The Pathologic Physiology of Dementia: With Indications for Diagnosis and Treatment

163 Pages·1978·4.987 MB·English

by  Professor Dr. Richard M. Torack (auth.)

Monographien
aus dem Gesamtgebiete
der Psychiatrie
20
Psychiatry Series
Herausgegeben von
H. Hippius, Munchen . W. Janzarik, Heidelberg
C. Muller, Prilly-Lausanne
Richard M. Torack
The Pathologic Physiology
of Dementia
With Indications for Diagnosis
and Treatment
Springer -Verlag
Berlin Heidelberg New York 1978
Professor Dr. RICHARD M. TORACK, Washington University, School of
Medicine, Department of Pathology, 660 South Euclid Avenue,
St. Louis, MO 63110/USA
ISBN-13: 978-3-642-88439-9 e-ISBN-13: 978-3-642-88437-5
DOl: 10.1007/978-3-642-88437-5
Library of Congress Cataloging in Publication Data. Torack. Richard M .• 1927 -. The patholo
gic physiology of dementia. with indications for diagnosis and treatment. (Monographien aus
dem Gesamtgebiete der Psychiatrie; v. 20). Bibliography: p. Includes index. I. Dementia. I. Title.
II. Series. RC386.2.T67. 616.8'9. 78-15102.
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2123/3130-543210
Contents
1. Historical Overview of Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . ....
Prelude to the Modem Era . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Age of Alzheimer and Kraepelin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
History of Alzheimer's Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 12
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 15
2. Clinical Manifestations as a Determinant of Dementia. . . . . . . . . . . . . . . .. 17
General Considerations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 17
Functional Mental Syndromes as a Manifestation of Brain Disease . . . . . . .. 19
Acute Confusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 23
Specialized Syndromes in Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . .. 26
Creutzfeldt-lakob Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 26
Kluver-Bucy Syndrome (Limbic Encephalitis) . . . . . . . . . . . . . . . . . . .. 28
Normal Pressure Hydrocephalus. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 32
Summary of Specialized Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . .. 34
Summary of Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . .. 34
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 35
3. Diagnostic Tests of Dementia as Research Tools. . . . . . . . . . . . . . . . . . .. 39
Psychological Tests of Intelligence . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 39
Electroencephalography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 43
Radiographic Technique. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 46
Morphologic and Chemical Assay of Brain Tissue. . . . . . . . . . . . . . . . . . .. 47
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 51
4. Treatment of Senile Dementia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 56
Acute Confusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 57
Circulatory Agents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 57
Metabolic Stimulants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 58
Psychoactive Drug Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 59
Antiviral Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 59
Surgical Management. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 60
Shunt Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 60
Carotid Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 60
Conclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 61
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 61
VI
5. Epidemiology of Dementia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 64
General Considerations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 64
Previous Surveys of Senile Dementia. . . . . . . . . . . . . . . . . . . . . . . . . . .. 65
Cross-Sectional Survey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 65
Larsson Survey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 68
Autopsy Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 68
The GM Survey. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 70
Characteristics of the Population . . . . . . . . . . . . . . . . . . . . . . . . . . .. 70
Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 70
Diagnosis of Dementia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 70
Results. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 71
Etiologic Implications of Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . .. 73
Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 73
Heredity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 73
Slow Virus Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 74
Concluding Remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 75
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 75
6. Current Evaluation of Pathologic Correlates of Dementia . . . . . . . . . . . . .. 77
Congophilic Angiopathy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 77
Senile Plaques. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 85
Endogenous Plaque Formation. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 87
Exogenous Origin From Circulating Immunoproteins. . . . . . . . . . . . . .. 88
Neurofibrillary Tangles. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 88
Creu tzfeld t -J akob Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ., 91
Other Pathologic Correlates. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 93
Aluminum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 93
Lipofuscin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 94
Granulovacuolar Degeneration. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 95
Pathogenetic Implications of Pathology. . . . . . . . . . . . . . . . . . . . . . .. 95
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 95
7. Arteriosclerotic Dementia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 101
