![]() Neurological presentations that suggest a CRMP-5-IgG-related syndrome include subacute chorea or cranial neuropathy (particularly loss of vision, taste, or smell), dementia, myelopathy and gastrointestinal dysmotility in a patient with risk factors for lung cancer, or encephalopathy or neuromuscular hyperexcitability in a patient with serological or clinical evidence of myasthenia gravis.(1) Fourteen percent of patients have thromboembolic phenomena. The neurological presentation of CRMP-5 seropositive patients is usually multifocal, and can affect any level of the neuraxis. Most are highly predictive of specific neoplasms that are metastatic when diagnosed, but usually limited in spread to regional lymph nodes and adjacent structures.(1-4)Ĭollapsin response-mediator protein-5 (CRMP-5) is highly expressed in small-cell lung carcinomas (SCLC), in neurons throughout the adult central and peripheral nervous systems, and in a subset of glial cells.(1) In Western blot analyses the native antigen is a 62-kDa protein (recombinant human CRMP-5 is 68-kDa).(1) CRMP-5-IgG (also known as anti-CV-2)(4,5) is a more common autoantibody accompaniment of SCLC than antineuronal nuclear antibodies-1 (ANNA-1 anti-Hu) and sometimes occurs with thymoma. Autoantibodies specific for neurons and muscle are important serological markers of neurological autoimmunity.
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