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Review
Normal and pathological gait: what we learn from Parkinson's disease
  1. David Grabli1,2,3,4,
  2. Carine Karachi1,2,3,4,5,
  3. Marie-Laure Welter1,2,3,4,
  4. Brian Lau1,2,3,6,
  5. Etienne C Hirsch1,2,3,
  6. Marie Vidailhet1,2,3,4,
  7. Chantal François1,2,3
  1. 1Université Pierre et Marie Curie-Paris 6, CR-ICM, UMR-S975, Paris, France
  2. 2INSERM, U975, Paris, France
  3. 3CNRS, UMR 7225, Paris, France
  4. 4Assistance Publique-Hôpitaux de Paris, Groupe Pitié-Salpêtrière, Paris, France
  5. 5CENIR, ICM, Paris, France
  6. 6Department of Neuroscience, Columbia University, New York, USA
  1. Correspondence to Dr Chantal François, CRICM, UMRS 975, Inserm, UPMC, Hôpital de la Salpetrière, 47 Bd de l'Hôpital, 75013, Paris, France; chantal.francois{at}upmc.fr

Abstract

Gait and balance disorders represent a major therapeutic challenge in Parkinson's disease (PD). These symptoms respond poorly to dopaminergic treatments, except in the early phase of the disease. Currently, no other treatment is particularly efficient and rehabilitation appears to be the most effective approach. Since these gait and balance deficits are resistant to dopaminergic drugs, their occurrence could be related to the development of extradopaminergic lesions in PD patients. We provide a comprehensive description of the clinical features of gait and balance disorders in PD. We also highlight the brain networks involved in gait and balance control in animals and humans with a particular focus on the relevant structures in the context of PD, such as the mesencephalic locomotor region. We also review other neuronal systems that may be involved in the physiopathology of gait and balance disorders in PD (noradrenergic and serotoninergic systems, cerebellum and cortex). In addition, we review recent evidence regarding functional neurosurgery for gait disorders in PD and propose new directions for future therapeutic research.

  • Parkinson's disease
  • gait disorders
  • pedunculopontine nucleus
  • acetylcholine
  • animal models

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Footnotes

  • Linked article 302461

  • Funding Part of the work presented in this review was funded by INSERM, the Fondation de l'Avenir and the Michael J. Fox Foundation.

  • Competing interests None.

  • Provenance and peer review Commissioned; externally peer reviewed.

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