Abstract
Prom these varied observations on pain, spontaneous and induced,
it is obvious that neither motor activity nor irritation by acid can
be the sole cause of the pain of peptic ulcer. It is true that
spasms of pain were observed which coincided with peristaltic waves
of the duodenum in a patient with a duodenal ulcer deformity. It
is also true that another patient was free of pain \?hen motility was
reduced to a minimum and at a time v/hen the acid level remained high.
On the other hand some patients had pain which was quite unrelated to
motility. This pain would stop for 10 minutes or more and then
resume while contractions continued uninterrupted. Even duodenal
spasm could occur in patients with duodenal ulceration without caus¬
ing pain. It could hardly be argued that the ulcer was insensitive
since a matter of a few minutes before or after the patient was in
pain. During one episode of duodenal spasm a patient had pain for
a minute but the pain then disappeared while the spasm continued for
another few minutes
It has been suggested that acid causes pain by causing spasm
(Hurst, I9H5 Kinsella, 19^4-8) but 35% of f*18 injections of 0.5% HC1
failed to produce any increase in tone or movement and the majority
of these injections were followed by pain. The converse of this
argument - that alkaline powders act by relaxing tone - is difficult
to /
20.
to sustain since 50>o of 18 injections of sodium "bicarbonate were
followed "by increased tone or movement, usually with relief of pain.
In one case the injection was followed' by duodenal spasm, relief of
pain and spasm coinciding.
The case for the acid theory of pain is not much better.
Certainly in some of the experiments there was a relationship between
increasing acid concentration and the onset of pain and also between
decreasing acidity and relief of pain. Other experiments, however,
showed no such relationship. Pain often disappeared when the acid¬
ity remained constant or even increased. Indeed pain was sometimes
intermittent when no change could be detected in either acidity or
motility. Relief of pain with sodium bicarbonate was usually poss¬
ible but there was sometimes a delay of 30 minutes before relief was
obtained. Palmer also encountered long delays between the giving
of alkali and the relief of pain. He found similar delay between
the injection of acid and the onset of pain. If one has to allow
for such long latent periods it makes interpretation of spontaneous
pain rather difficult because the acid level in the stomach is con¬
stantly varying. Pickering took samples of gastric juice half hourly
hut during this period there could have been considerable variations
in acidity. Dne has seen the acid concentration rise from 2.3 mg.
HCl/ml. of gastric juice to 3.35 nig. and fall again to 2 mg0 within
the space of half an hour. The pain sensitivity of the ulcer may
not be sufficiently great to follow such changes quickly. If pain
takes some time to develop and reach its acme it is difficult to
explain why it may disappear for a short time and then return while
the acidity remains constant. Pain can occur in the absence of
free acid as was shown in one case when there were several spasms of
pain during a spell of achlorhydria lasting 38 minutes.
Motility and acid may each cause pain but they obviously do nob
account for all the facts. It is possible that Kinsella may be
right in ascribing the intermittency of the pain to alterations in
"blood flow through an ulcer area which is sensitive "because of in¬
flammation and oedema. Much, however, remains to be done to prove
this theory
