Psychosomatics 46:458-460, October 2005
doi: 10.1176/appi.psy.46.5.458
© 2005 Academy of Psychosomatic Medicine
Acute Onset of Obsessive-Compulsive Disorder in an Adolescent With Acute Lymphoblastic Leukemia
Douglas R. Morris, M.D.,
Karen G. Meighen, M.D., and
Christopher J. McDougle, M.D.
Received Nov. 21, 2004; revision received Dec. 28, 2004; accepted Feb. 4, 2005. From the Section of Child and Adolescent Psychiatry, Department of Psychiatry, Indiana University School of Medicine, Bloomington; and the James Whitcomb Riley Hospital for Children. Address correspondence and reprint requests to Dr. Meighen, James Whitcomb Riley Hospital for Children, 702 Barnhill Dr., Rm. 4300, Indianapolis, IN 46202-5200; kmeighen{at}iupui.edu (e-mail).
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INTRODUCTION
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We describe the case of a 13-year-old boy who experienced an acute onset of obsessive-compulsive disorder (OCD) in the context of abrupt steroid cessation during treatment for acute lymphoblastic leukemia. Potential contributing factors to the rapid onset of this patient’s symptoms, including the possible role of either steroids or the patient’s underlying leukemia, are explored.
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Case Report
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Andy (not his real name) was a 13-year-old white boy diagnosed with isolated testicular relapse of acute lymphoblastic leukemia 40 days before coming to psychiatric attention. He was first diagnosed with acute lymphoblastic leukemia at age 10. After his initial diagnosis, he experienced remission at the end of chemotherapy induction and finished his treatment for acute lymphoblastic leukemia 3 years later.
Five months after completing chemotherapy, Andy developed leukemic blasts in his right testicle. He subsequently began treatment with a three-drug induction regimen consisting of dexamethasone (10 mg/m2/day) for 28 days; daunorubicin, vincristine, and intrathecal chemotherapy with hydrocortisone, Ara-C; and methotrexate. Spinal taps during intrathecal chemotherapy revealed no evidence of leukemic CNS involvement.
One month after beginning treatment for Andy’s relapse, the psychiatric consultation-liaison service evaluated him in the hematology/oncology clinic after he expressed bothersome obsessive thoughts, compulsive behaviors, and insomnia beginning 24–36 hours after he had completed the 28-day course of dexamethasone. Andy had no history of psychiatric illness or treatment.
At his initial interview, Andy described increasingly bothersome obsessions over the previous 2 days. He felt that he was "going crazy" and feared that he would forget how to talk and lose his cognitive abilities. He repeated mantras, reassuring himself that if he remained calm, these bothersome thoughts would pass. He sought reassurance from his mother and the interviewers, and he repeated the "ABCs" to reassure himself that he could think clearly. His mood was dysphoric, which he attributed both to insomnia and worry surrounding his constant bombardment of unwanted thoughts. He reported no depressive symptoms, perceptual disturbances, or suicidal thoughts. He displayed no manic symptoms. The team recommended sertraline, 25 mg/day, to target his obsessions and compulsions and oral risperidone, 0.5 mg at bedtime, to provide more immediate relief of his anxiety and aid with sleep.
Andy’s symptoms rapidly worsened within 24 hours. His thoughts became dominated by fears that he would be condemned to hell and that he deserved this fate. He noted images in his mind of self-harm and harming family members. He struggled against these thoughts and images, as well as guilt from having them, by repeatedly telling family members that he loved them. He continued to deteriorate and struck himself in the head with the blunt end of an ax. He stated that he had no desire to die but had become convinced of the validity of the emerging thoughts that he should harm himself. Although he did not sustain serious injury, he was admitted to a child and adolescent psychiatric inpatient unit for safety. Andy had received risperidone, 0.5 mg, on the night before admission. The sertraline had not yet been started by his family.
After admission, his oral risperidone dosage was increased to 1.5 mg b.i.d. Because of concern that the abrupt discontinuation of dexamethasone could be contributing to the rapid onset of symptoms, his previous dose of oral dexamethasone, 5 mg t.i.d., was reinstituted with plans to taper it over the following week. Over the next 3 days, Andy’s obsessions steadily subsided, and he was transferred to the hematology/oncology service at our affiliated children’s hospital for continued chemotherapy. During this admission, magnetic resonance imaging of his brain was unremarkable. The result of a test for streptolysin O antibody was negative. His marked improvement allowed for a reduction of the oral risperidone to 0.5 mg at bedtime, and he reported the absence of any notable obsessions on days 4 and 5 of his hospital stay, right before discharge.
