Camptocormia: pathogenesis, classification, and response to therapy.
Identifieur interne : 001033 ( Main/Exploration ); précédent : 001032; suivant : 001034Camptocormia: pathogenesis, classification, and response to therapy.
Auteurs : Shaheda. Azher [États-Unis] ; Joseph Jankovic [États-Unis]Source :
- Neurology ; 2005.
English descriptors
- KwdEn :
- Abdominal Muscles (physiopathology), Aged, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (therapeutic use), Brain (pathology), Brain (physiopathology), Dystonia (complications), Dystonia (physiopathology), Female, Humans, Male, Middle Aged, Neuromuscular Diseases (classification), Neuromuscular Diseases (physiopathology), Neuromuscular Diseases (therapy), Parkinson Disease (complications), Parkinson Disease (physiopathology), Posture (physiology), Spasm (etiology), Spasm (physiopathology), Spasm (therapy), Spinal Diseases (complications), Treatment Outcome.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents.
- classification : Neuromuscular Diseases.
- complications : Dystonia, Parkinson Disease, Spinal Diseases.
- etiology : Spasm.
- pathology : Brain.
- physiology : Posture.
- physiopathology : Abdominal Muscles, Brain, Dystonia, Neuromuscular Diseases, Parkinson Disease, Spasm.
- chemical , therapeutic use : Antiparkinson Agents.
- therapy : Neuromuscular Diseases, Spasm.
- Aged, Female, Humans, Male, Middle Aged, Treatment Outcome.
Abstract
Originally considered a psychogenic disorder, camptocormia, an abnormal posture with marked flexion of thoracolumbar spine that abates in the recumbent position, is becoming an increasingly recognized feature of parkinsonian and dystonic disorders. Prior reports were limited by sample size, short follow-up, and paucity of data on response to therapy. The authors reviewed 16 patients evaluated in their PD Center and Movement Disorders Clinic diagnosed with camptocormia. In addition to detailed neurologic assessment all patients were videotaped. The mean age was 64.9 +/- 17.4 years, mean age at onset of neurologic symptoms was 51.5 +/- 19.9 years, duration from onset of neurologic symptoms to development of camptocormia was 6.7 +/- 7.6 years, and the mean duration of camptocormia was 4.5 +/- 3.9 years. Of the 16 patients, 11 (68.8%) had Parkinson disease (PD); others had dystonia (n = 4) and Tourette syndrome (n = 1). Twelve patients received levodopa, with minimal or no improvement in the camptocormia. Nine patients received botulinum toxin type A injections into the rectus abdominus, with notable improvement in their camptocormia in four. One patient underwent bilateral subthalamic nucleus deep brain stimulation for PD, but there was no improvement in camptocormia. Based on this series and a thorough review of the literature of camptocormia, head drop, and bent spine syndrome, the authors propose etiologic classification of camptocormia and conclude that this heterogeneous disorder has multiple etiologies and variable response to systemic and local therapies.
DOI: 10.1212/01.wnl.0000171857.09079.9f
PubMed: 16087897
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Originally considered a psychogenic disorder, camptocormia, an abnormal posture with marked flexion of thoracolumbar spine that abates in the recumbent position, is becoming an increasingly recognized feature of parkinsonian and dystonic disorders. Prior reports were limited by sample size, short follow-up, and paucity of data on response to therapy. The authors reviewed 16 patients evaluated in their PD Center and Movement Disorders Clinic diagnosed with camptocormia. In addition to detailed neurologic assessment all patients were videotaped. The mean age was 64.9 +/- 17.4 years, mean age at onset of neurologic symptoms was 51.5 +/- 19.9 years, duration from onset of neurologic symptoms to development of camptocormia was 6.7 +/- 7.6 years, and the mean duration of camptocormia was 4.5 +/- 3.9 years. Of the 16 patients, 11 (68.8%) had Parkinson disease (PD); others had dystonia (n = 4) and Tourette syndrome (n = 1). Twelve patients received levodopa, with minimal or no improvement in the camptocormia. Nine patients received botulinum toxin type A injections into the rectus abdominus, with notable improvement in their camptocormia in four. One patient underwent bilateral subthalamic nucleus deep brain stimulation for PD, but there was no improvement in camptocormia. Based on this series and a thorough review of the literature of camptocormia, head drop, and bent spine syndrome, the authors propose etiologic classification of camptocormia and conclude that this heterogeneous disorder has multiple etiologies and variable response to systemic and local therapies.</div>
</front>
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