Year : 2013 | Volume
| Issue : 4 | Page : 453-460
Spasticity - Pathogenesis, prevention and treatment strategies
Anju Ghai1, Nidhi Garg1, Sarla Hooda1, Tushar Gupta2
1 Department of Anaesthesiology and Pain Medicine, Rohtak, Haryana, India
2 Department of Orthopaedics, All India Institute of Medical Sciences, New Delhi, India
H no: 19/9J, Medical campus, Rohtak, Haryana
Source of Support: None, Conflict of Interest: None
|Date of Web Publication||7-Nov-2013|
This review of the long-term management of spasticity addresses some of the clinical dilemmas in the management of patients with chronic disability. It is important for clinicians to have clear objectives in patient treatment and the available treatment strategies. The review reiterates the role of physical treatment in the management, and thereafter the maintenance of patients with spasticity. Spasticity is a physiological consequence of an injury to the nervous system. It is a complex problem which can cause profound disability, alone or in combination with the other features of an upper motor neuron syndrome, and can give rise to significant difficulties in the process of rehabilitation. This can be associated with profound restriction to activity and participation due to pain, weakness, and contractures. Optimum management is dependent on an understanding of its underlying physiology, an awareness of its natural history, an appreciation of the impact on the patient, and a comprehensive approach to minimizing that impact. The aim of this article is to highlight the importance, basic approach, and management options available to the general practitioner in such a complex condition.
Keywords: Long-term management, outcomes, peripheral nerve blockade, pharmacological treatment, phenol, spasticity
|How to cite this article:|
Ghai A, Garg N, Hooda S, Gupta T. Spasticity - Pathogenesis, prevention and treatment strategies. Saudi J Anaesth 2013;7:453-60
| Introduction|| |
Spasticity is a major challenge to the rehabilitation team. The word "spasticity" is derived from the Greek word "spasticus," which means "to pull or to tug." It is defined as "disordered sensory-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles."  It can range from mild muscle stiffness to severe, painful, and uncontrollable muscle spasm. It is associated with some common neurological disorders: Multiple sclerosis, stroke, cerebral palsy, spinal cord and brain injuries, and neurodegenerative diseases affecting the upper motor neuron, pyramidal and extrapyramidal pathways.  Left untreated, it gives rise to many problems, such as pain, spasms, limb contracture, and deformity. As a result, loss of mobility and dexterity, hygiene/self-care, and an inability to wear orthoses occur, which can lead to decreased functioning and participation, and poor self-esteem. The initial management should focus on the alleviation of external exacerbating causes before specific treatment is considered. The role of the multidisciplinary team in the management of spasticity has been well described, and good nursing care, optimal posture, and physical therapy underlie the basic principles of treatment.  The aims of treatment should be to improve function, to reduce the risk of unnecessary complication, to alleviate pain, and to assist with the maintenance of hygiene, dressing, and transferring. Peripheral nerve blocks and botulinum toxin are two local treatments which are proving very useful, but are undervalued and underused.  This article reviews the variety of options available for clinical management of spasticity.
| Pathophysiology|| |
Spasticity usually is accompanied by paresis and other signs, such as increased stretch reflexes, collectively called the upper motor neuron syndrome which results from damage to descending motor pathways at cortical, brainstem, or spinal cord levels. When the injury is acute, muscle tone is flaccid with hyporeflexia before the appearance of spasticity. The interval between injury and the appearance of spasticity varies from days to months according to the level of the lesion. 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. Loss of descending tonic or phasic excitatory and inhibitory inputs to the spinal motor apparatus, alterations in the segmental balance of excitatory and inhibitory control, denervation supersensitivity, and neuronal sprouting may be observed. Once spasticity is established, the chronically shortened muscle may develop physical changes such as shortening and contracture that further contribute to muscle stiffness [Figure 1]. 
| Assessment of Spasticity|| |
Before any intervention is undertaken to modulate hypertonicity, it is important to attempt to assess the severity of spasticity. Measuring spasticity is difficult, as there are no direct measures. Many grading scales are used to quantify spasticity. These assess the degree of muscle tone, frequency of spontaneous spasms, and the extent of hyperreflexia.
Ashworth Scale was developed in 1964. It is inadequate in measuring spasticity. 
0 = No increase in tone
1 = Slight increase in tone, giving a "catch" when the limb is moved in flexion or extension
2 = More marked increase in tone, but limb easily flexed
3 = Considerable increase in tone; passive movement difficult
4 = Limb rigid in flexion or extension.
