defect, which in some cases is very slight. Dr. Hurd is rather more hopeful of it than I am with my limited experience. I cannot recall a permanent recovery in any of my cases.

Now we may ask the question, are all these apparent discrepancies sufficient to invalidate our conception of this process as a disease? Is it not possible that there is a common cause underlying the whole disease, and can this common cause produce all the symptoms and the anatomical changes which have been described? It is to be hoped that future study will elucidate these apparent discrepancies.

Bonhoeffer calls the condition chronic alcoholic delirium, but he does admit that it may be caused by other toxins than alcohol. Korsakoff gives a whole series of ætiologies, but there is no doubt that alcohol is by far the most important ætiological factor. We see it is present in every case of · Dr. Hurd's but one. Of the four cases which I reported, three were alcoholic, and of the six cases which I have had in my service since that report, every one was alcoholic. I might add that of my reported cases two are still in the hospital and show practically no change; one has gone home and is earning a living, but could not, even for statistical purposes, be considered a recovery. He is emotional and has a very defective memory.

The question of association with peripheral neuritis has been well discussed by Dr. Hurd, and I do not consider that it is of fundamental importance whether the toxic effect is concentrated upon the peripheral or upon the central neurones, or upon both.

I came prepared to discuss the pathology of the disease, but I find that my time is up, so I will not further burden you. I wish again to thank Dr. Hurd for his very interesting reports.

A CASE OF VISUAL HALLUCINATIONS AND CROSSED AMBLYOPIA WITH VASCULAR AND DEGENERATIVE LESIONS IN THE CALCARINE CORTEX AND OTHER PORTIONS OF THE OCCIPITAL LOBE; ALSO WITH ATROPHY OF THE PREGENICULE AND OPTIC TRACTS.'

(From the Laboratory of Neuropathology The University of Pennsylvania.) BY CHAS. K. MILLS, M. D.

Professor of Neurology in the University of Pennsylvania, Neurologist to the Philadelphia General Hospital,

AND

C. D. CAMP, M. D.,

Assistant in Neuropathology in the University of Pennsylvania, Assistant Neurologist to the Philadelphia General Hospital.

The case briefly recorded below is of much interest from several points of view. It throws some light upon the question of the organic basis of visual hallucinations, and affords some valuable data regarding the pathological anatomy of the insanity of arterio capillary sclerosis. It also furnishes an illustration of a somewhat irregular form of crossed amblyopia, apparently due to lesion of the occipital cortex and subcortex.

The patient, a woman sixty-three years old, had suffered with impairment of vision in both eyes for nearly two years before coming under observation. This dimness of sight was attributed to glaucoma, for which a double iridectomy was performed. After this operation her vision was good in the left eye, but only fair in the right eye. She was not, however, blind in either eye and was able to do considerable near work, although she was careful in this respect. The following is a brief record of the state of her vision and of her fields shortly after the iridectomies, for which we are indebted to Dr. Geo. C. Harlan under whose care she was at that time and by whom the operations were performed. At this time the vision in the right eye was 20/40 and the

'Read at a meeting of the American Medico-Psychological Association, San Antonio, Texas, April 18-21, 1905.

field practically normal with a slight peripheral cut in the temporal side; the disc was cupped, 1.50 D; vision in the left eye was 20/50; the field and the ophthalmoscopic examinations were the same as in the other eye.

In September, 1904, one of us (Dr. Mills) was called to Virginia to see this patient. A few days before she was seen she had had a cerebral seizure in which the right eye became totally blind and vision in the left eye was greatly impaired. Examination showed this complete loss of vision in the right eye, and so great a contraction of the fields of the left eye as to give the case the appearance of one of so-called barrel vision. At the time of her attack she lost the power of coordinating her movements sufficiently to stand and she was slightly delirious. She was mildly excitable, talking rapidly and somewhat inconsequentially. The members of her family regarded her as simply excited over her loss of sight and inability to stand, but her condition was one suggestive of hypomania. From the first it seemed that active mental disorder was imminent.

After a few days she was brought to Philadelphia where she was attended until her death by Dr. Harlan and Dr. Mills. Shortly after her arrival Dr. Harlan made a careful examination of her eyes. In the right eye she had scarcely more than light perception. The fundus was the same as in the previously reported examination, except that the cupped nerve had filled up to the level of the retina which equalled a swelling of plus 1.50; tension was normal. In the left eye vision was reduced to 5/40. The field was peripherally contracted to 40 degrees on the mesal side and to 20 degrees on the temporal side. The color proportion of the field was normal. The disc was slightly cupped, the fundus was otherwise normal.

