Spasticity has been described as "a disorder of the sen-sorimotor system characterised by a velocity-dependent increase in muscle tone with exaggerated tendon jerks (deep tendon reflexes) resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome (UMNS).''2 The UMNS is the result of the changes to the normal functioning motor system following lesions to the CNS. These changes can be considered as both negative (i.e. things taken away from normal control) and positive (i.e. superimposed on normal motor control, not positive as "good"). The negative components include weakness, loss of dexterity, and fatigability. The positive components include velocity-dependent increase in tone and changes in deep tendon reflexes as described above. They also include changes in cutaneous-mediated reflexes (via disinhibition of flexor reflex afferents (FRA)), increased spread of cutaneous and deep tendon reflexes (via disinhibition of propriospinal pathways), abnormal reflexes (e.g. Babinski, Hoffmann), and flexor and extensor spasms.3 Many clinicians consider spasticity as not just the velocity-dependent increase in muscle tone, but the total picture of the positive component of the UMNS. These changes are summarized in Table 33.1.
It is also important to appreciate that in addition to the neurological changes there are also considerable muscle changes following lesions of the CNS. These changes include a relative increase in collagen compared to elastin, with an increase in tissue stiffness plus possible changes in muscle fiber type,4 contributing to the increase in stiffness.5
It is axiomatic that in spasticity there is hyperexcit-ability or disinhibition of the alpha motor neuron pool.6 The mechanism for this excitation is different for spasticity following lesions of the brain (cerebral origin spasticity) and for lesions of the spinal cord (spinal origin spasticity) (Table 33.2).
Cerebral origin spasticity has a rapid build up of reflex activity consistent with loss of inhibition of mono-and oligosynaptic pathways between brain stem nuclei, in particular rubro- and vestibulospinal pathways7 and the alpha motor neuron pool. Cerebral origin spasticity also
Table 33.1 Components of the upper motor neuron syndrome.
Spontaneous spasms Increased sensitivity to cutaneous mediated reflexes Increased sensitivity and spread of deep tendon reflexes Abnormal reflexes, e.g. pantar, adductor, etc. Increased tone velocity independent, i.e. spastic dystonia, as well as velocity dependent, i.e."spasticity"
Loss of dexterity beyond the degree of weakness Fatigability
Poor isolated movements differs from spinal origin spasticity in the expression of hemiplegic, or in the case of bilateral brain damage, double hemiplegic posturing with the typical features of shoulder adduction, elbow, wrist, and finger flexion and forearm pronation (flexor posturing), and hip adduction, knee extension, and ankle and foot plantar flexion (extensor posturing).
Spinal origin spasticity, on the other hand, has a relatively slow rise in reflex activity which is consistent with disinhibition of polysynaptic pathways between the dorsal column and the alpha motor neuron pool.3, 7, 8 This occurs particularly in Rexed laminae III and IV, where the FRA and C- and A8-fibers have their primary synapses. Spinal origin spasticity is also marked by disinhibition of propriospinal pathways resulting in longitudinal spread of reflexes. Consequently, a muscle response may occur many segments from the muscle stimulus. Unlike cerebral origin spasticity, flexor pattern spasticity and spasms tend to dominate the presentation, although, especially in severe spasticity, extensor patterning particularly of the trunk and lower limbs may dominate the clinical picture. Spasms are much more common in spinal origin spasticity9 than cerebral due to disinhibition of FRA.
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