Modified Ashworth Scale (MAS) developed in 1987 in response to concerns by the authors that the Ashworth grade "1" was indiscrete. The MAS has an additional value of 1+ and has demonstrated inter-rater reliability of 86.7% in assessment of elbow flexor muscle spasticity. 
0 = No increase in muscle tone
1 = Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion (ROM) when the part is moved in flexion or extension/abduction or adduction, etc.
1+ = Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM
2 = More marked increase in muscle tone through most of the ROM, but the affected part is easily moved
3 = Considerable increase in muscle tone, passive movement is difficult
4 = Affected part is rigid in flexion or extension (abduction or adduction, etc.).
Severity of pain is assessed on a visual analog scale (VAS) where zero represents no pain and 10 represents the worst possible pain. 
Triple flexion of the lower limb, consecutive to the flexor muscle spasm, is assessed using a 4-point scale: 
0 = Hip and/or knee flexion <30°, with or without mild gait disability
1 = Hip and/or knee flexion between 30° and 45°, with moderate gait disability
2 = Hip and/or knee flexion between 45° and 60°, with severe gait disability
3 = Hip and/or knee irreducible flexion with gait inability.
Range of Motion of the hip abductors is assessed passively by the abduction of the hip joint and graded as 0-3. 
0 = Ability to abduct the thigh easily to 45°
1 = Ability to abduct the thigh to 45° with mild effort
2 = Ability to abduct the thigh to 45° with major effort
3 = Inability to abduct the thigh to 45°.
Number of spasms experienced are recorded on spasm frequency scale. 
0 = No spasm
1 = One spasm or fewer per day
2 = Between one and five spasms per day
3 = Between five and nine spasms per day
4 = Ten or more spasms per day.
Perineal hygiene is assessed using a 4-point scale, considering the ability of the patient to perform perineal hygiene care, related to the degree of adductor muscles spasticity. 
0 = Hygiene performance with relative ease
1 = Hygiene performance with mild difficulty
2 = Hygiene performance with moderate difficulty
3 = Hygiene performance with severe difficulty.
Gait is assessed, when possible, using a 4-point score, representing the effect of obturator neurolysis on spasm and leg crossing: 
0 = Patient able to walk with mild difficulty
1 = Patient able to walk with moderate difficulty
2 = Patient able to walk with severe difficulty
3 = Patient unable to walk.
| Aims of Spasticity Management|| |
When the patient presents a pattern of spasticity that implies on functional or postural loss, management of spasticity must be considered within a progressive approach - from the most conservative to the most invasive therapy.  The aims of treatment should be the following:
- Improve function - mobility, dexterity
- Symptom relief
- Ease pain-muscle shortening, tendon pain, postural effects
-Decrease spasms - Orthotic wearing
- Postural - body image
- Decrease care burden - care and hygiene, positioning, dressing
- Optimize service responses - to avoid unnecessary treatments, facilitate other therapy, delay/prevent surgery.
Principles of Management
Positioning and seating
Correct positioning, for the immobile patient, is an important aspect of management. Incorrect positioning in bed, particularly in the early stages after stroke or brain injury, is a major cause of unnecessary spasticity. Side lying, sitting, and standing are of help in different circumstances, with the primary aim of producing stretch on the spastic muscles, thereby reducing spasticity as well as facilitating the use of antagonistic muscle groups.  Guidelines have been made to put each joint through a full range of movement for at least 2 h in every 24 h. The fundamental principle of seating is that the body should be contained in a balanced, symmetrical, and stable posture which is both comfortable and maximizes function. A proper seating system should aim at stabilization of pelvis without lateral tilt or rotation, but with a slight anterior tilt, so that the spine adopts its normal curves. 
Maintaining muscle length through passive or active exercise and stretching regimens including standing or splinting can be key to managing spasticity both in the short and the long term.
Cooling of muscles
This inhibits monosynaptic stretch reflex and lowers the receptor's sensitivity, thus inhibits spastic muscles, but the effect is short lived. Different techniques such as quick icing and evaporating spray like ethyl chloride are occasionally used. 
Heat may increase the elasticity of the muscles, causing relaxation of spastic muscles. Techniques used include ultrasound, fluidotherapy, paraffin, and superficial heat. These techniques should be combined with stretching and exercise. 
