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Editorial - Spasticity
M. Behari
Abstract
Almost a century ago, Sherrington transected a cat's brain stem above the vestibular nucleus and produced an animal with increased stretch reflexes and tone in antigravity extensor muscles.1,2 This was said to be 'decerebrate rigidity'. Although animal decerebrate rigidity is not considered analogous to human spastic states, Sherrington's seminal study of cat's myotactic stretch reflex established a model of an afferent - efferent neural circuit and paved way for better understanding of spasticity. Nathan described spasticity emphasizing the central role of stretch reflex. In his land mark paper he wrote 'spasticity is a condition in which stretch reflexes that are normally latent become obvious. The tendon reflexes have a lowered threshold to tap, the response of the tapped muscle is increased, and usually muscles besides the tapped one respond; tonic stretch reflexes are affected in the same way'.3 Frequently cited definition proposed by Lance states 'spasticity is a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflexes, as one component of the upper motoneuron syndrome'.4 Work of Sherrington and others defined an afferent - efferent model of stretch reflex and the role of proprioceptive, exteroceptive and descending supraspinal inputs such as reticulo-spinal, rubro-spinal and vestibulo-spinal afferent in the pathogenesis of spasticity. Role of alpha-motoneurons and inhibitory Renshaw interneurons in spasticity is well known. Though the phasic reflex arc is dependent on tendon lengthening and excitatory post synaptic potentials (EPSPs) carried by I-a afferents, inhibitory post synaptic potentials (IPSPs) arising from antagonistic muscle spindles, oligosynaptic and polysynaptic pathways also have important role in maintenance of tone.5-7 Spasticity results from prolonged disinhibition of components of this system. Damage to pyramidal tracts alone whether in the cortex, cerebral peduncle, basis points or medullary pyramids does not result in spasticity. It is only when lesions involves premotor and supplementary motor areas that the spasticity occurs.
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