
Psychosomatics 50:425-426, July-August 2009
doi: 10.1176/appi.psy.50.4.425
© 2009 Academy of Psychosomatic Medicine
Abrupt-Onset Obsessive-Compulsive Disorder (OCD) in a Child With Crohns Disease
Jennifer L. Derenne, M.D., Assistant Professor of Psychiatry and Behavioral Medicine and PediatricsDirector of Training, Div. of Child and Adolescent PsychiatryMedical College of WisconsinChildrens Hospital of WisconsinMilwaukee, WI
TO THE EDITOR: "Johnny," a 9-year-old boy with Crohns disease, experienced the abrupt onset of intrusive, ego-dystonic, sexualized obsessions (fears that he would lift up the shirts of random women to feel their breasts) which resulted in long nightly confessions to his mother. He was also overly scrupulous and worried that "the mistakes Ive made" (comments or actions that might be interpreted as being unkind) would result in harm to his family and friends. His symptoms gradually dissipated within 10 days, and he denied any ongoing symptoms. There was no history of OCD or OC-spectrum illnesses. Johnnys mother noted that transitioning had sometimes been a challenge. He had mild separation anxiety in kindergarten, but there were no other concerns about mood, anxiety, attention-deficit hyperactivity disorder, or pervasive developmental disorder. Family history was significant for generalized anxiety in Johnnys father.
Other than the Crohns disease (diagnosed at age 7), Johnnys medical history was unremarkable. His medications included methotrexate 7.5 mg weekly, adalimumab 10 mg biweekly, and multivitamin supplements. He laughed about his Crohns disease being "a pain in the butt," then became more somber when discussing the ways in which it had limited his ability to participate in school and sports. His parents described him as a responsible young man who was compliant with medications and treatments, yet still relied on his parents for reminders and did not attempt to coordinate his own care. He was also described as a popular, successful student. The pediatrician had asked about exposure to group-A beta-hemolytic streptococcal infection, but Johnny denied any sick contacts or symptoms. His parents and teacher confirmed that no one else in the home or classroom had recently been ill, and antistreptolysin-O titers were unremarkable. The only apparent event of interest was a transition from infliximab to adalimumab because of diminished response (irritable bowel disease [IBD] flare-up) approximately 3 weeks before the onset of symptoms. The flare-up had resolved nicely with the change to adalimumab.
Discussion
Patients with inflammatory bowel disease are frequently described as obsessive, rigid, and compulsive. Burke et al.1 found that OC symptoms in childhood IBD did not differ significantly from those found in children with cystic fibrosis, suggesting that symptoms were related to the demands of chronic medical illness, rather than IBD itself. The pathogenesis of IBD is not fully understood; it may be related to an abnormal mucosal immune system or specific defects in cellular and humoral immunity.2 Current treatments include anti-inflammatory and immunosuppressive medications. Infliximab and adalimumab bind tumor necrosis factor (TNF)-alpha and block interaction with the TNF receptors, thus inhibiting the induction of proinflammatory cytokines.3
A growing body of literature supported by functional-imaging studies implicates serotonin as well as the basal ganglia in the pathophysiology of OCD. Case reports have suggested that immune-complex formation may lead to OC-spectrum illnesses such as anorexia nervosa.4 Perhaps the most convincing evidence comes from Swedo et al.s work5 on pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Prepubertal patients may develop acute OCD symptoms / tics in the context of exposure to group A beta-hemolytic streptococcal (GABHS) infection. Through the process of molecular mimicry, nondestructive immune complexes localize in the basal ganglia and cause symptoms. Chronic antibiotics, tonsillectomy, intravenous immune globulin, and plasma exchange have been used, with varying success.6 Similar symptoms have been seen in non–strep-mediated illnesses, such as mycoplasma pneumonia.7 To my knowledge, there are no reported cases of OCD developing acutely in the context of an IBD exacerbation or as a response to immunosuppressive agents. It is possible that Johnnys symptoms were completely independent of his IBD status.
Many psychiatric illnesses present or worsen under stress; the stress of diminished response to infliximab may have triggered the OCD. There was also a family history of anxiety, and Johnny did have some preexisting traits of mild rigidity and separation anxiety. However, there did appear to be a temporal relationship between the switch from infliximab to adalimumab and symptom development. It is worthwhile noting that the switch to adalimumab improved IBD symptoms and that the OCD symptoms improved quite rapidly without intervention. There is likely no single explanation for Johnnys presentation. Rather, Johnny likely had a genetic vulnerability to anxiety disorders, which may have been triggered by the stress of illness. It is also possible that there was an unknown GABHS exposure or that there were other social stresses that the family did not divulge. However, given that there is evidence that OCD may be immunomodulated, it would follow that it could be associated with other autoimmune illnesses and that this might be a fruitful area for additional scientific inquiry.
REFERENCES
- Burke P, Meyer V, Kocoshis S, et al: Obsessive-compulsive symptoms in childhood inflammatory bowel disease and cystic fibrosis. J Am Acad Child Adolesc Psychiatry 1989; 28:525–527[CrossRef][Medline]
- Xavier RJ, Podolsky DK: Unraveling the pathogenesis of inflammatory bowel disease. Nature 2007; 448:427[CrossRef][Medline]
- Su C; Salzberg BA; Lewis JD, et al: Efficacy of anti-tumor necrosis factor therapy in patients with ulcerative colitis. Am J Gastroenterol 2002; 97:2577–2584[CrossRef][Medline]
- Harel Z, Hallett J, Riggs S, et al: Antibodies against human putamen in adolescents with anorexia nervosa. Int J Eating Disord 2001; 29:463–469[CrossRef][Medline]
- Swedo SE, Leonard HL, Garvey M, et al: Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. Am J Psychiatry 1998; 155:264–271[Abstract/Free Full Text]
- Swedo SE, Garvey M, Snider L, et al: The PANDAS subgroup: recognition and treatment. CNS Spectrums 2001; 22:419–426
- Ercan TE, Ercan G, Severge B, et al: Mycoplasma pneumoniae infection and obsessive-compulsive disease: a case report. J Child Neurol 2008; 23:338–340[Abstract/Free Full Text]
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