INTRODUCTION: Neurological manifestations are uncommon among the undesirable effects of systemic retinoid therapy. We observed a case of axial rigidity imputable to acitretine. Somesthesic evoked potentials were also altered. We therefore searched for such abnormal findings in patients given long-term systemic retinoid therapy. PATIENTS AND METHODS: A neurological exploration was performed in two groups of patients, G1 and G2, with psoriasis and no neurological complaint. The exploration included a physical examination, a study of the somesthesic evoked potentials of all 4 limbs and an electromyogram in case of abnormal findings. There were 8 patients (3 women, 5 men, mean age 56 years, age range 39-71) in G1 treated with systemic retinoids for a mean 140 months (80-185). Cumulative dose was 50 to 280 g with a daily dose of 0.2 to 0.6 mg/kg/day, i.e 20 to 50 mg/d of etretinate or acitretine. In G2, there were 5 subjects (mean age 42 years, range 21-52) with psoriasis (mean duration 20 years range 14-25) who had never been treated with systemic retinoids. RESULTS: Alterations in somesthesic evoked potentials were observed in 7 of the 8 patients in G1. Bilateral disturbances were seen in 6 cases, demonstrating abnormal lemniscal central nervous conduction in the dorsal and/or cervical level in 3 cases and the cervical level alone in 3 cases. There was one asymmetrical case involving the lumbar level on the right and the dorsal and/or cervical level on the right. Only one of the 5 controls in G2 had a minimal unilateral reduction in somesthesic evoked potentials involving the lower limb. Direct effect of systemic retinoids was retained in absence of any other cause due to metabolic, toxic or deficient disorders or spinal compression. CONCLUSION: Long-term use of systemic retinoids induces frequent latent neurological anomalies expressed as lemniscal central nervous conduction. It is hypothesized that pathogenesis involves changes in the lipid composition of the nervous membranes.
INTRODUCTION: Neurological manifestations are uncommon among the undesirable effects of systemic retinoid therapy. We observed a case of axial rigidity imputable to acitretine. Somesthesic evoked potentials were also altered. We therefore searched for such abnormal findings in patients given long-term systemic retinoid therapy. PATIENTS AND METHODS: A neurological exploration was performed in two groups of patients, G1 and G2, with psoriasis and no neurological complaint. The exploration included a physical examination, a study of the somesthesic evoked potentials of all 4 limbs and an electromyogram in case of abnormal findings. There were 8 patients (3 women, 5 men, mean age 56 years, age range 39-71) in G1 treated with systemic retinoids for a mean 140 months (80-185). Cumulative dose was 50 to 280 g with a daily dose of 0.2 to 0.6 mg/kg/day, i.e 20 to 50 mg/d of etretinate or acitretine. In G2, there were 5 subjects (mean age 42 years, range 21-52) with psoriasis (mean duration 20 years range 14-25) who had never been treated with systemic retinoids. RESULTS: Alterations in somesthesic evoked potentials were observed in 7 of the 8 patients in G1. Bilateral disturbances were seen in 6 cases, demonstrating abnormal lemniscal central nervous conduction in the dorsal and/or cervical level in 3 cases and the cervical level alone in 3 cases. There was one asymmetrical case involving the lumbar level on the right and the dorsal and/or cervical level on the right. Only one of the 5 controls in G2 had a minimal unilateral reduction in somesthesic evoked potentials involving the lower limb. Direct effect of systemic retinoids was retained in absence of any other cause due to metabolic, toxic or deficient disorders or spinal compression. CONCLUSION: Long-term use of systemic retinoids induces frequent latent neurological anomalies expressed as lemniscal central nervous conduction. It is hypothesized that pathogenesis involves changes in the lipid composition of the nervous membranes.