An orthosis or splint is an external device designed to apply, distribute, or remove forces to or from the body in a controlled manner to control body motions and/or alter the shape of body tissues, e.g., ankle foot orthosis, insoles, ankle supports, wrist/hand/elbow splints, knee splints, spinal brace, hip brace, neck collar. The application of splints and casts can prevent the formation of contractures in the spastic limb and serial casting can improve the range of movement in a joint that is already contracted - a new cast being applied every few days as the range improves. Some equipment can also aid positioning, e.g., T roles, wedges, cushions, and foot straps. These are usually used in combination with other modalities like botox therapy. ,
Functional electrical stimulation
This is an adjunct to physiotherapy that can be of benefit to selected individuals predominantly affected by upper motor neuron pathologies resulting in foot drop. 
Transcutaneous electrical nerve stimulation
This has been found to reduce spasticity through its nociceptive action and reduction of pain.
Medication should always be used as an adjunct to good general management and education though the effect is short lived. Aims should be to improve function and relieve troublesome symptoms.
| Delivery of medications|| |
- Enteral - orally, e.g., baclofen, benzodiazepines, dantrolene, clonidine, tizanidine, gabapentin
- Intrathecal - baclofen pump (other drugs used alone or in combination intrathecally include clonidine, morphine, fentanyl, midazolam, lidocaine)
- Intramuscular/focal injection, e.g., botulinum toxin
- Nerve blocks, e.g., phenol, ethanol.
The oral agents
Oral antispastic medications are helpful for milder cases. However, in more severe cases and for focal spasticity, the side effects, commonly drowsiness and weakness, can significantly restrict the usefulness of these drugs. The most commonly used drugs are baclofen, tizanidine, dantrolene, benzodiazepines, and gabapentin [Table 1]. ,
Baclofen: It is GABA B receptor agonist that has presynaptic inhibitory effects on the release of excitatory neurotransmitters such as glutamate, aspartate, and substance P. It is interesting to note that there is no convincing evidence of efficacy in spasticity of cerebral origin.  In double-blind, crossover, placebo-controlled trials, baclofen was reported to be effective, producing statistically significant improvements in spasticity.  The main adverse effects of oral baclofen include sedation or somnolence, excessive weakness, vertigo, and psychological disturbances. The incidence of adverse effects ranges from 10 to 75%. The majority of adverse effects are not severe; most are dose related and reversible. The main risks of oral baclofen administration are related to withdrawal; seizures, psychic symptoms, and hyperthermia. 
Tizanidine: It acts by preferential inhibition of polysynaptic spinal excitatory pathways by stimulating alpha 2 receptors. There is large evidence for the effective use of tizanidine monotherapy in the management of spasticity.  It has better tolerability; in particular, weakness was reported to occur less frequently with tizanidine than with baclofen. It is comparable to baclofen and may even be superior. 
Dantrolene sodium: It has a peripheral mode of action via a direct effect on suppression of release of calcium ions from the sarcoplasmic reticulum of muscle, with consequent inhibition of excitation, contraction, and coupling.  The recommended dosage is 25-400 mg daily with a slow titration. Doses higher than this can result in severe hepatotoxicity. 
Benzodiazepines: Diazepam is a GABA A agonist and it increases presynaptic inhibition of polysynaptic and monosynaptic reflexes. 
Peripheral nerve blockade using neurolytic agents is one of the therapeutic possibilities in the treatment of spasticity. Nerve block refers to the application of chemical agents to a nerve to impair, either temporarily or permanently, the conduction along that nerve. The agents most frequently used are phenol, alcohol, and local anesthetics. This can be done with the help of fluoroscopy or nerve stimulation [Table 2]. Khalili and co-workers were the first to describe the use of phenol for nerve block.  The obturator nerve is the commonest and most accessible nerve blocked for adductor spasticity. The posterior tibial nerve is the second common nerve blocked for calf muscle spasticity.  The main indication is debilitating or painful spasticity. Peripheral blocks with local anesthetics are used as tests to mimic the effects of motor blocks and determine their potential adverse effects. They are easy to perform, effective, and inexpensive.
| Indications for Chemical Neurolysis|| |
- Management of chronic, intractable, non-terminal pain that are not responsive to other modalities 
- Alternative to treat spasticity in order to improve balance, gait, self-care, and global rehabilitation. An important difference between neurolytic blocks for pain relief versus spasticity is that motor or mixed nerves are targeted preferentially in the management of spastic disorders. 
