4 Edward Liveing, in his work On Megrim, Sick Headache, and Some Allied Disorders, p. 404, thus expresses his conviction as to the neurotic theory of gout: "The view which is commonly entertained is, that the excessive generation or retention of uric acid in the system, which is regarded as the fundamental fact in the pathology of gout, exerts a toxic influence upon the nervous centres, while the particular character of the disorder is determined by the territory involved. This limited operation of a cause so general in its nature is a real obstacle to this view; on the other hand, there is much in the history of gout—its hereditary character, limitation to particular ages and sexes, periodicity, explosive character, sudden translations, and remarkable metamorphic relations with nervous disorders—which seems to stamp the malady as a pure neurosis; and even the fit itself, with its sudden nocturnal invasion, the late Dr. Todd was accustomed to compare to one of epilepsy or of asthma."
PATHOLOGICAL ANATOMY.—Blood-Changes.—Garrod's demonstration of the excess of uric acid in the blood of gouty persons constitutes the chief recognized hæmic change in this disease. That this is a constant change, and one that is essential to the existence of gout, cannot be said to be proved. The presence of uric acid in the blood is not always productive of gout, since it has often been found in the blood of healthy persons, and its temporary excess during pyrexia, and especially in the fevers and other morbid states in which spleen is congested, has already been noted. The excess of uric acid, however, in gouty blood may reach, according to Garrod, as much as 0.11 grain in 1000 grains of serum. It is probable that other excrementitious substances exist in the blood in gout which bear a closer etiological relation to this disease than uric acid, but they have not been demonstrated. The other blood-changes which are noted by Garrod—the diminished specific gravity of the serum from loss of albumen, the diminished alkalinity, and the increase of the fibrin in the inflammatory forms of the disease—are probably inconstant. In chronic gout the objective signs of anæmia which are often present would indicate a marked diminution in the red blood-corpuscles.
The tissues which are the chief seat of gouty lesions are the connective tissues. In the evolution of the disease the joints, where the connective tissue is most dense and the least vascular, suffer earliest; at a later period the connective tissue of the blood-vessels, nerves, and viscera becomes subject to gouty changes.
According to Garrod, the exudations in articular gout are rich in the urates of soda, lime, magnesia, and ammonia; they also contain some phosphate of lime and traces of organic matter. The watery portion is absorbed and the salts are deposited in crystalline forms. The location of these deposits varies: they are found on the synovial surfaces, in the cartilage-cells, and in the intercellular substance; in the tendons, ligaments, and bursæ, and in the subcutaneous connective tissue. The urate of soda occurs not on the free surface of the cartilage, and replacing the latter, as was formerly generally supposed, but as an infiltration into the substance of that tissue; and Garrod found that there is always a thin layer of unaffected cartilage lying between the deposit and the free articular surface—an observation which has been confirmed by Budd and quite recently by Ebstein.5
5 W. Ebstein, Die Natur und Behandlung der Gicht, Wiesbaden, 1882.
Very important are the recent investigations of the latter. After making numerous observations on the cartilages and other affected tissues of gouty subjects, besides studying the disease artificially produced in fowls, he has shown that those portions of cartilage and other tissues in which the deposit occurs are in a state of necrosis, as is evident from the fact that when the urates are dissolved out by warm water the area in which the deposit occurred, though apparently normal to the eye, refuses to be stained with aniline dyes, and lies plainly visible as a light spot in the midst of stained tissue. Since the work of Weigert we know that this is a sure sign of that peculiar form of death of a tissue to which the name of coagulation necrosis has been given. Ebstein regards this necrosis as primary and the deposition of the uratic salt as secondary. According to him, the urates circulating in the blood give rise to necrosis in parts where the circulation is sluggish (as the articular cartilages, the ears, and the extremities generally), and where, consequently, they remain a greater length of time in contact with the tissues. The necrotic portion has, however, an acid reaction, which causes a deposition, from the soluble neutral salt, of an acid urate in a crystalline form. Ebstein claims that this necrotic area, in which there is deposited a crystalline urate of soda, and around which there is a secondary inflammatory zone, is characteristic solely of gout. "I have never seen," he says, "in gout a crystalline deposit of urates occurring in normal tissue."
In addition to these so-called specific changes we find a hyperplasia of the connective tissue in the fibrous structures of the affected joints. The thickening thus induced, with the contraction of the new tissue and the atrophic changes resulting from pressure and disuse, are the causes of the deformities, subluxations, and impaired movements of gouty joints. Occasionally, the local irritation provoked by the pressure of the tophous deposits results in abscesses from which a mixture of pus and pasty urates may be discharged. These abscesses in feeble and anæmic subjects are sometimes difficult to heal. More frequently the skin undergoes gradual absorption and the chalk-like deposits are exposed.
The frequency with which the metatarso-phalangeal joint of the great toes is affected in gouty persons has always been noted. In Scudamore's tables the proportion of the first attacks in this joint was 72 per cent., and in 66 per cent. one or both great joints were affected to the exclusion of other joints. This frequency is due to the fact that this joint is the most vulnerable one in the body, bearing as it does the weight of the body and being exposed to most frequent shock. The phalangeal joints of the hands and the wrist-joints are also often the seat of acute gout, though these joints are more frequently affected by the subacute form of the disease. The larger joints may also be the seat of true gouty inflammation; indeed, no joint, not even the intervertebral, can be said to enjoy immunity, and the hip and shoulder are occasionally attacked to the exclusion of others. The cartilages of the ear and the arytenoid cartilages are sometimes the seat of gouty deposits.
The great frequency of arterial sclerosis, and the subsequent fatty and chalky metamorphosis in persons who have suffered from chronic gout, are well recognized. Next to syphilis, gout seems to be the most common cause of these arterial changes. The influence of these lesions in the arteries and capillaries in determining cardiac hypertrophy and cerebral hemorrhage is often seen in the accidents which terminate the lives of gouty patients.
In the heart a gouty endocarditis is of not uncommon occurrence, according to Ebstein, who cites Lancereaux as having found uric acid in concretions on the valves. Garrod, however, after examining a number of cases in which cardiac disease existed with gout, states that in his opinion the valvular changes are not due to a gouty deposit, he never having been able to demonstrate the presence of uric acid in them.