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CHAPTER 26
adrenergic receptors have been demonstrated in the ureter (Boyarski
et at.,
1966, 1971;
Rosset
et
a/., 1967). The difficulty in assessing the action of motor nerve innervation of
the ureter lies in the well-known fact that the ureter, completely deprived of its nerve
supply, still contracts to stimulation. Bors & Comarr (1952,1971) mention amongst other
points, as indirect evidence of the nervous influences on ureteral motor activity, a different
incidence of reflux occurring in upper as compared with lower motor lesions of the spinal
cord. This is not in accordance with my own observations on the relationship between
ureteric reflux and level of cord lesions. However, there is also some disagreement regard
ing the sensory innervation of the ureter. Head (1893) mapped out cutaneous areas of
referred ureteric pain over the Li-L2 segments. According to Foerster (1936) the radi-
cular sensory innervation of the ureter includes T9-L2. White & Garrey (1942) have
shown that division of the posterior spinal roots Ti2-L2 abolished pain resulting from
distension of the renal pelvis.
CONGENITAL STRUCTURAL ANOMALIES
Before considering details of the vesical neuro-physiology and pathophysiology, certain
congenital structural anomalies may be mentioned briefly which may prevent,
a priori,
a co-ordinated reciprocal function of the vesical closing and emptying mechanisms.
They may involve the bladder itself and may lead to intravesical obstruction. The more
common are the congenital bladder diverticulum, the extrophy (i.e. eversion of the dorsal
bladder wall which may be associated with absence of the ventral bladder and lower
abdominal walls), reduplication of the bladder which may be complete or incomplete
or trigonal folds which may result in obstruction of the vesical outlet. On the other hand,
urethral anomalies such as congenital urethral stricture resulting in stenosis of the external
meatus, hypospadias or congenital diverticulum may be the primary cause of vesical
dysfunction. Of special interest are urechal cysts. They develop as a result of persistence
of the lumen of the allantoic stalk which may result in a small cavity with epithelial
lining becoming filled with fluid and developing later into a larger cyst surrounded by a
thick wall of connective tissue (Kuntz, 1965). There may be no connection of such a
cyst with the bladder or external opening at the umbilicus; on the other hand such a
persistent allantois lumen, called a patent urachus, may connect with the bladder and
develop into an umbilico-urinary fistula. Recently I saw a young man with a complete
traumatic tetraplegia below C5/6 and chronic urinary infection, who developed, at the
end of 1969, 3 years after his injury, a swelling and inflammation around the umbilicus
with high temperature. Aspiration of this swelling by the family doctor revealed a large
amount of pus from a infected urechal cyst beneath the umbilicus. Following opening
of the cavity there was a temporary urine discharge through the umbilicus indicating
connection of the urechal cyst with the bladder. A contrast filling of the cyst carried out
on 18 December 1969 through the sinus of the umbilicus showed a cavity lying anterior-
ally above the bladder. At that time, no communication with the bladder was found
(Fig. 1373), neither did a cystography of the bladder show any communication of the
