Spasticity (from Greek, Modern spasmos-, meaning '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.



Spasticity mostly occurs in disorders of the central nervous system (CNS) affecting the upper motor neurons 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 sheaths and is thus unrelated to the types of spasticity present in neuromuscular cerebral palsy rooted spasticity disorders.

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 celebral palsy, brain injuries or a spinal chord injury, but it can happen to anybody e.g. having a stroke.

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 end 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.[1]

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".[2]

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 CNS as a result of stroke or spinal cord injury, alter the [net inhibition] of peripheral nerves 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 membranes 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.

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.[3] Some consider clonus as simply an extended outcome of spasticity.[3] Although closely linked, clonus is not seen in all patients with spasticity.[3] 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.[3] 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.[3] Clonus is commonly seen in the ankle but may exist in other distal structures as well, such as the knee or spine.[4]


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 is thought by some to be 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.

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, the Tardieu, and the modified Ashworth. 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, physicians (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 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 an occupational therapist, physical therapist, accredited exercise physiologist (AEP) 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). Alternatively, rehabilitation robotics can be used to provide high volumes of passive or assisted movement, depending on the individual's requirements;[5] this form of therapy can be useful if therapists are at a premium, and has been found effective at reducing spasticity in patients suffering from stroke.[6] 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[7]

Medical interventions may include such medications as baclofen, diazepam, dantrolene, or clonazepam. Phenol injections can be used, or botulinum toxin[8] 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.[9][10] Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits.[9] 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.

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.[11][12] 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.[11] 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.[12]


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.


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.[13] The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials.


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.[14]

Research has clearly shown that exercise is beneficial for spastic muscles,[15] 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.[16] While splinting is not considered effective for decreasing spasticity, a range of different orthotics are effectively used for preventing muscle contractures 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.

See also


  1. ^
  2. ^ {{subst:citation: JW. Lance (1980). Symposium synopsis. In: Feldman RG, Young RR, Koella WP (eds) Spasticity: disorders motor control. Miami: Year Book Medical Publishers. pp. 185–203. ISBN 0883721287}}
  3. ^ a b c d e Hilder, Joseph M.; Zev W. Rymer (September 1999). "A Stimulation Study of Reflex Instability in Spasticity: Origins of Clonus". IEEE Transactions on Rehabilitation Engineering. 7 (3): 327–340. doi:10.1109/86.788469.
  4. ^ Douglas, Wallace M.; Bruce H Ross; Christine K. Thomas (Aug 25, 2005). "Motor unit behaviour during clonus". Journal of Applied Physiology. 99 (6): 2166–2172. CiteSeerX doi:10.1152/japplphysiol.00649.2005. PMID 16099891.
  5. ^ Hillman, M. (2004). Rehabilitation robotics from past to present: A historical perspective. In Z.Z. Bien & D. Stefanov (Eds.), Advances in Rehabilitation Robotics (25-44). Berlin: Springer-Verlag.
  6. ^ Krebs H.I.; et al. (2003). "Rehabilitation robotics: Performance-based progressive robot-assisted therapy". Automatic Robots. 15: 7–20. doi:10.1023/A:1024494031121.
  7. ^ O'Sullivan, Susan (2007). Physical Rehabilitation. Philadelphia, PA: F.A Davis Company. pp. 496–497.
  8. ^ "UK Approves New Botox Use". 5 February 2014.
  9. ^ a b Taricco M, Adone R, Pagliacci C, Telaro E (2000). "Pharmacological interventions for spasticity following spinal cord injury". Cochrane Database of Systematic Reviews. 2 (2): CD001131. doi:10.1002/14651858.CD001131. PMID 10796750.
  10. ^ Shakespeare D, Boggild M, Young CA (2003). "Anti-spasticity agents for multiple sclerosis". Cochrane Database of Systematic Reviews. 4 (4): CD001332. doi:10.1002/14651858.CD001332. PMID 14583932.
  11. ^ a b Kesiktas N, Paker N, Erdogan N, Gülsen G, Biçki D, Yilmaz H (December 2004). "The use of hydrotherapy for the management of spasticity". Neurorehabil Neural Repair. 18 (4): 268–73. doi:10.1177/1545968304270002. PMID 15537997.
  12. ^ a b Beresneva J, Stirane D, Kiukucane E, Vetra A (2009). "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". International Journal of Rehabilitation Research. 32: S110. doi:10.1097/00004356-200908001-00145.
  13. ^ "The brain may be able to repair itself -- with help".
  14. ^ Ivanhoe CB, Reistetter TA (October 2004). "Spasticity: the misunderstood part of the upper motor neuron syndrome". Am J Phys Med Rehabil. 83 (10 Suppl): S3–9. doi:10.1097/01.PHM.0000141125.28611.3E. PMID 15448572.
  15. ^ Ada L, Dorsch S, Canning CG (2006). "Strengthening interventions increase strength and improve activity after stroke: a systematic review". Australian Journal of Physiotherapy. 52 (4): 241–248. doi:10.1016/s0004-9514(06)70003-4. PMID 17132118.
  16. ^ Bovend'Eerdt TJ, Newman M, Barker K, Dawes H, Minelli C, Wade DT (July 2008). "The effects of stretching in spasticity: a systematic review". Arch Phys Med Rehabil. 89 (7): 1395–406. doi:10.1016/j.apmr.2008.02.015. PMID 18534551.