The success and duration of the block may vary anywhere from partial to excellent pain relief lasting from weeks to months depending upon the type of block and the skill of the physician. The most common cause of an unsuccessful block is incorrect placement of the neurolytic agent.
Phenol is a chemical composite containing carbolic acid, phenic acid, phenylic acid, phenyl hydroxide, hydroxybenzene, and oxybenzene. It is available as colorless crystal and can be prepared to a maximum concentration of 6.7% solution in water. This substance is highly soluble in organic solvents such as alcohol and glycerol. The solution can be diluted with saline and is compatible when mixed with radiocontrast dye to allow fluoroscopic guidance during injection of the agent and to monitor spread of the solution. When mixed with glycerol, it slowly diffuses from the solution and is an advantage when injected intrathecally because it allows for limited spread and is localized in the area that needs to be destroyed. When mixed with water, it has a wider spread, causing a bigger area of nerve destruction. Aqueous solution of phenol is more potent than the glycerine solution.  The choice of diluent is dependent upon the extent of neurolysis desired. The use of higher concentrations of phenol might predispose to a higher incidence of vascular injury.
Shelf life exceeds 1 year when the solution is refrigerated and not exposed to light. Phenol turns red on exposure to sunlight and air because of oxidation. It is metabolized in the liver by conjugation to glucuronides and oxidation to equinol compounds or to carbon dioxide and water. Excretion of metabolites is via the kidneys. Systemic doses of more than 5 g can cause convulsive seizures and central nervous system depression. Doses less than 100 mg are less likely to cause serious side effects. 
Phenol causes nerve destruction by inducing protein precipitation. There is loss of cellular fatty elements, separation of the myelin sheath from the axon, and axonal edema. At a concentration of 2%-3% in saline, phenol seems to spare motor function. The efficacy of 3% phenol in saline is comparable to that of 40% alcohol. Protein denaturation occurs at concentrations less than 5%, and concentrations higher than 5% produce protein coagulation, nonspecific segmental demyelination, and orthograde degeneration. Wallerian degeneration More Details occurs approximately 2 weeks following the injection. The degree of damage correlates directly with the concentration and the total amount used. Concentrations of 3.3% and less are ineffective. Pain transmission is blocked at a concentration of 5%. Touch, proprioception, and nociceptive fibers are blocked at concentrations above 5%. The effect reaches maximum in 2 weeks, followed by maximum recovery in 14 weeks because eventually there is regrowth of most of the axons.  It has an immediate local anesthetic effect due to its immediate selective effect on smaller nerve fibers. This differential blocking ability is due to small vessel destruction that initially spares large fibers. However, the effects of the block cannot be evaluated until after 24-48 h, to allow time for the local anesthetic effect to dissipate. The neurolytic effect may be clinically evident only after 3-7 days. If inadequate pain relief is obtained after 2 weeks, this may indicate incomplete neurolysis and requires repetition of the procedure. , The subsequent fibrosis that occurs following phenol injection makes nerve regeneration more difficult, but not impossible. Nerve regeneration occurs as long as the nerve cell body is intact, at a rate of 1-3 mm/day. Nerve arborization and neuroma formation can also occur at the site of nerve disruption and can be a focus of neuropathic pain.
Ethyl alcohol has similar destructive effect as phenol and is more efficient in destroying nerve cell bodies. Its mechanism of nerve destruction is similar to that of phenol. It extracts phospholipids, cholesterol, and cerebroside from neural tissues and precipitates mucoprotein and lipoprotein.  Although 50%-100% alcohol is used as a neurolytic agent, the minimum concentration required for neurolysis has not been established. A concentration of 95% will reliably lyse sympathetic, sensory, and motor components of the nerve. It is hypobaric to the CSF, is readily soluble in body tissues, and produces severe burning pain on injection. It spreads quite rapidly from the injection site and requires 12-24 h before the effects of the injection can be assessed. 
| Complications of Chemical Neurolysis|| |
Skin and other non-target tissue necrosis and sloughing
This is due to damage of the vascular supply to the skin, causing ischemia, and chronic trauma to denervated tissue. Necrosis of muscles, blood vessels, and other soft tissues has also been reported. 
