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Pharmacological interventions other than botulinum toxin for spasticity after stroke

  1. Cameron Lindsay1,
  2. Anand D Pandyan2,*

Editorial Group: Cochrane Stroke Group

Published Online: 28 FEB 2013

Assessed as up-to-date: 10 NOV 2012

DOI: 10.1002/14651858.CD010362


How to Cite

Lindsay C, Pandyan AD. Pharmacological interventions other than botulinum toxin for spasticity after stroke (Protocol). Cochrane Database of Systematic Reviews 2013, Issue 2. Art. No.: CD010362. DOI: 10.1002/14651858.CD010362.

Author Information

  1. 1

    Sandwell and West Birmingham NHS Trust, Department of Physiotherapy, Birmingham, West Midlands, UK

  2. 2

    Keele University, School of Health and Rehabilitation, Keele, UK

*Anand D Pandyan, Professor for Rehabilitation Technology in Health, School of Health and Rehabilitation, Keele University, Keele, ST5 5BG, UK. a.d.pandyan@keele.ac.uk.

Publication History

  1. Publication Status: New
  2. Published Online: 28 FEB 2013

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Table 1. Pharmacological agents for treating spasticity after stroke

Generic nameMethod of administrationMethod of action

BaclofenOral, intrathecal pumpBaclofen is a centrally acting gamma-aminobutyric acid (GABA) analogue that limits the release of excitatory neurotransmitters in the spinal cord (Mukherjee 2010). It binds to GABA receptors at the presynaptic terminal and inhibits the influx of calcium in to the presynaptic terminal decreasing both mono and poly synaptic reflexes (Davidoff 1985; Krach 2001). It also binds on the post-synaptic terminal of the 1a sensory afferent (Howe 1987)

TizanidineOralAn imidazole derivative with agonist action on alpha-2-adrenergic receptors in the central nervous system (Mukherjee 2010). It has an effect both pre and post-synaptically and decreases the level of excitatory neurotransmitter between the spinal interneurons to the alpha motor neurons through pre-synaptic inhibition (Gallichio 2004). It may also inhibit abnormal activity by acting on locus coeruleus and inhibiting activity in the coerulospinal pathway (Palmeri 1990)

DantroleneOralThis drug acts at the muscle level rather than the neural level and affects both intra and extrafusal muscles (Gallichio 2004). It interferes with the release of calcium from the sarcoplasmic reticulum of the muscle (Mukherjee 2010). This decrease in available calcium reduces the force produced during a contraction (Gallichio 2004)

TolperisoneOralCentrally acting muscle relaxant that acts at the spinal cord level. Primarily acts pre-synaptically to inhibit both calcium and sodium channels. Decreases reflex activity by inhibiting release from the primary afferent (Vora 2010)

AlcoholInjectionThe effect of alcohol varies dependent on the concentration. At concentrations below 35% it acts as a local anaesthetic. In concentrations between 35% to 50% small fibre demyelination was observed but in stronger concentrations above this level Wallerian degeneration and fibrosis is observed (Kocabas 2010)

PhenolInjection, intrathecalThe effect of phenol also varies dependent on concentrations used. It can be injected into either the muscle or directly to the nerve. At concentrations greater than 3% protein denaturation and axonal degeneration destroys the neurons. 5% phenol injection to the motor points of the muscle lead to demyelination of the gamma fibres (Kocabas 2010)