Trastrorno obsesivo compulsivo en niños y adolescentes: una actualización. Primera parte

• Autores: Luis Alberto Vargas Alvarez, Lino Palacios Cruz, Guillermo González Thompson, Francisco de la Peña Olvera
• Localización: Salud mental, ISSN 0185-3325, Vol. 31, Nº. 3, 2008, págs. 173-179
• Idioma: español
• Títulos paralelos:
  • Obsessive–compulsive disorder in children and adolescents: an update. Part one
• Enlaces
  • Texto completo (pdf)
• Dialnet Métricas: 2 Citas
• Resumen
  • español

    El trastorno obsesivo compulsivo se ha reportado en los últimos tiempos con mayor prevalencia en la edad pediátrica que lo reportado anteriormente, esto se debe probablemente a una mejor caracterización de su presentación en niños y adolescentes y al desarrollo de mejores métodos de evaluación. Los criterios diagnósticos son los mismos para niños, adolescentes y adultos. Debido a su bajo nivel de conciencia, los niños pueden no considerar sus obsesiones como exageradas o ilógicas por lo que el DSM–IV no incluye este criterio en este grupo de edad. Aunque hay muchas similitudes sintomáticas a distintas edades, también hay importantes diferencias que convierten este padecimiento en un reto diagnóstico y de tratamiento en el TOC de inicio temprano. La prevalencia del TOC pediátrico se ubica en un rango de 2% a 4%, con una predominancia de los hombres en relación a las mujeres. En México aún no se cuenta con estudios que confirmen estas cifras en esta forma de presentación pediátrica. Frecuentemente los niños, más que los adolescentes y los adultos, pueden presentar conductas compulsivas, sin un componente obsesivo, lo cual probablemente se asocie al desarrollo cognitivo. Los síntomas obsesivos y compulsivos presentan diferencias en el contenido de acuerdo al grupo etario. Las obsesiones más comunes en el TOC de inicio temprano son las relacionadas a la contaminación y gérmenes con compulsiones relacionadas a lavado y revisión. Otras obsesiones frecuentes son el temor a dañar a otros. Se ha identificado que los adolescentes presentan con mayor frecuencia obsesiones sexuales o religiosas y, junto con los niños, más obsesiones agresivas y compulsiones de atesoramiento que los adultos.

    Por sus características el TOC de inicio en la infancia ha dado pauta a diversas clasificaciones, como son la presencia comórbida de tics y la agregación familiar con más de un integrante con el padecimiento. Algunos estudios han reportado diferencias entre los niños que padecen TOC con tics versus aquellos sin tics, como es la mayor frecuencia de rituales de repetición sin contexto de evitación al daño y menor frecuencia de síntomas relacionados con contaminación/lavado. Otra forma de clasificación que en la actualidad ha permitido la subdivisión del TOC en subtipos se ha apoyado en el análisis factorial, donde se han identificado subtipos en adultos y recientemente en niños y adolescentes con consistencia entre autores. Los subtipos propuestos son: lavado/contaminación, simetría/ orden, obsesiones sexuales/religiosas y atesoramiento. Respecto de las hipótesis etiológicas, las evidencias de agregación familiar y los estudios en gemelos han esclarecido el importante papel genético de este trastorno. Otras teorías biológicas no genéticas para el TOC que se han considerado son las lesiones cerebrales focales y secuelas inmunes generadas por infecciones con el estreptrococo beta–hemolítico del grupo A que podrían explicar alguna proporción de los individuos con TOC. Diversas líneas de investigación han evidenciado que la neuropatología del TOC se encuentra en el circuito cortico–estriado–tálamo–cortical, donde están implicadas la disfunción de la dopamina, la serotonina, el glutamato y el GABA. Particularmente existe evidencia sobre la serotonina, dada la amplia utilización y probada efectividad de los inhibidores selectivos de la recaptura de serotonina (ISRS) en el tratamiento del TOC. Los estudios electrofisiológicos y con potenciales relacionados con eventos (PREs) han sido limitados en adultos y no hay reportes en población pediátrica. Por medio de estudios de neuroimagen como la tomografía axial computarizada (TAC), se ha reportado: disminución de volumen bilateral en el núcleo caudado y cambios estructurales en los ganglios basales ante sintomatología obsesivo–compulsiva durante la adolescencia. La tomografía por emisión de positrones (TEP) en adultos ha sugerido un incremento en el metabolismo del giro orbital y la cabeza del núcleo caudado, mientras que en sujetos con una edad de aparición en la adolescencia se ha reportado un incremento en el metabolismo en regiones orbito–frontal izquierda, sensorio–motor derecha, giro del cíngulo anterior y prefrontal bilateral.

  • English

    The obsessive–compulsive disorder (OCD) is being reported now with increased prevalence in pediatric population than in the past, associated with the development of more specific assessment methods. This evolution has opened the possibility to characterize OCD presentation in children and adolescents. OCD in childhood is a chronic and distressing disorder that can lead to severe impairments in social, academic and family functioning. Currently, pediatric OCD criteria are the same than in adults. The presence of obsessive and compulsive symptoms are needed to establish the diagnosis but, because of the lower levels of cognitive awareness in children, they are less likely to consider their OCD symptoms as excessive or unreasonable. The DSM–IV does not require that symptoms be recognized as senseless or unrealistic for the diagnosis to be made in children. Overall, there are several clinical differences in the younger age groups that make this disorder a diagnostic and treatment challenge for clinicians.

    Epidemiologic studies have been conducted in adolescent population. These studies report a prevalence in the range of 2% to 4% with a slight predominance in males than females. In Mexico, there are no studies in this population to confirm these rates.