The reported incidence of neuritis is up to 10%. It is caused by partial destruction of somatic nerve and subsequent regeneration. Neuritis would occur only if the nerve cell body is not destroyed. It is clinically manifested as hyperesthesia and dysesthesia that may be worse than the original pain problem. It is one of the limiting factors in the use of chemical neurolysis.
The patient complains of distressing numbness caused by an imbalance in afferent input. It is caused by long-term loss of afferent input and the resultant CNS changes. A local anesthetic block done a few hours prior to the performance of the neurolytic block seems to prevent the development of this complication. Management of this problem is pharmacotherapy with the use of tricyclic antidepressants, major antipsychotic tranquilizers, and anticonvulsants.
Prolonged motor paralysis
This can be a major complication and is greatly feared by physicians, patients, and family. It occurs infrequently and is usually temporary.
These include hypotension secondary to sympathetic block and systemic toxic reactions, heart rate, and rhythm disturbances, blood pressure changes, and CNS excitation and depression.
Botulinum toxin injection
Botulinum toxin is the most widely used treatment for focal spasticity. The effect of the toxin is to inhibit the release of acetylcholine at the neuromuscular junction.  The clinical effect of injecting botulinum toxin is reversible due to nerve sprouting and muscle reinnervation, leading to functional recovery of the muscle in a few months. It is essential that botulinum toxin injections are given in conjunction with physiotherapy in order to obtain the maximum benefit. The toxin is injected directly into the targeted muscle and an effect is noticed in 2-3 days with a maximum effect seen by about 3 weeks, lasting at least 3 months. As it is not a permanent treatment, it may have to be repeated after a few months. 
If oral drug treatment is inadequate in controlling lower limb spasticity or is not tolerated, intrathecal delivery of baclofen should be considered.  The main risks of intrathecal baclofen infusion are symptoms related to overdose or withdrawal. These are mostly related to catheter disruption, failure to refill the pump reservoir, or failure of the pump's power source. Abrupt disruption of intrathecal baclofen can be a serious scenario with continuous spasms, tremors, temperature elevation, seizure, and death having been reported. 
Use of phenol is reserved for those individuals who do not have any functional movement in the legs, who have lost bladder and bowel function, and who have impaired leg sensation. Intrathecal phenol can be an effective treatment which requires expert administration and does not have the long-term maintenance or cost issues that are associated with intrathecal baclofen treatment. The effect of a single injection often lasts many months and can be repeated if necessary. 
Anterior and posterior rhizotomy, peripheral neurotomy,  percutaneous radiofrequency rhizotomy, spinal cord and deep cerebellar stimulation of the superior cerebellar peduncle,  functional neurosurgery 
Directly act on muscles and tendons, e.g., lengthening operation, tenotomy, neurectomies, and transfer of tendons.
| Conclusion|| |
The management of spasticity is complex involving contribution from physiotherapist, orthopedician, and pain physician. Most individuals, even with quite severe spasticity, can be managed by a combination of physiotherapy and local nerve block or botulinum toxin injection, sometimes combined with relatively low dose oral medication. Neurolytic block with phenol, when adequately indicated, is a tool that presents excellent cost-benefit relation, high margin of safety and rare complications, especially when administered by well-qualified professionals. More advanced intrathecal and surgical techniques are rarely needed. A multidisciplinary approach helps to deal with the problem and improve the quality of life.
