Pre/irpiparg Report, Clinical and 
Pathological, of a Case of 
Progressive Demeptia. 
By CUAS. K. MILLS, Aj, D., and hJrfRY 
SOW V ELY, M. D. 
REPRINTED FROM PROCEED!NCS OF THE 
AMERICAN MEDICO-PSYCHOLOGICAL ASSOCIATION 
BALTIMORE, MD. . PRELIMINARY REPORT, CLINICAL AND PATHOLOG- 
ICAL, OF A CASE OF PROGRESSIVE DEMENTIA.* 
By CHARLES K. MILLS, M. D., and MARY A. SCHIVELY, M. D., 
Philadelphia, Pa. 
The case presented the following history: Patient—aged sixty- 
four years; married; was always of a nervous, somewhat irritable 
temperament, but mentally bright and clever with linguistic and 
other accomplishments. After the birth of her first child she had 
an attack of mania. When about twenty-three years of age she 
had chorea which lasted for several weeks. When thirty-five 
years of age, apparently as the result of unusual worriment, 
she became more irritable and her temper was afterwards ca- 
pricious. For a period of ten years preceding her death, she 
was subject to spells of excitement which almost amounted to 
transient derangement, but she had no tangible delusions, al- 
though she had a tendency to persecutory ideas. About the same 
time, she began to show a decided amnesia for names; this gradu- 
ally, but surely, increased. She had, however, no motor aphasia 
but could converse and write well until within three years of her 
death. During the third year previous to her death, she became 
so unreasonable that it was almost impossible to live peaceably 
with her, she having at times outbursts of uncontrollable passion. 
During the second year previous to death she had two attacks 
of what appeared to resemble la grippe; during which time she 
complained of intense pain in the head and back; from the first 
of these attacks she recovered, but from the second she did not, 
the pain in the head being persistent and always referred to the 
right parietal region; insomnia was marked. General failure of 
memory was observed about this time and she became half bed- 
ridden. During the last eighteen months of her life she was 
* Read at the Annual Meeting of the American Medico-Psychological Association, 
held at Baltimore, Md-, May, 1897. 2 
REPORT OF CASE OF PROGRESSIVE DEMENTIA. 
confined to bed continuously. Her chief symptoms during this 
period were vertiginous attacks; difficulty in orientating herself, 
and marked amnesia not only for names but for recent events. 
She gradually became feebler mentally and during the few months 
preceding death was in a state of decided dementia with occa- 
sional spells of excitement. Her attempts at conversation 
were childish and she had numerous transient, unsystematized 
delusions. An ophthalmoscopic examination made one year 
previous to death was negative. There were no bed sores and 
no paralysis at any time. The case was one in which the entire 
fabric of the mind seemed gradually to break up and step by 
step failure of the mental and physical powers progressed. On 
November 5, 1896, she suddenly became comatose and died the 
next day. 
The post-mortem examination was made on November 7th by 
Dr. Burr and Dr. Kelly. The following pathological conditions 
were present: The dura was somewhat thickened; the pia-arach- 
noid was opaque. The vessels of the base of the brain were 
atheromatous; the anterior communicating artery showed aneur- 
ismal dilatation. The pial vessels on the ventral surface of the 
pons showed miiiary aneurisms. Portions from six regions of 
the cortex were removed and hardened in alcohol; the remainder 
of the brain was placed in Muller’s fluid. 
Microscopical examination reveals the following pathological 
changes: Sections stained with thionin (according to the method 
of Lenhossek) and by methylene-blue (Nissl’s method) show in- 
ternal changes in the neuron. These changes consist in irregular 
arrangement of the chromophilic particles of the cell-body— 
disappearance of these from some areas and aggregations in 
others—giving the cell-body a vacuolated appearance. The 
chromophilic particles are absent from or sparsely scattered 
through the cell processes. The nuclear changes consist in ab- 
sence of large chromophilic particles, while the finer dustlike 
particles and the normally clear karyoplasm stain irregularly; 
the nucleolus stains deeply. 
External cell changes (as demonstrated by the silver phospho- 
molybdate method of Berkley) consist in roughening and de- 
formity, extending in some cases to excavation of the cell corpus. 
