Lower Limb Spasticity: 5 Things Physiotherapists Should Know

Lower limb spasticity is one of the most common reasons a patient struggles to stand, walk and transfer after a stroke or spinal cord injury. It is also one of the most misunderstood findings in neurological rehabilitation. The resistance you feel when you move a leg passively is not automatically spasticity. Yet the label you choose decides what you treat.

This guide covers five things every physiotherapist should know about lower limb spasticity, also called lower extremity spasticity. You will learn what makes it spasticity, which muscles are usually involved, and when it helps or hurts. You will also see what it is often confused with, and why it develops.

1. Spasticity depends on the speed of the stretch

The most widely cited definition comes from Lance [1]. Spasticity is “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (‘muscle tone’) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.”

The key word is velocity. Move the knee slowly and you meet little resistance. Move it quickly and you feel a sudden catch. That catch is most likely the stretch reflex at work. A consensus statement on hypertonia describes the same feature: in spasticity, resistance grows with the speed of the stretch, or rises sharply above a threshold speed or joint angle [2].

In practice, the resistance in a spastic leg rarely comes from the reflex alone. Trompetto and colleagues divide hypertonia after an upper motor neuron lesion into two components [3]. The first is a neural component mediated by the stretch reflex, which is spasticity in the strict sense. The second is a non-neural component caused by changes in muscle and soft tissue, often called intrinsic hypertonia. The Modified Ashworth Scale cannot tell these two apart. The Tardieu Scale does better, because it compares stretches at different speeds [4].

We walk through the full exam in Spasticity Assessment: A Step-by-Step Clinical Exam.

2. Four muscle groups shape most lower limb spasticity patterns

After stroke, the most common lower limb pattern combines hip adduction, knee extension and an equinovarus foot [5]. Thibaut and colleagues list the muscles behind each part of this pattern and the problems each one causes. Four groups deserve your attention first.

• Hip adductors (adductor longus, brevis and magnus, gracilis, pectineus). Scissoring thighs interfere with perineal care, sitting, transfers, standing and walking [5]. A narrow base of support also makes standing balance harder, especially in older patients.
• Quadriceps (rectus femoris and the vasti). The knee stays stiff and extended through the gait cycle. The leg becomes functionally longer, so the toes drag and the risk of tripping rises [5].
• Hamstrings. The knee stays flexed. The patient walks in a crouched gait with compensatory knee flexion, which tires them quickly [5].
• Calf muscles and tibialis posterior. Gastrocnemius, soleus and tibialis posterior pull the foot into equinovarus, and tibialis anterior and the long toe muscles can add to it. The foot is hard to clear and the limb is hard to advance in swing [5].

Look at the whole limb, not one muscle. A plantarflexed, inverted foot changes what the knee and hip do in stance. In the same way, a stiff knee changes how the foot meets the ground.

3. Lower limb spasticity can help, and it can hurt

Spasticity is not always the enemy. Sepúlveda and colleagues point out that it is not always harmful and does not always need treatment [6]. Some of its effects can even help, for example during the support phase in walking rehabilitation. In the clinic, extensor tone in the stance leg sometimes lets a patient with weak extensors stand, pivot and transfer. If you reduce that tone without a plan for active control, the patient may lose the support that held them up.

The costs are just as real. In a cohort of 103 patients after stroke, those with spasticity had more pain and more nursing home placements [7]. They also had lower Barthel Index and quality of life scores than patients with normal tone. Exaggerated responses to skin stimuli can cause painful spasms that interfere with positioning and transfers [8]. These spasms also disturb sleep. Adductor and plantarflexor patterns make hygiene, dressing, seating and walking harder as well [5].

The goal of treating lower limb spasticity follows from this balance. Reduce the effects that limit the patient or cause pain, and keep the ones that help.

4. What lower limb spasticity is not

Several problems feel like spasticity at first touch. Telling them apart matters, because each one needs a different treatment.

