2006, Number 2
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Plasticidad y Restauración Neurológica 2006; 5 (2)
Spasticity. Who is and who is not?
Aznavurian AA, Aguilar RF
Language: Spanish
References: 30
Page: 152-159
PDF size: 163.26 Kb.
ABSTRACT
Severe muscle spasticity is a common problem in patient with chronic neurological disability resulting from lesions of the upper motor neuron. Although the increased muscle tone in these patients may result in impairment of voluntary movement and thus interferes with motor function, it is often invaluable for the maintenance of trunk posture, weight bearing of the weak lower limb, and for ambulation. Other possible beneficial effects of muscle spasticity are the prevention of deep vein thrombosis in the paretic limb and protection against osteoporosis. Common treatment goals are improvement of motor function, alleviation of painful muscle spasms, and prevention of fixed contractures and bone deformities an enabling comfortable positioning of the patient in bet or chair.
REFERENCES
Griffith ER, Mayer NH. Hypertonicity and movement disorders, in Rosenthal M et al. (eds) Rehabilitation of the adult and child with traumatic brain injury. 1990:127-46.
Mayer NH. Clinic physiologic concepts of spasticity and motor dysfunction in adults with an upper motor neuron lesion. Muscle Nerve 1997;20(Suppl 6):S1-13.
Hagbath K-E, Wallin G, Lofstedt L. Muscle spindle response to stretch in normal and spastic subjects. Scand J Rehabil Med 1973;5:156-9.
Pierrot-Deseillingny E, Mazieres L. Spinal mechanisms underlying spasticity. In: Delwaide PJ, Young RR eds. Clinical neurophysiology in spasticity. Amsterdam: Elsevier, 1985:63-76.
Young RR. Treatment of spastic paresis. New Engl J Med 1989;320:1553-5.
Corcos DM, Gottlieb GL, Penn RD et al. Movement deficits caused by hyperexcitable stretch reflexes in spastic humans. Brain 1986;109:1043-58.
Dietz V, Qintern J, Berger W. Electrophysiological studies of gait in spasticity and rigidity: evidence that altered mechanical properties of muscle contribute to hypertonia. Brain 1981;109:431-49.
Ashby P, Wiens M. Reciprocal inhibition following lesion of the spinal cord in man. J Physiol 1989;414:145-57.
Baldissera F, Hultborn H, Illert M. Integration in spinal neuronal systems. In: Brooks VB, ed. Handbook of physiology, sect I. The nervous system, vol. II Motor control part I. Bethesda: American Physiological Society, 1981:509-95.
Krenz NR, Weaver LC. Sprouting of primary afferent fibers after spinal cord transection in the rat. Neuroscience 1998;85:443-58.
Dewald JP, Pope PS, Given JD et al. Abnormal muscle coactivation patterns during isometric torque generation at the elbow and shoulder in hemiparetic subjects. Brain 1995;118:495-510.
Fellows SJ, Ross HF, Thilmann AF. The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity. J Neural Neurosurg Psychiatry 1993;56:531-7.
Katz R, Perrot-Deseillingny E. Recurrent inhibition of alpha motoneurones in patients with upper motoneurone lesions. Brain 1992;105:103-24.
Ashby P, Mailis A, Hunter J. The evaluation of “spasticity”. Can J Neurol Sci 1987;14:497-500.
Contad B, Benecke R, Meinck HM. Gait disturbances in spastic patients. In: Delwaide PJ, Young RR, eds. Clinical neurophysiology in spasticity. Amsterdam: Elsevier, 1985;155-74.
Landau WM. Spasticity: the fable of a neurological demon and the emperor’s new therapy. Arch Neurol 1974;31: 217-19.
Mayer NH. Clinicophysiologic concepts of spasticity. Muscle Nerve 1997;Suppl 6:S1-13.
Goldstein EM. Spasticity management: an overview. J Child Neurol 2001;16:16-23.
Worblewski JT, Danysz W. Modulation of glutamate receptors: molecular mechanisms and functional implications. Annu Rev Pharmacol Toxicol 1989;29:441-74.
Montague PR, Gancayo CD, Winn MJ et al. Role of NO production in NMDA receptor-mediated neurotransmitter release in cerebral cortex. Science 1994;263:973-7.
Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Roella WP, editors. Spasticity: disordered motor control. Chicago: Yearbook Medical; 1980:485-94.
Jankowska E. Interneurons. In: Adelman G, editor. Encyclopedia of neuroscience. Boston: Birkhaeuser; 1987:63-76.
Mayer N, Esquenazi A, Childers MK. Common patterns of clinical motor dysfunction. Muscle Nerve 1997;20(Suppl 6):S21-S35.
Sahrmann SA, Norton BJ. The relationship of voluntary movement to spasticity in the upper motor neuron syndrome. Ann Neurol 1977;2:460-5.
Roby-Brami A, Bussel B. Long-latency spinal reflex in man after flexor reflex afferent stimulation. Brain 1987;110: 707-25.
Gordon J. Spinal mechanisms of motor coordination. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of neural science. 3rd ed. Norwalk: Appleton & Lange, 1991:581-95.
Hagbarth K-E, Wallin G, Lofsted L. Muscle spindle response to stretch in normal and spastic subjects. Scand J Rehabil med 1973;5:156-9.
Corcos DM, Gottlieb GL, Penn RD et al. Movement deficits caused by hyperexcitable stretch reflexes in spastic humans. Brains 1986;109:1043-52.
Fellows SJ, Ross HF, Thilmann AF. The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity. J Neurol Neurosurg Psychiatry 1993;56:531-7.
Sanger T. Pathophysiology of pediatric disorders. Journal of Child Neurology 2003;18:S9-S24.