Rhabdomyolysis induced by severe levodopa induced dyskinesia in a patient with Parkinson’s disease

Abstract

A 74-year-old man with Parkinson’s disease (PD) who had been regularly taking levodopa for 17 years developed severe generalized dyskinesia of choreiform movement. He began to show bradykinesia and rigidity in right limbs at age 57 years. Levodopa treatment dramatically improved his parkinsonian symptoms. Three years after levodopa treatment, he began to feel wearing-off. At age 72 years, he suffered from levodopa-induced dyskinesia (LID) during levodopa on period and was immobile during the off period. Seven days before his first visit to emergency room, he began to feel deterioration of his symptoms with levodopa/ carbidopa 250/25 mg q.i.d. and controlled-release form of levodopa/benserazide 100/25 mg q.i.d. Although peak dose dyskinesia gradually worsened, he gradually increased the dosage until he was taking 12 tablets of levodopa/carbidopa 250/25 mg and four tablets of levodopa/benserazide 100/25 mg per day. The dyskinesia violently affected all four of his limbs and the trunk, and he could not stand or sit in a chair without support. His body temperature was 36.1 C, and serum creatine kinase (CK) level was 215 IU/L. The Unified Parkinson’s Disease Rating Scale (UPDRS) motor score was 64. Although the dosage of levodopa was lowered to levodopa/carbidopa 250/25 mg t.i.d. and controlled-release form of levodopa/benserazide 100/25 mg t.i.d., the violent dyskinesia persisted. We intermittently gave him 2 mg of midazolam intravenously, but failed to stop the dyskinesia when he was awake. After 2 days, he still showed dyskinesia with the same severity, but his mentality was clear. In contrast to his violent dyskinesia and immobility, he showed very mild rigidity in his arms and neck. His body temperature and serum CK level rose up to 38.2 C and 24,651 IU/L, respectively. Urine myoglobulin was markedly increased to 48.1 nmol/L. Leukocyte count in peripheral blood was 18,680/mm. Serum creatinine level was 176.8 lmol/L and serum potassium level 6.9 mmol/L. Rhabdomyolysis with acute renal failure was suspected. All dopaminergic medications were stopped and midazolam was continuously infused intravenously at a rate of 0.4–0.8 lg/min/kg. Five hours after the infusion, body temperature rapidly decreased to normal range. After 21 h of infusion, dyskinesia completely disappeared even without midazolam. Serum CK level decreased to 7,961 IU/L and normalized after following 5 days (Fig. 1). Because dyskinesia reappeared even with the trial of a levodopa/carbidopa 100/25 mg, he had to be maintained with selegiline, amantadine and pergolide. UPDRS motor score measured 1 month after this acute exacerbation of dyskinesia was 55. He was stabilized afterwards without recurrence of dyskinesia. In movement disorders, various causes of rhabdomyolysis have been reported, including status dystonicus, myoclonus, generalized chorea and parkinsonism-hyperpyrexia syndrome (PHS) in patients with parkinsonian diseases [1–4]. In PD, LID leading to rhabdomyolysis is a very rare phenomenon [5]. Two previously reported patients developed rhabdomyolysis by severe LID and C. H. Lyoo Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, 712 Eonjuro, Gangnam-gu, Seoul, South Korea e-mail: lyoochel@yuhs.ac