On day 15 of the follow-up by the consultation-liaison service, Andy was readmitted to the hematology/oncology inpatient unit with neutropenia and a low-grade fever. He explained that his obsessions and compulsions had increased in severity after his recent discharge. Prominent repetitive, ego-dystonic thoughts, both that he was homosexual and of inflicting harm to himself and to his mother, persisted. He continued compulsively seeking reassurance from the staff and his mother. His oral risperidone dosage was increased to 2 mg b.i.d., and oral sertraline was started at 25 mg in the morning with a recommendation to increase it to 50 mg in the morning after 7 days. Cognitive behavioral therapy, relaxation techniques, and guided imagery were also employed. Andy was referred to a local mental health center for medication management and cognitive behavioral therapy. Over the ensuing weeks, his obsessions decreased in intensity, he felt increasingly in control of his thoughts, and his affect brightened considerably.
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Discussion
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DSM-IV-TR criteria for OCD1 do not specify a necessary duration of symptoms; therefore, Andy was diagnosed with this illness. The abrupt onset of his obsessions and compulsions prompted concern as to whether the symptoms were the product of his medical condition or were related to the generalized stress of a significant medical illness and the need for intensive treatment. Whether his symptoms were steroid-induced, with the use of dexamethasone for his chemotherapy, or were due to abrupt steroid withdrawal were considered prominent possibilities. His negative antistreptolysin O titer limited concern that he might be suffering from a pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS).2
Few cases of steroid-induced obsessions and compulsions have been reported. Our literature review revealed four such cases, each rapidly resolving after steroid discontinuation.3–6 Notable among these cases were repetitive behavioral patterns and washing and cleaning rituals. Andy’s case differed somewhat in that obsessions, rather than compulsions, dominated his presentation. His compulsions were confined to repetitively seeking reassurance and involvement of family members, more commonly noted in childhood OCD,7 as well as some cognitive exercises, e.g., the ABCs.
In reviews of the psychiatric effects of steroids, several authors have frequently described cases of steroid-induced affective disorders (depressive, manic, and mixed), psychotic disorders, and delirium.8,9 Although most adverse effects appear to occur within the first 2 weeks of treatment,10 Sirois8 described a bimodal pattern of acute or subacute psychiatric symptoms. He noted the first peak appearing after several days and the second peak occurring approximately 3 weeks into the course of treatment.8 The onset of Andy’s symptoms, several weeks after beginning daily corticosteroid treatment, occurred near this second bimodal peak.
His other chemotherapy agents could also be considered potential substance-inducing causes of his symptoms. Although some chemotherapeutic agents have been implicated in causing adverse psychiatric effects, our literature review revealed few data on the specific agents to which our patient was exposed.
While Andy’s symptoms could have been substance induced, it is possible that steroid withdrawal could have been a more likely cause of his psychiatric illness. A diverse symptom pattern of steroid withdrawal has been noted with affective and psychotic states and symptoms of delirium.8 That the onset of Andy’s acute symptoms began the day after abrupt cessation of dexamethasone suggests a causal relationship in the development of his symptoms. Wantanabe et al.11 reported two cases of adolescent girls receiving dexamethasone for the treatment of acute lymphoblastic leukemia who developed acute psychiatric symptoms during dexamethasone tapering. The first girl experienced a manic episode, whereas the second experienced panic symptoms.
Pathways of steroid production and regulation may be involved in the development of obsessions and compulsions. McDougle et al.12 reviewed the literature associated with the possible role of hypothalamic-pituitary-adrenal (HPA) axis neuropeptides, corticotrophin-releasing factor, and adrenocorticotrophic hormone (ACTH) in OCD. Although preliminary, there does appear to be evidence of HPA axis dysregulation in patients with obsessive-compulsive symptoms.
Andy experienced rapid symptom resolution after reinstitution of dexamethasone. An increased dose of risperidone was also initiated at this time and makes it difficult to determine how much of his initial improvement could be ascribed to steroid replacement. However, even higher doses of risperidone later in his illness course did not provide as much symptom relief as that seen with larger doses of dexamethasone combined with risperidone. It is also possible that the addition of sertraline to ongoing risperidone treatment led to some improvement in Andy’s obsessive-compulsive symptoms.13
The question as to whether acute lymphoblastic leukemia itself or the physical and psychological stress associated with this serious medical condition could have contributed to the onset of Andy’s symptoms must be entertained. Studies have sought to determine whether children diagnosed with acute lymphoblastic leukemia are more susceptible to psychiatric illness. Brown et al.14 evaluated the psychiatric and family functioning of 55 children with acute lymphoblastic leukemia at three points in time: after a new diagnosis, 1 year postdiagnosis, and 1 year after the completion of chemotherapy. The results showed minimal psychopathology in this group and no increase in the rate of diagnosable psychopathology in these children. Sharan et al.15 assessed the frequency of psychiatric disorders in 30 consecutive children with acute lymphoblastic leukemia who came to a hematology clinic after their first remission. One-third of these children received an anxiety or depression spectrum diagnosis, according to ICD 9 criteria. All of these disorders were felt to be of mild to moderate intensity and perceived to be easily treatable.
