22:T523,An antineuronal autoantibody has been identified in serum from 14 patients, 8 women and 6 men, with small-cell lung carcinoma (SCLC) and a neurologic disorder. Neurologic symptoms began prior to diagnosis of the SCLC in 12 patients. The dominant neurologic disorder was a subacute sensory neuronopathy (SSN) in eight patients, SSN plus lower motor neuron weakness (2 patients), SSN plus autonomic neuropathy (1 patient), cerebellar ataxia (1 patient), myelopathy (1 patient), and multifocal nervous system disease (encephalomyelitis) in one patient. The presence of the same autoantibody in patients with SSN, encephalomyelitis, and autonomic neuropathy suggests that these diseases are different manifestations of the same nosologic process. With one exception, treatment of the tumor, immunosuppressive drugs, and plasmapheresis did not influence the course of the neurologic illness. The autoantibody was not identified in sera from more than 400 controls subjects, including patients with SSN associated with other tumors, SSN without malignancy, other paraneoplastic syndromes, and SCLC without neurologic symptoms. The autoantibody is a highly specific marker of the paraneoplastic syndromes associated with SCLC and its detection in a patient not known to have cancer should prompt a careful search for SCLC.23:T462,We retrospectively evaluated the effect of plasmapheresis (PE) in seven patients with paraneoplastic encephalomyelitis (PEM), small-cell lung carcinoma, and anti-Hu antibodies, and four patients with paraneoplastic cerebellar degeneration (PCD), ovarian or breast cancer, and anti-Yo antibodies. In addition to PE, patients received prednisone (nine), cyclophosphamide (eight), or treatment of the tumor (five). All but one patient were severely disabled by the time PE began. The clinical outcome was compared with that of five patients (PEM, four; PCD, one) who only had treatment of the tumor. Only one of these five patients had a severe neurologic deficit at the onset of the antineoplastic treatment. No patient improved. Two patients treated with PE and antineoplastic therapy and three who only received treatment of the tumor remained stable for at least 6 months. Four of the five patients with a stable course started the treatment when the neurologic deficit was not severe. We conclude that the efficacy of PE with other immunosuppressive therapies in the stabilization of the neurologic deficit is uncertain.24:T47c,POLYMYOSITIS is an inflammatory disease of striated muscle, which has been attributed to a vasculopathy. Although the pathogenesis is unknown, studies suggest that an immune mechanism may contribute to this disorder. The evidence consists of the presence of tissue-bound immunoglobulins and complement within blood vessels of involved muscle¹and the in vitro cytotoxic effect of patients' lymphocytes on muscle cells grown in culture.^2,3 The mainstay of therapy in polymyositis is corticosteroids. This treatment results in improvement of prognosis and life-style in most patients with this disorder.^4-10However, some individuals are refractory to steroid therapy or demonstrate only a partial response.^11,12In other patients, short- or long-term toxic reactions to corticosteroids force discontinuation of the drug. Such patients who are resistant to or intolerant of corticosteroids have been treated with immunosuppressive agents, including methotrexate sodium,^13-17azathioprine sodium,^18-20cyclophosphamide,^17,21,22and cyclosporine.²³ Although patients may

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