Clinical Significance:

Elevated Cerebellar antibodies are an indication of neuroautoimmunity. Infection, or exposure to toxic chemicals, can induce production of antibodies against Purkinje’s cells.

Due to cross-reactivity between Gliadin and Cerebellar antigens or peptides, an autoimmune reaction occurs.

Medical conditions related to Purkinje cells range from toxic exposure (mercury, alcohol) to autoimmune disorders (Celiac disease), and from genetic mutations (spinocerebellar ataxias) to neurodegenerative diseases of no known genetic basis (cerebellar multiple system atrophy, sporadic ataxias).

Although the etiology of paraneoplastic cerebellar degeneration (PCD), which generally occurs in patients with neoplasms of the lung, breast, ovary, or with Hodgkin’s disease, is unknown, scientists speculate it is autoimmune in nature.

The known cross-reactivity between cerebellar peptides and gliadin and milk butyrophilin, as seen in patients with gluten sensitivity, which includes many individuals with autism spectrum disorder (ASD), may be responsible for molecular level gluten ataxia, tremors and alterations of coordination, balance and sensations.

Exacerbating cerebellar degeneration, and bringing about the subsequent clinical conditions in ASD patients is mercury –induced disruption in cerebellar synaptic transmission between parallel fibers or climbing fibers of Purkinje cells.

According to Bernard and colleagues, due to the anti-cerebellar antibodies present in the sera of ASD patients, ongoing damage may arise as these antibodies find and react with neuronal antigens.