Currently, autoimmunity is postulated to underlie the pathophysiology of PNS. Tumor cells can sometimes express antigens normally found only in the nervous system, an immunologically privileged site. Onconeural antigens on tumors can be identified as foreign by the immune system and an immune attack can be elicited against them. In the subset of PNS patients, the immune system could also recognize and attack onconeural antigens in normal nervous tissue. This autoimmune hypothesis for the pathogenesis of PNS is supported by a series of arguments: Onconeural antibodies are found in serum and CSF; Cerebrospinal fluid studies show inflammation in 93% of patients; In the acute phase of paraneoplastic cerebellar degeneration hypermetabolism in 18F-Fluoro-2-Desoxy-Glucose Positron Emission Tomography (FDG-PET) scan and increased perfusion on Single Photon Emission Computed Tomography (SPECT) have been described and attributed to inflammatory changes; Pathological examination of the nervous system from patients with anti-Hu associated paraneoplastic encephalomyelitis demonstrates loss of neurons in affected areas with extensive T-cells infiltration and immunohistochemical studies on damaged neural tissue after autopsy reveal inflammatory infiltrations.