Journal of Neurology, Neurosurgery, and Psychiatry 2006;77:1229-1234
PAPER
A specific clinical pattern of camptocormia in Parkinsons disease
1 Department of Neurology, EA2683, IFR 114, Lille University Medical Centre, Lille, France
2 Department of Rehabilitation, Swynghedauw Hospital, EA2683, IFR 114, Lille University Medical Centre
3 Department of Anatomo-pathology, INSERM U 422, Lille University Medical Centre
4 Department of Neurophysiology, Lille University Medical Centre
5 Department of Radiology, Lille University Medical Centre
Correspondence to:
Correspondence to:
D Devos
Hôpital R Salengro, Clinique Neurologique, CHRU, F-59037 Lille Cedex, France;d-devos{at}chru-lille.fr
Background: Camptocormia, characterised by extreme forward flexion of the thoracolumbar spine and severe stooping in the supine position, seems to be prevalent in Parkinsons disease. Objective: The aim of this study was to identify features of parkinsonian camptocormia and to describe the main clinical characteristics of patients with Parkinsons disease who develop the condition. Methods: An extensive range of clinical, biochemical and imaging data were gathered for 23 patients with Parkinsons 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 Parkinsons 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 Parkinsons 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 Parkinsons disease is likely to be important for preventing axial disorders and spinal deformations.
Abbreviations: MRI, magnetic resonance imaging; STIR, short inversion time inversion recovery; UPDRS, Unified Parkinsons Disease Rating Scale
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J. Neurol. Neurosurg. Psychiatry 2006 77: 1223-1228.
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