INTRAVENOUS IMMUNOGLOBULIN TREATMENT IN PARANEOPLASTIC NEUROLOGICAL SYNDROMES WITH ANTINEURONAL AUTOANTIBODIES

Objective-To evaluate the effect of intravenous high dose human immuno globulin (IVIg) therapy on the clinical course and autoantibody titres of patients with neurological paraneoplastic syndromes. Methods-Twent y two patients with paraneoplastic encephalomyelitis and sensory neuro nopathy syndrome associated with anti-au antibodies (18) or paraneopla stic cerebellar degeneration (PCD) with anti-Yo antibodies (four), wer e treated with 1-26 (mean 5.8) cycles of IVIg. The Rankin scale was us ed to evaluate the response. Results-The only serious toxicity was one case of haemolytic anaemia. Twenty one patients were evaluable for th erapeutic response. One patient, with subacute sensory neuronopathy (S SN), improved for at least 15 months, 10 remained stable (eight with a nti-Hu and two with anti-Yo antibodies), and 10 deteriorated (eight wi th anti-Hu and two with anti-Yo antibodies). In seven of the 10 patien ts who stabilised, the syndrome had already made a plateau when the tr eatment was started but three patients (one with anti-au and two with anti-Yo antibodies) who had still been progressing stabilised for six, eight, and more than 48 months, including one patient with SSN who ac hieved stabilisation when the neurological dysfunction was only modera te (Rankin scale = 3). Another patient with SSN and initial stable res ponse worsened when Mg was reduced and improved when it was increased. No significant predictive factors of outcome could be identified but improvement or stabilisation was more frequent in patients with isolat ed involvement of the peripheral nervous system (62%) than in patients with evidence of CNS damage (37%) at the onset of treatment. Stabilis ation in patients with CNS involvement was only achieved when the neur ological dysfunction was already severe (Rankin scale > 3). The titres of autoantibodies did not change significantly. Conclusion-Treatment with IVIg at the doses given in the present protocol was not effective in paraneoplastic CNS syndromes associated with antineuronal antibodi es. The role of this regime in the treatment of SSN should be further evaluated.