The pathophysiology of spasticity is poorly understood. The final common pathway underlying the mechanism is over-reactivity of the alpha motor neuron. Descending spinal pathways (corticospinal, reticulospinal, vestibulospinal) exert control over alpha motor neurons via monosynaptic and polysynaptic pathways. Complete destruction or partial interruptions of these descending pathways from cortical and brainstem structures can reduce the inhibitory tone on the spinal cord alpha motor neurons. This disinhibition can increase the resting tone of motor neurons. However, the most severe pathologic effect may be the excessive and exaggerated response to peripheral excitatory input.

The muscle spindle consists of several bundles of intrafusal muscle fibers surrounded by a connective tissue capsule. It represents the most complex sensory structure of the muscle and conveys information about muscle length. The central part of this specialized structure is composed of a noncontractile nuclear bag region. Spindles lie in parallel with extrafusal fibers, large muscle fibers that effect gross movement. Stretching the noncontractile bag region, or stretching the extrafusal fibers, constitutes the mechanical stimulus to fire the primary afferent or group Ia fiber. Group Ia afferents from the muscle spindle make synaptic contact with the cells of the dorsal nucleus of the spinal cord and with alpha motor neurons. Shortening of the extrafusal muscle fibers shortens the spindle and silences the Ia afferents. The intrafusal muscle fibers of the spindle complex are innervated by gamma motor neurons in the anterior horns of the spinal cord, which increase the tension of the intrafusal fiber when it is shortened. This resets the spindle after shortening, so that it is again sensitive to changes in muscle length.3

When the muscle is lengthened by tendon tap or stretch, Ia afferents produce excitatory postsynaptic potentials on agonist motoneurons. Although this monosynaptic connection plays a role in the reflex, most excitatory activity in the stretch reflex is mediated by oligosynaptic and polysynaptic pathways.2 Interneurons play a major role in the reflex arc. Antagonist muscle spindles also send Ia afferents to produce excitatory postsynaptic potentials on agonist inhibitory interneurons, which then evoke inhibitory postsynaptic potentials on motoneurons. The firing of the motoneuron depends on the summation of excitatory and inhibitory postsynaptic potentials. Additional inhibitory interneurons act on Ia afferents to inhibit the afferent signal presynaptically. Gamma-aminobutyric acid (GABA) is the neurotransmitter mediating this selective presynaptic inhibition.4

The spinal segmental reflexes require the participation of muscle spindles, fusimotor innervation (gamma motor neurons), Ia primary afferents, and alpha motor neurons, as well as Renshaw recurrent inhibition, disynaptic reciprocal inhibition, nonreciprocal autogenic Ib inhibition, presynaptic inhibition, and remote inhibition-excitation of alpha motor neurons.2 Spasticity results from prolonged disinhibition of components of this system, but the exact mechanism remains unclear.

Adapted from: Bassi V, Kita M, Feldman DS, and Devinsky O. Spasticity. In: Devinsky O and Westbrook LE, eds. Epilepsy and Developmental Disabilities. Boston: Butterworth-Heinemann; 2001;231–247.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.