mentally ill, for instance, were built in the eighth century in Fez, Morocco, and in Baghdad. The first European hospital exclusively organized for the mentally ill was inaugurated in 1409 in the Spanish city of Valencia
• #9: The eighteenth century witnessed a flowering of the revival of the clinical–empirical tradition in medicine, with advanced descriptions of mania and melancholia, such as the following by Richard Mead (1751) Medical writers distinguish two kinds of Madness, and describe them both as a constant disorder of the mind without any considerable fever; but with this difference, that the one is attended with audaciousness and fury, the other with sadness and fear: and that they call mania, this melancholy. But these generally differ in degree only. For melancholy very frequently changes, sooner or later, into maniacal madness; and, when the fury is abated, the sadness generally returns heavier than before. El primer libro todo en inglés fue publicado en 1621 y escrito por Robert Burton: La Anatomía de la Melancolía
• #10: In 1854, Jean Falret (5) described a circular disorder (la folie circulaire), which for the first time expressly defined an illness in which ‘this succession of mania and melancholia manifests itself with continuity and in a manner almost regular'. The same year, Baillarger (6) described essentially the same thing (la folie double forme), emphasizing that the manic and depressive episodes were not different attacks but rather different stages of the same attack Despite these contributions, most clinical investigators continued to regard mania and melancholia as separate entities, chronic in nature, which follow a deteriorating course.
• #11: Eric Kandel: premio Nobel de medicina 2000, Kraepelin It was left to Emil Kraepelin (9) to segregate psychotic illnesses from each other and clearly draw a perimeter around manic–depressive illness. Aspectos: the periodic or episodic course, the more benign prognosis, and a family history of manic–depressive illness. Kraepelin was one of the first to point out that psychological stresses could precipitate individual episodes. Julius von Wagner-Jaurregg, curó un paciente con neurosífilis inyectando malaria: ¿único premio Nobel ganado por un psiquiatra? Given these therapeutic difficulties, the Kraepelinian school was criticized for being practically unhelpful.
• #12: Freud For most of the twentieth century, however, the psychoanalytic ‘climate of opinion' prevailed. Freud's classic work on mood disorders, ‘Mourning and melancholia',(12) set the tone. It argues that melancholia is essentially analogous to the depressive feelings of normal experiences, like bereavement. To Freud, the depressive process in mourning arises from the tension between ambivalent feelings toward the dead parent, like love and aggression. Melancholia was conceived to involve similar ambivalent feelings. Freud's basic insight into the connection between mourning and melancholia was expanded by later psychoanalysts into the general theory that depression is related to feelings of hostility towards another person, often one's parents. These unacceptably hostile feelings turned inwards toward oneself, rather than outwards toward others, leading to depression.
• #13: Karl Jaspers wrote General Psychopathology,(13) which emphasized the importance of unbiased extensive clinical description of psychopathological states. Adolf Meyer Meyer believed that psychopathology emerged from interactions between an individual's biological and psychological characteristics and his or her social environment. While allowing for biological and genetic factors, the Meyerians understood them as part of an individual's vulnerability to specific psychological and social influences. Meyer's approach differs from the standard disease model, in which clinical phenomena in a given patient are understood (and, therefore, potentially predictable) in terms of a given disease with a specific natural history and pathophysiology.