Dementia Following Multiple Strokes .......................... , 102
Little Strokes .......................................... , 104
Diffuse Cerebral Ischemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 105
Ischemia Due to Macrovascular Disease . . . . . . . . . . . . . . . . . . . . . . .. 105
Carotid Artery Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 105
Vertebrobasilarinsufficiency. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 105
Ischemia Due to Microvascular Disease . . . . . . . . . . . . . . . . . . . . . . .. 106
Cerebral Blood Flow Study of Dementia ........................ , 106
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 108
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 108
VII
8. Critical Evaluation of the Concept of Mental Aging . . . . . . . . . . . . . . . . .. 110
Functional Aspects of the Elderly Brain. . . . . . . . . . . . . . . . . . . . . . . . .. 112
Mental Behavior in the Aged . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 112
Memory ........................................... 112
Cognitive Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 113
Psychoses After 65 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ., 113
Electroencephalography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 114
Routine EEG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 114
Visual Evoked Response (VER) . . . . . . . . . . . . . . . . . . . . . . . . . .. 115
Cerebral Blood Flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 116
Immunologic Indices of Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 116
Pathology of the Aged Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 118
Brain Weight as a Determinant of Atrophy. . . . . . . . . . . . . . . . . . . . .. 118
Neuron Loss With Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 120
Senile Plaques, Neurofibrillary Tangles, Granulovacuolar Degeneration . .. 121
Lipofuscin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 122
Abnormalities of the Peripheral Neuron. . . . . . . . . . . . . . . . . . . . . . .. 123
Epidemiology of Mental Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 124
Cross-Sectional Survey of Effectiveness. . . . . . . . . . . . . . . . . . . . . . .. 124
Longitudinal Survey of Aging . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 127
Summary of Longitudinal Surveys . . . . . . . . . . . . . . . . . . . . . . . .. 128
Psychological Test of In telligence. . . . . . . . . . . . . . . . . . . . . . . . .. 128
Psychometrics as Determinants of Longevity . . . . . . . . . . . . . . . . .. 129
Biologic Factors of Longevity . . . . . . . . . . . . . . . . . . . . . . . . . . .. 130
Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . .. 130
Summary of Mental Aging. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 131
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 132
9. Nature and Cause of Alzheimer's Disease: The Case for Slow Virus Infection. 138
Nature of AD. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 138
Clinical Indicators. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 138
Diagnostic Criteria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 139
Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 140
Pathologic Data. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 140
Etiologic Potential for AD. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 142
Metabolic Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 142
Autoimmune Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 142
Metallic In toxication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 143
Slow Virus Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 145
Concept of Slow Virus Infection . . . . . . . . . . . . . . . . . . . . . . . . .. 145
Comparison of AD and Slow Virus Infection . . . . . . . . . . . . . . . . .. 146
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 148
Subject Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 151
1. Historical Overview of Dementia
The evolution of senile dementia has traditionally been considered to represent an aspect
of senescence which, in turn, is the normal final phase of human performance that occurs
as a prelude to death. Yet t}1ere has always been vast disagreement regarding the mean
ing of this statement. Let us begin with senescence itself (Tibbitts, 1957):
The character of elderly men - men who are past their prime may be said to be formed for the
most part of elements that are the contrary of all those in youth. They have lived many years; they
have often been taken in, and often made mistakes; and life on the whole is a bad business. (Aristotle,
384-322 B.C.).
Aristotle's negataive opinion is exactly opposite that of his mentor Plato as he pre
sents his plan for gerontocracy (Tibbitts, 1957):
And he who at every age, as boy and youth and in mature life, has come out of the trial victo
rious and pure, shall be appointed a ruler and guardian of the State; he shall be honored in life and
death.
There can be no doubt that the elder must rule to younger. (Plato, 427 -34 7 B. C.).
A very astute appraisal of aging was that of Cicero in his famous essay "De Senectute"
(Couch,1959):
The blame seems to me misdirected. If the faults are due to old age, the same misfortunes would
have befallen me and other men, but I have known many men who have no complaints. (Cicero,
106-43 B.C.).
The controversy regarding aging inevitably transfer to that condition we call senile
dementia, since as senility, it personifies the ultimate force of aging. There have always
been those who advocate the concept that senility, like senescence, is that bad product
of brain aging and decay to which all of us will succumb if we live long enough. Their
adversaries argue that this idea is untenable because there is no age by which everyone
has been shown to become senile. The complexity of this problem is evidenced by the
fact that this issue has not been resolved despite the efforts of modern medical science.
