Lower extremity spasticity is a motor disorder characterized by an involuntary increase in muscle tone. This condition differs from general muscle stiffness or rigidity because the increase in muscle resistance is dependent on the speed of movement (velocity-dependent response). When a clinician rapidly moves a spastic limb, the resistance felt is much greater than during a slow movement. Spasticity is the result of hyperexcitability of the stretch reflex, causing muscles to contract too strongly in response to being lengthened.
The Neurological Mechanism Behind Spasticity
Spasticity arises from damage to the Upper Motor Neurons (UMNs), which are nerve cells located in the brain and spinal cord responsible for controlling movement. These UMNs form descending pathways, such as the corticospinal tract, that travel down from the brain to the spinal cord, modulating local reflex circuits. A primary function of these pathways is to send inhibitory signals that dampen spinal reflexes.
When UMN damage occurs, this inhibitory control is disrupted, creating a state of disinhibition in the spinal cord. The spinal reflexes, which normally cause a muscle to contract when stretched, become hyperexcitable because descending inhibitory signals are no longer effectively regulating them. This imbalance favors excitation, meaning even a small stretch can trigger an exaggerated reflex response and uncontrolled muscle overactivity.
Primary Conditions Leading to Lower Extremity Spasticity
The UMN damage that causes spasticity can be triggered by a variety of neurological conditions impacting the brain or spinal cord. Stroke (Cerebrovascular Accident) is a common cause, where interrupted blood flow leads to the death of brain tissue, damaging the UMN pathways. Spasticity affects a significant percentage of stroke survivors within the first year.
Multiple Sclerosis (MS) is another frequent cause, as this autoimmune disease attacks the myelin sheath of nerve fibers in the central nervous system. This demyelination impairs the brain’s ability to communicate with the muscles. Spinal Cord Injury (SCI) directly disrupts the descending UMN pathways, leading to disinhibition of reflexes below the level of the lesion.
Cerebral Palsy (CP) is the most frequent cause of spasticity in children, resulting from damage to the developing brain before or shortly after birth. Traumatic Brain Injury (TBI) can also cause UMN damage through severe head trauma, physically disrupting the brain’s ability to send proper signals to the muscles.
Physical Manifestations and Functional Impact
Lower extremity spasticity presents with a range of observable signs that severely limit movement and function. Common presentations include increased muscle tone that makes passive joint movement difficult, involuntary muscle contractions (spasms), and ankle clonus. Ankle clonus is a rapid, rhythmic, and involuntary contraction and relaxation of the ankle muscles.
These signs translate into significant functional limitations, particularly impacting gait and mobility. Spasticity in the hip adductors and knee extensors can cause a “scissoring gait,” where the legs cross over each other during walking. Foot drop or equinovarus, where the ankle is pointed down and the foot turns inward, is frequently seen, limiting ambulation and increasing fall risk.
Sustained muscle contraction can lead to contractures, which are permanent shortenings of the muscle and soft tissues, resulting in fixed joint postures. This makes activities of daily living, such as dressing and bathing, much more challenging. The continuous muscle activity also leads to fatigue and discomfort, reducing quality of life.
Comprehensive Management Strategies
The management of lower extremity spasticity requires a tailored, multi-modal approach combining physical, pharmacological, and interventional strategies. Non-pharmacological treatments are foundational and typically begin with physical therapy focused on maintaining muscle and joint length. This includes prolonged stretching and regular range of motion exercises to prevent contractures.
Non-Pharmacological Treatments
- Occupational therapy helps individuals adapt to functional limitations.
- Bracing and orthotics support proper joint alignment and maintain limbs in a stretched position.
- Locomotor training with body-weight support may help reduce spasticity.
- Hydrotherapy can offer subjective relief.
Pharmacological interventions include oral medications that work systemically to reduce nerve excitability throughout the central nervous system. Baclofen, a GABA-B receptor agonist, and Tizanidine, an alpha-2 adrenergic agonist, are frequently prescribed to reduce muscle tone and dampen reflex activity. While effective, oral medications can cause side effects like drowsiness and generalized weakness, which can limit their use.
For spasticity localized to specific muscles, Botulinum toxin injections (Botox) are highly effective focal treatments. The toxin is injected directly into the overactive muscle, blocking the release of acetylcholine at the neuromuscular junction to cause temporary, targeted muscle weakening.
For severe, generalized spasticity that does not respond adequately to oral medications, advanced interventions may be necessary. The Intrathecal Baclofen (ITB) pump delivers baclofen directly into the spinal fluid via an implanted device, allowing for higher concentrations at the spinal cord with fewer systemic side effects. Selective Dorsal Rhizotomy (SDR) is a neurosurgical procedure primarily for severe leg spasticity, involving surgically cutting selected sensory nerve rootlets in the spinal cord to permanently reduce muscle stiffness.