| References|| |
|1.||Pandyan AD, Gregoric M, Barnes MP, Wood D, Van Wijck F, Burridge J, et al. Spasticity: Clinical perceptions, neurological realities and meaningful measurement. Disabil Rehabil 2005;27:2-6. |
|2.||Bavikatte G, Gaber T. Approach to spasticity in general practice. Br J Med Pract 2009;2:29-34. |
|3.||Ward AB. Long-term modification of spasticity. J Rehabil Med 2003;41:60-5. |
|4.||Barnes MP. Management of spasticity. Age Ageing 1998;27:239-45. |
|5.||Dietz V, Quintern J, Berger W. Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia. Brain 1981;104:431-49. |
|6.||Ashworth B. Preliminary trial of carisoprodal in multiple sclerosis. Practitioner 1964;192:540-2. |
|7.||Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale of muscle spasticity. Phys Ther 1986;67:206-7. |
|8.||Langley GB, Sheppeard H. The visual analogue scale: Its use in pain management. Rheumatol Int 1985;5:145-8. |
|9.||Viel EJ, Perennou D, Ripart J, Pelissier J, Eledjam JJ. Neurolytic blockade of the obturator nerve for intractable spasticity of adductor thigh muscles. Eur J Pain 2002;6:97-104. |
|10.||Snow BJ, Tsui JK, Bhart MH, Varelas M, Hashimoto SA, Calne DB. Treatment of spasticity with botulinum toxin: A double blind study. Ann Neurol 1990;28:512-5. |
|11.||Bittencourt PC, Tournier MB. Phenol block for spasticity management. Acta Fisiatr 2008;15:189-91. |
|12.||Carr EK, Kenney FD. Positioing of the stroke patient: A review of the literature. Int J Nurs Stud 1992;29:355-69. |
|13.||McQuilton G, Johnson GR. Cost effective moulded seating for the handicapped child. Prosthet Orthot Int 1981;5:37-41. |
|14.||Price R, Lehmann JF, Boswell-Bessette S, Burleigh A, deLateur BJ. Influence of cryotherapy on spasticity of the human ankle. Arch Phys Med Rehabil 1993;74:300-4. |
|15.||Lehmann JF, de Lateur BJ. Therapeutic heat. In: Lehmann JF, editor. Therapeutic Heat and Cold. 3 rd ed. Baltimore: Williams and Wilkins; 1982. |
|16.||Ricks NR, Eilert RE. Effects of inhibitory casts and orthoses on bony alignment of foot and ankle during weight bearing in children with spasticity. Dev Med Child Neurol 1993;35:11-6. |
|17.||Wellen M, Mackay S. An evaluation of the soft splint in the acute management of elbow hypertonicity. Occup Ther J Res 1995;15:3-6. |
|18.||Burridge JH, Taylor PN, Hagan SA, Wood DE, Swain ID. The effects of common peroneal stimulation on the effort and speed of walking: A randomised controlled clinical trial with chronic hemiplegic patients. Clin Rehabil 1997;11:201-10. |
|19.||Campistol J. Orally administered drugs in the treatment of spasticity. Rev Neurol 2003;37:70-4. |
|20.||Rode G, Maupas E, Luaute J, Courtois-Jacquin S, Boisson D. Medical treatment of spasticity. Neurochirurgie 2003;49:247-55. |
|21.||Sawa GM, Paty DW. The use of baclofen in the treatment of spasticity in multiple sclerosis. Can J Neurol Sci 1979;6:351-4. |
|22.||Dario A, Tomei G. A benefit-risk assessment of baclofen in severe spinal spasticity. Drug Saf 2004;27:799-818. |
|23.||Stevenson VL, Thompson AJ, Jarrett L. Text book of Spasticity Management A practical multidisciplinary guide. UK: Informa Healthcare publishers; 2006. p. 96-9. |
|24.||Hoogstraten MC, van der Ploeg RJ, vd Burg W, Vreeling A, van Marle S, Minderhoud JM. Tizanidine versus baclofen in the treatment of spasticity in multiple sclerosis patients. Acta Neurol Scand 1988;77:224-30. |
|25.||Young RR, Delwaide PJ. Spasticity. N Engl J Med 1981; 304:28-23. |
|26.||Zafonte R, Lombard L, Elovic E. Antispastic medications: Uses and limitations of enteral therapy. Am J Phys Med Rehabil 2004;83:S50-8. |
|27.||Naftchi NE, Schlosser W, Horst WD. Correlation of changes in the GABA-ergic system with the development of spasticity in paraplegic cats. Adv Exp Med Biol 1979;123:431-50. |
|28.||Khalili AA, Betts HB. Peripheral nerve block with phenol in the management of spasticity: Indications and complications. JAMA 1967;200:1155-7. |
|29.||Spira R. Management of spasticity in cerebral palsied children by peripheral nerve block with phenol. Dev Med Child Neurol 1971;13:164-73. |
