Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 38

• Published in: Journal of the peripheral nervous system Vol. 8; no. 1; pp. 29 - 58
• Main Authors: Beronio, A, Ghiglione, E, Reni, L, Abbruzzese, M
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Inc 01.02.2003
• ISSN: 1085-9489; 1529-8027
• DOI: 10.1046/j.1529-8027.2003.00038.x

Thalidomide has immunomodulatory and antiangiogenic properties. An important dose limiting side‐effect of long term thalidomide treatment is peripheral neuropathy. Thalidomide induces mainly an axonal sensory neuropathy whose incidence is scarcely known. We prospectively evaluated thalidomide‐induced neuropathy using neurological examination and neurophysiological studies. 50 patients with diagnosed Multiple Myeloma were studied. Thalidomide was given at a dosage ranging from 100 to 400 mg/die, orally. Neurological examination and nerve conduction studies (NCS) were evaluated prior and at 3, 6 and 12 months of treatment. Neurological examination included Neurological Symptom Score and Neurological Disability Score. For NCS, amplitude of sensory and motor action potentials (SNAP and MAP) and conduction velocities of median, peroneal and sural nerves, with F wave recording, were evaluated. All patients were asymptomatic at baseline, with a normal neurological examination and NCS. A decline of the SNAP index of 40 % or more (SNAP amplitude at first examination was considered 100 %) was set as the diagnostic marker of axonal neuropathy. Out of 50 patients, 15 discontinued thalidomide for lack of therapeutic response, 15 remained on therapy for 3 months and 20 completed the treatment at 12 months. Incidence of neuropathy, as judged by clinical and neurophysiological criteria, was high (90%) in the group of patients with a 12 months follow up. On the contrary, the incidence of neuropathy in the group of patients with a 3 months follow up and in those treated with a lower dosage, was low (10–20%). In all the patients, who developed a neuropathy, the subjective symptoms preceded NCS abnormalities. Most common symptoms were paresthesias and reduced sensation with a stock and glove distribution. Our data support the view that thalidomide induces very frequently a dose‐dependent axonal neuropathy with only a partial reversibility, and that NCS findings lack of a predictive value.