External links

External resources
  • 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),
  • Maureen E. Neistadt and Elizabeth Blesedell Crepeau, ed. (1998). Willard and Spackman's occupational therapy. Philadelphia: Lippincott-Raven Publishers. p. 233. ISBN 978-0-397-55192-7.CS1 maint: Extra text: authors list (link)
  • This article contains text from the public domain document at
  • Douglas, Wallace M.; Bruce H Ross; Christine K. Thomas (Aug 25, 2005). "Motor unit behaviour during clonus". Journal of Applied Physiology. 99 (6): 2166–2172. CiteSeerX doi:10.1152/japplphysiol.00649.2005. PMID 16099891.
  • Hilder, Joseph M.; Zev W. Rymer (September 1999). "A Stimulation Study of Reflex Instability in Spasticity: Origins of Clonus". IEEE Transactions on Rehabilitation Engineering. 7 (3): 327–340. doi:10.1109/86.788469.

An antispasmodic (synonym: spasmolytic) is a pharmaceutical drug or other agent that suppresses muscle spasms.


Baclofen, sold under the brand name Lioresal among others, is a medication used to treat muscle spasticity such as from a spinal cord injury or multiple sclerosis. It may also be used for hiccups and muscle spasms near the end of life. It is taken by mouth or by delivery into the spinal canal.Common side effects include sleepiness, weakness, and dizziness. Serious side effects may occur if baclofen is rapidly stopped including seizures and rhabdomyolysis. Use in pregnancy is of unclear safety while use during breastfeeding is probably safe. It is believed to work by decreasing neurotransmitters.Baclofen was approved for medical use in the United States in 1977. It is avaliable as a generic medication. A month supply in the United Kingdom costs the NHS about one £ as of 2019. In the United States the wholesale cost of this amount is about 8.40 USD. In 2016 it was the 124th most prescribed medication in the United States with more than 5 million prescriptions.


Clonus is a series of involuntary, rhythmic, muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions involving descending motor pathways, and in many cases is, accompanied by spasticity (another form of hyperexcitability). Unlike small, spontaneous twitches known as fasciculations (usually caused by lower motor neuron pathology), clonus causes large motions that are usually initiated by a reflex. Studies have shown clonus beat frequency to range from three to eight Hz on average, and may last a few seconds to several minutes depending on the patient’s condition. The term is from the Greek for "violent, confused motion".


This article refers to permanent shortening of muscles, tendons, or ligaments. For short-term contraction of muscles, see Muscle contraction.

A muscle contracture is a permanent shortening of a muscle or joint. It is usually in response to prolonged hypertonic spasticity in a concentrated muscle area, such as is seen in the tightest muscles of people with conditions like spastic cerebral palsy.

Contractures are essentially muscles or tendons that have remained too tight for too long, thus becoming shorter. They develop when these normally elastic tissues are replaced by inelastic tissues. This results in the shortening and hardening of these tissues, ultimately causing rigidity, joint deformities, and a total loss of movement around the joint. Most of the physical therapy, occupational therapy, and other exercise regimens targeted towards people with spasticity focuses on trying to prevent contractures from happening in the first place. However, research on sustained traction of connective tissue in approaches such as adaptive yoga has demonstrated that contracture can be reduced, at the same time that tendency toward spasticity is addressed.

Contractures can also be due to ischemia, as in Volkmann's contracture.

Excessive matrix metalloproteinase and myofibroblast accumulation in the wound margins can result in contracture.

