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accepted this view with regard to the vasodilator effect and I came to the same conclusion
with regard to sudomotor inhibition. However, this concept is not in accordance with
Bayliss' views. This author, while confirming the vasodilator effect of posterior root
stimulation as found by Stricker (1876), denied the existence of true efferent fibres and
advanced the theory of 'antidromic' conduction through the posterior roots. Lewis
(1928)5 agreeing with Bayliss' theory, postulated that the antidromic conduction liberates
histamine (H-Substance) which is responsible for the vasodilator effect. In this connec
tion, it may be noted that in man there is always a long latent period following faradic
stimulation of the peripheral part of a divided posterior root, until vasodilatation appears
in the cutaneous distribution of that root, which is in contrast to the immediate effect
of faradic stimulation of anterior root fibres on the muscular system as well as sudomotor
function. If Lewis' concept of the release of the H-Substance evoked by antidromic
conduction is correct, this would also explain the inhibition of sweating, since Kara
(1932) described an inhibitory action of histamine on sweating. As far as the anatomical
proof of the existence of efferent inhibitory nerve fibres in the posterior root is concerned,
Ken Kure's and Gagel's conclusions were not accepted by other workers in this field
(Barron & Mathews, 1935; Hinsey, 1934; Okelberry, 1935; Sheehan, 1935; Story,
Corbin & Hinsey, 1936; Toennies, 1938), and from all evidence available so far no
definite conclusion can be drawn in this rather complex problem.
Effects of complete and incomplete transverse lesions of the spinal cord on
sudomotor function
Complete interruption of the sudomotor pathways between the hypothalamic region
and the sympathetic outflow abolishes the thermoregulatory function of the sweat glands,
resulting in anhidrosis. Since Riddoch's & Head and Riddoch's classical studies (1917)
during the First World War on soldiers with spinal cord transection, details of the
disturbances of sweating in complete and incomplete lesions of the spinal cord have been
repeatedly reported (Guttmann & List, 1928; Guttmann, 1931, 1953, I954> 1969;
Guttmann & Whitteridge, 1947; List & Peet, 1938-39).
The extent of thermoregulatory loss of sweat gland activity following complete lesion
depends on the level of the lesion and the time which has elapsed after injury. In the
early stage following cord transection, the sudomotor deficit is more extensive and
corresponds more closely to the level of sensory loss than in later stages, when the last
normal segment above the level of the transection through its anterior root connection
with its corresponding sympathetic ganglia has developed its maximal function overlap
ping into several dermatomes below the level of the sensory loss. In complete lesions of
the cervical cord, including C8 and Ti, the thermoregulatory sweat test shows anhidrosis
over the whole body, apart from a few pin-points of sweat over face and neck if some
sudomotor fibres of the cervico-thoracic junction have escaped damage. Such patients
cannot stand heat well and on increasing heat stimulation in the sweat cabinet feel
uncomfortable and soon mobilize auxiliary heat regulatory mechanisms, such as increased
rate of respiration (panting), mottled cutaneous vasodilatation over the body and increased
renal function. However, in later stages of complete tetraplegia, the patient acquires a
