View source for Spasticity

{{Short description|Abnormal stiffness of skeletal muscle}}
{{About||the societal implications of the term when applied as a label for a particular person|Spastic (word)|the most common type of spasticity-based neuromuscular disorder|spastic diplegia}}
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'''Spasticity ''' ({{ety|gre|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 [[motor neurons]], causing excessive velocity-dependent [[muscle contraction]]. This ultimately leads to [[hyperreflexia]], an exaggerated deep tendon reflex. Spasticity is often treated with the drug [[baclofen]], which acts as an [[agonist]] at [[GABA]] receptors, which are inhibitory.

[[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 is usually caused by damage to nerve pathways within the brain or spinal cord that control muscle movement.<ref>{{Cite web|url=https://www.uhsussex.nhs.uk/sussex-trauma-network/rehabilitation/conditions/spasticity/|title=Spasticity|date=August 3, 2023|website=University Hospitals Sussex NHS Foundation Trust}}</ref><ref>{{Cite web|url=https://www.hopkinsmedicine.org/health/conditions-and-diseases/spasticity#:~:text=What%20is%20spasticity?,brain%20or%20spinal%20cord%20injury|title=Spasticity &#124; Johns Hopkins Medicine}}</ref> This can cause an imbalance in the inhibitory and excitatory signals sent to the muscles.<ref>{{Cite web | title=Spasticity – Penn Medicine | url=https://www.pennmedicine.org/for-patients-and-visitors/patient-information/conditions-treated-a-to-z/spasticity | archive-url=https://web.archive.org/web/20191011162555/https://www.pennmedicine.org/for-patients-and-visitors/patient-information/conditions-treated-a-to-z/spasticity | access-date=2025-08-22 | archive-date=2019-10-11}}</ref> 

Spasticity mostly occurs in disorders of the [[central nervous system]] (CNS) affecting the [[upper motor neuron]]s in the form of a [[lesion]], such as [[spastic diplegia]], or [[upper motor neuron syndrome]], and can also be present in various types of [[multiple sclerosis]], where it occurs as a symptom of the progressively-worsening attacks on [[myelin sheath]]s and is thus unrelated to the types of spasticity present in neuromuscular [[cerebral palsy]] rooted spasticity disorders.{{citation needed|date=December 2020}}

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|date=December 2020}}<ref>{{cite web | publisher = American Heart Association | date = April 2022 | title = Spasticity | work = www.stroke.org | access-date = 26 June 2022 | url = https://www.stroke.org/en/about-stroke/effects-of-stroke/physical-effects-of-stroke/physical-impact/spasticity#:~:text=Spasticity%20is%20a%20common%20post,soft%20tissue%20can%20become%20tight }}</ref>

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.<ref>{{cite web | work = WeMove.org | title = Spasticity: Pathophysiology | url = http://www.mdvu.org/library/disease/spasticity/spa_mpath.asp | archive-url = https://web.archive.org/web/20100227062731/http://www.mdvu.org/library/disease/spasticity/spa_mpath.asp | archive-date = 27 February 2010 }}</ref>
[[File:02 Types of hypertonia.svg|thumb|Characteristic features, analogy, and pathophysiology of common types of hypertonia. GTO – Golgi Tendon Organ]]
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".<ref>{{cite book | vauthors = Lance JW | chapter = Symposium Synopsis | veditors = Feldman RG, Young RR, Koella WP | title = Spasticity: Disordered Motor Control | location = Chicago | publisher = Yearbook Medical Publishers | date = 1980 | isbn = 978-0-88372-128-5 |pages=185–203 }}</ref>

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 [[Central nervous system|CNS]] as a result of stroke or spinal cord injury, alter the [net inhibition] of [[peripheral nerve]]s 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 membrane]]s 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 (spasticity). 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]].{{citation needed|date=December 2020}}

== 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.<ref name="Hidler_1999">{{cite journal | vauthors = Hidler JM, Rymer WZ | title = A simulation study of reflex instability in spasticity: origins of clonus | journal = IEEE Transactions on Rehabilitation Engineering | volume = 7 | issue = 3 | pages = 327–340 | date = September 1999 | pmid = 10498378 | doi = 10.1109/86.788469 | s2cid = 18315004 }}</ref> Some consider clonus as simply an extended outcome of spasticity.<ref name="Hidler_1999" /> Although closely linked, clonus is not seen in all patients with spasticity.<ref name="Hidler_1999" /> 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.<ref name="Hidler_1999" /> 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 [[Anatomical terms of location#Proximal and distal|distal]] muscle groups.<ref name="Hidler_1999" /> Clonus is commonly seen in the ankle but may exist in other distal structures as well, such as the knee or spine.<ref name="Wallace_2005">{{cite journal | vauthors = Wallace DM, Ross BH, Thomas CK | title = Motor unit behavior during clonus | journal = Journal of Applied Physiology | volume = 99 | issue = 6 | pages = 2166–2172 | date = December 2005 | pmid = 16099891 | doi = 10.1152/japplphysiol.00649.2005 | s2cid = 8598394 | citeseerx = 10.1.1.501.9581 }}</ref>

