David A Gelber

Springfield Clinic Neuroscience Institute, Springfield, IL, USA

Spasticity is commonly defined as excessive motor activity characterized by a velocity-dependent increase in tonic stretch reflexes. It is often associated with exaggerated tendon jerks, and is often accompanied by abnormal cutaneous and autonomic reflexes, muscle weakness, lack of dexterity, fatigability, and co-contraction of agonist and antagonist muscles (Young, 1987; Young, 2002; Sanger et al., 2003). It is a common complication of central nervous system disorders, including stroke, traumatic brain injury, cerebral palsy, multiple sclerosis, anoxic brain injury, spinal cord injury, primary lateral sclerosis, and hereditary spastic paraparesis (Young, 2002).

In many individuals, the presence of spasticity has negative consequences, interfering with mobility and activities of daily living. Disability may result from spasticity-related impairment of posture, abnormal quality of movement, painful spasms, and poor hygiene. In these patients treatment of spasticity is often considered. This chapter will review the patho-physiology of spasticity, outline the rationale for treatment and the development of treatment goals. In addition, pharmacologic and surgical management strategies will be discussed.

17.1 Physiology

Muscle tone, defined as the resistance to externally imposed muscle movement, is modulated by central nervous system influences on the alpha motor neuron in the spinal cord (Rossi, 1994). The pathways that regulate tone are similar to those that regulate voluntary and involuntary motor movements and, as a final common pathway, involve the spinal reflex arc. Alpha motor neurons that innervate muscle fibers are located in the ventral horns of the spinal cord, and comprise the efferent limb of this reflex arc. Afferent sensory impulses from muscle spindles are relayed to the spinal cord via Ia fibers. Some of these fibers synapse directly on alpha motor neurons that innervate agonist muscles. This is a monosynaptic reflex pathway and allows for sensory feedback necessary for motor movements. Collateral fibers from the Ia afferents also synapse on inhibitory interneurons in the dorsal horn, which in turn synapse on alpha motor neurons of antagonist muscles to inhibit their contraction; this is a polysynaptic reflex (Rossi, 1994). These pathways allow for coordinated action of agonist and antagonist muscles necessary for fine and gross motor movements.

There are several descending central nervous system pathways that synapse directly or indirectly (via internuncial pathways) on motor neurons and allow for suprasegmental control of movement (Volume II, Chapter 2). The corticospinal tract synapses directly on motor neurons and is responsible for voluntary control of the extremities, as well as inhibition of anti-gravity muscles of the trunk and limbs (Rossi, 1994). The reticulospinal tract has two components that influence motor movement. The pontine reticu-lospinal tract is excitatory to alpha motor neurons, while the medullary reticulospinal tract is inhibitory. The vestibulospinal tract is excitatory to the motor neurons of antigravity muscles (Merritt, 1981).

Upper motor neuron lesions result in spasticity from a number of mechanisms. Collateral branches from these descending motor pathways excite inhibitory presynaptic interneurons. With an upper motor neuron lesion this excitation is removed leading to decreased "presynaptic inhibition" of the motor neuron pool and overactivity of the spinal reflex pathways (Young, 2002).

Ia inhibitory interneurons to antagonist muscles are also activated by descending motor pathways (reciprocal inhibition) (Young, 2002). Removal of this excitation by an upper motor neuron insult leads to overactivity of antagonist muscle motor neurons, resulting in co-contraction of agonist-antagonist muscles commonly seen in association with spasticity.

Alpha motor neurons send collateral axons to internuncial Renshaw cells that normally act to inhibit the motor neuron pool (feedback or recurrent inhibition). Descending motor pathways typically activate Renshaw cells; supraspinal lesions often result in decreased recurrent inhibition with subsequent overactivity of spinal reflex pathways (Katz and Pierrot-Deseilligny, 1982).

In summary, lesions of the brain and spinal cord that interfere with the descending motor pathways often result in spasticity. Removal, in particular, of these descending inhibitory influences leads to an overactivity of the spinal reflex arc resulting in an increase in muscle tone, hyperreflexia, extensor plantar response (Babinski sign), flexor spasms, clonus, and co-contraction of agonist and antagonist muscles. Lesions that specifically involve the corti-cospinal tract may also cause concurrent motor weakness and decreased dexterity (Rossi, 1994).

17.2 Pharmacology

A number of neurotransmitters are involved in the sensory and motor pathways that regulate muscle tone. Acetylcholine is released by motor neuron axons that terminate on Renshaw interneurons (Young, 2002). Glutamate, an excitatory neurotrans-mitter, is released by the descending corticospinal tract and by primary spinal cord Ia afferent fibers (Davidoff, 1985). Gamma aminobutyric acid (GABA), the predominant inhibitory neurotransmitter in the spinal cord, is contained in interneurons in the dorsal and intermediate grey matter of the spinal cord and acts to mediate presynaptic inhibition of primary Ia afferent inputs on motor neurons (Young and Delwaide, 1981). Presynaptic inhibition acts to suppress sensory signals from skin and muscle receptors and to decrease the amount of glutamate released by the primary afferent fibers (Davidoff, 1985). Glycine interneurons (Renshaw cells) are also inhibitory, and mediate postsynaptic recurrent inhibition of alpha motor neurons and reciprocal Ia fiber inhibition, discussed above (Davidoff, 1985).

Substance P is released by small, predominantly unmyelinated sensory afferent fibers that mediate pain, and enhances the postsynaptic effect of glutamate (Young, 2002). Nociceptive stimuli can result in an increase in flexor reflexes causing painful flexor spasms that often accompany spasticity (Rossi, 1994). Enkephalins, which modulate pain, are located in the dorsal horn of the spinal cord and may also play a role in the pain-spasticity interaction (Young, 2002).

Descending pathways containing catecholamines and serotonin are also involved in the regulation of spinal cord reflexes. These pathways primarily affect the transmission of impulses from primary sensory afferent fibers and affect the excitability of interneurons (Merritt, 1981).

17.3 Clinical manifestations of spasticity

Spasticity is one of the components of the "upper motor neuron syndrome," which includes both positive and negative phenomena (Table 17.1). Injury to the corticospinal tract, which has facilatory influence on motor neurons in the spinal cord, causes the "negative" manifestations including muscle weakness, fatigability, and decreased dexterity (Rossi, 1994). These features are the major determinant of motor disability associated with upper motor neuron lesions. Conversely, injury to the reticulospinal or vestibulospinal tracts, which normally inhibit

Table 17.1. Positive and negative symptoms of spasticity.

Negative symptoms

Positive symptoms

Muscle weakness

Increased muscle tone


Co-contraction of agonist and

Decreased dexterity

antagonist muscles

Slowed initiation of

Flexor and extensor muscle spasms



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