Spasticity

For the societal implications of the term when applied as a label for a particular person, see spastic. For the most common type of spasticity-based neuromuscular disorder, see spastic diplegia.

Spasticity
Classification and external resources
DiseasesDB	20872
eMedicine	neuro/706 pmr/177
MeSH	D009128

Spasticity is a feature of altered skeletal muscle performance in muscle tone involving hypertonia, which is also referred to as an unusual "tightness" of muscles. Clinically spasticity is defined as velocity dependent resistance to stretch, where a lack of inhibition from the CNS results in excessive contraction of the muscles, ultimately leading to hyperflexia.

It mostly occurs in disorders of the central nervous system (CNS) impacting the upper motor neuron in the form of a lesion, such as spastic diplegia, but it can also present in various types of multiple sclerosis, which are autoimmune conditions.

Precise cause aside, whenever there is a loss of muscle tone inhibition from the brain to the spinal cord such that muscles become overactive, this loss of inhibitory control can cause an ongoing level of contraction, with decreased ability for the affected individual to volitionally control the muscle contraction, and increased resistance felt on passive stretch.

The clinical underpinnings of two of the most common spasticity conditions, spastic diplegia and multiple sclerosis, can be described as follows: in spastic diplegia, the upper motor neuron lesion arises often as a result of neonatal asphyxia, while in conditions like multiple sclerosis, spasticity comes as a result of the autoimmune destruction of the myelin sheaths around nerve endings — which in turn can mimic the gamma amino butyric acid deficiencies present in the damaged nerves of spastic diplegics, leading to roughly the same presentation of spasticity, but which clinically is fundamentally different from the latter.

Overall, a defining feature of spasticity is that the increased resistance to passive stretch is velocity-dependent. Lance (1980) describes it this way: “...a motor disorder, characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone (UMN) syndrome”.^{[citation needed]} Strangely, however, rather than being in the motor nerves as might be assumed to be the case, spasticity actually stems from the sensory nerves.^{[citation needed]}

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. Muscles affected in this way have many other potential features of altered performance in addition to spasticity, including muscle weakness; decreased movement control; clonus (a series of involuntary rapid muscle contractions often symptomatic of muscle over-exertion and/or muscle fatigue); exaggerated deep tendon reflexes; and decreased endurance.

Historical progression of spasticity hypotheses

The understanding of spasticity and the upper motor neuron lesion it is based on has progressed considerably in recent decades. However, the term "spasticity" is still often used interchangeably with "Upper Motor Neuron Syndrome" in the clinical settings, and it is not unusual to see patients labeled as spastic who demonstrate an array of upper motor neuron findings^[1]

Research has clearly shown that exercise is beneficial for spastic muscles,^[2] even though in the very early days of research it was assumed that strength exercise would increase spasticity. Also, from at least the 1950s through at least the 1980s, there was a strong focus on other interventions for spastic muscles, particularly stretching and splinting, but the evidence does not support these as effective.^[3] In the case of spastic diplegia there is also a permanent neurosurgical treatment for spasticity, selective dorsal rhizotomy, that directly targets nerves in the spine that cause the spasticity, and destroys them, so that the spasticity can't be activated at all.

Presentation and assessment

Spasticity is assessed by feeling the resistance of the muscle to passive lengthening in its most relaxed state. A spastic muscle will have immediately noticeable, often quite forceful, increased resistance to passive stretch when moved with speed and/or while attempting to be stretched out, as compared to the non-spastic muscles in the same person's body (if any exist). As there are many features of the Upper Motor Neuron Syndrome, there are likely to be multiple other changes in affected musculature and surrounding bones, such as progressive misalignments of bone structure around the spastic muscles (leading for example to the scissor gait in spastic diplegia. Also, following an upper motor neuron lesion, there may be multiple muscles affected, to varying degrees, depending on the location and severity of the upper motor neuron damage. The result for the affected individual, is that they may have any degree of impairment, ranging from a mild to a severe movement disorder. A relatively mild movement disorder may contribute to a loss of dexterity in an arm, or difficulty with high level mobility such as running or walking on stairs. A severe movement disorder may result in marked loss of function with minimal or no volitional muscle activation. There are several scales used to measure spasticity, such as the King’s Hypertonicity Scale^{[citation needed]}, the Tardieu^{[citation needed]}, and the Modified Ashworth^{[citation needed]}. Of these three, only the King’s Hypertonicity Scale measures a range of muscle changes from the UMN lesion, including active muscle performance as well as passive response to stretch.

Assessment of a movement disorder featuring spasticity may involve several health professionals depending on the affected individual's situation, and the severity of their condition. This may include physical therapists, doctors (including neurologists and rehabilitation physicians), orthotists and occupational therapists. Assessment is needed of the affected individual's goals, their function, and any symptoms that may be related to the movement disorder, such as pain. A thorough assessment will include analysis of posture, active movement, muscle strength, movement control and coordination, and endurance, as well as spasticity (response of the muscle to stretch). Spastic muscles typically demonstrate a loss of selective movement, including a loss of eccentric control (decreased ability to actively lengthen). While multiple muscles in a limb are usually affected in the Upper Motor Neuron Syndrome, there is usually an imbalance of activity, such that there is a stronger pull in one direction, such as into elbow flexion. Decreasing the degree of this imbalance is a common focus of muscle strengthening programs. Spastic movement disorders also typically feature a loss of stabilisation of an affected limb or the head from the trunk, so a thorough assessment requires this to be analysed as well.

