Spasticity
Spasticity | |
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Specialty | Neurology |
Spasticity (from Greek spasmos- 'drawing, pulling') is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.
Clinically, spasticity results from the loss of inhibition of
Spastic cerebral palsy is the most common form of cerebral palsy, which is a group of permanent movement problems that do not get worse over time. GABA's inhibitory actions contribute to baclofen's efficacy as an anti-spasticity agent.
Pathophysiology
Spasticity mostly occurs in disorders of the
The cause of spasticity is thought to be where an imbalance occurs in the excitatory and inhibitory input to α motor neurons caused by damage to the spinal cord and/or central nervous system. The damage causes a change in the balance of signals between the nervous system and the muscles, leading to increased excitability in muscles. This is common in people who have cerebral palsy, brain injuries or a spinal cord injury, but it can happen to anybody e.g. having a stroke.[citation needed][1]
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 result of spasticity is problems with the muscles, spasticity is actually caused by an injury to a part of the central nervous system (the brain or spinal cord) 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 increased activity (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.[2]
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".[3]
Spasticity is found in conditions where the
Spasticity and clonus
Clonus (i.e. involuntary, rhythmic, muscular contractions and relaxations) tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins.[4] Some consider clonus as simply an extended outcome of spasticity.[4] Although closely linked, clonus is not seen in all patients with spasticity.[4] Clonus tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of clonus.[4] Clonus results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups.[4] Clonus is commonly seen in the ankle but may exist in other distal structures as well, such as the knee or spine.[5]
Characteristics of spasticity
A commonly known feature of spasticity, known as Clasp-knife response is the sudden decrease of tone after initial resistance, also referred to as a lengthening reaction or a "catch-yield sequence".[6] This is because of inverse stretch reflex activation mediated by the Golgi tendon organ on sustained muscle stretching resulting in sudden relaxation of the muscle.[7] Another characteristic of spasticity, which may be referred to as "seatbelt effect" of spasticity, is different as the amount of resistance offered by the muscle is directly proportional to velocity of the passive movement.[8] It is caused by increased muscle spindle excitability and velocity sensitivity of Ia spindle afferent nerve fibres, resulting in excessive activation of alpha motor neurons of the spinal cord.[9] It is similar to the tug we feel initially while pulling the seatbelt of a car beyond a certain velocity, hence the name "seatbelt effect"[7]
Diagnosis
The clinical underpinnings of two of the most common spasticity conditions, spastic
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). Spasticity can be differentiated from rigidity with the help of simple clinical examination, as rigidity is a uniform increase in the tone of agonist and antagonist muscles which is not related to the velocity at which the movement is performed passively and remains the same throughout the range of movement while spasticity is a velocity-dependent increase in tone resulting from the hyperexcitability of stretch reflexes.[10] It primarily involves the antigravity muscles – flexors of the upper limb and extensors of the lower limb. During the passive stretch, a brief "free interval" is appreciated in spasticity but not in rigidity because the resting muscle is electromyographically silent in spasticity. In contrast, in rigidity, the resting muscle shows firing.[7]
As there are many features of the
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
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.[citation needed]
Treatment
Treatment should be based on assessment by relevant health professionals. For spastic muscles with mild-to-moderate impairment, exercise should be the mainstay of management, and is likely needed to be prescribed by a physiatrist (a doctor specialized in rehabilitation medicine), occupational therapist, physical therapist, accredited exercise physiologist (AEP) or other health professional skilled in neurological rehabilitation.[citation needed]
Muscles with severe spasticity are likely to be more limited in their ability to exercise, and may require help to do this. In spastic cerebral palsy children the main treatment modality of spasticity is conservative in the form of botulinum toxin A injection and various physical therapy modalities such as serial casting, sustained stretching and medical pharmacologic treatment.[14][15] Spasticity in cerebral palsy children is usually generalized although with varying degrees of severity across the affected extremities and trunk musculature.[14][15] Neglected or inappropriately treated spasticity can eventually lead to joint contractures. Both spasticity and contractures can cause joint subluxations or dislocations and severe gait difficulties.[16][11] In the event of contracture there is no role for conservative treatment. Hip dislocation and ankle equinus deformity are known to arise from muscle spasticity primarily. Orthopedic surgical reconstruction of the hip is commonly practiced to improve sitting balance, nursing care and relieve hip pain.[16][11] Treatment should be done with firm and constant manual contact positioned over nonspastic areas to avoid stimulating the spastic muscle(s). Alternatively, rehabilitation robotics can be used to provide high volumes of passive or assisted movement, depending on the individual's requirements;[17] this form of therapy can be useful if therapists are at a premium, and has been found effective at reducing spasticity in patients with strokes.[18] 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.[citation needed]
A general treatment guideline can be followed that involves:[19]
- 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 exercise
Medical interventions may include oral medications such as
Incorporating
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.[citation needed]
Research
Doublecortin positive cells, similar to stem cells, are extremely adaptable and, when extracted from a brain, cultured and then re-injected in a lesioned area of the same brain, they can help repair and rebuild it.[27] The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials.[citation needed]
History
Historical progression of spasticity and the upper motor neuron lesion on which it is based 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 actually demonstrate not just spasticity alone, but also an array of upper motor neuron findings.[28]
Research has clearly shown that exercise is beneficial for spastic muscles,
See also
- Brunnstrom Approach
- Gamma-aminobutyric acid
- Pronator drift
- Rhizotomy
- Stroke rehabilitation
- Tizanidine
- Transverse myelitis
References
- ^ "Spasticity". www.stroke.org. American Heart Association. April 2022. Retrieved 26 June 2022.
- ^ "Spasticity: Pathophysiology". WeMove.org. Archived from the original on 27 February 2010.
- ISBN 978-0-88372-128-5.
- ^ S2CID 18315004.
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- ^ PMID 35936584.
- PMID 30692856.
- ISBN 978-981-19-0227-7, retrieved 2023-07-31
- ISBN 9780521689786, retrieved 2023-07-31
- ^ PMID 28279852.
- PMID 30816087.
- S2CID 7432802.
- ^ PMID 32224633.
- ^ PMID 31591703.
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- ^ Hillman M (2004). "Rehabilitation robotics from past to present: A historical perspective.". In Bien ZZ, Stefanov D (eds.). Advances in Rehabilitation Robotics. Berlin: Springer-Verlag. pp. 25–44.
- S2CID 39313352.
- ^ O'Sullivan S (2007). Physical Rehabilitation. Philadelphia, PA: F.A Davis Company. pp. 496–497.
- ^ ISBN 978-0-07-179329-2.
- ^ "UK Approves New Botox Use". 5 February 2014.[dead link]
- ^ PMID 10796750.
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- ^ Bloch J (15 February 2016). "The brain may be able to repair itself -- with help". Ted Talks.
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Further reading
- "Other Complications of Spinal Cord Injury: Spasticity". Louis Calder Memorial Library/Jackson Memorial Medical Center. University of Miami. 3 October 2002.
- Neistadt ME, Crepeau EB, eds. (1998). Willard and Spackman's occupational therapy. Philadelphia: Lippincott-Raven Publishers. pp. 233. ISBN 978-0-397-55192-7.
- Wallace DM, Ross BH, Thomas CK (December 2005). "Motor unit behavior during clonus". Journal of Applied Physiology. 99 (6): 2166–2172. S2CID 8598394.
- Hidler JM, Rymer WZ (September 1999). "A simulation study of reflex instability in spasticity: origins of clonus". IEEE Transactions on Rehabilitation Engineering. 7 (3): 327–340. S2CID 18315004.