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A biological marker has been discovered that may identify children susceptible to obsessive-compulsive symptoms and tic-like disorders in the aftermath of the ubiquitous streptococcal infection.
So report Susan Swedo, M.D., chief of the section on behavioral pediatrics, and her colleagues at the National Institute of Mental Health. They first announced an association between strep infection and childhood OCD at APA's annual meeting last year in New York.
Swedo and colleagues believe the strep-induced OCD is an autoimmune response triggered when antibodies produced to counter the strep infection "misrecognize" the body's own host cells and attack healthy cells in the basal ganglia region of the brain.
This sets up an inflammatory response leading to obsessive-compulsive symptoms--a syndrome Swedo and colleagues have labeled "pediatric autoimmune neuropsychiatric disorders and associated disorders" (PANDAS).
The current thinking about an association between strep and childhood OCD grew out of research begun by Swedo and colleagues in 1986 investigating obsessive-compulsive behaviors in children who had developed Sydenham's chorea, a variant of rheumatic fever characterized by neurological dysfunction. That work led to the observation of a subset of children who developed OCD and tic-like symptoms in the aftermath of B-hemolytic streptococcal infections.
As an example, Swedo described a 9-year-old boy who virtually overnight developed extreme hoarding behaviors, including holding onto scraps of paper; obsessive fears of contamination; and other compulsive actions. A review of his medical record revealed that he had had a streptococcal infection a month previously.
Following up on that research, Swedo and colleagues discovered what appears to be a positive biological predictor for PANDAS--a monoclonal antibody designated as D8/17 that attaches to the surface of cells and that has been previously associated with rheumatic fever.
In a case control study reported in this month's American Journal of Psychiatry, 23 out of 27 children with PANDAS were found to be D8/17 positive; in contrast, only four of 24 healthy children were D8/17 positive, Swedo and colleagues report.
"If the D8/17 marker is able to identify PANDAS-susceptible individuals, not only would it be the first such marker for a psychiatric disorder, but it would have both immediate and long-term benefits," Swedo writes. "In the short term, it would improve research into the etiology and pathophysiology of obsessive-compulsive disorder . . .by allowing us to define a more homogeneous subgroup of patients for study; it would provide patients and their families with more accurate descriptive and prognostic information; and it would promote the development of treatments designed to address the underlying pathophysiology of the disorder, rather than mere symptom palliation."
In an interview with Psychiatric News, Swedo said that the link between strep and childhood OCD, and the discovery of a biological marker for strep-induced OCD, can lead to new insights about the nature of obsessive-compulsive disorder generally and about its cause and treatment in adults.
"PANDAS can probably teach us about the neural circuitry involved in OCD because the antibodies may allow us to target the specific receptors [in the basal ganglia region of the brain] involved" in obsessive-compulsive disorder, Swedo said.
Swedo said that NIMH is involved in testing several treatments that appear to have dramatic success in children with PANDAS: plasma pheresis, a "blood cleaning" process whereby plasma is exchanged to decrease by more than 95 percent the circulating antibodies that set up the inflammatory response, and intravenous immunoglobulin.
Preliminary results suggest that these treatments are successful enough that they could replace the use of psychoactive medications for children with PANDAS, Swedo said.
She added that preliminary data suggest that some cases of adult OCD may also be immunological and may respond to similar treatments, though more research is necessary.
(Psychiatric News, January 17, 1997)