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Physiopathologie de l’hyperactivité vésicale

Pathophysiology of bladder overactivity

  • Article de Synthèse / Review Article
  • Published:
La Lettre de médecine physique et de réadaptation

Résumé

L’hyperactivité vésicale est définie comme un trouble de la continence associant une urgenturie avec ou sans incontinence, et fréquemment associée à une pollakiurie et à une nycturie. Un ensemble d’observations récentes permet en effet, désormais, d’établir que l’hyperactivité vésicale correspond d’abord à une anomalie du traitement sensoriel régulant la continence. Les différents cadres étiopathogéniques chez l’homme partagent un ensemble de désordres similaires au niveau de l’urothélium, des nerfs et du muscle lisse du détrusor. Ces désordres s’inscrivent pour partie dans le cadre d’une neuroplasticité orchestrée par les facteurs de croissance nerveuse.

Abstract

Overactive bladder (OAB) is characterised by the storage symptoms of urgency, with or without incontinence, and usually with urinary frequency and nocturia. Recent findings establish that OAB may first refer to abnormal sensory processing of continence. The various pathologic conditions associated with OAB share common features of altered function of urothelium, innervation and detrusor smooth muscle, and may partly rely on growth factors that orchestrate neural plasticity.

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Références

  1. Abrams P, Cardozo L, Fall M, et al (2002) The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 21(2):167–78

    Article  PubMed  Google Scholar 

  2. Fall M, Geirsson G, Lindström S (1995) Toward a new classification of overactive bladders. Neurourol Urodyn 14(6):635–46

    Article  CAS  PubMed  Google Scholar 

  3. de Groat WC (1997) A neurologic basis for the overactive bladder. Urology 50(6A Suppl):36–52

    Article  PubMed  Google Scholar 

  4. Brading AF (1997) A myogenic basis for the overactive bladder. Urology 50(6A Suppl):57–67

    Article  CAS  PubMed  Google Scholar 

  5. Griffiths D, Derbyshire S, Stenger A, et al (2005) Brain control of normal and overactive bladder. J Urol 174(5):1862–7

    Article  PubMed  Google Scholar 

  6. Araki I, Du S, Kamiyama M, et al (2004) Over expression of epithelial sodium channels in epithelium of human urinary bladder with outlet obstruction. Urology 64(6):1255–60

    Article  PubMed  Google Scholar 

  7. O’Reilly BA, Kosaka AH, Knight GF, et al (2002) P2X receptors and their role in female idiopathic detrusor instability. J Urol 167(1):157–64

    Article  PubMed  Google Scholar 

  8. Yoshida M, Homma Y, Inadome A, et al (2001) Age-related changes in cholinergic and purinergic neurotransmission in human isolated bladder smooth muscles. Exp Gerontol 36(1):99–109

    Article  CAS  PubMed  Google Scholar 

  9. Geirsson G, Fall M, Lindström S (1993) Toward a new classification of overactive bladders. Neurourol Urodyn 14(6):635–46

    Google Scholar 

  10. Seki S, Sasaki K, Igawa Y, et al (2004) Suppression of detrusorsphincter dyssynergia by immunoneutralization of nerve growth factor in lumbosacral spinal cord in spinal cord injured rats. J Urol 171(1):478–82

    Article  PubMed  Google Scholar 

  11. Steers WD, Kolbeck S, Creedon D, Tuttle JB (1991) Nerve growth factor in the urinary bladder of the adult regulates neuronal form and function. J Clin Invest 88(5):1709–15

    Article  CAS  PubMed  Google Scholar 

  12. Krenz NR, Meakin SO, Krassioukov AV, Weaver LC (1999) Neutralizing intraspinal nerve growth factor blocks autonomic dysreflexia caused by spinal cord injury. J Neurosci 19(17):7405–14

    CAS  PubMed  Google Scholar 

  13. Clemow DB, Steers WD, Tuttle JB (2000) Stretch-activated signaling of nerve growth factor secretion in bladder and vascular smooth muscle cells from hypertensive and hyperactive rats. J Cell Physiol 183(3):289–300

    Article  CAS  PubMed  Google Scholar 

  14. Hohlfeld R, Kerschensteiner M, Stadelmann C, et al (2000) The neuroprotective effect of inflammation: implications for the therapy of multiple sclerosis. J Neuroimmunol 107(2):161–6

    Article  CAS  PubMed  Google Scholar 

  15. Fowler CJ, Jewkes D, McDonald WI, et al (1992) Intravesical capsaicin for neurogenic bladder dysfunction. Lancet 339(8803):1239

    Article  CAS  PubMed  Google Scholar 

  16. Sui GP, Rothery S, Dupont E, et al (2002) Gap junctions and connexin expression in human suburothelial interstitial cells. BJU Int 90(1):118–29

    Article  CAS  PubMed  Google Scholar 

  17. Drake MJ, Mills IW, Gillespie JI (2001) Model of peripheral autonomous modules and a myovesical plexus in normal and overactive bladder function. Lancet 358(9279):401–3

    Article  CAS  PubMed  Google Scholar 

  18. Drake MJ, Hedlund P, Harvey IJ, et al (2003) Partial outlet obstruction enhances modular autonomous activity in the isolated rat bladder. J Urol 170(1):276–9

    Article  PubMed  Google Scholar 

  19. Coolsaet BL, Van Duyl WA, Van Os-Bossagh P, De Bakker HV (1993) New concepts in relation to urge and detrusor activity. Neurourol Urodyn 12(5):463–71

    Article  CAS  PubMed  Google Scholar 

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Correspondence to J. Kerdraon.

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Kerdraon, J., Manunta, A., Coignard, P. et al. Physiopathologie de l’hyperactivité vésicale. Lett Med Phys Readapt 26, 69–73 (2010). https://doi.org/10.1007/s11659-010-0228-x

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  • DOI: https://doi.org/10.1007/s11659-010-0228-x

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