VOL. XXIII.

Of importance to the general practitioner because it may frequently be diagnosed even in its early stages, by the presence of well-known physical signs; its dire prognosis foreseen, and very serious consequences at times averted, and because it is liable to attack persons in the better walks of life, well known in the community, men who have probably no inherited. weakness, whose work has been crowned with success and gives promise of still better things; professional and business men, authors and actors, preachers and phy

sicians.

Moreover there seems but little doubt that among the population of the cities at least, this disease is upon the increase.

Paretic dementia may be defined as a progressive degenerative disease of the central nervous system characterized usually by mental enfeeblement with delusions frequently of grandeur, and physically by motor, reflex, and speech defects.

If we consider broadly that hereditary

*Read before the Indiana State Medical Association May 19, 1904.

No. 2.

taint represents one-half of the aetiological factors concerned in the production of insanity, and stress and strain, disease, worry, etc., the other half, it will be found that paretic dementia derives its aetiological factors as a rule from the second class of causes.

It is a half brother of tabes dorsalis, and in most instances is to be regarded as an acquired disease; yet even here we can hardly doubt that the subject of hereditary neuropathic taint falls a more ready vic

tim to the causative factors than does he of sounder and more stable organization.

Syphilis is no doubt the most frequent single factor. Some investigators have gone as far as to ascribe every case to a former specific infection. Yet its relationship to syphilis has not been shown to be so nearly constant as in the case of tabes. It seems safe to assert that in about half the cases, syphilitic infection has been the determining factor.

As in the case of locomotor ataxia we do not consider it among the manifestations of syphilis however. Syphilis of the central nervous system is really a disease of the vessels and membranes, and injures nerve tissue only secondarily, by pressure, by exudation, by occlusion of vessels, gummatous deposit, membranous thickening, etc., while in tabes and paretic dementia, early if not primarily the neurons themselves are the seat of retrograde changes, which may occur in the absence of gross syphilitic lesions. It may be that in the syphilitic toxines we must look for the agency whose prolonged effect saps the vitality of cells, and leads to the development of the so-called para-syphilitic affections.

Other causes are of undoubted potency: exhausting diseases, alcoholism, mental anxiety, overwork and high tension, irregular hours and excesses of various kinds, physical and mental shock, each come in

for a share of the blame in a proportion of

cases.

The onset of the disease is usually in the active period of adult life-between 30 and 45 years and in males more frequent. The proportion in the United States being probably 8 or 10 men to 1 woman. Its development is usually slow and it has been found convenient to divide the course of the disease, as in ataxia, into three stages.

First. The prodromal period. Second. The period of active mental disturbances.

Third. The period of dementia and general physical decrepitude.

As the purpose of this paper is to lay emphasis upon certain diagnostic features, rather than to give a description of the course of the disease with its great variations or types, I will refer to these three periods of the disease rather from the diagnostic standpoint.

Unless the practitioner be on his guard the disease may be readily overlooked. Within the year a patient was sent home from the city hospital of this city with a diagnosis of paretic dementia. At the request of his wife an insanity commission was held, and he was declared of sound mind. Within a month he became unmanageable. In making the diagnosis the cardinal point to bear in mind is that the patient presents a mental change associated with certain physical signs.

Frequently the so-called prodromal period is so insidious in its development as to lack any striking mental or physical phenomena. The little lapses of memory, or errors in judgment, with perhaps disordered sleep, headache and irritability are readily ascribed to overwork, a disordered liver or at most to neurasthenia.

In this stage a tentative diagnosis may however be made at times. Any mental change, any change in temperament, whetherexaltation or depression, any alteration of character in a man during the period of middle adult life, should arouse the suspicion of beginning paresis and lead to a search for physical signs as well as mental symptoms.

These signs, appearing early at times, are mainly motor, speech and reflex disturbances.

A fine or coarse jerky tremor about the

lips and tongue may appear at the beginning of an effort to speak, or to innervate the facial muscles. Of these I consider the coarse more diagnostic. A peculiar articulation, tremulous, scanning, stumbling, changing at times the quality of the voice, giving it a sort of drawl or even sing-song character, associated with difficulty of enunciation notably of the linguals and labials is noted.

The patient may be able to give expression to his own thoughts without showing a speech defect, and yet show a marked stumbling when required to repeat test phrases rich in labials and linguals. A little excitement may greatly increase the disability; or, in the early stages overcome it. The handwriting may be as characteristic as the speech.

The patellar reflexes are altered in most all cases. More frequently they are exaggerated, almost warranting the term spastic. In others again they are lostso-called atactic cases.

