Introduction
In the SOAP note, the background information on MW led to a diagnosis of Pediatric Autoimmune Neuropsychiatric Disorder (PANDIS). This autoimmune condition manifests as neurological and behavioral problems triggered by streptococcal infections (Swedo et al., 2015). It is characterized by sudden manifestations of obsessive-compulsive disorder (OCD), depressed mood, and anxiety, among others. This paper examines the relationship between PANDIS and an abrupt incline in symptoms of OCD, mood dysregulation, and depression identified in MW.
PANDIS and A Sudden Onset of Symptoms
The pathophysiology of PANDIS is associated with group A streptococcal infections. Antibodies produced against Streptococcus pyogenes are believed to pass through the blood-brain-barrier (BBB) to stimulate calcium-calmodulin-dependent protein kinase II (CaM kinase II), an enzyme associated with inflammation of basal ganglia (Sjöholm, Karlsson, Linder, & Malmström, 2014). This autoimmune response manifests as an abrupt onset of various neuropsychiatric symptoms. Thus, an elevated CaM kinase II activation and related inflammatory responses induced OCD, mood dysregulation, and depressive disorders in MW. S. pyogenes express diverse virulence factors that help the bacteria to invade cells and avoid the host immune system (Sjöholm et al., 2014). Additionally, this pathogen can acquire new structures to evade detection.
Research has examined the neural basis for OCD and tics associated with PANDIS. The primary focus has been directed at the basal ganglia, which is the part of the brain involved in motor control, and therefore, it plays a role in the development of neurobiological disorders (Sjöholm et al., 2014). This structure has functional connections with different areas of the cortex forming the “corticostriatal-thalamocortical (CSTC) circuits” (Sjöholm et al., 2014, p. 1703). Their role is to control psychomotor and cognitive functioning. Therefore, autoimmune inflammation of the CSTC circuits would result in abrupt symptom onset.
The development of OCD has been linked to sensorimotor imbalances in the CSTC circuits (Swedo et al., 2015). Sensory disturbances in these systems manifest as obsessions and compulsions, mood dysregulation, and depressive symptoms that appear suddenly after a streptococcal infection. Therefore, antibody levels are important in a PANDIS diagnosis. Concentrations of anti-streptolysin O (ASLO) and anti-DnaseB (ADB) near or beyond the upper limit titers indicate a streptococcal infection, which can trigger PANDIS symptoms (Swedo et al., 2015). Thus, exposure to streptococcus is a precondition to PANDIS flares.
As indicated above, the cortical damage resulting from misdirected inflammatory responses to streptococcal infections is the real cause of OCD and depressed mood in children diagnosed with PANDIS. The relationship between a positive diagnosis of this disorder and a sudden onset of symptoms can be explained in the context of an autoimmune response to S. pyogenes invasion. Host defenses or antibodies activate CaM kinase II, which triggers the inflammation of the basal ganglia, causing motor and behavioral problems.
Sudden exacerbations of OCD, mood dysregulation, and depressive symptoms are associated with new or recrudescent streptococcal infection. A longitudinal analysis of serological concentrations of host anti-neural antibodies (ASLO and ADB) can be used to establish this association. Their levels are expected to increase following S. pyogenes infection. A subsequent sudden exacerbation of OCD and depressed mood is expected following a PANDIS diagnosis.
Conclusion
The obsessive and compulsive behaviors, depression, and dysregulated moods associated with the PANDIS diagnosis in MW resulted from CaM kinase II-mediated damage of brain dopamine receptors due to human anti-neural antibodies produced against S. pyogenes infection. The sudden onset of these symptoms is related to serologically detectable levels of ASLO and ADB that pass through the BBB to activate CaM kinase II. Therefore, immune therapy in combination with antibiotics can help achieve symptom remission in this patient.
References
Sjöholm, K., Karlsson, C., Linder, A., & Malmström, J. (2014). A comprehensive analysis of the Streptococcus pyogenes and human plasma protein interaction network. Molecular BioSystems, 10(7), 1698–1708. Web.
Swedo, S. E., Seidlitz, J., Kovacevic, M., Latimer, M. E., Hommer, R., Lougee, L., & Grant, P. (2015). Clinical presentation of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections in research and community settings. Journal of Child and Adolescent Pyschopharmacology, 25(1), 26-30. Web.