Vargas ÁLA, Palacios CL, González TG, Peña OF

Language: Spanish
References: 55
Page: 173-179
PDF size: 114.61 Kb.

ABSTRACT

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 ticrelated 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 betahemolytic 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 betahemolytic 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.

REFERENCES

1. Rapoport J. Childhood obsessive-compulsive disorder. J Clin Psychiatry 1998;53:11-16.

2. Stewart S, Geller D, Jenike M. Long term outcome of pediatric obsessive- compulsive disorder: a meta-analysis and qualitative review of the literature. Acta Psychiatr Scand 2004;110:4-13.

3. Pauls D, Alsobrook J, Goodman W, Rasmussen S, Leckman J. A family study of obsessive-compulsive disorder. Am J Psychiatry 1995;152:76-84.

4. Riddle M. Obsessive-compulsive disorder in children and adolescent. Br J Psychiatry 1998;173(supl 35):91-96.

5. Weissman M, Bland R, Canino G. The cross national epidemiology of obsessive compulsive disorder. J Clin Psychiatry 1994;(supl 55):5-10.

6. Nicolini H, Orozco B, Giuffra L. Age of onset, gender and severity in obsessive-compulsive disorder. A study on a Mexican population. Salud Mental 1997;20:1-4.

7. Caraveo-Anduanga J, Colmenares B, Saldivar H. Morbilidad psiquiátrica en la Ciudad de México: prevalencia y comorbilidad a lo largo de la vida. Salud Mental 2000;22:62-67.

8. American Psychiatry Association. Manual Diagnóstico y Estadístico de los Trastornos Mentales. Cuarta edición, texto revisado (DSM-IV-TR). Washington: Masson; 1995.

9. Apter A, Fallon T, King R et al. Obsessive-compulsive characteristics: from symptoms to syndrome. J Am Acad Child Adolesc Psychiatry 1996;35:907-912.

10. Geller D, Biederman J, Faraone S, Agrant A, Cradock K et al. Developmental aspects of obsessive-compulsive disorder: Findings in children, adolescents and adults. J Nerv Ment Dis 2001;189:471-477.

11. King R, Leonard H, March J. Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1998;37(supl 10):27s-45s.

12. Leonard H, Goldberg E, Rapapord J, Cheslw D, Swedo S. Childhood rituals: normal development or obsessive-compulsive symptoms? J Am Acad Child Adolesc Psychiatry 1990;29:17-23.

13. Geller D, Biederman J, Jones J, Parrk k, Schwatz S et al. Is juvenile obsessive- compulsive disorder a developmental subtype of the disorder? A review of the pedriatric literaure. J Am Acad hild Adolesc Psychiatry 1998; 37:420-427.

14. Du Toit P, Van Krandenburg J, Niehas D, Stein D. Comparisons of obsessive-compulsive disorder patients with and without comorbid putative obsessive-compulsive spectrum disorder used a structured clinical interview. Compreh Psychiatry 2001;42:291-300.

15. Leckman J, Gice, D, Boardman J, Zhang H, Vitale A et al. Symptoms of obsessive-compulsive disorder. Am J Psychiatry 1997;154(7):911-917.

16. Bienveniu O, Samuels J, Riddle M, Hoen-Saric R, Liang K, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: A results from a family study. Biol Psychiatry 2000;48:287-293.

17. Hollander E. Obsessive-compulsive spectrum disorders: An overview. Psychiatric Ann 1993;23:355-358.

18. Mcdougle C, Goodman W, Price L. Dopamine antagonists in Tic-related and psychotic Spectrum Obsessive compulsive disorder. J Clin Psychiatry 1994;55 3(supl):24-31.

19. Lensi PG B, Corredu G, Ravagli S, Kunovac J, Akiskal H. Obsessivecompulsive disorder. Familial developmental history, symptomathology, comorbidity and course with special reference to gender-related differences. British J Psychiatry 1996;169:101-107.

20. Hanna G, Veenstra-Vanderweele J, Cox N. Genome -wide linkage analysis of families with obsessive-compulsive disorder ascertained through pediatric probands. Am J Med Genet 2002;114:541-552.

21. Riddle M, Scahill L, King R, Hardin M, Towin K et al. Obsessive-compulsive disorder in children and adolescents: phenomenology and family history. Am J Acad Child Adolesc Psychiatry 1990;29:766-772.

22. Piacientini J, Bergman L. Obsessive-compulsive disorder in children. Psychiatry Clin North Am 2000;23:519-533.

23. Baer L. Factor analysis of symptom subtypes of obsessive-compulsive disorder and their relation to personality and tic disorders. J Clin Psychiatry 1994;55(3 supl):18-23.

24. Khann S, Kaliaperumal V, Channabasavanna S. Cluster of obsessivecompulsive phenomena in obsessive-compulsive disorder. British J Psychiatry 1990;156:51-54.

25. Lochner C, Stain D. Heterogeneity of obsessive-compulsive disorder: A literature review. Harv Rev Psychiatry 2003;11:113-132.

26. Mataix-Cols D, Rauch S, Manzo P, Jenike M, Baer L. Relation of factoranalyzed symptom dimensions of obsessive-compulsive disorder to personality disorders. Acta Psychiatric Scand 2000;102:199-202.

27. Masi G, Millepiedi S, Mucci. A naturalistic study of referred children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 2005;44:673-681.

28. Ivarsson T, Valderhaug R. Symptom patterns in children and adolescents with obsessive-compulsive disorder. Behav Res Ther 2006;44:1105-1116.

