By Prodyut Das

What is Spasticity

by Max

Spastic hand

Spastic hand

What is Spasticity?

Spasticity is defined as Velocity dependent Resistance to movement. Spasticity is derived from the Greek word spasticus, which means to pull. Spasticity is a component of the upper motor neuron syndrome (UMNS). The upper motor neuron syndrome is caused by a lesion proximal to the anterior horn cell; in the spinal cord, brainstem, or brain. It has both positive and negative components. Weakness, paralysis, and fatigue are the negative signs of the syndrome, whereas spasticity, athetosis, hyperreflexia, release of primitive reflexes, and dystonia are the positive. Hyperreflexia, spread of reflexes beyond muscles stimulated, hypertonicity, clonus, and rigidity are often seen in association with spasticity.

Pathophysiology and Causes of Spasticity

So from where does spasticity come? Dietz and Berger have suggested that intrinsic properties of the muscle itself could explain the changes seen with spasticity. Based on work from animal models, the concept of rigidity was raised. With overfiring of the γ motor neuron, the spindle would be too taut and the Ia interneurons would be hyperexcitable. Efforts at identifying this with microneurography failed to confirm this hypothesis. Delwaide felt that spasticity resulted from a loss of descending, facilitatory, inhibitory influences that act on Ia interneuron inhibition. This loss would make it impossible for the inhibitory influence of the interneuron to shut off antagonist muscles, with resultant increased velocity-dependent resistance to movement mediated by the muscle spindle. The concept of a hyperexcitable motor neuronal pool has been recently raised. In essence these neurons would be hypervigilant and initiation of firing would occur with less excitation. This may result from a loss of tonic inhibition secondary to a loss of supraspinal influences. Some have expressed the belief that the ionic properties of the membrane itself are changed as well. Other theories that may explain spasticity include central collateral sprouting, presynaptic disinhibition, and denervation hypersensitivity. Neurotransmitters may also play some role in spasticity. Some suspects include serotonin and substance P. In animal literature, serotonin has been noted to prolong responses and facilitate extensor responses.

A number of options are available for the treatment of spasticity. Drugs with systemic effects are now used primarily in patients who are confined to a wheelchair or bed. These drugs are used to facilitate relaxation of muscles, allowing easier transfers from bed to chair and facilitating hygiene as well as alleviating painful flexor spasms; however, the effects may be of marginal benefit to some patients when one considers the rather high frequency of side effects. The drugs used are baclofen, diazepam, tizanidine, and dantrolene.

Injections of botulinum toxin into specific muscles can also be used in ambulatory patients to facilitate normal gait patterns while preserving spasticity in muscles that are necessary for walking. Injections into the gastrocnemius-soleus muscle can facilitate a conversion from toe walking to plantigrade foot placement. Botulinum toxin injections are useful when a dynamic spasticity is present but very little, if any, permanent contracture. If a fixed contracture has developed, it may be necessary to release the contracted tendons surgically. These procedures are most commonly done to release the Achilles, adductor, and hamstring tendons.Implantation of pumps for the continuous infusion of intrathecal baclofen for severe spasticity not amenable to targeted injections of botulinum toxin has shown promise in properly selected cases.

Physiotherapy for Spasticity Control


The first step in any program to manage spasticity is the reduction of noxious stimulation. Spasticity and muscle overactivity have been shown to be increased as a result of this input. Stimulation of the flexor reflex afferents may lead to an increase in pathologic activity. The term noxious stimulation encompasses a wide variety of conditions such as pressure ulcers, ingrown toenail, contracture, kinked catheter, urolithiasis, urinary tract infection, DVT, heterotopic ossification, fecal impaction, sepsis, and fracture. This is just a partial list. Addressing these conditions should almost always be the first approach in spasticity management.


Proper positioning is an extremely important component of spasticity management. Poor positioning can result in an increase in spasticity and in in decreased ROM, contractures, increased noxious stimulation, pain, and exacerbation of a vicious cycle that can lead to worsening spasticity. Postures that should be avoided include a scissoring posture (bilateral hip extension, adduction, internal rotation), windswept position (hip flexion, abduction, external rotation on one side and relative hip extension, adduction, and internal rotation on the other), and frog-leg position, which can exacerbate the problem. Positioning is also important in the wheelchair. Tone can be minimized by placing the patient with the hips and knees at 90 degrees and by maintaining good torso position.