The basilar dendrites show moniliform swellings along their 
course or present clubbed extremities; in some cells there is loss Fig. I.—Long pyramidal cell from the middle occipital convolution, showing 
roughening of the cell corpus and apical dendrite; moniliform swellings 
on the basilar dendrites; also loss of gemmuhe. 
Fig. II.—Long pyramidal and fusiform cells from the second frontal convolu- 
tion, showing irregularity in contour ; also excavation of the cell corpus ; 
deformity of basilar dendrites; also moniliform swellings of the apical 
dendrites. Fig. III.—Photo-micrograph of a long pyramidal cell from the ascending 
frontal convolution, showing roughening of the cell corpus and of the 
apical dendrite ; also moniliform swellings of some of the basal dendrites. Fig. IV.—Long pyramidal cells from the second frontal convolution, showing 
vacuolated appearance of ttie cell body; diminution of chromophilic par- 
ticles in cell processes; and nuclear changes. 
Fig. V. — Protoplasmic glia cell, showing loss of fine mossy granulation, and 
the presence of varicosities on the pseudopodia. Fig. VI.—Section from the middle frontal convolution, showing stasis, over- 
distension of the vessel walls, enlargement of perivascular lymphatic 
space ; also area of softening. Fig. VII.—Section from the ascending parietal convolution, showing stasis; 
over-distension of the vessel walls; tortuosity and multiplication of 
vessels. Fig. VIII.—Section in the second temporal region, showing changes in the 
meninges; thickening of the pia-araclinoid; evidences of extravasated 
blood; thickening of vessel walls. Fig. IX.—Section of basilar artery, showing atlieromatous condition of walls; 
also thrombus. 
Fig. X.—Area of softening from the ascending parietal region, containing 
portions of blood-vessels, blood corpuscles and haematoidin crystals. BY DRS. CHAS. K. MILLS AND MARY A. SCHIVELY. 
3 
of several dendrites. The apical dendrite is roughened and de- 
formed in contour. The axis cylinder remains intact. The long 
pyramidal cells seem to be most affected by these changes. The 
Purkinje cells show thickened stems with short, stumpy branches 
in place of the complex feathery dendrites of the normal cell. 
The protoplasmic glia cells present a series of transitional 
changes; the fine mossy granulation appearance of the pseudo- 
podia is lost and varicose swellings appear in their course. 
Other cells take on an irregular, botryoidal appearance and 
finally evidences of disintegration are to be observed. Deiter’s 
cells are numerous both in cerebrum and cerebellum. 
The basilar and internal carotid arteries show increase in the 
number of true endothelial cells and a growth of new connective 
tissue derived from the endothelium. This growth consists of 
branching cells, proliferated nuclei and basement substance with 
areas of atheromatous degeneration. In the posterior communi- 
cating arteries the intima, media and adventitia are about equally 
thickened. The anterior communicating shows aneurismal dila- 
tation. Thrombi are present in all these vessels. 
The pial vessels show stasis, aneurismal dilatations, tortuosity 
and thickening of their walls, with nuclear proliferation. In all 
regions there are evidences of extravasated blood in the form of 
groups of corpuscles and haematoidin crystals. The region of 
miliary aneurisms shows similar changes. 
All cortical vessels are over-distended with blood corpuscles; 
they are exceedingly irregular and tortuous in their course and 
appear to be greatly increased in number. The perivascular 
lymphatics are distended. 
Areas of softening occur in the right ascending parietal region; 
they consist of a reticulated stroma surrounding a central cavity 
which contains portions of blood vessels, blood corpuscles, 
haematoidin crystals and fragments of nerve and neuroglia tissue. 
Areas of coagulation necrosis are present in the left ascending 
parietal region. 
Medullated fibres of the ascending parietal region, optic chiasm, 
and of scattered areas in the pons and medulla show different 
stages of myelin degeneration. 
In addition to the methods above referred to, sections were 
stained with hsematoxylin and eosin; haematoxylin, picric acid 
and fuchsin, and according to the Weigert-Pal method. 4 
REPORT OF CASE OF PROGRESSIVE DEMENTIA. 
In conclusion the pathological features of the case may be 
summarized as follows: First, Internal and external changes in 
the neuron; second, changes in the protoplasmic glia cells; third, 
changes involving the cortical and pial vessels, also the vessels 
at the base of the brain; fourth, multiple areas of softening in 
the ascending parietal region; fifth, myelin degeneration.