Hare contended also that excessive intake of starch and sugar by inducing a state of “glycogenic distension” of the liver, might through compression of the intra-hepatic portal capillaries, lead to congestion of the retro-hepatic portal venous system, and sequentially of the gastric and intestinal mucosa. Through consequent inhibition of digestion and absorption, a condition of hyperpyræmia is induced. This, under varying conditions, may eventuate in acute gout, the coincident pyrexia of which is curative of the underlying hyperpyræmic state, and of all those hyperpyræmic manifestations (irregular or suppressed gout) which so often are the harbingers of an on-coming articular outbreak.
Nervous Theories
It may be noted en passant that the influence of the nervous system was frequently invoked directly or indirectly in many of the theories already discussed. Stahl, it will be recalled, was the pioneer in this direction, and later Cullen and Henle propounded the view that “the origin of the affection was probably to be found in the central nervous system.” Gairdner, too, by implication, as also Laycock, postulated a neural origin for at any rate some of, the phenomena of gout.
But it was reserved for Edward Liveing (1873) explicitly to advocate the nervous origin of the disease, his reflections on the paroxysmal nature of the attacks, its tendency to periodicity leading him to suspect its kinship with other neuroses.
Those inclining towards the neural conception were later strengthened in their convictions by Charcot’s momentous identification of the nervous origin of certain arthropathies. Accordingly, in 1880, we find Sir Dyce Duckworth advocating the view that gout was “a primary neurosis,” “a functional disorder of a definite tract of the nervous system.”
The gouty neurosis, Duckworth contended, may “be acquired, intensified, and transmitted; also that it may be modified variously and commingled with other neuroses; that it may suffer metamorphic transformations, or be altogether repressed.” Arguing by analogy, Duckworth saw in the paroxysmal attacks, the tendency to periodicity and alternation in the manifestations, evidence of an alliance between gout and the various neuroses.
He further postulated that “this diathetic neurosis determined a disorder of nutrition and led to the perverted relations of uric acid and sodium salts in the economy.” He also held that the localisation of attacks, and the determination of urate of soda to the affected part was also due, in all probability to nervous influence. And the temporary renal incapacity for excretion of uric acid was also attributed by him to the same nerve inhibition.
We see, therefore, from the above, that Duckworth was well justified in describing his view as a combine of the humoral and neural hypotheses. His pathological differentiation between primary or inherited gout and secondary or acquired gout is as follows: In the primary type “the toxæmia is dependent on the gouty neurosis ... and is therefore a secondary manifestation.”
In secondary or acquired gout, “the toxæmia is directly induced by such habits as overload the digestive and excretory organs, and consequently prevents complete secondary disposal of nutritional elements of food; that if, together with such toxæmia, distinctly depressing and exhausting agencies, affecting the nervous system, come into operation, the special neurotic manifestations of the gouty diathesis will occur, and be impressed more or less deeply upon the individual and his offspring.” It is generally conceded that Duckworth’s theory as to the genesis of gout is pre-eminently catholic in conception, because, as Ewart rightly remarks, “it represents the most complete theory published in this country on the general pathology of gout,” and because “the able advocacy of its propounder has given it the support of arguments derived from pathological analogy and from clinical influence which will demand careful examination and searching criticism before they can be either disproved or adopted.”
Albeit, it must be frankly admitted that Duckworth’s perception of gout as a tropho-neurosis of central nervous origin has never gained wide acceptance; this no doubt largely because it was insusceptible of proof. In an endeavour to remove this reproach. Sir Willoughby Wade promulgated the view that the causal change in gout was partly in the central nervous system, partly in the peripheral nerves of the inflamed limb. In other words, he regarded gouty arthritis as the outcome of a local neuritis, this latter being set up in the first instance by the faulty blood state, viz., uricæmia. On the other hand, the central nerve centres might occasion or aggravate the general gouty tendency through their influence over “recognised seats of metabolic activity.” Also the same might, through the medium of the vaso-motor nerves, determine the incidence of local attacks. It will be seen that Wade’s theory is but a variant of that propounded by Duckworth, viz., neuro-humoral.