Management of Spasticity After Spinal Cord Injury: Current Techniques and Future Directions

Elbasiouny, Sherif M.; Moroz, Daniel; Bakr, Mohamed; Mushahwar, Vivian K.

doi:10.1177/1545968309343213

Cited by 186 publications

(160 citation statements)

References 73 publications

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“…While classic symptoms of UTI include dysuria, increased frequency and urgency, neurogenic bladder patients can present differently with increased spasticity, autonomic dysreflexia, urinary incontinence, and vague pains [12]. Spasticity (hypertonia) develops when an imbalance in excitatory and inhibitory inputs lead to hyperexcitability of alpha motor neurons occurs [13]. Muscle tone is maintained by regulation of stretch reflex arc which is balanced between the inhibitory influences by corticospinal tract and dorsal reticulospinal tract, and the facilitatory influences (on extensor tone) by medial reticulospinal and verstibulospinal tract (supraspinal control) [14].…”

Section: Discussionmentioning

confidence: 99%

Usefulness of Coupling Transcutaneous Electrical Nerve Stimulation with Routine Physical Therapy in Spinal Spasticity with Intolerant Drug Sideeffects: A Case Report

Oo¹,

Bo²

2016

Int J Phys Med Rehabil

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Spasticity is a common complaint in patients with spinal cord injury. Clinically, spasticity is characterized by increased muscle tone, exaggerated tendon reflex, frequent muscle spasm and clonus. We report a case of worsening spasticity in a patient with incomplete cervical spinal cord injury (ASIA B) as a consequence to urinary tract infection. The initial baclofen dose of 5 mg/dose three times per day was increased to 15 mg/dose three times/day with dosage increment at 3-day intervals by 15 mg (5 mg/dose). Marked weakness and vertigo was reported. He continued to suffer from severe spasms and trunk tightness that limited his daily activities and induced intolerable pain. The Modified Ashworth Score was increased from 1+ initially to 3, and the Pen Spasm frequency Score deteriorated from initial 1 to 3. After eradication of urinary tract infection with ciprofloxacin, spasticity did not improve, and so was administered with high-frequency transcutaneous electrical nerve stimulation at the parameters of frequency 100 Hz, pulse-width 0.2 millisecond, intensity 15 mA for the duration of 60 minutes for 3 weeks, coupling with routine physical therapy. After 3 week of TENS therapy, final Modified Ashworth Score reduced to 1+ , and Final Penn Spasm frequency Score was decreased to 2 with much improved quality of life. We also discuss the role of coupling transcutaneous electrical nerve stimulation with physical therapy in spinal spasticity.

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Section: Discussionmentioning

confidence: 99%

Usefulness of Coupling Transcutaneous Electrical Nerve Stimulation with Routine Physical Therapy in Spinal Spasticity with Intolerant Drug Sideeffects: A Case Report

Oo¹,

Bo²

2016

Int J Phys Med Rehabil

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“…22 However, onabotulimtoxin-A may cause marked weakness of the injected muscles. 1,22 Less frequently, its effects may spread from the area of injection, resulting in generalized muscle weakness and other potentially serious AEs. This study has some limitations.…”

Section: Discussionmentioning

confidence: 99%

“…1 Up to 311 000 Americans are living with SCI, 2 and 65-78% of patients with chronic SCI (persisting X1 year after injury) have symptoms of spasticity. 3 Further, more than 80% of people with multiple sclerosis have varying degrees of spasticity.…”

Section: Introductionmentioning

confidence: 99%

Efficacy and safety study of arbaclofen placarbil in patients with spasticity due to spinal cord injury

Nance

Huff²,

Martinez‐Arizala

et al. 2011

Spinal Cord

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Study design: Randomized, double-blind, placebo-controlled, two-period crossover. Objectives: To evaluate the efficacy and safety of arbaclofen placarbil (AP) in patients with spasticity secondary to spinal cord injury (SCI). Setting: United States and Canada. Methods: Patients received extended-release AP tablets 10, 20 or 30 mg every 12 h in one of two AP/placebo sequences, with 26 days of each treatment. The primary analysis compared Ashworth scale assessments of muscle tone between AP and placebo for the muscle group with maximum baseline Ashworth score. Secondary endpoints included a patient-rated Severity of Spasticity Scale. Results: In the primary analysis, AP significantly improved Ashworth scores compared with placebo over the dosing interval: least-squares mean reduction versus placebo was 0.60 for AP 20 mg (P ¼ 0.0059) and 0.88 for AP 30 mg (P ¼ 0.0007). The difference was significant for the pre-morning dose time point, 12 h after the prior evening dose, indicating that efficacy was maintained throughout the dosing interval. Treatment differences for AP 10 mg versus placebo were not significant. Severity of Spasticity ratings were significantly reduced for the combined 20/30-mg group versus placebo (P ¼ 0.018). No statistically significant differences between AP and placebo were observed for muscle strength. AP-related AEs were generally mild to moderate in intensity, and none led to early withdrawal or were serious. Conclusion: AP was well tolerated at all investigated dosages and, when administered at doses of 20 or 30 mg twice daily, was efficacious in reducing spasticity due to SCI.

