Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, referred to by the acronym PANDAS, is autoimmune disorder with obsessive-compulsive disorder or tic disorder manifestations associated with GAS.

Proposed Pathogenesis

The hypothesis for PANDAS involves several factors, including pathologic strains of GAS bacteria, host susceptibility (e.g., genetics, development, or other), and abnormal immune response. A pathogenesis model has been proposed to describe the disorder . Ongoing research is being conducted to understand the pathologic mechanisms involved in the PANDAS subgroup. As part of the diagnostic criteria, temporal association with GAS infection and neuropsychiatric exacerbation is very important. It is essential to distinguish exacerbations of PANDAS resulting from GAS infection from the waxing and waning course seen in Tourette disorder and some cases of childhood-onset obsessive-compulsive disorder. According to Swedo,host susceptibility is thought to result from genetic, developmental, and immunologic factors. Children in the PANDAS subgroup may have similar genetic susceptibility for poststreptococcal sequelae, as children with Sydenham chorea. Development also seems to play a role in the pathogenesis of PANDAS, because the peak age of onset of symptoms is 6 to 7 years and prepubertal onset is characteristic. PANDAS is described as an autoimmune process, and many think there are antineuronal cross-reactive antibodies similar to the autoantibodies found in Sydenham chorea. These antibodies are meant to react against GAS, but in the case of PANDAS cross-react with cells in the basal ganglia. Studies using MRI volumetric scans have shown bilateral enlargements of the caudate, putamen, and globus pallidus among patients in the PANDAS subgroup.

These criteria as further described by Swedo and coworkers are as follows:

The presence of a tic disorder and/or obsessive-compulsive disorder.

Prepubertal age at onset, usually between 3 and 12 years of age.

Abrupt symptom onset and/or episodic course of symptom severity.

Temporal association between symptom exacerbations and streptococcal infections.

Presence of neurologic abnormalities during periods of symptom exacerbation.

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