Original Editor - Timothy Assi
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The most well-known and referenced description of spasticity is the physiological definition proposed by Lance in 1980:
Spasticity is a motor disorder characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neurone syndrome.
- Spasticity as described by European working group, EUSPASM  is disordered sensorimotor control,resulting from an upper motor neuronelesion, presenting as intermittent or sustained involuntary activation of muscles.
- Spasticity is a velocity-dependent disorder of the stretch reflex that results in increased muscle tone. 
Spasticity is a complex topic and in truth, is poorly understood. Generally speaking it can be said that spasticity develops when an imbalance occurs in the excitatory and inhibitory input to α motor neurons which is caused by damage to the spinal cord and/or central nervous system. This damage then results in an imbalance between messages from the nervous system to the muscles causing increased excitability.
One factor that is thought to be related to spasticity is the stretch reflex. This reflex is important in coordinating normal movements in which muscles are contracted and relaxed and in keeping the muscle from stretching too far. Although the end result of spasticity is problems with the muscles, spasticity is actually caused by an injury to a part of the central nervous system that controls voluntary movements. The damage causes a change in the balance of signals between the nervous system and the muscles. This imbalance leads to excitability in the muscles. Receptors in the muscles receive messages from the nervous system, which sense the amount of stretch in the muscle and sends that signal to the brain. The brain responds by sending a message back to reverse the stretch by contracting or shortening.
Spasticity is found in conditions where the brain and/or spinal cord are damaged or fail to develop normally; these include cerebral palsy, multiple sclerosis, spinal cord injury and acquired brain injury including stroke.Damage to the CNS as a result of stroke or spinal cord injury, alter the inhibition of peripheral nerves in the affected region. This change in input to bodily structures tends to favor excitation and therefore increase nerve excitability. CNS damage also causes nerve cell membranes to rest in a more depolarized state. The combination of decreased inhibition and an increased depolarized state of cell membranes, decreases action potential threshold for nerve signal conduction, and thus increases activity of structures innervated by the affected nerves. Muscles affected in this way have many other potential features of altered performance in addition to spasticity, including muscle weakness; decreased movement control; clonus; exaggerated deep tendon reflexes; and decreased endurance.
When the brain or spinal cord is damaged, the stretch reflex can be insufficiently inhibited. An exaggerated reaction in the muscle could occur, which can lead to spasticity. 
Important problems that rise because of spasticity are for example limited joint movement, abnormal postures that can produce pain, impaired functional capacity, aesthetic or hygiene disorders. Spasticity is frequently present in childhood, mainly because of cerebral palsy, and in adults, which is mostly caused by traumatic brain injuries, strokes and spinal cord injuries.
The Ashworth scale is the most widely used assessment tool to measure resistance to limb movement in a clinic setting, although it is unable to distinguish between the neural and non-neural components of increased tone.
The scale is as follows:
0 No increase in muscle tone
1 Slight increase in tone giving a catch when the limb is moved
2 More marked increase in tone but limb easily moved
3 Considerable increase in tone – passive movement difficult
4 Limb is rigid in flexion or extension
This scale quantifies muscle spasticity by assessing the response of the muscle to stretch applied at specified velocities.
Grading is always performed at the same time of day, in a constant position of the body for a given limb. For each muscle group, reaction to stretch is rated at a specified stretch velocity.
Velocity to stretch
V1 As slow as possible
V2 Speed of the limb segment falling
V3 As fast as possible (> natural drop)
Quality of muscle reaction
0 No resistance throughout passive movement
1 Slight resistance throughout,with no clear catch at a precise angle.
2 Clear catch at a precise angle followed by release
3 Fatigable clonus (<10secs) occurring at a precise angle
4 Unfatigable clonus (>10secs) occurring at a precise angle
5 Joint Immobile
R1- Angle of catch seen at Velocity V2 or V3
R2- Full range of motion achieved when muscle is at rest and tested at V1 velocity
- A large difference between R1 & R2 values in the outer to middle range of normal m. length indicates a large dynamic component.
