Paraneoplastic cerebellar degeneration III. Cerebellar degeneration, cancer, and the Lambert‐Eaton myasthenic syndrome
1992
We studied nine patients with a subacute onset of a pancerebellar syndrome. Six had known cancer (three small-cell carcinoma of the lung [SCLC], one metastatic small-cell carcinoma, one small-cell carcinoma of the prostate, and one non-Hodgkin9s lymphoma). Six of eight who had neurophysiologic testing, including the three patients without detectable cancer, had coexistent Lambert-Eaton myasthenic syndrome (LEMS). In two of the patients, LEMS was discovered only by neurophysiologic testing. We looked for anti-Purkinje cell autoantibodies in all patients9 sera and in four patients9 CSF. We also looked for autoantibodies to voltage-gated calcium channels (VGCCs) in seven patients9 sera and two patients9 CSF, using the 125 I-ω-conotoxin radioimmunoassay. We were unable to detect anti-Purkinje cell autoantibodies in any patients9 serum or CSF. However, there were raised titers of anti-VGCC autoantibodies in five of seven patients9 serum, including one patient with SCLC who did not have LEMS, and in the CSF of one of two patients. We conclude that the frequency of presentation of a pancerebellar syndrome with LEMS is higher than expected by chance and is usually associated with cancer. In some of these patients, LEMS may be clinically occult. The presence of LEMS and raised titers of anti-VGCC autoantibodies in some patients with subacute cerebellar degeneration is suggestive of an autoimmune etiology even though anti-Purkinje cell antibodies could not be detected. Anti-VGCC autoantibodies are not confined to LEMS. They may be found at high titer in CSF as well as serum.
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