Acute camptocormia induced by olanzapine: A case report

被引:12
|
作者
Robert F. [1 ]
Koenig M. [2 ]
Robert A. [3 ]
Boyer S. [4 ]
Cathébras P. [2 ]
Camdessanché J.-P. [1 ]
机构
[1] Department of Neurology, University Hospital, Saint-Etienne
[2] Department of Internal Medicine, University Hospital, Saint-Etienne
[3] Department of Radiology, University Hospital, Saint-Etienne
[4] Department of Psychiatry, University Hospital of Saint-Etienne
关键词
Amyotrophic Lateral Sclerosis; Risperidone; Olanzapine; Neuroleptic Malignant Syndrome; Paraspinal Muscle;
D O I
10.1186/1752-1947-4-192
中图分类号
学科分类号
摘要
Introduction. Camptocormia refers to an abnormal posture with flexion of the thoraco-lumbar spine which increases during walking and resolves in supine position. This symptom is an increasingly recognized feature of parkinsonian and dystonic disorders, but may also be caused by neuromuscular diseases. There is recent evidence that both central and peripheral mechanisms may be involved in the pathogenesis of camptocormia. We report a case of acute onset of camptocormia, a rare side effect induced by olanzapine, a second-generation atypical anti-psychotic drug with fewer extra-pyramidal side-effects, increasingly used as first line therapy for schizophrenia, delusional disorders and bipolar disorder. Case presentation. A 73-year-old Caucasian woman with no history of neuromuscular disorder, treated for chronic delusional disorder for the last ten years, received two injections of long-acting haloperidol. She was then referred for fatigue. Physical examination showed a frank parkinsonism without other abnormalities. Routine laboratory tests showed normal results, notably concerning creatine kinase level. Fatigue was attributed to haloperidol which was substituted for olanzapine. Our patient left the hospital after five days without complaint. She was admitted again three days later with acute back pain. Examination showed camptocormia and tenderness in paraspinal muscles. Creatine kinase level was elevated (2986 UI/L). Magnetic resonance imaging showed necrosis and edema in paraspinal muscles. Olanzapine was discontinued. Pain resolved quickly and muscle enzymes were normalized within ten days. Risperidone was later introduced without significant side-effect. The camptocormic posture had disappeared when the patient was seen as an out-patient one year later. Conclusions. Camptocormia is a heterogeneous syndrome of various causes. We believe that our case illustrates the need to search for paraspinal muscle damage, including drug-induced rhabdomyolysis, in patients presenting with acute-onset bent spine syndrome. Although rare, the occurrence of camptocormia induced by olanzapine must be considered. © 2010 Robert et al; licensee BioMed Central Ltd.
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