afterward taken west for rest and recuperation, and in a dispute on the plains was so injured that he died in the spring of 1892.

Case VII.-J. W. H., æt. 43.

First seen on October 27, 1891.

Complains of discomfort in use of eyes when busy. It was hard to

Exophoria,

get his previous history without exciting too much suspicion, but he may have had syphilis. V-8 o. u., with correction. three degrees at twenty feet; discs creamy pink; whiter on the temporal side, not abnormally vascular; vessels prominent and of

normal caliber. Retina normal except a few patchy spots. Has been seen at intervals since, and at last visit exhibited the characteristics of general paresis. Has now white discs; fields as per chart VI. He will no doubt soon become the inmate of some institution.

Case VIII-Dr. G. E. H., æt. 35. First seen professionally in 1891, when he was fitted with glasses. Had good previous history. Had been a constant but not excessive cigarette smoker, and a very moderate drinker. Had a good practice and was ambitious. V-8 with correction, discs creamy or leathery white, no cupping, vessels prominent and normal. Field as per chart VII. Color perception good, especially red. Seen again in May, 1892, when he complained that his eyes gave out occasionally, and that then he could not study or read with comfort. Advised rest, and cautioned a relative, also a physician. In October, 1892, he was seen again, complaining that he was worse. V-38-; fields as per chart No. VIII, nerves bluish-white, and vessels prominent and not much diminished in caliber. Field for red larger than for white. He soon after became violent and was admitted to the asylum at Middletown, N. Y., where he died a few months after admission.

Besides the above, several cases are now under observation, but the termination is as yet too uncertain to render them of any value as corroborative evidence.

In three of the cases mentioned above, the diagnosis of general paresis was made by examiners who did not know the results of the eye examination, and consequently based their diagnosis upon the general manifestations of the affection.

The number of cases thus far observed is of course too small to more than suggest investigation, but the following appear to occur with sufficient regularity to be fairly good diagnostic marks in the early period before the classical symptoms are well enough developed to attract attention:

The appearance of the optic nerve entrance creamy pink or leathery. A better idea of this appearance may, perhaps, be conveyed if it is stated that in this, the earliest period, the surface looks of the normal reddish white hue, with numerous laminated striations through it of a slightly deeper color. Over this is an extremely fine layer of transparent nerve tissue on which the vessels of the disc appear to lie. In one of the cases observed, one could almost imagine he could see behind or around the vessel, so

These vessels

apparent was the stratum of transparent tissue. show no change from the normal in their appearance or direction.

Later the disc becomes gradually whiter and whiter, then takes on a bluish tint, from the connective tissue changes in the deposit, and becomes slightly cupped, which changes are accompanied by changes in the blood-vessels that are much less marked than in cases of ordinary atrophy.

In the retina there is some connective tissue deposit in between the nerve fibers in small striæ or patches, confined to the nasal side till an advanced period of the disease, but later invading the temporal side rapidly.

Of the extrinsic ocular muscles, the interni appear to be most often affected, though all the muscles moving the eyeball may be affected to a greater or less degree. Cutting off of the field of vision on the temporal side to a moderate degree may be looked on as a fairly constant symptom, and the rate of its increase as a measure of the progress of the disease. Steady deterioration of vision, especially when accompanied by the patient's statement of improvement in vision, looks to a rapid course of the general affection. Inequality in size of pupils is by no means a constant symptom, and where it exists the case is likely to be complicated by some constitutional taint or habit.

Should the above conclusions be confirmed by further observation, an important factor will be the gain of from one to three years in the time of diagnosis, thus affording opportunity for the arrangement of affairs of business, etc., and, perhaps, of postponing the termination by judicious treatment, as well as presenting a means of positive determination not so liable to dispute as are some of the symptoms at present recognized as pathognomonic. This was one of the most marked characteristics of all the cases above related, and would appear to show that the progress of general paresis is slow, but at no time stationary.

The clinical appearances suggest that the affection of the optic nerves and retina is a connective tissue hyperplasia, or an interstitial optic neuritis, which results in substitution of connective tissue for true nerve substance, resulting in true atrophy, and strong corroboration of this view is found in the results of the researches made by Dr. J. A. Oliver, and published in the March number of the University Medical Magazine.

