Spasticity and Paralytic Disorders

Spasticity and Paralytic Disorders

R. David Warren

Spasticity was defined by Lance as a motion 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 (1). This chapter attempts to give some insight into the causes of spasticity. Even though spasticity affects the upper extremities as well as the lower extremities, the focus is on how it affects the lower extremity with regard to diagnosis, and rationale for establishing a treatment plan, either conservative (therapy, pharmacologic) or surgical.

In reality, spasticity is difficult to define comprehensively presumably because the neurobiology remains largely a mystery (2). In fact, Young (2) states that although spasticity is difficult to define, neurologists recognize spasticity when they see it—at least they think they do. Spasticity as a term is widely used by clinicians to describe abnormalities in patients with lesions of the central nervous system, but the signs and symptoms found in this group vary widely from patient to patient as does the response to any given therapy (3). What is frequently forgotten is that spasticity is but one component of the upper motor neuron syndrome and many confuse the other findings of upper motor neuron syndrome and use them interchangeably with spasticity (4).

Upper motor neuron syndrome is characterized by impaired motor control, muscle paresis, and muscle spasticity. This net imbalance of muscle forces across joints can lead to both dynamic and static joint deformities (5). Some authors believe spasticity is such a strongly integrated part of upper motor neuron syndrome that it cannot be separated from the other components (6).

Upper motor neuron syndrome is the result of damage to the descending motor pathways at the cortical, brainstem, or spinal cord level (7). Some of the more common causes are stroke, cerebral palsy, spinal cord injury, multiple sclerosis, and traumatic brain injury. This results in both positive and negative findings. The positive findings are athetosis, clonus, dystonia, primitive reflexes, rigidity, and spasticity (4). This is the result of the release of a more or less intact motor subsystem for precise rostral control (2). The negative findings are fatigue, impaired coordination, impaired motor control, impaired motor planning, and muscle weakness (4). This is thought to be a direct result of disconnecting lower motor centers from higher motor centers (2). It is difficult, if not inadequate, to discuss the single positive sign of spasticity in the absence of addressing its overlap of similarities with other findings of upper motor neuron syndrome (4).

To adequately discuss upper motor neuron syndrome, a consensus on terminology needs to be achieved. An interdisciplinary workshop sponsored by the National Institutes of Health in 2001 defined the terms spasticity, dystonia, and rigidity (8). Spasticity was defined as hypertonia with one or both of the following present:

  • Resistance to externally imposed movement that increases with increasing speed of stretch and varies with the direction of joint movement

  • Resistance to externally imposed movement increases above a threshold speed or joint angle (8)

Dystonia is defined as a movement disorder in which “involuntary sustained or intermittent muscle contractions cause twisting and repetitive movements, abnormal postures, or both” (8). And finally, rigidity is defined as hypertonia with all the following present:

  • Resistance to externally imposed joint movement is present at very low speeds of movement, does not depend on imposed speed, and does not exhibit a speed or angle threshold.

  • Simultaneous cocontraction of agonists and antagonists may occur and is reflected in an immediate resistance to a reversal of the direction of movement about a joint.

  • The limb does not tend to return to a particular fixed posture or extreme joint angle.

  • Voluntary activity in distant muscle groups does not lead to involuntary movements about the rigid joints, although the rigidity may worsen (8).

To confuse the picture, in clinical practice these terms are often used interchangeably.


This section gives a basic overview of the conditions or disease states that may have spasticity as a component in either the upper or lower extremity. It is not intended as an in-depth review of the condition or disease state, but rather these more commonly seen entities will be reviewed in relation to their propensity to produce spasticity in the lower extremity as a sequela. These include stroke (cerebrovascular accident), cerebral palsy, spinal cord injury, multiple sclerosis, and traumatic brain injury.


Stroke is defined as a neurologic deficit lasting more than 24 hours caused by reduced blood flow in a particular artery supplying the brain. It is characterized by a sudden onset of clinical signs related to the site in the brain where the morbid process occurs (28). The most common artery affected is the middle cerebral artery. This results in significant damage to the cerebral cortex. Damage to the pyramidal tract and its accompanying pyramidal (corticoreticulospinal) fibers gives rise to the upper motor neuron syndrome (29).

In the classic stroke involving the middle cerebral artery, the affected limbs are completely paralyzed, with loss of tendon reflexes (30). Initially, some 80% of stroke patients experience motor impairments of the contralateral limb(s) (29,31). The longer the limb remains flaccid, the poorer the prognosis for recovery (30). In most cases, the first changes noted in the flaccid limb are hyperactive tendon reflexes and increased resistance to passive movement, that is, spasticity. Spasticity is most pronounced distally but progresses to involve all muscles and, in the case of the lower extremity, most prominently the extensors and adductors (30). Spasticity after a stroke has been shown to peak at 1 to 3 months, with some patients who were not initially spastic now spastic and some who were initially spastic now with normal muscle tone (32). One study reported that 39% of patients with first ever stroke were spastic after 12 months (33). In general, neurologic return tends to be complete within 6 months of injury (30).

When movement begins to return, it does so with synergistic patterns. Return of voluntary lower extremity movement begins proximally with hip flexion and proceeds distally. Flexor synergies are the first to develop and are usually followed by, or overlap with, extension synergies. As voluntary movement increases, spasticity decreases in a proximal-to-distal distribution with increase of individual muscle group movement independent of synergistic patterns and gradual return of individual muscle speed, coordination, and endurance. While recovery proceeds in an orderly and sometimes overlapping manner, it may stop permanently at any stage (30).

Lower extremity spasticity following a stroke takes on certain patterns. The pelvis is elevated and the hip is extended, adducted, and internally rotated with the knee extended and the ankle in plantar flexion (30,33). If the patient has no functionally useful voluntary limb movement, spasticity can maintain an abnormal resting limb posture leading to contracture formation.


Cerebral palsy has been defined as a nonprogressive condition affecting those parts of the brain that control movements and postures. It is clear, therefore, that the term cerebral palsy does not refer to a single disease entity but rather represents a combination of motor disorders, sensory deficits, and mental impairment, varying from mild to severe, caused by injury to the central nervous system in the perinatal period (34).

The incidence of cerebral palsy is said to be 4.2 per 1,000 live-born infants according to the large collaborative perinatal study published in the United States in 1978 (35). The prevalence of moderately severe to severe cerebral palsy is from 1.5 to 2.5 per 1,000 live births (36). More than 100,000 Americans under the age of 18 years are estimated to have some degree of neurologic disability attributed to cerebral palsy (37). Contrary to initial expectations, with improvements in perinatal medicine including the use of fetal monitoring and cesarean section, the prevalence of cerebral palsy has not decreased (38). At present, there seems to be little we can do to reduce the prevalence cerebral palsy (39).

Cerebral palsy is classified based on topographical as well as neuromuscular deficit. The topographical breakdown is diplegia (30% to 40%), being the most common, with hemiplegia (20% to 30%) and quadriplegia (10% to 15%) comprising the bulk of the remainder. Monoplegia and triplegia are relatively uncommon (40). Neuromuscular deficit classification is comprised of spastic, dyskinetic (inclusive of choreoathetoid and dystonic), ataxic, hypotonic, and mixed. Spastic cerebral palsy is far and away the most common and accounts for 70% to 75% of all cases, with dyskinetic (10% to 15%) and ataxic (<5%) accounting for the remainder (40).

Jul 26, 2016 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Spasticity and Paralytic Disorders

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