• #15: Donald Winnicott,(23) for instance, described the ‘depressive position' in infant development, when the infant is helpless and unable to master his or her surroundings. The infant, Winnicott taught, responds to the mother's inability to provide everything for him or her with a necessary phase of depressive mood and activity. Winnicott felt that some adult psychopathology related to a reversion to or inability to conquer(vencer) that depressive phase of development. Contemporary neo-Kraepelinian nosology: DSM-III and DSM-IV The current nosology, codified in DSM-III in 1980, is neo-Kraepelinian. The empirical evidence for it is based on classical validity studies, deriving from the pioneering work of Robins and Guze,(25) who laid out a groundwork (levantaron las bases) for establishing the validity of a psychiatric diagnosis based on the four criteria of clinical phenomenology, genetics, course, and treatment response. This group of thinkers, centred at the Washington University in St Louis in the 1970s, swam against the tide of psychoanalytic orthodoxy, empirically tested competing nosologies, and developed diagnostic criteria which became the basis for the first empirically based psychiatric nosology. While some studies have failed to find evidence in support of DSM-III's nosology, most of the empirical evidence continues to support the basic structure of the neo-Kraepelinian nosology.(26,27 and 28)
• #16: Prevalencia de vida más alta de cualquier trastorno psiquiátrico: 17%. A los 12 meses: 7%. Independiente del país y la cultura mujeres:hombres 1.5 - 3:1 (¿Diferencias hormonales, efectos del parto, diferentes estresores psicosociales, modelos comportamentales?) Edad media: 40 años. (50% inicio entre los 20-50 años). De 18-29 años es 3:1 que en >60 años. Incremento incidencia en población <20 años (¿abuso de alcohol y drogas?). >Divorciados o separados. No correlación con estrato socioeconómico. Más común en áreas rurales. No diferencia entre razas.
• #18: Enfermedades crónicas: artritis, enfermedades pulmonares, depresión y migraña. Dentro de las 4 enfermedades crónicas no transmisibles que más producen ausentismo y ausentismo presencial. Nilños (7-11) - Prevalencia últimos 30 días: de- presión mayor se describe en 0,04 % (IC95 %: 0-0,2) y la disti- mia no se detectó. Últimos 12 meses: depresión ma- yor una prevalencia de 0,1 % y la distimia no está presente, esto es, tiene una prevalencia no detectable con el presente estudio. Adolescentes (12-17): toda la vida 2.4%, últimos 12 meses es el trastorno depresivo mayor (0,8 %). Todos los trastornos son más prevalentes en las mujeres. Evaluar con precaución. proporción de ideación suicida total del 6,6 %, distribuida en 7,4 % en adolescentes mujeres y 5,7 % en hombres. plan sui- cida está presente en el 1,8 % de los adolescentes, siendo 2,5 % en mujeres y 1,0 % en hombres. intento de suicidio se da en 2,5 % de los adolescentes (2,9 % en mujeres y 2,1 % en hombres). Adultos: prevalencias de los afectivos 2.1%, mujeres mayores son mayores que las prevalencias de los varones, y el trastorno más prevalente es la depresión mayor (1,6 %) con una relación hombre: mujer de 1:2,6. Los estimativos de depresión menor, distimia son poco precisos. ideación suicida se evidencia que 7,4 % de los adultos lo han pensado. Tiene estas ideas suicidas el 5,5 % de los hombres y el 7,6 % de las mujeres. El plan suicida se presenta en el 2,7 % de las mujeres y 2,0 % para hombres (CVE = 20,4) Por su parte el intento de suicidio se observa en el 1,9% de los hombres y en el 3,3% de las mujeres.
• #19: Muchos estudios que documentan la heredatibilidad de los trastornos afectivos. (Prevalencia en miembros familiares de alguien con trastorno depresivo mayor que la población general?). Entre más miembros de la familia se encuentren afectados, más riesgo.
• #20: The identification of single candidate genes associated with major depression has been difficult because of the likelihood that complex psychiatric illnesses are under polygenic influence and are associated with interactions between genetic variants and environmental exposures.23 major depressive disorder has been associated with polymorphisms in the glucocorticoid receptor gene NR3C1,25 the monoamine oxidase A gene,26 the gene for glycogen synthase kinase-3β (which has a key role in the phosphorylation and regulation of metabolic enzymes and many transcription factors27), and a group-2 metabotropic glutamate receptor gene (GRM3). Many studies have focused on the functional insertion- deletion promoter variant (serotonin transporter-linked polymorphic region [5HTTLPR]) in the serotonin trans- porter gene (SLC6A4) Estudiados en la predicción de outcomes en el manejo con ISRS. Several single-nucleotide polymorphisms (SNPs) in the gene for the serotonin type-2a receptor are associated with outcomes of SSRI treatment. Genome-wide association studies further suggest that effectiveness of antidepressants can be predicted by genetic markers other than traditional candidate genes.