29. Delmore R, Bille A, Betancur C, Mathieu F, Cahabane N et al. Exploratory analysis of obsessive-compulsive symptom dimensions in children and adolescents: A prospective follow-up study. BMC Psychiatry 2006;6:1.

30. Mckay D, Piacentini J, Greisberg S, Graae F, Jaffer M et al. The structure of childhood obsessions and compulsions: Dimensions in an outpatient sample. Behav Res Ther 2006;44:137-146.

31. Stewar E, Rosario M, Brown T, Carter A, Leckman J et al. Principal components analysis of obsessive-compulsive disorder symptoms in children and adolescents 2007;61:285-291.

32. Hemmings S, Kinnear C, Lochner C et al: Early- versus late-onset obsessive- compulsive disorder: Investigating genetic and clinical correlates. Psychiatry Res 2003;128:175-182.

33. Delmore R, Krebs M, Chabane F. Frequency and transmission of glutamate receptors GRIK2 and GRIK3 polymophisms in patients with obsessive-compulsive disorder. Neuroreport 2004;15(4):699-702.

34. Hemmings S, Stein D. The current status of association studies in obsessive compulsive disorders. Psychiatry Clin N Am 2006;29:411-444.

35. Grados MA, Riddle M, Samuels J, Liang K, Hoehn-Saric R et al. The familial phenotype of obsessive-compulsive disorder in relation to tic disorders: the Hopkins OCD family study. Biol Psychiatry 2001;50:559-565.

36. Nestadt G, Samuel S, Riddle M, Bienvenu O, Liang K et al. A family study of obsessive-compulsive disorder. Arch Gen Psychiatry 2000;57:358-363.

37. Lenane M, Swedo S, Leonard H, Pauls D, Sceery W et al. Psychiatric disorders in first degree relatives of children and adolescents with obsessive- compulsive disorder. J Am Acad Child Adolesc Psychiatry 1990;29:407-412.

38. Dickel D, Veenstra-Vanderweele J, Chiu BN, Wu X, Fischer D et al. Association studies of serotonine system candidate genes in early-onset obsessivecompulsive disorder. Biol Psychiatry 2007;61:322-329.

39. Hanna G. Demographic and clinical features of obsessive-compulsive disorder in children and adolescents. J Am Acad Child Adolesc Psychiatry 1995,45:19-27.

40. Van Grootheest D, Barteles M, Cath D, Beekman A, Hudziak J et al. Genetic and environmental contributions underlying stability in childhood obsessive- compulsive behavior. Biol Psychiatry 2007;61:308-315.

41. Walitza S, Wewetzer C, Warnke A, Gerlach M, Gellerf et al. 5-HT2A promoter polymorphism -1438G/A in children and adolescents with obsessive-compulsive disorder. Mol Psychiatry 2002;7:1054-1057.

42. Berthier M, Kulievsky J, Goronell A, Heras J. A family study of obsessive- compulsive disorder. Neurology 1992;49:362-368.

43. Pujol JMC, Alonso P, Cardoner N, Menchon J, Deus J et al. Mapping Structural Brain Alterations in Obsessive-compulsive disorder. Arch Gen Psychiatry 2004;61:720-730.

44. Swedo S, Schapiro M, Grady C, Cheslow D, Leonard H et al. Cerebral glucose metabolism in childhood-onset obsessive-compulsive disorder. Arch Gen Psychiatry 1989;46:518-226.

45. Witheside S, Port J, Abramowitz J. A meta-analysis of functional neuroimaging in obsessive-compulsive disorder. Psychiatry Res Neuroimag 2004;132:69-79.

46. Zohar J, Insel T, Berman T, Foa E, Hill J et al. Anxiety and cerebral blood flow during behavioral challenge. Dissociation for central from peripheral and subjective measures. Arch Gen Psychiatry 1989;46:505-510.

47. Swedo S, Rapaport J, Cheslow D, Schapiro M, et al. Hight prevalence of obsessive-compulsive symptoms in patients with Sydenham´s chorea. Am J Psychiatry 1989;146:246-249.

48. Swedo S. Syndeham´S chorea A model for childhood autoinmune neuropsychiatric disorders. J Am Med Assoc 1994;272:1788-1791.

49. Mcdonough M, Kennedy N. Pharmacological management of obsessive- compulsive disorder: A Review for clinicians. Harv Rev Psychiatry 2002;10:127-137.

50. Towbin K, Riddle M. Obsessive-compulsive disorder. Child and adolescent psychiatry. A comprehensive textbook. Baltimore, Maryland: Williams & Wilkins; 1991;p.685-695.

51. Prichep L, Mas F, Hollander E, Liebowitz M, John E et al. Quantitative electroencephalographic subtyping of obsessive-compulsive disorder. Psychiatric Res 1993;50:25-32.

52. Behar D, Rapoport J, Berg C, Denckla M, Mann L et al. Computerized tomography and neuropsychological test measures in adolescents with obsessive-compulsive disorder. Am J Psychiatry 1984;141:363-369.

53. Rosenberg D, Benazon N, Gilbert A, Lorch E, Moore G. Thalamic volume in pediatric obsessive-compulsive disorder. Biol Psychiatry 2000;48:294-300.

54. Gilbert A, Moore G, Keshavan M, Paulson L, Narula V et al. Decrease thalamic volumes of pediatric obsessive-compulsive disorder patients taking paroxetine. Arch Gen Pschiatry 2000;57:449-456.

55. Rosenberg D, Mirza Y, Russel A. Reduced anterior cingulated gluthamatergic concentrations in childhood OCD and mayor depression vs healthy controls. J Am Acad Child Adolesc Psychiatry 2004;43:1146-1153.