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Parkinson’s disease with camptocormia
  1. F Bloch1,
  2. J L Houeto2,10,
  3. S Tezenas du Montcel2,
  4. F Bonneville3,
  5. F Etchepare4,
  6. M L Welter1,
  7. S Rivaud-Pechoux5,
  8. V Hahn-Barma1,6,
  9. T Maisonobe7,
  10. C Behar1,
  11. J Y Lazennec8,
  12. E Kurys3,
  13. I Arnulf9,
  14. A M Bonnet1,
  15. Y Agid1
  1. 1Centre d’Investigation Clinique-Fédération des Maladies du Système Nerveux, Groupe-Hospitalier Pitié-Salpêtrière, Paris, France
  2. 2Service de Biostatistiques et Information Médicale, Groupe-Hospitalier Pitié-Salpêtrière
  3. 3Fédération de Neuroradiologie, Groupe-Hospitalier Pitié-Salpêtrière; UPR640 CNRS LENA, Poitiers, France
  4. 4Service de Rhumatologie, Groupe-Hospitalier Pitié-Salpêtrière
  5. 5INSERM U679, Groupe-Hospitalier Pitié-Salpêtrière; IFR 70, Paris
  6. 6INSERM U610, Groupe-Hospitalier Pitié-Salpêtrière
  7. 7Fédération de Neurophysiologie, Groupe-Hospitalier Pitié-Salpêtrière
  8. 8Service d’Orthopédie, Groupe-Hospitalier Pitié-Salpêtrière
  9. 9Fédération des Pathologies du Sommeil, Groupe-Hospitalier Pitié-Salpêtrière (Assistance Publique—Hôpitaux de Paris), Paris
  10. 10Service de Neurologie, CHU la Milétrie, Poitiers
  1. Correspondence to:
 Y Agid
 Centre d’Investigation Clinique, Hôpital de la Salpêtrière, 47 Boulevard de l’Hôpital, 75013 Paris, France; agid{at}ccr.jussieu.fr

Abstract

Background: Camptocormia is defined as an abnormal flexion of the trunk that appears when standing or walking and disappears in the supine position. The origin of the disorder is unknown, but it is usually attributed either to a primary or a secondary paravertebral muscle myopathy or a motor neurone disorder. Camptocormia is also observed in a minority of patients with parkinsonism.

Objective: To characterise the clinical and electrophysiological features of camptocormia and parkinsonian symptoms in patients with Parkinson’s disease and camptocormia compared with patients with Parkinson’s disease without camptocormia.

Methods: Patients with parkinsonism and camptocormia (excluding patients with multiple system atrophy) prospectively underwent a multidisciplinary clinical (neurological, neuropsychological, psychological, rheumatological) and neurophysiological (electromyogram, ocular movement recording) examination and were compared with age-matched patients with Parkinson’s disease without camptocormia.

Results: The camptocormia developed after 8.5 (SD 5.3) years of parkinsonism, responded poorly to levodopa treatment (20%) and displayed features consistent with axial dystonia. Patients with camptocormia were characterised by prominent levodopa-unresponsive axial symptoms (ie, axial rigidity, gait disorder and postural instability), along with a tendency for greater error in the antisaccade paradigm.

Conclusion: We suggest that (1) the salient features of parkinsonism observed in patients with camptocormia are likely to represent a specific form of Parkinson’s disease and camptocormia is an axial dystonia and (2) both camptocormia and parkinsonism in these patients might result from additional, non-dopaminergic neuronal dysfunction in the basal ganglia.

  • MRI, magnetic resonance imaging
  • MSA, multiple systemic atrophy
  • UPDRS, Unified Parkinson’s Disease Rating Scale

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Footnotes

  • Published Online First 5 June 2006

  • Funding: The study was supported by INSERM and the Assistance Publique des Hôpitaux de Paris.

  • Competing interests: None declared.

  • Patient consent was obtained for publication of fig 1.

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