THE TROPHO-NEUROSES OF PARETIC DEMENTIA.

BY FRANK C. HOYT, M. D.,

Superintendent State Hospital for the Insane, Clarinda, Iowa.

In presenting for your consideration a brief review of the vasomotor abnormalities exhibited in the clinical history of paretic dementia, I do so, not that I am able to offer anything new, but to accentuate the important part which neuro-angio-paralysis plays in the production of many of the most interesting phenomena of this dreaded malady.

The vaso-motor and trophic changes, which are observed in both the early and late stages of the disease, are characteristic and important. Glancing hastily over the clinical picture presented by the early stage of paretic dementia, we find an array of symptoms, some of which, if not all, are found in every case. Among these may be mentioned vertigo, flushing of the face, and other evidences. of transient anæmia and hyperæmia of the brain; alterations in the tension of the pulse, it being high in the more active forms of the disease and low in the depressive form (Spitzka), frequent attacks of headache, associated with a sense of pressure in the head; occasional slight apoplectiform attacks, and many other symptoms familiar to all who have observed cases of paretic dementia in their incipiency. These symptoms are, however, evanescent in character, failing to furnish satisfactory evidence of structural changes in the interstitial or parenchymatous tissues of the brain, they are explicable only on the hypothesis of vaso-motor paralysis. The mental symptoms at this stage of the disease also bear evidence of very slight cerebral disturbance, and are accounted for more satisfactorily by the theory of functional circulatory disturbances than by the belief that real structural changes in the cerebral tissues have occurred.

The slight impairment of the mind, which makes its appearance and progresses so slowly; the sudden attacks of mental confusion, synchronous with the flushing of the face and the attacks of cerebral congestion; the blunting of, the finer sensibilities, the mild exhilaration, the abnormal development of the Ego, the unnatural changeableness of the moods and temper of a formerly well-balanced individual; the irritability and the frequent attacks of excitement or melancholy, are suggestive of vascular abnormalities and of vaso

motor disturbances. It is in this prodromal stage that Meynert, Folsom, and others believe that the line of demarcation between functional and organic diseases can be drawn; and by proper treatment and regimen the malady be stayed in its progress, if not actually cured. Later in the history of paretic dementia, we have the episodical attacks of epileptiform and apoplectiform seizures which not infrequently, after a few days of mental and physical impairment, result in the patient emerging from the attack with apparent rejuvenation of mental power. These attacks are often recovered from too quickly to have been due to any inflammatory process, as is claimed by some writers.

As the disease advances, the progressive impairment of mental vigor, the frequency of profound apoplectiform and epileptiform attacks, the marked ataxic and other symptoms of progressive paralysis of all striated muscles, mark the era of more serious brain changes. We now find the vaso-motor and trophic abnormalities presenting themselves in more tangible form. The vaso-motor paralysis is evidenced by changes in every tissue of the body. The oedema of the feet and limbs, hyperidrosis, malnutrition of the cutaneous surfaces, localized anesthesias and hyperesthesias, herpetic eruptions following the course of branches of the trigeminus, brittleness of the hair, sponginess of the gums, ulceration of the mucosa of the cheeks, acute decubitus, neuro-paralytic congestion of the lungs, othæmatoma, sub-dural hæmatoma duræ matris, etc., all are consequent upon trophic changes. Post-mortem, the findings are still indicative of grave vaso-motor changes, which, by long-continued disturbances, have produced organic lesions of the cerebral structures. These may be briefly summarized as follows: An atrophy of the brain as a whole or in part, degeneration of the cells and neuroglia, of so pronounced a character as to lead Clouston to speak of general paresis as "essentially a death of that tissue, and equivalent to a premature and sudden senile condition; senility being the slow physiological process of ending, general paralysis the quick pathological one."

The vascular changes are as important as constant, the vessels of the pia and cortex being tortuous, looped, varicose, their walls thinned, the peri-vascular lymph spaces dilated. The membranes of the brain, especially the pia-mater, are almost constantly changed, being injected, infiltrated, thickened and opaque, the vessels giving ocular evidences of their inability to bear the strain put upon them.