Spasticity is an increased resistance to the passive movement of a joint due to abnormally high muscle tone (hypertonus) which varies with the amplitude and speed of displacement of a joint (cf. rigidity). The excessive resistance evident at the extremes of joint displacement may suddenly give way, a phenomenon known as clasp-knife (or, confusingly, clasp-knife rigidity). Spasticity may vary in degree from mild, (e.g., a spastic catch on supination/pronation of the forearm), to extreme (e.g., immobile limbs in fixed flexion with secondary contractures and painful spasms: paraplegia in flexion). Spasticity may need to be differentiated clinically from rigidity and stiffness.
The amount and pattern of spasticity depends on the location of the lesion and tends to be greater with spinal cord than cortical lesions. Scales to quantitate spasticity are available (Ashworth, modified Ashworth, Wartenberg pendulum test) but have shortcomings. Spasticity may also vary in distribution: for lesions above the spinal cord it typically affects the arm flexors and the leg extensors to a greater extent (hemiparetic posture).
Spasticity is a clinical feature of the upper motor neurone syndrome, and may be accompanied by both positive (clonus, hyperreflexia, Babinski’s sign, flexor or extensor spasms) and negative phenomena (weakness in a pyramidal distribution, motor underactivity): the latter may be more significant determinants of disability. Slow, labored speech, with slow voluntary tongue movements, may be referred to as spastic dysarthria, which may occur in the context of a pseudobulbar palsy.
The pathogenesis of spasticity has traditionally been ascribed to damage to the corticospinal and/or corticobulbar pathways at any level from cerebral cortex to spinal cord. However, various lines of evidence (e.g., the failure of pyramidotomy to produce spasticity in animals, rare human cases of isolated pyramid infarction causing hyperreflexia and weakness without spasticity) has led to the implication of other motor tracts in the genesis of spasticity, viz.:
- The dorsal reticulospinal tract, which lies in the lateral funiculus of the spinal cord and hence is often damaged concurrently with the adjacent lateral corticospinal tract (e.g., in MS, which seems to have a predilection for the lateral funiculus); this descending path- way has an inhibitory effect on stretch reflexes which is under cor- tical control;
- The medial reticulospinal tract and vestibulospinal tracts which are not under cortical control and whose excitatory effects on extensor tone may remain unopposed.
Physiologically, spasticity has been characterized as an exaggeration of the muscle stretch reflexes, with reduced threshold (hyperexcitable α-motor neurones) and abnormal reflex transmission (increased gain). The role of neurotransmitters (glutamate, glycine, catecholamines, serotonin) in the pathogenesis of spasticity is unclear, but the efficacy of baclofen (a GABAB agonist) and benzodiazepines
suggest impaired GABAergic transmission may contribute, perhaps
through a loss of presynaptic inhibition mediated by interneurones or the inhibition of glutamate release.
Treatment of severe spasticity, for example in multiple sclerosis, often requires a multidisciplinary approach. Urinary infection, constipation, skin ulceration and pain can all exacerbate spasticity, as may inappropriate posture; appropriate management of these features may ameliorate spasticity. Drugs which may be useful include baclofen, dantrolene (a blocker of muscle excitation-contraction coupling), and tizanidine (α2
adrenoreceptor agonist). Intrathecal baclofen given via a pump may also
be of benefit in selected cases, and for focal spasticity injections of botulinum toxin may be appropriate. For painful immobile spastic legs with reflex spasms and double incontinence, irreversible nerve injury with intrathecal phenol or alcohol may be advocated to relieve symptoms. The place of cannabinoids has yet to be fully determined.
Shakespeare DT, Boggild M, Young C. Anti-spasticity agents for multiple sclerosis. Cochrane Database of Systematic Reviews 2003; 4: CD001332 Sheean G. Neurophysiology of spasticity. In: Barnes MP, Johnson GR (eds.). Upper motor neurone syndrome and spasticity. Clinical manage-ment and neurophysiology. Cambridge: CUP, 2001: 12-78