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However, it must be admitted that the details of pain mechanism are still obscure,
as so many nervous pathways, relay stations and chemical transmitters are involved which
may act not only as mediator but also as modulator of nociceptive responses. Keele
(1957) believes that there are at least three chemical substances involved in the produc
tion of pain. There is also the problem of pain inhibition by centrifugal tracts or at
segmental level. The question of relationship of the unmyelinated *C' fibres to burning
pain and that of small myelinated delta fibres of the 'A' group to pricking (fast) pain is
still a matter of conjecture (Bishop, 1946; Landau & Bishop, 1958; Jones, 1956). The
same applies to the question where 'A' fibres and 'C' fibres synapse within the spinal
cord.
With regard to the problem of control of pain in the spinal man, it must be stressed
that, for a proper evaluation of these sensations, full consideration must be given to the
pre-paraplegic personality of the individual and his habitual pattern of reaction to painful
stimuli. It must be kept in mind that, while the threshold of pain perception is relatively
uniform in man, the expression of the individual's response to pain varies widely not only
from individual to individual in accordance with his whole psychological make-up, but
also in the same individual under different circumstances. Moreover, there are psycho
logical factors, which, on the one hand, lower the pain reaction threshold, such as
anxiety, apprehension, fatigue, fear and frustration, and on the other there are those
which raise the reaction threshold and act as pain depressors or inhibitors. Therefore,
it must be the task of everyone concerned with the management of pain in paraplegics,
be he physician or surgeon, to take all these factors into account and to mobilize, from
the beginning, those readjustment forces in the nervous system which promote the
development of the suppressor mechanisms to sensory irritation. I have found that, from
the early stages of clinical treatment, distraction of the patient's attention from his
affliction and diversion and mobilization of his concentration to regular work and early
pre-vocational training, as well as sport, is most helpful in the control of pain in para
plegics. In this connection, it is of utmost importance to be very circumspect in prescrib
ing heavy pain killers, in particular opiates, and sleeping drugs in the immediate and
early stages of paraplegia. Their action on the central nervous system, especially if
given routinely and prolonged, have very undesirable side effects.
From the beginning of our work on paraplegics, we have been extremely reluctant
and selective in the administration of barbiturates and, in particular, opiates, for the
control of pain in these patients and have discarded them very early, as these drugs no
doubt act adversely on the mobilization of the natural inhibitors to sensory irritation
and the concentration of the patient on his readjustment to his disability. I feel that the
thoughtless and indiscriminate prescription of heavy drugs, in which I also include
pethidine, valium and librium, has no more place in the management of these patients
than the hasty and early cordotomy or posterior rhizotomy, let alone sympathectomy.
In the very few instances of intractable, nociceptive border-zone reactions at and above
the level of complete spinal cord lesion, I have been satisfied with the intrathecal alcohol
block above the spinal cord lesion (the same could also apply to phenol), which is infinitely
less destructive than the operative procedures mentioned above.