== Characteristics of spasticity ==
[[File:03 Resistance vs stretch.svg|thumb|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".<ref>{{Cite journal |last1=Mukherjee |first1=Angshuman |last2=Chakravarty |first2=Ambar |date=2010 |title=Spasticity Mechanisms – for the Clinician |journal=Frontiers in Neurology |volume=1 |page=149 |doi=10.3389/fneur.2010.00149 |pmid=21206767 |issn=1664-2295|pmc=3009478 |doi-access=free }}</ref> 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.<ref name=":0">{{Cite journal |last1=Ramanathan |first1=Venkateswaran |last2=Baskar |first2=Dipti |last3=Pari |first3=Hariswar |date=2022 |title='Seatbelt Effect' of spasticity: Contrasting velocity dependence from the clasp knife phenomenon |url=http://www.annalsofian.org/text.asp?2022/25/3/517/338853 |journal=Annals of Indian Academy of Neurology |language=en |volume=25 |issue=3 |pages=517–519 |doi=10.4103/aian.aian_817_21 |pmid=35936584 |issn=0972-2327|pmc=9350785 |doi-access=free }}</ref> 

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.<ref>{{Cite journal |last=Petek Balci |first=Belgin |date=2018 |title=Spasticty measurement |url=http://submission.noropsikiyatriarsivi.com/default.aspx?s=public~kabul&mId=23339 |journal=Archives of Neuropsychiatry |volume=55 |issue=Suppl 1 |pages=S49–S53 |language=en |doi=10.29399/npa.23339 |pmid=30692856 |issn=1309-4866|pmc=6278623 }}</ref> 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.<ref>{{Citation |last=Ko |first=Hyun-Yoon |title=Functional Neuroanatomy of the Spinal Cord |date=2022 |work=Management and Rehabilitation of Spinal Cord Injuries |pages=41–68 |place=Singapore |publisher=Springer Nature Singapore |doi=10.1007/978-981-19-0228-4_3 |isbn=978-981-19-0227-7}}</ref> 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"<ref name=":0" />

== Diagnosis ==
The clinical underpinnings of two of the most common spasticity conditions, spastic [[cerebral palsy]] 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 is thought by some to be as a result of the [[autoimmune]] destruction of the [[myelin sheath]]s around nerve endings—which in turn can ''mimic'' the [[gamma amino butyric acid]] deficiencies present in the damaged nerves of spastic [[cerebral palsy]] children, leading to roughly the same ''presentation'' of spasticity, but which clinically is fundamentally different from the latter.{{citation needed|date=December 2020}}

===Grading===
Spasticity can be graded on scales including the modified Ashworth scale, the Tardieu scale and the Penn spasm frequency scale.<ref>{{Cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK507869/|title=StatPearls|first1=Yulia|last1=Rivelis|first2=Nowera|last2=Zafar|first3=Karen|last3=Morice|chapter=Spasticity |date=December 14, 2024|publisher=StatPearls Publishing|via=PubMed|pmid=29939646}}</ref>

===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). 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.<ref>{{cite book |last=Rushton |first=David N. |chapter=Intrathecal baclofen for the control of spinal and supraspinal spasticity |date=2008 |title=Upper Motor Neurone Syndrome and Spasticity |pages=181–192 |publisher=Cambridge University Press|doi=10.1017/cbo9780511544866.011 |isbn=978-0-521-68978-6 }}</ref> 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.<ref name=":0" />

