According to the definition by Lance, spasticity is: “a motor disorder characterized by a velocity-dependent increase of tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome”. Spasticity is obviously a heterogenous set of clinical states. As a matter of fact the release of the proprioceptive reflex can be the consequence of a lesion of the corticofugal pathways at any level of Central Nervous System (C.N.S).
KeywordsPresynaptic Inhibition Dantrolene Sodium Polysynaptic Pathway Skeletal Muscle Sarcoplasmic Reticulum Motor Neuron Syndrome
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- Betz H (1987) Biology and structure of the mamalian glycine receptor. TINS 10:113–117Google Scholar
- Delwaide JP, Dresse A (1984) Les myorelaxants. Sem Hop Paris 60(40):2897–2929Google Scholar
- Eyssette M, Rohmer F, Serratrice G, Warter JM, Boisson D (1988) Multi-centrer, double-blind trial of a novel antispastic agent, Tizanidine, in spasticity associated with multiple sclerosis. Curr Med Res Opin 10(10)Google Scholar
- Gonsette RE, Desmet Y, Demonty L (1984) Tizanidine, a new antispastic agent: 6 years clinical experience in 152 MS sclerosis. MTD Press Ltd, Lancaster Boston The Hauge Dordrecht, pp 219–225Google Scholar
- Katz RT (1988) Management of spasticity. Am J Phys Med Rehabil 67(3)Google Scholar
- Lance JW (1980) Pathophysiology of spasticity and clinical experience with Baclofen. In: Feldman RG, Young RR, Koella WP (eds) Spasticity: disordered motor control. Year book, Chicago, pp 185–203Google Scholar
- Young RR, Delwaide PJ (1981) Drug therapy in spasticity. N Engl J Med 304:28–33, 96–99Google Scholar