Muscle Disorders and the Relaxants.

1 Muscle weakness is a feature of many illnesses but the present discussion will be confined mainly to conditions in which it is a manifestation of defects in the anterior horn cells, the motor nerves, the neuromuscular junction, or the muscle itself. The pathogenesis of these disorders is often ill-understood and more than one component of the neuromuscular system may be involved. Moreover, knowledge about the effect of muscle relaxant drugs upon patients with such conditions is often inadequate and in some conditions entirely absent. This situation is easily understood in view of the rarity of many of these diseases, the relative infre-quency with which operations are performed on such patients, and the natural reluctance of anaesthetists to administer relaxant drugs to patients with known weakness. The purpose of this article is to review the information available on this subject with emphasis on the clinical implications in regard to anaesthesia. Disorders of neuromuscular transmission will be considered first with particular reference to myas-thenia gravis. The functional pathology of this condition has been extensively studied and it is the most important of all the muscle disorders as far as the anaesthetist is concerned, because of its unique effect on the response to muscle relaxants. The general principles of the anaesthetic management of patients with myasthenia gravis can, however , be applied to all other disorders involving muscle weakness. Although this term implies severe muscular weakness , it is really a condition of pathological fatig-ability in which muscle power is rapidly exhausted by activity and slowly recovers with rest. The estimated incidence of the disease in Great Britain is 1 in 40,000 (Garland and Clark, 1956). It is twice as common in women and the mean age of onset is about 26 years (Simpson, 1960). The initial 558 symptoms are frequently ocular (diplopia or ptosis) with weakness of the limb girdles and neck as the next commonest complaint. Other features of this disease are its insidious onset and the spontaneous remissions which occur especially during the first three years (Simpson, 1960). It has been appreciated for many years that myasthenia gravis is due fundamentally to a defect in neuromuscular transmission. For a fuller understanding of the effects of the muscle relaxants in this disease, it is necessary to consider the functional pathology of the neuromuscular junction, which may be considered under four main theories. Altered response by the motor endplates. A number …