Debate About PANDAS

It should be noted that in the literature there is ongoing debate regarding the validity of PANDAS as a unique disease entity. Kurlan and Kaplan (2004) have challenged the five diagnostic criteria of PANDAS and have suggested that there has not been substantial evidence to confirm that the onset or exacerbations of neuropsychiatric symptoms are directly linked to GABHS infection, which is the distinguishing feature of the PANDAS diagnosis as compared with pediatric OCD and/or tic disorder. Kurlan and Kaplan believe that because many authors have suggested that OCD and tic behavior may not be the only psychiatric symptoms associated with PANDAS, the true boundaries (and inclusion of symptoms) of the PANDAS clinical spectrum have not been scientifically validated or standardized. They also believe that the degree and characteristics of symptom severity required for a diagnosis have not been obtained against control studies. Kurlan and Kaplan have stated that the criteria of prepubertal onset is heavily based on the referral patterns of the first 50 described patients and have suggested that there is no immune-mediated explanation for why PANDAS would only occur in 3- to 12-year-olds.

Furthermore, the cause and effect of GABHS infection and neuropsychiatric symptoms are not so clear. It is well established that stress and illness of any kind cause a worsening of OCD and tic symptoms; thus, the neuropsychiatric symptoms associated with GABHS might be caused by illness in general and not the specific GABHS infection (Kurlan and Kaplan 2004). There are no strict or universal guidelines of what "temporal association" of onset of psychiatric symptoms and GABHS infection means. Swedo et al. (1998) implied that evidence of a GABHS infection up to 9 months prior to symptom onset is acceptable criteria for the diagnosis of PANDAS, but it has also been stated that the presence of GABHS in the upper respiratory tract may not be detectable until weeks after onset or exacerbation of infection. This lack of strict guidelines makes it difficult to establish PANDAS as a distinct syndrome. The lack of regular, continuous, and prospective throat cultures along with the lack of universal streptococcal antibody determinations has further hindered the ability to establish a valid temporal relationship between streptococcal infection and onset or exacerbation of neuropsychiatric symptoms (Kurlan and Kaplan 2004).

Singer et al. (2004) have focused on the lack of consistent laboratory tests aimed at determining whether patients with PANDAS have elevated levels of anti-basal ganglia antibodies when compared with healthy control subjects. Singer et al. (2004) measured anti-basal ganglia antibodies and found no major antibody changes in 15 children diagnosed with PANDAS as compared with healthy control subjects. These authors presented five inclusion criteria for evidence of an autoimmune mechanism in any neuropsychological disorder. These included 1) identification of antibodies; 2) presence of immu-noglobulins at the pathological site; 3) positive response to immunomodulatory therapy; 4) induction of symptoms with antigens; and 5) ability to passively transfer the disorder to animal models.

However, recently these criteria have been met to establish an autoimmune mechanism for PANDAS in experimental mouse models (Hoffman et al. 2004; Yaddanapudi et al. 2009). In 2004 Hoffman et al. developed a PANDAS mouse model and found motor and behavioral changes in the mice immunized with a GABHS homogenate. Yaddanapudi et al. (2009) further confirmed this mechanism by which a humoral immune response to GABHS can cause CNS dysfunction and lead to PANDAS. It is believed that antibodies induced by GABHS antigens cross-react with CNS epitopes, disrupting normal neuronal function and result in repetitive behaviors (Yaddanapudi et al. 2009). Naive mice transfused with immunoglobulin G (IgG) from PANDAS mice showed abnormal behavior similar to the GABHS donor mice. Specifically, the posttransfusion naive mice displayed deficits in motor coordination, learning/memory, and social interaction; these impairments are similar to those seen in PANDAS children. This study demonstrated that IgG is the active component of the GABHS donor serum; injection of the IgG sera caused abnormal PANDAS-like behavior, while injection of IgG-depleted GABHS sera did not induce behavioral changes in the mice (Yaddanapudi et al. 2009). These two studies are some of the first to elucidate a physiological mechanism of PANDAS in an animal model, which will help to inform understanding and treatment of PANDAS in children.

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