CHAPTER 31
CLINICAL MANAGEMENT OF SPASTICITY
The heightened reflex activity of the isolated cord, following transection or severe lesions
in continuity resulting in violent flexor or extensor spasms and rigidity of the muscular
system below the level of the lesion, represents one of the most incapacitating of compli
cations and is a formidable obstacle to the rehabilitation of paraplegics and tetraplegics.
However, with the advances made in a better understanding of the factors promoting
and, in particular, preventing excessive spasticity, and consequently the introduction of
selective modern techniques of treatment, this complication has lost much of its dread.
The management of spasticity consists of a combination of conservative and surgical
procedures according to type, severity and extent of the heightened reflex activity.
Nurses and physiotherapists have to play a most essential part in dealing with this
problem.
A. CONSERVATIVE TREATMENT
I. Elimination of factors lowering the threshold of spinal reflex activity
A number of intrinsic and extrinsic factors may act as nociceptive stimuli to the unres
trained activity of the isolated cord. Distension of any internal organ in the paralysed
area, particularly the bladder, is one of the most important violent initiators of reflex
spasms. It is obvious that the smaller the capacity of the bladder (as found in contracted
bladders following suprapubic cystostomy and prolonged indwelling catheter drainage)
the smaller the amount of urine necessary to elicit the reflex response of the skeletal
muscles and the more frequent the spasms. Of equal importance is distension of the
rectum and colon through stagnation of faeces. Indeed, the beneficial effect of the
evacuation of an overloaded rectum on the intensity of reflex spasms is often remarkable
as also is the prevention of stagnation of the faeces in the higher parts of the colon by
the administration of adequate laxatives. Furthermore, intervening infection—in parti
cular urinary flare-up or toxaemia from pressure sores and, last but by no means least,
anaemia—also lowers the threshold of reflex activity of the damaged spinal cord. Fre
quently, the increased spasticity of the paralysed limbs was found to be the first sign of
active urinary infection, long before the temperature rose and other symptoms appeared.
Moreover, the successful treatment of these infectious conditions has often resulted in a
decrease in the intensity of flexor spasms.
Another factor conducive to reflex spasms is the irritation of sensory organs in con
tracted tendons and joints. In non-paralysed persons, the irritation of these sensory
organs is appreciated as pain. In complete and also severe incomplete transverse lesion
of the spinal cord, sensation is lost in the paralysed area, but nevertheless the afferent
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