- A small difference in the R1 & R2 measurement in the middle to inner range indicates predominantly fixed contracture.
Since the severity of Spasticity may vary from one neurological condition to another and even from one patient to other with the same condition, disease specific spasticity measurement scales are developed.
For example, in the multiple sclerosis (MS) population (The Multiple Sclerosis Society Spasticity Scale, MSSS-88). This is an 88-item, patient-based, interval level scale that not only looks at spasticity symptoms but also incorporates the person’s experience of spasticity and how spasticity affects their daily life.
However, in general the outcome measures include:
- Goniometric Measurement
- Range of passive Hip Abduction
- Ashworth Scale
- Adductor Tone Rating- five-point ordinal rating of tone, but is confined to the adductors.
- Spasm Frequency Scale -ordinal rank scale (0–4) based on self-reporting of lower-limb spasm frequency in people with spinal cordrelated spasticity. It is scored depending on how many spasms are experienced in an average hour.
- Clonus and spasms score (self-report). This is a further ordinal scale (0–3), based on self-reporting of the frequency and provocation of both spasms and clonus.
- Numeric rating scale for leg stiffness.
- Walking and falls score- an estimate of fall frequency scored in an ordinal fashion (0–4), with 0 being no falls and 4 equating to more than 1 per day. If appropriate, a timed 10-metre walk is also recorded.
- Overall comfort rating.
Management / Interventions
- Progressive resistance strength training: no evidence shows that strength training increases spasticity in patients with stroke. Musculoskeletal impairment are significantly reduced after resistance strength training.
- Biofeedback combined with functional electrical stimulation and occupational therapy does not increase the degree of spasticity after treatment. It also showed a greater reduction in spasticity compared to patients who performed functional electrical stimulation and occupational therapy alone.
- Shock wave therapy on flexor hypertonic muscles of the forearm and interosseus muscles of the hand in patients with stroke showed significant reduction of muscle tone (>3months).
- Amelio reported significant reduction of muscle tone (>12 weeks) of plantar flexors in children with cerebral palsy.
- Significant reduction of ankle plantar flexor spasticity in patients with stroke after fifteen 10-minute sessions of continuous ultrasound therapy over a 5-week period (frequency 1MHz and intensity 1,5 W/cm2).
- Cryotherapy, using cold packs (12°C) for 20-minutes, can lower the muscle temperature to reduce the spasticity.
- Electric stimulation : agonist stimulation showed a significant improvement in Ashworth scores. Antagonist stimulation showed an increase of stretch reflex-initiating angle.
**Early treatment is important to avoid or reduce the severe complications due to this phenomenon.**
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- ↑ Lance JW. Symposium synopsis. In: Feldman RG,fckLRYoung RR, Koella WP (eds). Spasticity: Disordered Motor Control. Chicago, IL: Year Book 1980:485–94.
- ↑ Pandyan AD, Gregoric M, Barnes MP et al. Spasticity: clinical perceptions, neurological realities and meaningful measurement. Disabil Rehabil 2005;27:2–6.
- ↑ 3.0 3.1 Lance JW. The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology. 1980;30(12): 1303-13.
- ↑ http://www.nationalmssociety.org/Symptoms-Diagnosis/MS-Symptoms/Spasticity
- ↑ 5.0 5.1 5.2 http://en.wikipedia.org/wiki/Spasticity
- ↑ http://www.nice.org.uk/guidance/cg145
- ↑ Gracies JM, Bayle N, Vinti M, Alkandari S, Vu P, Loche CM, Colas C. Five-step clinical assessment in spastic paresis. Eur J Phys Rehabil Med. 2010 Sep;46(3):411-21.
- ↑ http://www.nlm.nih.gov/medlineplus/ency/article/003297.htm
- ↑ http://emedicine.medscape.com/article/2207448-overview#aw2aab6b2b2
- ↑ Ashworth B. Preliminary trial of carisoprodal in multiple sclerosis. Practitioner 1964;192:540–2.