Contracture

Contracture is a non-neural problem. Shortened muscle and connective tissue resist stretch at any speed. Contracture develops when a weak limb stays in a shortened position. Gracies names relative immobilization of the paretic limb as a cause of adaptive muscle shortening and joint contracture [9].

Contracture is not only a late complication. In animal studies, these muscle changes appear very early during immobilization [3]. Malhotra and colleagues followed stroke patients with no arm function [10]. They found changes associated with wrist contracture at every assessment, starting a few weeks after the stroke.

Contracture and spasticity also interact. O’Dwyer and colleagues studied the elbow in 24 patients after stroke [11]. Increased resistance to passive stretch went with contracture, not with reflex hyperexcitability. Increased tonic stretch reflexes appeared only in some patients with contracture. The authors suggested that contracture may potentiate spasticity, rather than the other way round.

Clonus

Clonus is a series of involuntary, rhythmic contractions and relaxations. It comes from self re-excitation of a hyperactive stretch reflex [5]. Clonus belongs to the same upper motor neuron syndrome and shares its reflex mechanism, but it is a separate sign. You test it with a sustained stretch, most often at the ankle. Record it separately from the resistance you feel. We cover the test in Ankle Clonus: Causes, Testing and What It Means.

Rigidity

Rigidity is typical of basal ganglia disorders rather than of an upper motor neuron lesion. A consensus definition lists its features [2]. Resistance is present even at very low speeds and does not depend on speed. There is no speed or angle threshold. Co-contraction of agonists and antagonists gives immediate resistance when you reverse the direction of movement.

5. Why lower limb spasticity develops after stroke or spinal cord injury

A lesion of the upper motor neuron pathways upsets the balance between inhibitory and excitatory input to the spinal cord. The result is a disinhibited stretch reflex [3]. Three levels contribute: the brainstem, the spinal cord and the muscle.

Loss of descending control

After stroke, Li and Francisco argue that the reticulospinal system plays the central role [12]. Cortical and internal capsule lesions often damage two pathways at once: the corticospinal tract and the corticoreticular fibers. These fibers normally drive an inhibitory center in the medulla. Without that drive, the facilitatory medial reticulospinal tract is left unopposed, because it does not depend on cortical control.

The reticulospinal system supports posture against gravity. When it is unopposed, the balance shifts toward antigravity muscles: the flexors of the upper limb and the extensors of the lower limb [12]. This is why the typical pattern of lower limb spasticity after stroke is extension, not flexion.

Changes in the spinal cord

Normally, a voluntary command that activates a muscle also inhibits its antagonist. This is reciprocal inhibition. After an upper motor neuron lesion, its loss during voluntary movement produces co-contraction [3]. Trompetto and colleagues consider co-contraction probably the most disabling form of muscle overactivity, because it hampers force and movement. Sheean and McGuire also link spastic co-contraction to failed reciprocal inhibition during active movement [4].

Timing tells you something too. In the cohort of 103 patients mentioned above, 24.5% developed increased muscle tone within 2 weeks of stroke [7]. According to Trompetto and colleagues, this delay speaks against a simple release phenomenon [3]. It points to plastic changes in the spinal cord and brain instead. One example is a progressive loss of post-activation depression during immobilization.

Changes in the muscle

Finally, the muscle itself changes. Immobilization at short lengths reduces the number of sarcomeres in series. It also increases the share of connective tissue in the muscle. These changes raise resistance to stretch and make muscle spindles more sensitive [3]. Weakness, disuse and immobilization then feed each other. Gracies calls this the vicious cycle of paresis, disuse and paresis [9].

What this means for treatment

Lower limb spasticity is a mix of a hyperexcitable stretch reflex and changing muscle tissue. Both get worse when the leg stops moving. Trompetto and colleagues conclude that limb mobilization is essential to prevent and treat both spasticity and intrinsic hypertonia [3]. So treat what limits the patient, and protect the tone that helps them stand. Above all, keep the limb moving through active, task-based practice.