Download Myth # 1: The definition of spasticity as presented by JW Lance (1980)

Challenging Longstanding Myths in Equinus
Deformity Management - Beverly Cusick, PT, MS, C/NDT, COF
Myth # 1: The definition of spasticity as presented by JW Lance (1980) has been
proven to be valid.
According to Lance (1980), spasticity is “a motor disorder characterized by a velocity-dependent increase in tonic
stretch reflexes (“muscle tone”) with exaggerated phasic reflexes, such as tendon jerks, resulting from
hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.” p. 485 One element in
this definition that compromises clarity is the parenthetical (“muscle tone”), which is actually defined as the degree of
muscle tension during rest or the degree of resistance to passive stretch at any velocity.1
A group of clinicians who called themselves SPASM spent three years investigating the literature on the issue of
spasticity and its assessment and management. In one of their publications led by Pandyan (2005), they suggest that
if Lance’s definition of spasticity is valid, then it should be possible to demonstrate the truth of the following four
resulting myths. I have contributed to the evidence that the four myths lack factual certainty:
1) The increased muscle activity seen on EMG during the imposed stretching phase results exclusively
from increased activity in the stretch reflex pathways - often described using the terms “hyperexcitable” or “exaggerated”.
o One of the main features of physiologic, nonreflexive soft tissue adaptation in calf muscle contracture is the
stiffening and proliferation of a connective tissue matrix throughout the perimysium and endomysium of the
shortened muscle. Peripheral nerves and blood vessels are contained within neurovascular tracts that are
connected to the periphery of muscles along most of their belly lengths. Each neurovascular tract has branches
through which the major blood vessels and the collagen fiber reinforced nerves enter the muscle at specific
locations. The intramuscular connective tissues are the intramuscular part of the neurovascular tract since they
also embed nerves as well as blood and lymph vessels (Yucesoy et al 2007).
Peripheral nerve entrapment and the formation of peripheral nerve cell adhesion molecules have been reported
in transformed muscle that is considered to be “spastic” (Barber et al 2011, Booth et al 2001, Butler DS et al 1991,
Castle et al 1979, Huijing 2007).
o Frascarelli et al (2005) performed nerve conduction and needle EMG tests in 29 patients with “spastic” CP and
severe limb deformities, 11 of whom showed abnormal nerve conduction in 32 of 400 sensory or motor nerves,
indicating one or more entrapment neuropathies. Severe joint contractures and deformities can cause nerve
damage, possibly as a result of the stretching, angulation, or compression mechanisms in the anatomic fibroosseous passages where nerves are particularly susceptible.
o Stecker et al (2011) state, “Clinically, the presence of spontaneous EMG activity is one of the factors used in
determining when there is a significant injury to a nerve.” p. 7 They add, “The presence of EMG activity mainly
occurred during stretch at the higher force levels and during recovery after a severe [nerve] stretch injury.” p. 8
2) The increased muscle activity during imposed stretching will contribute to an increase in resistance
to passive movement.
o Several studies indicate that it is not possible to support this statement with confidence. “Although one would
expect to be able to measure reliably the muscle activity contributions to stiffness from tonic stretch reflex
activity (this will probably involve long latency polysynaptic pathways), it is surprising to note that it has also
not been possible. The key confounding factors are likely to be inertial components from the limb segments,
changes in the visco-elastic properties of soft tissues and joints, abnormal voluntary muscle activity, abnormal
involuntary muscle activity resulting from phenomena other than stretch reflex hyperexcitability and the
patient’s cognitive and/or perceptuomotor abilities.... spasticity-related muscle activity may contribute to
increased joint stiffness. However, under routine clinical or research conditions, the exact relationship between
spasticity-related muscle activation and increased stiffness is yet to be modelled reliably.” p. 4-5
1
Source: Stedman's Medical Dictionary for the Health Professions and Nursing, 7th edition. 2012.
(c) 2014 Beverly Cusick, PT, MS, C/NDT, COF/BOC
3) Velocity dependent increase in the resistance to passive movement is exclusive to spasticity.
o Abundant evidence refutes this myth. The velocity-dependent change in stiffness is a characteristic response of
soft-tissue structures (e.g. muscles, tendons, ligaments, etc.) and their normal viscoelastic properties.
4) Spasticity is a pure ‘motor disorder’.
o Though spasticity is an abnormal motor phenomenon, current evidence indicates that it would be wrong to treat
it as a pure motor disorder. Stretch reflex activity is influenced by activity in cutaneous and proprioceptive
pathways – as is shown in the beneficial effects of electrical stimulation and lycra garments – and is modulated
by the higher centers in the nervous system. It is also possible that disordered feed-forward, corticospinal
modulation of reflex activity, under both active and passive conditions, may also contribute to spasticity.
At this time, it is clear that spasticity is not:
·
·
·
A movement disorder. It is hyperreflexia. The movement disorder is due to corticospinal dysfunction with
impaired reciprocal inhibition.
Distinctly evident in EMG activity observed during rapid passive elongation of resting muscles and soft tissues.
The source of soft-tissue stiffness – diminished extensibility due to physiologic transformation and peripheral
nerve adhesion following a history of tonic recruitment in shortened state.
References:
1. Barber L, Hastings-Ison T, Baker R, Barrett R, Lichtwark G. 2011. Medial gastrocnemius muscle volume and fascicle
length in children aged 2 to 5 years with cerebral palsy. Dev Med Child Neurol. 53(6):543-8.
2. Booth CM, Cortina-Borja MJ, Theologis TN. 2001. Collagen accumulation in muscles of children with CP and correlation
with severity of spasticity. Dev Med Child Neurol. 43(5): 314-320.
3. Butler DS, Jones MA. 1991. Mobilisation of the Nervous System. New York, NY: Churchill Livingstone.
4. Castle ME, Reyman TA, Schneider M. 1979. Pathology of spastic muscle in cerebral palsy. Clin Orthop Relat Res. 142:
223-232.
5. Frascarelli M, Frascarelli F, Gentile MG, et al. 2005. Entrapment neuropathy in patients with spastic cerebral palsy. Acta
Neurol Scand. 112(3): 178-182.
6. Huijing PA. 2007. Epimuscular myofascial force transmission between antagonistic and synergistic muscles can explain
movement limitation in spastic paresis. J Electromyogr Kinesiol. 17(6): 708-724. Review.
7. Lance JW. 1980a. Symposium synopsis. In Feldman RG, Young RR, Koella WP. ( Eds.) : Spasticity: Disordered Motor
Control,. p. 485-494. Chicago IL:: Year Book Medical Publisher.
8. Pandyan AD, Gregoric M, Barnes MP, et al. 2005. Spasticity: clinical perceptions, neurological realities and meaningful
measurement. Disabil Rehabil. 27(1-2):2-6.
9. Stecker MM, Baylor K, Wolfe J, Stevenson M. 2011. Acute nerve stretch and the compound motor action potential. J
Brachial Plex Peripher Nerve Inj. 6(1):4.
10. Yucesoy CA, Huijing PA. 2007. Substantial effects of epimuscular myofascial force transmission on muscular mechanics
have major implications on spastic muscle and remedial surgery. J Electromyogr Kinesiol. 17(6): 664-679. Review.
(c) 2014 Beverly Cusick, PT, MS, C/NDT, COF/BOC