As there are many features of the [[Upper Motor Neuron Syndrome|upper motor neuron syndrome]], there are likely to be multiple other changes in affected musculature and surrounding bones, such as progressive malalignments of bone structure around the spastic muscles (leading for example to the [[scissor gait]] and tip-toeing gait due to ankle equinus or ankle planter flexion deformity in spastic [[cerebral palsy]] children, [[scissor gait]] is caused by spasticity of the hip adductor muscles while tip-toeing gait is caused by spasticity of the gastrocnemius-soleus muscle complex or calf musculature.<ref name="Galey2017">{{cite journal | vauthors = Galey SA, Lerner ZF, Bulea TC, Zimbler S, Damiano DL | title = Effectiveness of surgical and non-surgical management of crouch gait in cerebral palsy: A systematic review | journal = Gait & Posture | volume = 54 | pages = 93–105 | date = May 2017 | pmid = 28279852 | doi = 10.1016/j.gaitpost.2017.02.024 | pmc = 9619302 }}</ref><ref>{{cite journal | vauthors = Gendy S, ElGebeily M, El-Sobky TA, Khoshhal KI, Jawadi AH | title = Current practice and preferences to management of equinus in children with ambulatory cerebral palsy: A survey of orthopedic surgeons | journal = SICOT-J | volume = 5 | page = 3 | date = 2019 | pmid = 30816087 | pmc = 6394235 | doi = 10.1051/sicotj/2019003 }}</ref>  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, the Tardieu, and the [[Modified Ashworth scale|modified Ashworth]].<ref>{{cite journal | vauthors = Aloraini SM, Gäverth J, Yeung E, MacKay-Lyons M | title = Assessment of spasticity after stroke using clinical measures: a systematic review | journal = Disability and Rehabilitation | volume = 37 | issue = 25 | pages = 2313–2323 | date = 18 February 2015 | pmid = 25690684 | doi = 10.3109/09638288.2015.1014933 | s2cid = 7432802 }}</ref> 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.{{citation needed|date=December 2020}}

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]], physicians (including [[neurologists]] and [[American Academy of Physical Medicine and Rehabilitation|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 [[core stability|stabilisation]] of an affected limb or the head from the [[torso|trunk]], so a thorough assessment requires this to be analysed as well.{{citation needed|date=December 2020}}

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|date=December 2020}}

== Treatment ==
Treatment should be based on assessment by relevant health professionals.  For spastic muscles with mild-to-moderate impairment, [[strength training|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|date=December 2020}}

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.<ref name=farag2020>{{cite journal | vauthors = Farag SM, Mohammed MO, El-Sobky TA, ElKadery NA, ElZohiery AK | title = Botulinum Toxin A Injection in Treatment of Upper Limb Spasticity in Children with Cerebral Palsy: A Systematic Review of Randomized Controlled Trials | journal = JBJS Reviews | volume = 8 | issue = 3 | article-number = e0119 | date = March 2020 | pmid = 32224633 | pmc = 7161716 | doi = 10.2106/JBJS.RVW.19.00119 }}</ref><ref name=Blumetti2019>{{cite journal | vauthors = Blumetti FC, Belloti JC, Tamaoki MJ, Pinto JA | title = Botulinum toxin type A in the treatment of lower limb spasticity in children with cerebral palsy | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | issue = 10 | article-number = CD001408 | date = October 2019 | pmid = 31591703 | pmc = 6779591 | doi = 10.1002/14651858.CD001408.pub2 }}</ref> Spasticity in [[cerebral palsy]] children is usually generalized although with varying degrees of severity across the affected extremities and trunk musculature.<ref name=farag2020/><ref name=Blumetti2019/> 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.<ref name=elsobky2018>{{cite journal | vauthors = El-Sobky TA, Fayyad TA, Kotb AM, Kaldas B | title = Bony reconstruction of hip in cerebral palsy children Gross Motor Function Classification System levels III to V: a systematic review | journal = Journal of Pediatric Orthopedics. Part B | volume = 27 | issue = 3 | pages = 221–230 | date = May 2018 | pmid = 28953164 | doi = 10.1097/BPB.0000000000000503 | s2cid = 4204446 }}</ref><ref name=Galey2017/> 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.<ref name=elsobky2018/><ref name=Galey2017/>
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;<ref>{{cite book | vauthors = Hillman M | date = 2004 | chapter = Rehabilitation robotics from past to present: A historical perspective. | veditors = Bien ZZ, Stefanov D | title = Advances in ''Rehabilitation Robotics'' | pages = 25–44 | location = Berlin | publisher = Springer-Verlag }}</ref> this form of therapy can be useful if therapists are at a premium, and has been found effective at reducing spasticity in patients with [[stroke]]s.<ref>{{cite journal | vauthors = Krebs HI, Palazzolo JJ, Dipietro L, Ferraro M, Krol J, Rannekleiv K, Volpe BT, Hogan N | year = 2003 | title = Rehabilitation robotics: Performance-based progressive robot-assisted therapy | journal = Automatic Robots | volume = 15 | pages = 7–20 |display-authors = 6 | doi = 10.1023/A:1024494031121 | s2cid = 39313352 }}</ref>  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|date=December 2020}}