On account of the patient's nervous condition it was not considered wise to make a minute outline of the fields.

Early in the history of this case there was something hard to describe in her mental state and attitude. She talked and acted as one somewhat emotionally exalted and lacking in inhibition. As she had not at first any hallucinations or illusions, some of those around her were inclined to regard her as not suffering from any mental unbalance, she normally being vivacious and inclined, on slight cause, to excitement. At first she was not able to stand or walk, but in the course of ten days she became able to walk

without support for a few feet. How far her inability was mental and how far physical, it was difficult to say, as under strong encouragement she stood and walked better.

Two weeks after arriving in Philadelphia she suddenly became violently delirious during the night, talking and screaming and showing signs of visual hallucinations. She leaped from the bed and became difficult to manage. From this time on until a few. days before her death, when she became quieter through weakness, she was acutely maniacal.

A record of a few of her hallucinations will be of interest. Four days after she had given clear evidences of the existence of acute mania, she saw men in the room with knives and pistols assaulting her son and husband as well as herself; she said that her own life was in danger but she did not care for that if only her son and husband were saved. At about this time she also saw fire occasionally, but she still continued to recognize those around her, and talked with them more or less rationally. She also now and then spoke of some dead relatives. Up to this period she had shown no fever, although her temperature had occasionally arisen to 99 or even to 100 degrees.

About one month after coming under continuous observation she developed a glandular swelling on the under right side of the face which disappeared in a few days. She died about three months after coming under care in Philadelphia. During most of this time illusions and hallucinations of sight were the most marked features of the case. She would, for example, suddenly cry out that she saw persons or objects threatening her or passing before her. She sometimes mistook the nurse or the doctor for someone with evil designs against her. With an effort her attention could be temporarily fixed, but she would suddenly cry out with great fear, pointing in the direction of some imaginary person or object. The hallucinations and illusions of sight kept up until a state of thorough exhaustion came on a few days before her death. They were not associated with hallucinations of sound, and there was no involvement of other senses unless the statements which she made at one time early after the development of visual hallucinations, that her legs were being or had been cut off, might be so considered.

Examinations of her urine were frequently made and on one or two occasions showed a few casts and on one or two others a

ance.

trace of albumin; otherwise there was nothing of special importThe blood examination made about ten weeks before her death showed: red cells 4,280,000; white cells 8700; hemoglobin 85 per cent.

Her mental condition grew steadily worse as shown by incoherence mingled with wild hallucinations and illusions, chiefly of terror, and steady mental reduction. A week or two before her death the optic discs, which were cupped, began to present the appearance of an optic neuritis, but this did not fully develop. About this time her evacuations became involuntary. Later she became stuporous and developed Cheyne-Stokes breathing. She died of all the evidences of cerebral and general physical exhaustion.

Dr. Cadbury, one of the internes at the Pennsylvania Hospital, has kindly furnished notes of the case.

The necropsy was performed by Dr. Geo. S. Crampton, one of the resident physicians to the Pennsylvania Hospital. The results of the gross examination summarized were, chronic interstitial nephritis; chronic mitral and aortic endocarditis; acute vegetative aortic endocarditis; cardiac hypertrophy with fatty degeneration of the myocardium; congestion of the lungs with acute bronchopneumonia; fatty degeneration of the liver, and a high degree of atheroma of the vessels at the base of the brain. The brain was sent to the laboratory of neuropathology of the University of Pennsylvania where it was examined both macroscopically and microscopically by Dr. C. D. Camp under the supervision of Dr. Wm. G. Spiller, professor of neuropathology.

Further macroscopical examination of the brain showed the convexity and other regions of the brain apparently normal. The arteries at the base, as already stated, were intensely sclerotic. The pregeniculæ were much atrophied on both sides. No areas of softening were found in the thalamus, other basal ganglia, optic radiations, or in any part of the cerebrum.

After hardening in ten per cent formalin solution, pieces of tissue from various parts were examined histologically with the following results:

The preparacentral regions on each side were normal by the hematoxylin, acid-fuchsin, and Weigert-hematoxylin methods, though the blood vessels here as elsewhere in the cortex, were slightly thickened and the perivascular spaces enlarged. There