    Frequently children, more than adolescents and adults, may present compulsive behavior without obsessions, which are related to immature cognitive development. The obsessive–compulsive symptoms have differences between age groups (children, adolescents and adults). Children may be somewhat more likely to engage in compulsive reassurance– seeking and involve their parents in their rituals. The most common obsessions in childhood are related to contamination and germs, followed by fears to harm others. The most common compulsions are washing, repeating and checking. Adolescents present more frequently religious and sexual contents in their obsessions, and similar about aggression as children. Related to compulsions, children and adolescents develop hoarding more frequent than adults. Several studies suggest a mean age of childhood OCD from 6 to 11 years of age, but there are two peaks of more frequent cases presentation: in early childhood and early adolescence. Regarding the OCD early–onset, course studies have reported chronicity in most subjects, 50% of them meeting full OCD criteria seven years later. Meta–analytic studies about predictors and persistence of pediatric OCD diagnoses show persistence in 41% of the sample with full OCD and 60% full or sub–threshold OCD. Early beginning of OCD increase duration of illness and is a predicted of major persistence. Comorbid psychiatric illnesses and poor initial treatment response were poor prognostic factors. Regarding symptoms during illness course, the pattern and type frequently shift over time, although the number of symptoms typically remains constant.

    Pediatric OCD has evoked distinct classifications related to the familiar presentation form and comorbidity, especially with tics disorders. Studies have reported that children with tics disorders show several differences in their reported symptom types when compared with the group with no history of tics, for example, they are more likely to endorse repetition of routine behaviors unrelated to harm avoidance. Contamination and washing rituals are more common in the OCD child without tics. Findings are consistent with several studies in clinical assessed adult samples which have shown that the tic–related OCD can be distinguished as a subtype of OCD. These adults are more likely to report obsessions involving a need of symmetry and compulsions involving touching, starting and counting. There are also evidence that the tic–related OCD may be lees likely to monotherapy with a selective serotonin reuptake inhibitor. Another way to understand this disorder is subtyping symptoms using factorial analysis. Several authors have proposed at least four subtypes or factors (washers, hoarders, checkers and sexual/religions symptoms). Some studies with children and adolescents have shown limitations to conduct a factorial analysis, although some others with better methods have showed similarity between OCD symptoms dimensions structure in children and adults.

    The etiology of OCD is not clear, but the evidence in familiarity, segregation analysis and twins studies have established the role of genetics in the cause factors and is considered as a complex genetic disorder. Twin studies find a high concordance rate for monozygotic twins (53–87%) and dizygotic twins (22–47%). The prevalence of OCD is higher among first degree relatives of affected subjects, early–onset OCD has a higher rate of first degree relatives with TOC. Association studies with candidate genes have been done in early–onset OCD but significant results have not been replicated.

    Another etiologic aspects that have been studied and have helped in the comprehension of some types of pediatric OC symptoms are the focal cerebral lesions in basal ganglia and the symptoms occurrence related to immune response against Group A beta–hemolytic streptococcus (GABHS). Cerebral focal lesions are rare and involve basal ganglia, which evoke obsessive–compulsive symptoms. According to immune response to GAHBS infections, data support the basis of a immune role of OC symptoms with or without tics, because of the symptoms appearance and exacerbation associated to the recent infection. This disorder is named PANDAS (Pediatric Autoimmune Neuropsychiatry Disorders Associated with Streptococcal Infections). The PANDAS syndrome considers five clinical criteria: prepubertal onset, neurological abnormalities including motor hyperactivity and clumsiness, temporal relation with Group A beta–hemolytic streptococci, episodic course of severity and OCD or tics symptoms. The dramatic nature of the onset of symptoms and the rapid resolution with immune–based therapy is well described versus gradual resolution and onset on more typical OCD cases. In fact OCD symptoms cases are more often male, younger and have a very high rate of disruptive behavior and tics disorders. Although Sydenham chorea is proposed as a medical model for the PANDAS syndrome, the hypothesis mechanism of immune complex disease in basal ganglia remains unproven. In brief, studies do not support the routine use of immunomodulatory agents and even less clear is the use of antibiotic prophylaxis but current practice should include assessment for GABHS including throat cultures in all young patients with abrupt onset or exacerbation of OCD or tics symptoms.

    Clinical and basic investigation studies have elucidated that the OCD neuropathology includes the cortical–striata–talamic–cortical pathways, those implying serotonin and dopamine, GABA and glutamate dysfunction. Several studies supported the hypothesis that the serotonin neurotransmitter system plays a crucial role in OCD. First, the administration of selective serotonin reuptake inhibitors (SSRI) was demonstrated to be more effective than that of noradrenergic reuptake inhibitors in the treatment of OCD. To date all SSRIs in patients with OCD have been found to be more or less effective for the treatment.

    Several neuroimaging studies have shown differences and abnormalities in OCD patients. Abnormalities in the prefrontal cortex are believed to be involved in causing obsessive–compulsive symptoms. Although the ventral prefrontal cortex was previously more implicated in the pathogenesis of OCD, dorsolateral prefrontal cortex plays a critical rolle too. Bilateral reduction volume in basal ganglia caudate nucleus and structural changes in basal ganglia have been reported in OCD juvenile onset in axial tomography. In MR there are reports of frontal cortex, cingular gyrus and lenticular nucleus abnormalities. Positron emission tomography studies have shown hypermetabolism in the orbitofrontal cortex, anterior cingulate gyrus and head of caudate nucleus and finding evaluating OCD adolescent onset reported increase hypermetabolism in left orbitofrontal, right sensory–motor regions, anterior cingulate gyrus and bilateral prefrontal cortex.

    Pediatric OCD is a severe, chronically disabling illness with a broad scope of active research into this subject. Epidemiologic, genetic and neurobiologic advances have contributed to increase treatment strategies and characterization of early onset OCD.