Secondary effects are likely to impact on assessment of spastic muscles. If a muscle has impaired function following an upper motor neuron lesion, other changes such as increased muscle stiffness are likely to affect the feeling of resistance to passive stretch. Other secondary changes such as loss of muscle fibres following acquired muscle weakness are likely to compound the weakness arising from the upper motor neuron lesion. In severely affected spastic muscles, there may be marked secondary changes, such as muscle contracture, particularly if management has been delayed or absent.

Treatment

Treatment should be based on assessment by the relevant health professionals. For spastic muscles with mild-to-moderate impairment, exercise should be the mainstay of management, and is likely to need to be prescribed by a physical therapist or other health professional skilled in neurological rehabilitation.

Muscles with severe spasticity are likely to be more limited in their ability to exercise, and may require help to do this. They may require additional interventions, to manage the greater neurological impairment and also the greater secondary complications. These secondary complications involve the development of contractures, deformity and postural asymmetries. Interventions may include icing, serial casting, sustained stretching, inhibitory pressure and medical interventions. Treatment should be done with firm and constant manual contact positioned over nonspastic areas to avoid stimulating the spastic muscle(s). For muscles that lack any volitional control, such as after complete spinal cord injury, exercise may be assisted, and may require equipment, such as using a standing frame to sustain a standing position. A general treatment guideline can be followed that involves:

• The initial focus on first activating contraction of antagonist muscles to provide reciprocal inhibition and lengthen spastic muscles
• Reciprocal actions are attempted. Agonist contractions are performed first in small ranges progressing to larger arcs of movement
• Highly stressful activities be minimized early in training
• Functional skills are targeted for training
• Patients and family/caregivers should be educated about the importance of maintaining range of motion and doing daily exercises^[4]

Medical interventions may include such medications as baclofen, diazepam, dantrolene, or clonazepam. Phenol injections can be used, or botulinum toxin injections into the muscle belly, to attempt to dampen the signals between nerve and muscle. The effectiveness of medications vary between individuals, and vary based on location of the upper motor neuron lesion (in the brain or the spinal cord). Medications are commonly used for spastic movement disorders, but research has not shown functional benefit for some drugs.^[5][6] Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits.^[5] Surgery could be required for a tendon release in the case of a severe muscle imbalance leading to contracture. In spastic CP, selective dorsal rhizotomy has also been used to decrease muscle overactivity.

Prognosis

The prognosis for those with spastic muscles depends on multiple factors, including the severity of the spasticity and the associated movement disorder, access to specialised and intensive management, and ability of the affected individual to maintain the management plan (particularly an exercise program). Most people with a significant UMN lesion will have ongoing impairment, but most of these will be able to make progress. The most important factor to indicate ability to progress is seeing improvement, but improvement in many spastic movement disorders may not be seen until the affected individual receives help from a specialised team or health professional.

See also

• Stroke rehabilitation
• Strength training
• Cerebral palsy
• Spinal cord injury
• Transverse myelitis
• Gamma-aminobutyric acid
• Rhizotomy
• Phenol
• Baclofen
• Diazepam
• Dantrolene
• Tizanidine
• Pronator drift
• Brunnstrom Approach

References

1. ^ Ivanhoe CB, Reistetter TA: Spasticity: The misunderstood part of the upper motor neuron syndrome. Am J Phys Med Rehabil 2004;83(suppl):S3–S9.
2. ^ Ada L, Dorsch S, Canning C G. Strengthening interventions increase strength and improve activity after stroke: a systematic review. Australian Journal of Physiotherapy. 2006;52(4):241-248.
3. ^ Bovend'Eerdt TJ, Newman M, Barker K, Dawes H, Minelli C, Wade DT. The effects of stretching in spasticity: a systematic review. Arch Phys Med Rehabil. 2008 Jul;89(7):1395-406.
4. ^ O'Sullivan, Susan (2007). Physical Rehabilitation. Philadelphia, PA: F.A Davis Company. pp. 496–497. 
5. ^ ^{a b} Taricco M, Adone R, Pagliacci C, Telaro E. Pharmacological interventions for spasticity following spinal cord injury. Cochrane Database of Systematic Reviews 2000, Issue 2. Art. No.: CD001131.
6. ^ Shakespeare D, Boggild M, Young CA. Anti-spasticity agents for multiple sclerosis. Cochrane Database of Systematic Reviews 2003, Issue 4. Art. No.: CD001332.

• Lance JW: Symposium synopsis, in Feldman RG, Young RR, Koella WP (eds): Spasticity: Disordered Motor Control. Chicago, Yearbook Medical Publishers, 1980

• "Other Complications of Spinal Cord Injury: Spasticity." (Louis Calder Memorial Library of the University of Miami/Jackson Memorial Medical Center, October 3, 2002), http://calder.med.miami.edu/pointis/spasticity.html

• Maureen E. Neistadt and Elizabeth Blesedell Crepeau, ed. (1998). Willard and Spackman's occupational therapy. Philadelphia: Lippincott-Raven Publishers. pp. 233. ISBN 0-397-55192-4. 

• This article contains text from the public domain document at http://www.ninds.nih.gov/health_and_medical/disorders/spasticity_doc.htm

External links

• Patient site with information on intrathecal baclofen treatment for spasticity as a result of cerebral palsy
• The Spastic Centre - Sydney, Australia