We use the Cunningham Panel which determines the likelihood of neuropsychiatric symptoms being caused by an infection-triggered autoimmune response, which is a driver in numerous psychiatric symptoms, rather than a primary psychiatric disorder.
The Cunningham Panel provides laboratory which can pinpoint infection-induced autoimmune neuropsychiatric disorders. The panel measures the level of circulating antibodies directed against antigens concentrated in the brain, and measures the ability of these and other autoantibodies to increase the activity of an enzyme (CaMKII) that upregulates brain neurotransmitter activity.
The panel consists of five tests. These tests measure circulating levels of autoantibodies directed against specific neuronal antigens, including: Dopamine D1 receptor (DRD1), Dopamine D2L receptor (DRD2L), Lysoganglioside GM1, and Tubulin.
Autoimmune antibodies that bind to these targets may interfere or potentially lead to a blocking or stimulation of the function of these antigen. This, in turn, may trigger movement and neuropsychiatric disorders, along with OCD and abnormal neurologic behavior.
The 5th test, CaM Kinase II (CaMKII, Calcium-dependent Calmodulin Protein Kinase II) activation measures CaMKII activity. This is a key enzyme that is involved in the upregulation of many neurotransmitters such as dopamine. CaMKII is also understood to increase the “plasticity” or sensitivity and responsiveness of neurologic transmitters to neurotransmitters.
These autoantibodies have been associated with both PANS and PANDAS. The term “PANDAS” indicates that the infectious agent is related to a streptococcal infection. The term “PANS” indicates that the origin of the neurologic condition is undefined.