Hereditary spastic paraplegia

Hereditary spastic paraplegia (HSP) is a group of inherited diseases whose main feature is a progressive gait disorder. The disease presents with progressive stiffness (spasticity) and contraction in the lower limbs. HSP is also known as hereditary spastic paraparesis, familial spastic paraplegia, French settlement disease, or Strumpell-Lorrain disease. The symptoms are a result of dysfunction of long axons in the spinal cord. The affected cells are the primary motor neurons; therefore, the disease is an upper motor neuron disease. HSP is not a form of cerebral palsy even though it physically may appear and behave much the same as spastic diplegia. The origin of HSP is different from cerebral palsy. Despite this, some of the same anti-spasticity medications used in spastic cerebral palsy are sometimes used to treat HSP symptoms.

HSP is caused by defects in transport of proteins, structural proteins, cell maintaining proteins, lipids, and other substances through the cell. Long nerve fibers (axons) are affected because long distances make nerve cells particularly sensitive to defects in these mentioned mechanisms.The disease was first mentioned in 1876 by Adolph Seeligmüller, a German neurologist, who described a family of four affected children with spasticity. Further cases were described in 1883 by Adolph Strümpell, a German neurologist. Those cases were described more extensively in 1888 by Maurice Lorrain, a French physician. Due to their contribution in describing the disease, it is still named Strümpell-Lorrain disease in French speaking countries. The term hereditary spastic paraplegia was coined by Anita Harding in 1983.


Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug and/or physical therapy.

Movement disorders

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- hyperkinetic and hypokinetic.

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

Muscle relaxant

A muscle relaxant is a drug that affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause temporary paralysis. Spasmolytics, also known as "centrally acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only.


Nabiximols (USAN, trade name Sativex) is a specific extract of Cannabis that was approved as a botanical drug in the United Kingdom in 2010 as a mouth spray to alleviate neuropathic pain, spasticity, overactive bladder, and other symptoms of multiple sclerosis; it was developed by the UK company GW Pharmaceuticals. The drug is a pharmaceutical product standardised in composition, formulation, and dose. Its principal active cannabinoid components are the cannabinoids: tetrahydrocannabinol (THC) and cannabidiol (CBD). Each spray delivers a dose of 2.7 mg THC and 2.5 mg CBD.

In May 2003 GW Pharmaceuticals and Bayer entered into an exclusive marketing agreement for GW's cannabis-based medicinal extract product, to be marketed under the brand name Sativex. "Bayer has obtained exclusive rights to market Sativex in the UK. In addition, Bayer has the option for a limited period to negotiate the marketing rights in other countries in European Union and selected other countries around the world."

In April 2011, GW licensed to Novartis the rights to commercialise nabiximols in Asia (excluding China and Japan), Africa and the Middle East (excluding Israel).


Oxotremorine (i.e. oxo M) is a parasympathomimetic drug that acts as a selective muscarinic acetylcholine receptor agonist.Oxotremorine produces ataxia, tremor and spasticity, similar to those symptoms seen in Parkinsonism, and has thus become a research tool in experimental studies aimed at determining more effective anti-Parkinsonian drugs.Oxotremorine also produces antipsychotic effects.


Paraplegia is an impairment in motor or sensory function of the lower extremities. The word comes from Ionic Greek παραπληγίη "half-stricken". It is usually caused by spinal cord injury or a congenital condition that affects the neural (brain) elements of the spinal canal. The area of the spinal canal that is affected in paraplegia is either the thoracic, lumbar, or sacral regions. If four limbs are affected by paralysis, tetraplegia or quadriplegia is the correct term. If only one limb is affected, the correct term is monoplegia.

Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis.

The American Spinal Injury Association classifies spinal cord injury severity. ASIA A being the complete loss of sensory function and motor skills below the injury. ASIA B is having some sensory function below the injury, but no motor function. ASIA C some motor function below level of injury, but half the muscles cannot move against gravity. ASIA D, more than half of the muscles below the level of injury can move against gravity. ASIA E which is the restoration of all neurologic function.

Primary lateral sclerosis

Primary lateral sclerosis (PLS) is a rare neuromuscular disease characterized by progressive muscle weakness in the voluntary muscles. PLS belongs to a group of disorders known as motor neuron diseases. Motor neuron diseases develop when the nerve cells that control voluntary muscle movement degenerate and die, causing weakness in the muscles they control.

PLS only affects upper motor neurons. There is no evidence of the degeneration of spinal motor neurons or muscle wasting (amyotrophy) that occurs in amyotrophic lateral sclerosis (ALS).

Pronator drift

In medicine, pronator drift (also known as pyramidal drift) refers to a pathologic sign seen during a neurological examination. Jean Alexandre Barré is credited with having first described it; thus it is sometimes known as the Barré test or sign. A positive result indicates spasticity. This sign can appear due to an upper motor neuron lesion or various other conditions (including inborn errors of metabolism) which include spasticity as a symptom.

