Editing Spasticity (section)

== 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>{{Citation |last=Rushton |first=David N. |title=Intrathecal baclofen for the control of spinal and supraspinal spasticity |date=2008-04-24 |url=http://dx.doi.org/10.1017/cbo9780511544866.011 |work=Upper Motor Neurone Syndrome and Spasticity |pages=181–192 |access-date=2023-07-31 |publisher=Cambridge University Press|doi=10.1017/cbo9780511544866.011 |isbn=9780521689786 |url-access=subscription }}</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 | pages = 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}}