A general treatment guideline can be followed that involves:<ref>{{cite book| vauthors = O'Sullivan S |title=Physical Rehabilitation|year=2007|publisher=F.A Davis Company|location=Philadelphia, PA|pages=496–497}}</ref>
* 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 [[baclofen]], [[clonazepam]], [[clonidine]], [[diazepam]], or [[dantrolene]]. If refractive to oral agents, spasticity may be treated with [[intrathecal]] baclofen therapy (IBT) when spasticity. IBT may also be used in patients with limited tolerance to other modalities.<ref name=Saulino2014>{{cite book | vauthors = Saulino M, Goldman L | date = 2014 | chapter = Spasticity | veditors = Maitin IB, Cruz E | title = CURRENT Diagnosis & Treatment: Physical Medicine & Rehabilitation. | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=1180&sectionid=70376430 | isbn = 978-0-07-179329-2 }}</ref> [[Phenol]] injections can be used, or [[botulinum toxin]]<ref name=Saulino2014/><ref name=farag2020/><ref name=Blumetti2019/><ref>{{cite web|url=http://www.dddmag.com/news/2014/02/uk-approves-new-botox-use?et_cid=3751256&et_rid=657808477&type=cta|archive-url=https://archive.today/20140206045026/http://www.dddmag.com/news/2014/02/uk-approves-new-botox-use?et_cid=3751256&et_rid=657808477&type=cta|archive-date=February 6, 2014|title=UK Approves New Botox Use|date=5 February 2014}} </ref> 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.<ref name="Taricco M 2000">{{cite journal | vauthors = Taricco M, Adone R, Pagliacci C, Telaro E | title = Pharmacological interventions for spasticity following spinal cord injury | journal = The Cochrane Database of Systematic Reviews | volume = 2000 | issue = 2 | article-number = CD001131 | year = 2000 | pmid = 10796750 | pmc = 8406943 | doi = 10.1002/14651858.CD001131 }}</ref><ref>{{cite journal | vauthors = Shakespeare DT, Boggild M, Young C | title = Anti-spasticity agents for multiple sclerosis | journal = The Cochrane Database of Systematic Reviews | volume = 4 | issue = 4 | article-number = CD001332 | year = 2003 | pmid = 14583932 | pmc = 7028001 | doi = 10.1002/14651858.CD001332 }}</ref> Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits.<ref name="Taricco M 2000"/> [[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.<ref>{{Cite journal |last1=Grunt |first1=Sebastian |last2=Fieggen |first2=A Graham |last3=Vermeulen |first3=R Jeroen |last4=Becher |first4=Jules G |last5=Langerak |first5=Nelleke G |year=2014 |title=Selection criteria for selective dorsal rhizotomy in children with spastic cerebral palsy: a systematic review of the literature |journal=Developmental Medicine & Child Neurology |language=en |volume=56 |issue=4 |pages=302–312 |doi=10.1111/dmcn.12277|pmid=24106928 |doi-access=free }}</ref>

Incorporating [[hydrotherapy]] in the treatment program may help decrease spasm severity, promote functional independence, improve motor recovery and decrease medication required for spasticity, which may help reduce the side effects that are possible with oral drug treatments.<ref name="Kesiktas">{{cite journal | vauthors = Kesiktas N, Paker N, Erdogan N, Gülsen G, Biçki D, Yilmaz H | title = The use of hydrotherapy for the management of spasticity | journal = Neurorehabilitation and Neural Repair | volume = 18 | issue = 4 | pages = 268–273 | date = December 2004 | pmid = 15537997 | doi = 10.1177/1545968304270002 | s2cid = 40066099 | doi-access = free }}</ref><ref name="Beresneva">{{cite journal | vauthors = Beresneva J, Stirane D, Kiukucane E, Vetra A | year = 2009 | title = The use of aquatic therapy in stroke patients for the management of spasticity...Proceedings of the 10th Congress of the European Federation for Research in Rehabilitation, Riga, Latvia | journal = International Journal of Rehabilitation Research | volume = 32 | page = S110 | doi=10.1097/00004356-200908001-00145| s2cid = 147336547 }}</ref>   A 2004 study compared the effects of hydrotherapy on spasticity, oral [[baclofen]] dosage and [[Functional Independence Measure]] (FIM) scores of patients with a [[spinal cord injury]] (SCI). It was found that subjects who received hydrotherapy treatment obtained increased FIM scores and a decreased intake of oral baclofen medication.<ref name ="Kesiktas" />  A 2009 study looked at the effect of hydrotherapy to decrease spasticity on post-[[stroke]], [[hemiparetic]] patients with limited mobility and concluded that there was a significantly larger increase in FIM scores compared to the control group that did not receive hydrotherapy.<ref name ="Beresneva" />