Pseudobulbar palsy

Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements (such as chewing and speaking) and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech (which is often the initial presentation of the disorder), sometimes also demonstrating uncontrolled emotional outbursts.The condition is usually caused by the bilateral damage to corticobulbar pathways, which are upper motor neuron pathways that course from the cerebral cortex to nuclei of cranial nerves in the brain stem.


This article deals with Selective Dorsal Rhizotomy (SDR) rather than the rhizotomy procedures for pain relief; for those procedures, which have begun to take the name "rhizotomy" in certain instances, see facet rhizotomy and similar. A facet rhizotomy is just one of many different forms of radiofrequency ablation, and its use of the "rhizotomy" name should not be confused with the SDR procedure.A selective dorsal rhizotomy (SDR), also known as a rhizotomy, dorsal rhizotomy, or a selective posterior rhizotomy, is a neurosurgical procedure that selectively destroys problematic nerve roots in the spinal cord. This procedure has been well-established in the literature as a surgical intervention and is used to relieve negative symptoms of neuromuscular conditions such as spastic diplegia and other forms of spastic cerebral palsy. The specific sensory nerves inducing spasticity are identified using electromyographic (EMG) stimulation and graded on a scale of 1 (mild) to 4 (severe spasticity). Abnormal nerve responses (usually graded a 3 or 4) are isolated and cut, thereby reducing symptoms of spasticity.Spasticity is defined as a velocity-dependent increase in muscle tone in response to a stretch. This upper motor neuron condition results from a lack of descending input from the brain that would normally release the inhibitory neurotransmitter gamma amino butyric acid (GABA), which serves to dampen neuronal excitability in the nervous system. Spasticity is thought to be caused by an excessive increase of excitatory signals from sensory nerves without proper inhibition by GABA. Two common conditions associated with this lack of descending input are cerebral palsy and acquired brain injury.

Spastic cerebral palsy

Spastic cerebral palsy is the type of cerebral palsy wherein spasticity is the exclusive impairment present. Itself an umbrella term encompassing spastic hemiplegia, spastic diplegia, spastic quadriplegia and — where solely one limb or one specific area of the body is affected— spastic monoplegia. Spastic cerebral palsy affects the cerebral cortex and is overwhelmingly the most common type of overall cerebral palsy.

The Society for Cerebral Palsy in Europe (SCPE) estimates that the spasticity-only cerebral palsy classification sweeps in 90% of global cerebral palsy cases. But even if the 90% assertion is an exaggeration, more conservative scientific estimates still place the prevalence of spasticity-dominant or spasticity-only cerebral palsy at anywhere from 70–80% of all cases, leaving cases dominated by ataxic cerebral palsy, dyskinetic cerebral palsy and athetoid cerebral palsy trailing at 20–30%.

Spastic diplegia

Spastic diplegia, historically known as Little's disease, is a form of cerebral palsy (CP) that is a chronic neuromuscular condition of hypertonia and spasticity—manifested as an especially high and constant "tightness" or "stiffness"—in the muscles of the lower extremities of the human body, usually those of the legs, hips and pelvis. Doctor William John Little's first recorded encounter with cerebral palsy is reported to have been among children who displayed signs of spastic diplegia.

Spastic diplegia accounts for about 22% of all diagnoses of cerebral palsy, and together with spastic quadriplegia and spastic triplegia make up the broad classification spastic cerebral palsy, which accounts for 70% of all cerebral palsy diagnoses.


Tetraplegia, also known as quadriplegia, is paralysis caused by illness or injury that results in the partial or total loss of use of all four limbs and torso; paraplegia is similar but does not affect the arms. The loss is usually sensory and motor, which means that both sensation and control are lost. Tetraparesis or quadriparesis, on the other hand, means muscle weakness affecting all four limbs. It may be flaccid or spastic.


Tizanidine, sold under the brand name Zanaflex among others, is a medication that is used to treat muscle spasticity due to spinal cord injury or multiple sclerosis. Effectiveness appears similar to baclofen or diazepam. It is taken by mouth.Common side effects include dry mouth, sleepiness, weakness, and dizziness. Serious side effects may include low blood pressure, liver problems, psychosis, and QT prolongation. It is unclear if use in pregnancy and breastfeeding is safe. It is a α2-adrenergic agonist and how it works is not entirely clear.Tizanidine was approved for medical use in the United States in 1996. It is avaliable as a generic medication. A month supply in the United Kingdom costs the NHS about 3.45 £ as of 2019. In the United States the wholesale cost of this amount is about 4.20 USD. In 2016 it was the 118th most prescribed medication in the United States with more than 6 million prescriptions.

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