As a result of the upper motor neuron syndrome, muscles can be shortened for several reasons. One, is the immobilization of paralyzed muscles in shortened positions. This resultant decrease in longitudal tension (muscle unloading) can predispose to contracture. Other factors include a reduction in protein synthesis in immobilized muscles, which promotes atrophy. Spasticity and muscle overactivity also play a part in muscle shortening. This can in turn result in an increase in spindle activity and sensitivity. Gracies et al. have discussed the need to promote the commencement of stretch early in the treatment of any neurologic condition. Stretch has the advantage of being a focal treatment that can combat the development of the previously mentioned muscle shortening and increase in spindle sensitivity. Schmidt et al. have demonstrated the benefit of a relatively brief stretch in the management of spasticity . However, the benefit is very short lived, as the tone returns after a single contraction. Therefore, stretch needs to be applied for a longer period of time to have potential functional benefit. A study involving the use of a Lycra garment that provided a stretch of 3 hours demonstrated both an improvement in spasticity and good patient tolerance. Stretch has been shown to be useful in volitional movement in both agonist and antagonist muscles. Chronic stretch via casting or splints changes reflexive activity and reduces the stretch reflex. In summary, stretching activities have the advantage of being a local treatment, with limited risk that has demonstrated proven effect in the management of spasticity.


Cooling of muscles is beneficial in the management of spasticity. It both inhibits the monosynaptic stretch reflexes and lowers receptor sensitivity after it is removed. Cooling can be used in different ways. The quick icing technique, with ice applied with a light striking movement, results in facilitation of α and γ motor neurons and is used to facilitate antagonist function, whereas prolonged cooling can result in decreased conduction velocity and a reduction in the maximal motor CMAP.
Heat is another modality that can be applied in various forms. Ultrasound, paraffin, fluidotherapy, superficial heat, and whirlpool are some of the most common ways heat is applied. Heat's effect is short lived, and, like cold, its application should be followed immediately by stretching and exercise. The effects of heat on spasticity have been studied in only a limited way. Its major effect seems to be related to an increase in elasticity that may assist in stretching activities. Deeper heating modalities have also been used in the management of spasticity.


Electrical stimulation is another modality that can help spasticity management. Transcutaneous electrical nerve stimulation (TENS) units have been shown to be useful in the management of pain. Through its nociceptive action and resultant reduction in pain it was felt that it could reduce spasticity. Specifically, by reducing the flexor reflex afferents that are facilitated by nociceptive stimulation, Bajd et al. demonstrated a reduction in SCI-related spasticity in three of six patients in a dermatomal pattern, while a group applying TENS in an acupuncture method demonstrated a substantial reduction in spasticity that was partially reversed by co-administration of naloxone. Other potential mechanisms of action for spasticity reduction include inhibition or fatiguing of spastic muscles and possible activation of antagonist muscles through the Ia interneurons.

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Jan 11, 2019
Hypertonicity/ Spacticity
by: Senior Physiotherapist

Do not prefer quick Ice and muscle stimulation (Galvanic) for hypertonic muscles. Pain can be reduced even by simply sleeping.

Aug 24, 2016
Tens with hyperreflexia is awful
by: Anonymous

when you have severe hyperreflexia the tens unit causes severely fatiguing muscle jerks/movements and increases pain. Seems like this should be obvious to most doctors but so many seem to push use of Tens units without understanding how miserable it can make patients with hyperreflexia.

May 23, 2016
Tens unit for Hyperreflexia
by: Donna whites

The tens unit does not work for Hyperreflexia at all. It makes it so much worse I cried for six weeks because I was following dr orders. Q

Mar 10, 2015
physio treatment
by: rakesh kumar yadav

iam very happy as physiotherapist because we can easily update our knowledgw.

Feb 24, 2013
Great job
by: Mellyanna

This information is very helpful and also simple enough to understand.
As a student studying physiotherapy,its real tough but such information help alot.

Apr 09, 2012
good job
by: zara

its really very good information.. as i am becoming physiotherapist so its really good for me..keep it up

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