== 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|date=December 2020}}

== 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.<ref>{{cite web | vauthors = Bloch J | work = Ted Talks |url=https://www.ted.com/talks/jocelyne_bloch_the_brain_may_be_able_to_repair_itself_with_help|title=The brain may be able to repair itself -- with help|date=15 February 2016 }}</ref> 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|date=December 2020}}

== 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.<ref name="pmid15448572">{{cite journal | vauthors = Ivanhoe CB, Reistetter TA | title = Spasticity: the misunderstood part of the upper motor neuron syndrome | journal = American Journal of Physical Medicine & Rehabilitation | volume = 83 | issue = 10 Suppl | pages = S3–S9 | date = October 2004 | pmid = 15448572 | doi = 10.1097/01.PHM.0000141125.28611.3E | s2cid = 45445777 }}</ref>

Research has clearly shown that exercise is beneficial for spastic muscles,<ref>{{cite journal | vauthors = Ada L, Dorsch S, Canning CG | title = Strengthening interventions increase strength and improve activity after stroke: a systematic review | journal = The Australian Journal of Physiotherapy | volume = 52 | issue = 4 | pages = 241–248 | year = 2006 | pmid = 17132118 | doi = 10.1016/s0004-9514(06)70003-4 | doi-access = free }}</ref> 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 [[orthotics|splinting]], but the evidence does not support these as effective.<ref name="pmid18534551">{{cite journal | vauthors = Bovend'Eerdt TJ, Newman M, Barker K, Dawes H, Minelli C, Wade DT | title = The effects of stretching in spasticity: a systematic review | journal = Archives of Physical Medicine and Rehabilitation | volume = 89 | issue = 7 | pages = 1395–1406 | date = July 2008 | pmid = 18534551 | doi = 10.1016/j.apmr.2008.02.015 }}</ref> While splinting is not considered effective for decreasing spasticity, a range of different orthotics are effectively used for preventing [[muscle contracture]]s on patients with spasticity. 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 cannot be activated at all.{{citation needed|date=December 2020}}

== See also ==
{{col div|colwidth=30em}}
* [[Brunnstrom Approach]]
* [[Gamma-aminobutyric acid]]
* [[Pronator drift]]
* [[Rhizotomy]]
* [[Stroke rehabilitation]]
* [[Tizanidine]]
* [[Transverse myelitis]]
{{colend}}

== References ==
{{Include-NIH | title = NINDS Spasticity Information Page | url = https://web.archive.org/web/20040603053252/http://www.ninds.nih.gov/health_and_medical/disorders/spasticity_doc.htm }}

{{Reflist}}

== Further reading ==
{{refbegin}}
* {{cite web | title = Other Complications of Spinal Cord Injury: Spasticity. | work = Louis Calder Memorial Library/Jackson Memorial Medical Center | publisher = [[University of Miami]] | date = 3 October 2002 | url = http://calder.med.miami.edu/pointis/spasticity.html }}
* {{cite book | veditors = Neistadt ME, Crepeau EB |title=Willard and Spackman's occupational therapy |publisher=Lippincott-Raven Publishers |location=Philadelphia |year=1998 |pages=[https://archive.org/details/willardspackmans0000unse/page/233 233] |isbn=978-0-397-55192-7 |url=https://archive.org/details/willardspackmans0000unse/page/233 }}
* {{cite journal | vauthors = Wallace DM, Ross BH, Thomas CK | title = Motor unit behavior during clonus | journal = Journal of Applied Physiology | volume = 99 | issue = 6 | pages = 2166–2172 | date = December 2005 | pmid = 16099891 | doi = 10.1152/japplphysiol.00649.2005 | s2cid = 8598394 | citeseerx = 10.1.1.501.9581 }}
* {{cite journal | vauthors = Hidler JM, Rymer WZ | title = A simulation study of reflex instability in spasticity: origins of clonus | journal = IEEE Transactions on Rehabilitation Engineering | volume = 7 | issue = 3 | pages = 327–340 | date = September 1999 | pmid = 10498378 | doi = 10.1109/86.788469 | s2cid = 18315004 }}
{{refend}}

{{Medical resources
| ICD10           = {{ICD10|R25.2}}
| ICD9            = <!--{{ICD9|xxx}}-->
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| OMIM            =
| DiseasesDB      = 20872
| MedlinePlus     = 003297
| eMedicineSubj   = neuro
| eMedicineTopic  = 706
| MeshID          = D009128
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{{Movement and gait symptoms and signs}}
{{Central nervous system disease}}
{{Cerebral palsy}}
{{Authority control}}

[[Category:Cerebral palsy types]]