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“…dont les effets secondaires restent nombreux (somnolence, vertiges, etc.) [9]. La découverte d'un nouveau traitement plus efficace reste aujourd'hui une nécessité clinique.…”

Section: Qu'est-ce Que La Spasticité ?unclassified

Une nouvelle cible thérapeutique dans le traitement de la spasticité après une lésion de la moelle épinière : la calpaïne

Plantier

Brocard

2017

Med Sci (Paris)

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> À la suite d'un traumatisme de la moelle épi-nière, la plupart des patients développent une exagération du tonus musculaire, appelée spasticité, qui aboutit souvent à une incapacité motrice. Dans cette revue, nous résumerons les principaux mécanismes physiopathologiques de la spasticité qui découlent d'une lésion médul-laire, puis décrirons l'apport de nos récents travaux identifiant une protéase, la calpaïne, comme le promoteur de ces mécanismes physiopathologiques. Cette découverte ouvre de nouvelles pistes thérapeutiques dans le traitement de la spasticité. < . En raison de ses nombreuses étiologies, nous ne disposons pas d'estimation fiable de l'incidence mondiale de la spasticité, mais on évalue à environ 12 millions le nombre de personnes atteintes. La première défi-nition de la spasticité provient des travaux de Lance en 1980, qui la décrit comme « un désordre moteur caractérisé par une augmentation vitesse-dépendante du réflexe d'étirement (hypertonie musculaire), qui est associée à l'hyperexcitabilité de l'arc réflexe myotatique… » [4]. Concrètement, l'étirement d'un muscle lors d'une mobilisation passive de l'articulation provoque une contraction réflexe (voir plus loin « l'arc réflexe myotatique ») qui s'opposera au mouvement, et dont l'exagération définit la spasticité. Cette résistance au mouvement sera proportionnelle à la vitesse de mobilisation de l'articulation. Cependant, le tableau clinique de la spasticité est bien plus large que la définition de Lance [5]. Elle s'accompagne de troubles variés, associés à la pluralité des atteintes lésionnelles. Par exemple, l'hypertonie permanente (dystonie) peut apparaître en l'absence de tout étirement et modifie les propriétés viscoélastiques du muscle en le rendant moins extensible (raideur). À plus long terme, des raccourcissements musculo-tendineux (rétractions musculaires) déforment les articulations (Figure 1a). Il n'est pas rare que la spasticité s'accompagne de clonies (des contractions brèves et répétées du muscle) et de spasmes (des contractions involontaires transitoires du muscle) qui peuvent survenir spontanément ou en réponse à une stimulation Le fonctionnement du système nerveux repose sur un équilibre entre l'activité des neurones excitateurs et celle des neurones inhibiteurs. Cette balance excitation/inhibition permet une régulation fine des différentes actions de notre corps (respiration, mastication, locomotion, etc.). Elle permet notamment une coordination de nos mouvements locomoteurs qui repose sur une alternance des contractions entre les muscles fléchisseurs et extenseurs lors de la marche. Après une lésion de la moelle épinière, un déséquilibre de la balance excitation/inhibition perturbe la coordination locomotrice en raison d'une exagération du tonus musculaire (hypertonie) et de co-contractions des muscles fléchisseurs et extenseurs. Ces troubles moteurs, qui s'apparentent à de la spasticité, émergent chez la plupart (environ 75 %) des personnes présentant une lésion de la moelle épinière, plusieurs mois après le traumatisme [...

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Management of Spasticity After Spinal Cord Injury: Current Techniques and Future Directions

Cited by 186 publications

References 73 publications

Usefulness of Coupling Transcutaneous Electrical Nerve Stimulation with Routine Physical Therapy in Spinal Spasticity with Intolerant Drug Sideeffects: A Case Report

Usefulness of Coupling Transcutaneous Electrical Nerve Stimulation with Routine Physical Therapy in Spinal Spasticity with Intolerant Drug Sideeffects: A Case Report

Efficacy and safety study of arbaclofen placarbil in patients with spasticity due to spinal cord injury

Une nouvelle cible thérapeutique dans le traitement de la spasticité après une lésion de la moelle épinière : la calpaïne

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