F- CLINICAL ASPECTS OF SPINAL CORD INJURIES
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antiperistaltic action by increasing the tone of the anal sphincter, relaxing the colon. The
contents move back into the colon and the desire to defaecate will disappear.
Hypothalamic influence on intestinal peristalsis and secretion has been reported by
Beattie (1932), Beattie & Sheehan (1934) and others. Haemorrhages and ulceration of the
gastrointestinal tract may occur as a result of acute lesions in the course of descending
autonomic tracts from the level of the anterior hypothalamus to the level of the cervical
cord.
The dominant nervous control of the gastrointestinal tract is divided into three
systems: (a) Sympathetic ganglia and chain, which receive their impulses from the spinal
segments Th5 to L2/3 via anterior roots. The thoracic and lumbar splanchnic nerves
connect with the coeliac, superior and inferior mesenteric plexuses and, arising from the
ganglia of these plexuses, postganglionic fibres travel with the blood vessels to the various
parts of the gastrointestinal tract, (b) The parasympathetic control which is provided
by the vagus for the stomach, the small intestines and the major part of the large intes
tines, while the sacral parasympathetic innervation, which originates in the sacral segments
82-4, innervates through the pelvic nerves the rectum and sigmoid colon. Parasympathetic
fibres, especially from the vagi, also join the plexuses mentioned above and pass through
them and end around ganglion cells in the mesenteric and submucosal plexuses of the
intestinal wall (Fulton, 1945). The usual antagonistic action between sympathetic and
parasympathetic innervation—the former reducing peristalsis and digestion, the latter
increasing peristalsis and stimulating the production of digestive juices—may change into
synergistic action in the control of gastrointestinal function, especially in conducting
afferent impulses to the spinal cord, (c) Intramural autonomous innervation of the intesti
nal wall by the Meissner's and Anerbach's plexuses.
Changes in the peristaltic passage of food from the upper to the lower intestinal
tract, its storage and solidification in the descending colon and sigmoid and finally
intermittent defaecation from the sigmoid colon through rectum and anal canal are the
inevitable results of complete as well as incomplete lesions of the spinal cord or conus-
cauda equina. Since Lister (1858) demonstrated the inhibitory action of the sympathetic
system on peristalsis in the rabbit, the physiology and pathophysiology of the various
components of the intestinal tract have been the subject of intensive research (Masius,
1868; Gowers, 1877; Bayliss & Starling, 1900; Head & Riddoch, 1917; Hurst, 1921;
Learmouth & Rankin, 1930; Denny-Brown & Robertson, 1935; Heslop, 1938; Sheehan,
1940; Munro, 1953; Floyd & Walls, 1953; Dagradi, 1953; Guttmann, 1959; Connell,
1962; Connell, Frankel & Guttmann, 1963; Melzak & Porter, 1964; Paeslack, 1965,
1967; Frankel, 1967; and others).
Studies in man have been concerned mainly with the rectal and colonic response to
distension, since Masius (1968) and Gowers (1877) recorded reflex activity of the
sphincter ani in response to rectal distension (Nathan & Smith, 1953).
My colleagues Melzak & Porter (1964) in their electromyographic studies on the
external anal sphincter in 42 paraplegics and tetraplegics of Stoke Mandeville, found that
with each increase of intrarectal volume the external sphincter at first responds by
contracting. The rectal wall relaxes to accommodate the increased volume, but as soon as
the rectal wall contracts the external anal sphincter relaxes until defaecation is complete.
