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Postgraduate Medical Journal 2001;77:700-702; doi:10.1136/pmj.77.913.700
© 2001 BMJ Publishing Group Ltd and The Fellowship of Postgraduate Medicine.
Postgrad Med J 2001;77:700-702 ( November )

Review

Pathophysiological and clinical aspects of breathing after stroke

R S Howarda, A G Ruddb, C D Wolfec, A J Williamsd

a Department of Neurology, Guy's and St Thomas' Hospital Trust, London and Batten Harris Neuromedical Intensive Care Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London, b Department of Elderly Care, Guy's and St Thomas' Hospital Trust, London, c Department of Public Health Medicine, Guy's, King's and St Thomas' School of Medicine, London, d Lane Fox Unit, St Thomas' Hospital Trust, London

Correspondence to: Dr Robin Howard, Department of Neurology, St Thomas' Hospital, Guy's and St Thomas' Hospital Trust, Lambeth Palace Road, London SE1 7EH, UK

Submitted 2 April 2001; Accepted 15 May 2001

The first 150 words of the full text of this article appear below.

    Introduction

Stroke may disrupt breathing either by (A) causing a disturbance of central rhythm generation, (B) interrupting the descending respiratory pathways leading to a reduced respiratory drive, or (C) causing bulbar weakness leading to aspiration.


    Pathophysiology of respiratory control in stroke

Neural control of respiration in man depends on a central drive to the respiratory muscles which is modulated by chemical and mechanical inputs.1 While many of the factors controlling established respiratory rhythm in mammals are understood, the neural mechanisms of rhythm generation remain obscure.2-4 It has proved difficult, in man, to attribute precise respiratory function to localised anatomical substrates because lesions are rarely localised and coexisting pulmonary, cardiovascular, or autonomic influences may complicate the clinical picture. Furthermore accurate diagnosis of respiratory insufficiency has led to earlier therapeutic intervention with controlled ventilation. Also there is probably considerable redundancy and plasticity of the neural substrate of respiratory control, thus congenital, longstanding, or slowly progressive and destructive mass lesions . . . [Full text of this article]


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This article has been cited by other articles:

  • Howard, R. S, Davidson, C. (2003). Long term ventilation in neurogenic respiratory failure. J. Neurol. Neurosurg. Psychiatry 74: iii24-30 [Full Text]  

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