- ↑ Tardieu G, Rondont 0, Mensch J, Dalloz J-C, Monfraix C, Tabary J-C. Responses electromyographiques a l'etirement musculaire chez l'homme normal. Rev Neurol 1957; 97: 60-61.
- ↑ Boyd R, Graham K. Objective Measurement of clinical findings in the use of Botox type A for the management of children fckLR with Cerebral Palsy. European Journal of Neurology 6(Supp 4) S23-35
- ↑ Hobart J, Riazi A, Thompson A et al. Getting the measure of spasticity in MS: The Multiple Sclerosis Society Spasticity Scale (MSSS-88). Brain 2006;129(Pt1):224–34.
- ↑ Valerie L Stevenson, Louise J Lockley and Louise Jarrett, In: Assessment of the individual with spasticity, chapter 2, SPASTICITY MANAGEMENT:A PRACTICAL MULTIDISCIPLINARY GUIDE,Pg-20-21.
- ↑ Snow BJ, Tsui JKC, Bhatt MH et al. Treatment of spasticity with botulinum toxin: a double blind study.Ann Neurol 1990;28:512–15.
- ↑ Penn RD, Savoy SM, Corcos D et al. Intrathecal baclofen for severe spinal spasticity. N Engl J Med 1989;320:1517–21.
- ↑ Smith C, Birnbaum G, Carlter JL et al. Tizanidine treatment of spasticity caused by multiple sclerosis:results of a double-blind, placebo-controlled trial. US Tizanidine Study Group. Neurology 1994;44:S34–42.
- ↑ Wade DT, Wood VA, Heller A et al. Walking after stroke: measurement and recovery over the first three months. Scand J Rehabil Med 1987;19:25–30.
- ↑ Morris SL, Dodd KJ, Morris ME. Outcomes of progressive resistance strength training following stroke: a systematic review. Clin Rehabil. 2004 Feb;18(1):27-39.
- ↑ Lourenção MI, Battistella LR, de Brito CM, Tsukimoto GR, Miyazaki MH. Effect of biofeedback accompanying occupational therapy and functional electrical stimulation in hemiplegic patients. Int J Rehabil Res. 2008 Mar;31(1):33-41
- ↑ Manganotti P, Amelio E. Long-term effect of shock wave therapy on upper limb hypertonia in patients affected by stroke. Stroke. 2005 Sep;36(9):1967-71. Epub 2005 Aug 18.
- ↑ Amelio E, Manganotti P.Effect of shock wave stimulation on hypertonic plantar flexor muscles in patients with cerebral palsy: a placebo-controlled study. J Rehabil Med. 2010 Apr;42(4):339-43.(B)
- ↑ Ansari NN, Adelmanesh F, Naghdi S, Tabtabaei A.The effect of physiotherapeutic ultrasound on muscle spasticity in patients with hemiplegia: a pilot study. Electromyogr Clin Neurophysiol. 2006 Jul-Aug;46(4):247-52.(B)
- ↑ Ansari NN, Naghdi S, Bagheri H, Ghassabi H. Therapeutic ultrasound in the treatment of ankle plantarflexor spasticity in a unilateral stroke population: a randomized, single-blind, placebo-controlled trial. Electromyogr Clin Neurophysiol. 2007 May-Jun;47(3):137-43. (B)
- ↑ Harlaar J, Ten Kate JJ, Prevo AJ, Vogelaar TW, Lankhorst GJ. The effect of cooling on muscle co-ordination in spasticity: assessment with the repetitive movement test. Disabil Rehabil. 2001 Jul 20;23(11):453-61.
- ↑ Van der Salm A, Veltink PH, Ijzerman MJ, Groothuis-Oudshoorn KC, Nene AV, Hermens HJ. Comparison of electric stimulation methods for reduction of triceps surae spasticity in spinal cord injury. Arch Phys Med Rehabil. 2006 Feb;87(2):222-8.