Probably the most important of all physical signs is the Argyll-Robertson pupilreflex iridoplegia. In this condition the pupil fails to contract when exposed to light, but does contract when the patient converges for near vision. The optic and third intact, but association neurons in showing the ganglion probably at fault.

In 90% of cases Argyll-Robertson pupil the patient is suffering from tabes dorsalis or from general paresis.

Unequal or irregular pupils are suspicious, but not so diagnostic.

If a case were presented to me presenta marked ing a mental alienation, or change in his manner of feeling and acting, and I found the Argyll-Robertson pupil, I should make the diagnosis almost without qualification.

I should consider the peculiar speech defects almost as diagnostic as the ArgyllRobertson pupil. The tremor and the patellar changes while helpful in establishing the diagnosis, yet are not so significant, being more often present in neuroses.

The mental symptoms are rarely diagnostic at first. In some cases there is depression, amountingalmost to melancholia; in others there is even now an expansive state. There may be no actual delusion, and yet what might be called a delusive. state, a delusive manner of seeing or inter

preting things. I recall a prosperous wholesale merchant who was approached at different times by a life insurance agent with negative result. After an interval of about a year the agent again called upon him. He was received almost effusively; the man said he was just in shape for an additional $10,000 policy, the application was written and the man brought to my office. He answered all questions flawlessly, but there was a suspicious tremor about the mouth corners at times. On my making a friendly inquiry about his business, he launched into a disquisition about the character and volume of their stock, which would have done for an advertisement. He wrote a fair signature to his answers, but when given a piece of paper and asked to write a few words upon dictation he made almost a complete failure. This man was fully able to carry the insurance asked for; his firm was carrying a large stock of goods and was prosperous, and yet his manner of feeling and acting was already a delusive one, and if the intentions of his partner to take a vacation trip to Europe and leave the entire care of a large business in the hands of this man for some months had been carried out very grave results might have ensued.

Neurasthenia, the lesions of chronic alcoholic intoxication and the cerebral lesions of syphilis are most apt to simulate the disease notably in its initial stage.

As regards the physical signs, chronic alcoholism is usually marked by changes in skin and mucous membranes, a history of catarrhal condition of stomach, etc. The peculiar defect in speech and writing does not appear and the Argyll-Robertson pupil

is rare.

Cerebral syphilis with its endarteritis, chronic meningitis, encephalitis, etc., etc., cannot at all times be excluded, and if any doubt exist, the patient should be given the benefit of the doubt in treatment, and final judgment be reserved.

Mentally depressed cases may resemble neurasthenia. The presence of the ArgyllRobertson pupil would settle the question. Otherwise the sum of the mental and physical signs must serve for a tentative diagnosis. When well advanced the manifestations of the disease are so marked, that the diagnosis is readily made. Physical mental crises, a violent furious mania, or

an apoplectiform attack may usher in the second stage.

Delusions are marked by great exaggeration. geration. Shiploads of gold, feelings of undue well-being amounting to actual happiness, a smile that is child-like and bland; or exaggerated depressing delusions without real mental pain, general tremor, increased speech defects, awkward gait and general muscular enfeeblement. Diminished sensibility to pain, grinding of teeth, bolting of food, untidiness, uncleanliness, mark the gradual approach to complete mental and physical disintegration.

As regards the pathology, I will be brief. Whether we consider the disease primarily a slow meningo-encephalitis, or whether we believe that the inflammatory and thickening processes are secondary to the degeneration of the neurons and resulting choking and stasis and intoxication of lymph and venous channels, we observe both conditions are found early. On the part of the cells, swelling, chromatolysis, fatty degeneration, vacuolization, pigmentation and finally atrophy of the cell body, involving and at times preceded by similar changes in the axis cylinder occur.

These changes involve the entire cortex, but may be more pronounced in the frontal and parietal regions. No part of the brain. is exempt and the cord is involved in about 10% of the cases.

The vessels at first show hyperemia and stasis, increase of nuclei, exudation into the lymph spaces; there is proliferation of neuroglia to the extent finally of a diffuse sclerosis. Retraction occurs, the brain becomes smaller and harder, vacuoles may appear here and there. The membranes are thickened and the cerebro-spinal fluid is increased and fills in the spaces between the shrunken convolutions.

In making the prognosis, which, of course is bad, it must be borne in mind that some cases are rather remittent in character.

Symptoms may be far in advance of the actual destruction of tissue. The function of nerve tissues is often disturbed or lost as we all know in so-called neuroses with no palpable lesion, and so in tabes and in paretic dementia the symptoms may be out of proportion to say the least in the pathological change, and considerable improvement occur. This is especially liable to be