Focal Versus General Spasticity

In considering the management of spasticity and hence, as will be discussed, spasticity-associated pain, it is necessary to look at the clinical presentation of spasticity in terms of focal and general presentations.

Focal or regional spasticity typically results from cerebral origin.7 This refers to spasticity primarily affecting one limb, e.g. upper limb with the flexion/pronation/ adduction patterning described above or lower limb with the extension/adduction patterning. However, flexion spasticity of the hamstrings and sometimes the psoas

Table 33.2 Spinal versus cerebral origin spasticity.

Spinal origin spasticity Cerebral origin spasticity

Loss of supraspinal control of spinal pathways

Loss of interneuron inhibition from flexor reflex afferents

Loss of propriospinal inhibition

Loss of descending catecholamines and rubrospinal inhibition of interneurons Limb flexor and extensor spasms common Trunk extensor spasms

Marked increase in cutaneous mediated reflexes Abnormal spread and sensitivity of reflexes Polysynaptic pathways, relatively drug sensitive

Interruption to corticoreticular and corticovestibular pathways Loss of cortical inhibition to ipsilateral vestibulospinal and reticulospinal pathways Oligo- and monosynaptic connections from vestibular and reticular nuclei to a and g motor neurones Movement patterning common

Rigidity (velocity independent), as well as spasticity Spasms less common Relatively drug resistant may also occur. Clearly, upper and lower limb spasticity resulting from a cerebral lesion often occur together.

General spasticity typically results from spinal origin UMNS.10 It depends on the level of the spinal cord lesion. Lumbar and thoracic spasticity will affect both legs and possibly the trunk, depending on the level and nature of the lesion. The upper limbs are likely to be involved with cervical lesions.

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