1 4 . H O W T O U S E T H E W I R E L E S S P R O F E S S I O N A L O N S P E C I F I C
I N D I C AT I O N S
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WIRELESS PROFESSIONAL
14.11.2 Spasticity
reminder
Spasticity or spastic hypertonia is a term which describes the condition of paretic or paralysed muscles
showing different symptoms to varying degrees, including in particular, an increase in muscle tonus mainly
in the antigravity muscles, hyperreflexia, and clonus.
During passive stretching of a spastic muscle, there is resistance at the beginning of the movement, which
then diminishes in the course of extension.
The more rapid the passive stretching movement, the stronger this resistance.
If passive stretching is very rapid and is maintained, clonus may occur, i.e. a contractile oscillation of 5 to 7
Hz, which persists for 40 to 60 cycles for as long as the stretching is maintained.
Spasticity is caused by a lesion in the central nervous system which affects the tractus pyramidalis
(cerebral-spinal tract).
This interruption in central control releases the activity of the myotatic stretch reflex, which becomes
hyperactive. As this stretch reflex is responsible for muscular tonus, hypertonia develops affecting mainly
the antigravity muscles (extensions of the lower limbs and flexors of the upper limbs), since these contain
more neuromuscular spindles than their antagonist muscles.
In time, spasticity leads to the shortening of muscle-tendon structures and a reduction in the range of
articular movement, which can lead to stiffening and misalignment of the joints.
Use of neuromuscular electrical stimulation (NMES)
Starting in the neuromuscular bundles are afferent proprioceptive nerve fibres, which are directly
associated with the α motor neurons of the same muscle and which are indirectly associated (via
interneurons) with the α motor neurons of the antagonist muscle.
Stretching a muscle therefore stimulates the afferent proprioceptive nerve fibres of the neuromuscular
bundles and they monosynaptically activate the α motor neurons of the muscle being stretched (myotatic
stretch reflex) and inhibit, via an interneuron, the α motor neurons of the antagonist muscle (reciprocal
inhibition reflex).
NMES of a muscle excites not only the α motor neurons of that muscle but also, and even more readily,
the afferent proprioceptive nerve fibres which are contained in the neuromuscular bundle of the muscle
and which have a lower stimulation threshold.
Stimulating these activates the α motor neurons of this muscle and also inhibits the α motor neurons of
the antagonist muscle (reciprocal inhibition reflex). It is this last action that NMES uses in the treatment of
spasticity: NMES of a muscle antagonist to a spastic muscle makes it possible to reduce the spasticity by
inhibiting the α motor neurons of the spastic muscle via the reciprocal inhibition reflex.
This phenomenon of inhibiting α motor neurons through NMES of the antagonist muscle is clearly
demonstrated by electromyography.