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من طرف black ice الجمعة سبتمبر 26, 2008 3:54 pmTreatment of post-stroke spasticity
Spasticity is a condition that commonly affects muscles in people following upper motor neuron lesions, such as stroke. It has been estimated that approximately 65% of individuals develop spasticity following stroke, and studies have revealed that approximately 40% of stroke victims may still have spasticity at 12 months post-stroke. Spasticity has been described as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex”. It can also be described as a “wicked charley horse”, and once spasticity is established, the chronically shortened muscle may develop physical changes such as shortening and contracture that further contribute to muscle stiffness. These tight, stiff muscles can make movement, especially of the arms or legs, difficult or uncontrollable. The pathophysiologic basis of spasticity is incompletely understood. The changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord, and the absence of an intact corticospinal system. In other words, there is damage to the part of the brain or spinal cord that controls voluntary movement.
After-stroke spasticity can occur in any muscle group, but it most commonly affects the arm, with typical posturing being a clenched fist, bent elbow, and arm pressed against the chest; this can significantly interfere with a stroke victim’s ability to perform daily activities such as dressing and eating.
Various means are available for the treatment of post-stroke spasticity. These include: nonpharmacologic therapies, oral drug therapy, intrathecal drug therapy, injections, and surgery.
Nonpharmacologic therapies
Nonpharmacologic therapies include stretching, splinting, serial casting, dynamic splinting, biofeedback, and electrical stimulation. These therapies have been the traditional forms of treatment for spasticity and should be begun as early as possible. The aim of these therapies is to lengthen the overactive muscle, improve range of motion, prevent further contracture, and decrease the noxious stimuli that may affect the spinal circuit of spasticity. Applying contracture preventative positioning has been shown to slow down development of shoulder abduction contractures, and using Lycra garments for the upper extremity may also be beneficial.
Injections
Injections are focal treatments administered directly into the spastic muscle. Drugs used include: Botulinum toxin (BTX), Phenol, alcohol, and Lidocaine. Phenol and alcohol cause local muscle damage by denaturing protein, and thus relaxing the muscle. Botulinum toxin is a neurotoxin and it relaxes the muscle by preventing the release of a neurotransmitter (acetylcholine). Many studies have shown the benefits of BTX and it has also been demonstrated that repeat injections of BTX show unchanged effectiveness
Surgery
Surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy. Rhizotomy, usually reserved for severe spasticity, involves cutting selective sensory nerve roots, as they probably play a role in generating spasticity
References
J Gallichio. Pharmacologic management of spasticity following stroke. Phys Ther. 2004;84(10):973-981.
2. CL Watkins, et al. Prevalence of spasticity post stroke, Clinical Rehabilitation. 2002;16:515-522.
ZF Vanek. Spasticity. eMedicine article, May, 2005,
http://www.emedicine.com/neuro/topic706.htm.
http://www.stroke.org.
http://www.excite.wustl.edu/newsletters/vol%20207%20spasticity.pdf. 6.
http://strokeassociation.org.
AD Pandyan, et al. Contractures in the post-stroke wrist: a pilot study of its time course of development and its association with upper limb recovery. Clinical Rehabilitation. 2003;17:88-95.
N Mayer, et al. Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, We Move, September 2002.
BJ Young, et al., Physical Medicine and Rehabilitation Secrets, 2nd Edition, Hanley & Belfus, Inc. 2002, pp442-446.
LD de Jong, et al. Contracture preventive positioning of the hemiplegic arm in subacute stroke patients: a pilot randomized controlled trial. Clinical Rehabilitation
Spasticity is a condition that commonly affects muscles in people following upper motor neuron lesions, such as stroke. It has been estimated that approximately 65% of individuals develop spasticity following stroke, and studies have revealed that approximately 40% of stroke victims may still have spasticity at 12 months post-stroke. Spasticity has been described as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex”. It can also be described as a “wicked charley horse”, and once spasticity is established, the chronically shortened muscle may develop physical changes such as shortening and contracture that further contribute to muscle stiffness. These tight, stiff muscles can make movement, especially of the arms or legs, difficult or uncontrollable. The pathophysiologic basis of spasticity is incompletely understood. The changes in muscle tone probably result from alterations in the balance of inputs from reticulospinal and other descending pathways to the motor and interneuronal circuits of the spinal cord, and the absence of an intact corticospinal system. In other words, there is damage to the part of the brain or spinal cord that controls voluntary movement.
After-stroke spasticity can occur in any muscle group, but it most commonly affects the arm, with typical posturing being a clenched fist, bent elbow, and arm pressed against the chest; this can significantly interfere with a stroke victim’s ability to perform daily activities such as dressing and eating.
Various means are available for the treatment of post-stroke spasticity. These include: nonpharmacologic therapies, oral drug therapy, intrathecal drug therapy, injections, and surgery.
Nonpharmacologic therapies
Nonpharmacologic therapies include stretching, splinting, serial casting, dynamic splinting, biofeedback, and electrical stimulation. These therapies have been the traditional forms of treatment for spasticity and should be begun as early as possible. The aim of these therapies is to lengthen the overactive muscle, improve range of motion, prevent further contracture, and decrease the noxious stimuli that may affect the spinal circuit of spasticity. Applying contracture preventative positioning has been shown to slow down development of shoulder abduction contractures, and using Lycra garments for the upper extremity may also be beneficial.
Injections
Injections are focal treatments administered directly into the spastic muscle. Drugs used include: Botulinum toxin (BTX), Phenol, alcohol, and Lidocaine. Phenol and alcohol cause local muscle damage by denaturing protein, and thus relaxing the muscle. Botulinum toxin is a neurotoxin and it relaxes the muscle by preventing the release of a neurotransmitter (acetylcholine). Many studies have shown the benefits of BTX and it has also been demonstrated that repeat injections of BTX show unchanged effectiveness
Surgery
Surgical treatment for spasticity includes lengthening or releasing of muscle and tendons, procedures involving bones, and also selective dorsal rhizotomy. Rhizotomy, usually reserved for severe spasticity, involves cutting selective sensory nerve roots, as they probably play a role in generating spasticity
References
J Gallichio. Pharmacologic management of spasticity following stroke. Phys Ther. 2004;84(10):973-981.
2. CL Watkins, et al. Prevalence of spasticity post stroke, Clinical Rehabilitation. 2002;16:515-522.
ZF Vanek. Spasticity. eMedicine article, May, 2005,
http://www.emedicine.com/neuro/topic706.htm.
http://www.stroke.org.
http://www.excite.wustl.edu/newsletters/vol%20207%20spasticity.pdf. 6.
http://strokeassociation.org.
AD Pandyan, et al. Contractures in the post-stroke wrist: a pilot study of its time course of development and its association with upper limb recovery. Clinical Rehabilitation. 2003;17:88-95.
N Mayer, et al. Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, We Move, September 2002.
BJ Young, et al., Physical Medicine and Rehabilitation Secrets, 2nd Edition, Hanley & Belfus, Inc. 2002, pp442-446.
LD de Jong, et al. Contracture preventive positioning of the hemiplegic arm in subacute stroke patients: a pilot randomized controlled trial. Clinical Rehabilitation
