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Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)

Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
If there are no structural brain abnormalities, then what might cause abnormal brain functioning? Recently, there has been increased speculation that at least some children who develop obsessive-compulsive disorder may do so in response to an external pathogen (in this case -hemolytic streptococcal infection). Studies of Sydenham’s chorea, childhood onset OCD, and Tourette’s syndrome isolated a subgroup of children with either OCD or Tourette’s who had a symptom course marked by abrupt, dramatic exacerbations which were temporally related to -hemolytic streptococcal infection. Additional studies then identified a group of children whose f irst onset of OCD occurred after streptococcal infection. This group was identified by the term PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections). Several studies identified an antigen marker (D8/17) which appears more frequently in children with PANDAS or Sydenham’s chorea compared to normal controls. Importantly, those with PANDAS did not have Sydenham’s chorea, thus leading the authors to suggest that these two disorders may share a similar poststreptococcal autoimmunity. Although these findings are intriguing, it is important to recognize that even if PANDAS is associated with one form of OCD, it apparently accounts for only a small percentage of childhood OCD cases. For example, beginning by soliciting 270 children who had a sudden onset of symptomatology, fifty (18.5%) had PANDAS. However, even among that f ifty, only ten (20%) had OCD only, whereas 16% had tics alone and the remainder of the sample (64%) had subclinical OCD and tics or OCD and tics. Therefore, this means that only 3% of those originally identified by this abrupt onset symptom picture had ‘‘classic’’ OCD. Furthermore, because the rate of streptococcal infection decreases dramatically after puberty, this explanation would not account for onsets of OCD that occur during adolescence and adulthood.
In summary, the conclusions that could be drawn from the current literature are remarkably similar to those drawn by Turner et al.. In short, much of the current evidence regarding altered brain functioning in patients with OCD is conflictual. Although some data suggest that the ventral prefrontal cortical region is the most likely area that is involved, the evidence is far from overwhelming. As presented earlier, Tallis noted that a number of neuropsychological investigations have not found differences in those with OCD, but these negative studies are often discounted in favor of those finding group differences. Similarly, Aylward et al. did not find any consistent abnormalities of the caudate nucleus when meta-analytic procedures were used to analyze the available data. They noted that, although there might be a theoretical basis suggesting a dysfunction of the caudate nucleus, structural and functional MRI studies do not provide empirical support. The issue of a theoretical basis is important because in many instances, it appears that the biological assessment studies are not grounded in any theory explaining why abnormalities might be expected. Rather, much of the data generated appear to have been collected because of the availability of technology or proce dures rather than a clear theory-driven research program. Another major issue is that even if specific abnormalities are identified, do these abnormalities represent activity specific to OCD, or do they merely reflect a general stress response? Certainly, the few studies that used clinical comparison groups did not identify any abnormalities specific to OCD. Furthermore, none of these data necessarily indicate a biological etiology for this disorder and, except for Rosenberg and Keshavan and perhaps Swedo et al., no one has yet addressed the question of what produces the altered or abnormal brain function. Even if the D8/17 antigen plays a role, PANDAS accounts for only a few cases of those who meet diagnostic criteria for OCD. In conclusion, it is clear that all of the data presented are fully consistent with the alternative proposal that these data represent epiphenomena, or correlates of this disorder and although biological structures and functions might be altered as a result of the disorder, the current database indicates that it is premature to refer to OCD as a neuropsychiatric disorder.

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