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J Neurol Neurosurg Psychiatry 77:1229-1234 doi:10.1136/jnnp.2005.083998
  • Paper

A specific clinical pattern of camptocormia in Parkinson’s disease

  1. A-C Lepoutre1,
  2. D Devos1,
  3. A Blanchard-Dauphin2,
  4. V Pardessus2,
  5. C-A Maurage3,
  6. D Ferriby1,
  7. J-F Hurtevent4,
  8. A Cotten5,
  9. A Destée1,
  10. L Defebvre1
  1. 1Department of Neurology, EA2683, IFR 114, Lille University Medical Centre, Lille, France
  2. 2Department of Rehabilitation, Swynghedauw Hospital, EA2683, IFR 114, Lille University Medical Centre
  3. 3Department of Anatomo-pathology, INSERM U 422, Lille University Medical Centre
  4. 4Department of Neurophysiology, Lille University Medical Centre
  5. 5Department of Radiology, Lille University Medical Centre
  1. Correspondence to:
 D Devos
 Hôpital R Salengro, Clinique Neurologique, CHRU, F-59037 Lille Cedex, France;d-devos{at}chru-lille.fr
  • Received 9 November 2005
  • Accepted 15 May 2006
  • Revised 18 April 2006
  • Published Online First 30 May 2006

Abstract

Background: Camptocormia, characterised by extreme forward flexion of the thoracolumbar spine and severe stooping in the supine position, seems to be prevalent in Parkinson’s disease. Objective: The aim of this study was to identify features of parkinsonian camptocormia and to describe the main clinical characteristics of patients with Parkinson’s disease who develop the condition. Methods: An extensive range of clinical, biochemical and imaging data were gathered for 23 patients with Parkinson’s disease with camptocormia, notably including magnetic resonance imaging (MRI) of the brain and spine, electromyographic recordings of the paravertebral muscles and muscle biopsies. Results: Camptocormia occurred in severe Parkinson’s disease with axial predominance, motor fluctuations and dysautonomic symptoms. The condition was often associated with spondyloarthritic changes and pain. MRI showed paraspinal muscle signal abnormalities in five patients and fatty involution in seven patients. The seven patients had motor unit reductions on the spinal erector electromyogram. The MRI results for the girdle muscles were normal. Cranial MRI showed signal abnormalities for the basal ganglia in three patients. Discussion: Various mechanisms may contribute to the development of parkinsonian camptocormia: dopaminergic depletion in Parkinson’s disease induces functional changes in the organisation of the corticospinal and reticulospinal tracts, where dysfunction could contribute to axial rigidity. Furthermore, rigidity of the spinal flexion muscles could lead to under-use of the spinal extension muscles, which become progressively atrophic. Rigidity may also induce spinal deformations, leading to a neurogenic syndrome via compression of the spinal nerves. Conclusion: The screening and early management of camptocormia in Parkinson’s disease is likely to be important for preventing axial disorders and spinal deformations.

Footnotes

  • Published Online First 30 May 2006

  • Competing interests: None declared.

  • Informed consent was obtained for publication of fig 1.

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