|30.||Trainer N, Bowser BL, Dahm L. Obturator nerve block for painful hip in adult cerebral palsy. Arch Phys Med Rehabil 1986;67:829-30. |
|31.||Gunduz S, Kaylon TA, Dursun H, Möhür H, Bilgiç F. Peripheral nerve block with phenol to treat spasticity in spinal cord injured patients. Paraplegia 1992;30:808-11. |
|32.||Yadav SL, Singh U, Dureja GP, Singh KK, Chaturvedi S. Phenol block in the management of spastic cerebral palsy. Indian J Pediatr 1994;61:249-55. |
|33.||Kong KH, Chua KS. Outcome of obturator nerve block with alcohol for the treatment of hip adductor spasticity. Int J Rehabil Res 1999;22:327-9. |
|34.||Chua KS, Kong KH. Alcohol neurolysis of the sciatic nerve in the treatment of hemiplegic knee flexor spasticity: Clinical outcomes. Arch Phys Med Rehabil 2000;81:1432-5. |
|35.||Kumar ER, Tharion G, Bhattacharji S. A study to evaluate the effectiveness of phenol blocks to peripheral nerves in reducing spasticity in patients with paraplegia and brain injury. Indian J Phys Med Rehabil 2008;19:13-7. |
|36.||Akkaya T, Unlu E, Alptekin A, Gumus HI, Umay E, Cakci A. Neurolytic phenol blockade of the obturator nerve for severe adductor spasticity. Acta Anaesthesiol Scand 2010;54:79-85. |
|37.||Khalili AA, Harmel MH, Forster S, Benton JG. Management of spasticity in selective peripheral nerve block with dilute phenol solutions in clinical rehabilitation. Arch Phys Med Rehabil 1964;45:513-9. |
|38.||Gehdoo RP. Neurolytic agents and neurodestructive techniques. In: Baheti DK, Bakshi S, Gupta S, Gehdoo RP, editors. International pain management - A practical approach. 1 st ed. New Delhi: Jaypee Brothers; 2009. p. 27-38. |
|39.||Georgescu VA. Drugs and agents used in neurolysis and fluoroscopy. In: Chelly, Jacques E, editors. Peripheral nerve blocks: A color atlas. 3 rd ed. Philadelphia: Lippincott Williams and Wilkins; 2009. p. 410-5. |
|40.||Anderson RS. Chemical Neurolytic Agents. In: Raj PP, editor. Clinical Practice of Regional Anesthesia. New York: Churchill Livingston; 2002. p. 229-39. |
|41.||Felsenthal G. Pharmacology of phenol in peripheral nerve blocks: A review. Arch Phys Med Rehabil 1974;55:13-6. |
|42.||Braun RM, Hoffer MM, Mooney V, McKeever J, Roper B. Phenol nerve block in the treatment of acquired spastic hemiplegia in the upper limbs. J Bone Joint Surg Am 1973;55:580-5. |
|43.||Meyers RR, Powell HC. Galacose neuropathy: Impact of chronic endoneurial edema on the nerve blood flow. Ann Neurol 1984;16;587-94. |
|44.||Peng Philips WH, Chan Vincent WS. Complications of regional anesthesia in chronic pain therapy. In: Finucane BT, editor. Complications of regional anesthesia. 2 nd ed. New York: Springer; 2007. p. 301-32. |
|45.||Brashear A, Gordon MF, Elovic E, Kassicieh VD, Marciniak C, Do M, et al. Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. N Engl J Med 2002;347:395-400. |
|46.||Rosales RL, Chua-Yap AS. Evidence-based systematic review on the efficacy and safety of botulinum toxin-A therapy in post-stroke spasticity. J Neural Transm 2008;115:617-23. |
|47.||Bensmail D, Ward AB, Wissel J, Motta F, Saltuari L, Lissens J, et al. Cost-effectiveness modeling of intrathecal baclofen therapy versus other interventions for disabling spasticity. Neurorehabil Neural Repair 2009;23:546-52. |
|48.||Jarrett L, Nandi P, Thompson AJ. Managing severe lower limb spasticity in multiple sclerosis: Does intrathecal phenol have a role? J Neurol Neurosurg Psychiatry 2002;73:705-9. |
|49.||Maarrawi J, Mertens P, Luaute J, Vial C, Chardonnet N, Cosson M, et al. Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb:Prospective study in 31 patients. J Neurosurg 2006;104:215-25. |
|50.||Harat M, Radziszewski K, Ruda? M, Okoñ M, Galanda M. Clinical evaluation of deep cerebellar stimulation for spasticity in patients with cerebral palsy. Neurol Neurochir Pol 2009;43:36-44. |
|51.||Siegfried J, Lazorthes Y, Broggi G, Claverie P, Deonna T, Frerebeau P, et al. Functional neurosurgery of cerebral palsy. Neurochirurgie 1985;31 Suppl 1:1-118. |
[Table 1], [Table 2]
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