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Spasticity
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== 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 | Johns Hopkins Medicine}}</ref> This can cause an imbalance in the inhibitory and excitatory signals sent to the muscles.<ref>https://www.pennmedicine.org/for-patients-and-visitors/patient-information/conditions-treated-a-to-z/spasticity</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 Ξ± 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 β 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=185β203 }}</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}}
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