Developmental factors germane to this case and requiring further research include the specific role of testicular cancer in the development of psychiatric illness, especially in pubertal boys. The psychological response to cancer relapse compared with that at the initial diagnosis is also a consideration in this case.
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Conclusion
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This case describes the acute onset of OCD in an adolescent boy undergoing treatment for relapse of acute lymphoblastic leukemia. The acute onset of his symptoms following abrupt steroid cessation warrants this as a possible cause of his symptoms. Conversely, steroid induction of symptoms or factors involving the patient’s underlying leukemia are also considerations. Clinicians must be alert to the emergence of uncommon psychiatric symptoms in conjunction with corticosteroid use and discontinuation and in the context of significant medical illness. Further study is warranted to better characterize both the diverse psychiatric effects involved with corticosteroid treatment and the psychological sequelae of cancer at different developmental stages.
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REFERENCES
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- American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders (4th ed, Text Revision) DSM-IV-TR. Washington DC, American Psychiatric Association, 2000, pp 456–463
- Swedo SE, Leonard HL, Mittleman BB, Allen AJ, Rapoport JL, Dow SP, Kanter ME, Chapman F, Zabriskie J: Identification of children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections by a marker associated with rheumatic fever. Am J Psychiatry 1997; 154:110–112[Abstract]
- Bick PA: Obsessive-compulsive behavior associated with dexamethasone treatment. J Nerv Ment Dis 1983; 171:253–254[Medline]
- Jonasson G, Wilkinson SR: Prednisolonindusert obsessive kompulsiv atferd hos barn. Tidsskr Nor Laegeforen 1993; 25:3161
- Grabe H, Freyberger HJ, Maier W: Obsessive-compulsive symptom exacerbation following cortisone treatment. Neuropsychobiology 1998; 37:91–92[Medline]
- Scheschonka A, Bleich S, Buchwald AB, Ruther E, Wiltfang J: Development of obsessive-compulsive behavior following cortisone treatment. Pharmacopsychiatry 2002; 35:72–74[Medline]
- Piacentini J, Bergman RL: Obsessive-compulsive disorder in children. Psychiatr Clin North Am 2000; 23:519–533[Medline]
- Sirois F: Steroid psychosis: a review. Gen Hosp Psychiatry 2003; 25:27–33[CrossRef][Medline]
- Patten SB, Neutel CI: Corticosteroid-induced adverse psychiatric effects: incidence, diagnosis and management. Drug Safety 2000; 22:111–122[CrossRef][Medline]
- Perantie DC, Brown ES: Corticosteroids, immune suppression, and psychosis. Curr Psychiatry Rep 2002; 4:171–176[Medline]
- Wantanabe TK, Sylvester CE, Manaligod JM: Mania or panic associated with dexamethasonechemotherapy in adolescents. J Adolesc Health 1994; 15:345–347[CrossRef][Medline]
- McDougle CJ, Barr LC, Goodman WK, Price LH: Possible role of neuropeptides in obsessive compulsive disorder. Psychoneuroendocrinology 1999; 24:1–24[CrossRef][Medline]
- McDougle CJ, Epperson CN, Pelton GH, Wasylink S, Price LH: A double-blind, placebo-controlled study of risperidone addition in serotonin reuptake inhibitor-refractory obsessive-compulsive disorder. Arch Gen Psychiatry 2000; 57:794–801[Abstract/Free Full Text]
- Brown RT, Kaslow NJ, Hazzard AP, Madan-Swain A, Sexson SB, Lambert R, Baldwin K: Psychiatric and family functioning in children with leukemia and their parents. J Am Acad Child Adolesc Psychiatry 1992; 31:495–502[Medline]
- Sharan P, Mehta M, Chaudhry VP: Psychiatric morbidity in children suffering from acute lymphoblastic leukemia. Pediatr Hematol Oncol 1999; 16:49–54[Medline]
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INTRODUCTION
Case Report