The history of dementia affords an opportunity to understand how the present situation
evolved. There is another benefit that accrues from a study of history, one which was
described very well by Harry Truman in his memoirs (Truman, 1956):
I learned of the unique problems of Andrew Johnson, whose destiny it was to be thrust suddenly
into the presidency to fill the shoes of one of history's great leaders. When the same thing happened
to me, I knew just how Johnson had coped with his problems, and I did not make the mistakes he
made.
2
Prelude to the Modern Era
One initial impact of mental problems like dementia was the result of the fact that chan
ges in the brain accompanied the disorder. This indicated a relationship between mind
and brain, which certainly was appreciated by Hippocrates, who discussed the nature of
consciousness in his book, Sacred Disease (Jones, 1923):
Wherefore I assert that the brain is the interpreter of consciousness. Some people say that the
heart is the organ with which we think, and that it feels pain and anxiety. But is not so ... Men ought
to know that from the brain, and from the brain only, arise our pleasures, joys, laughter and jests,
as well as our sorrows, pains, griefs and tears. Through it, in particular, we think, see, hear, and dis
tinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant ...
It is the same thing which makes us mad or delirious, inspires us with dread and fear, whether by night
or by day, brings sleeplessness, inopportune mistakes, aimless anxieties, absentmindedness, and acts
that are contrary to habit. These things that we suffer all come from the brain, when it is not healthy.
Hippocrates seems to be concerned with the notion that the heart, rather than the
brain, is the organ of the mind, so we can assume that many people believed this to be
true. His concept of mind and brain was perpetuated by Galen, who not only affirmed
this view, but added a belief that dementia was due to a "coldness in the brain". How
ever, the collapse of Rome and Greco-Roman culture ushered in an era of intellectual
confusion in which the fears of Hippocrates were confirmed. The mind moved from the
brain to the heart. Presumably, the nature of this heroic age required an association
between consciousness, strength, and heart. At any rate, this alien habitat seems like a
good explanation for the intellectual confusion. Our heritage from this era is best mani
fest in the rich endowment of our vocabulary linking heart with all those things that
Hippocrates talked about: hearty, heartfelt, hartless, heart strings, heartache, etc. The
whole idea culminates in the sentiment expressed on Valentines Day. For those who
only believe the dictionary, one current definition of heart is: "the vital center of one's
being, emotions and sensibilities; the seat or repository of emotions."
Hippocrates and Galen were resurrected during the renaissance along with Socrates
and Plato and, at this time, the relationship between mind and brain was renewed.
Although renaissance man adopted the classics, he also fel t compelled to enlarge and
improve this culture by his own hunger for knowledge. Among other things, brains were
studied avidly and one of the points of greatest interest was the ventricular system with
its fluid content. This is a direct outgrowth of the concern with body humors in the
medical classics. This interest expanded when Harvey published his theory on the circula
tion of blood in 1628. The circulation of a fluid peculiar to the brain was considered by
some to have comparable importance for mental performance. Some astonishing ideas
of brain function were formulated and those of Rene Descartes achived greatest notoriety.
In Descartes, we find that renaissance ideal of "universality" expressed in a complete
ness comparable to Da Vinci. Primarily a mathematician, he produced essays on music,
on the development of the fetus, and on legal doctrine. Late in life, he became obsessed
with the function of the mind; his "Je pense donc je suis" is still a milestone in the
history of philosophy. He was also engrossed in the topic of matter and mind (or soul).
Complicating his science was a strong religious conviction, which embodied God as an
infmite source, a fountainhead. He conceived of the brain as another spiritual system,
needing a similar initiator of all activity. He ascribed this power to the pineal gland
which has been ridiculed ever since Descartes' folly (Haldane and Ross, 1911):
3
It is, "the principal seat of the soul, and the place where all its thoughts occur." As the "animal
spirits, which are like a tenuous wind, or rather like a pure or vital flame", pass along "the passage
from the anterior to the posterior cavities of the brain", it takes advantage of its strategic position
(it is "suspended above the passage") to exert itself upon them, and is reciprocally affected by the
changes they undergo." (Descartes, 1596-1650.)
Within a short time, Gall and those who followed him showed that the neocortex was
the seat of consciousness and any similar function of the pea-sized pineal was considered
absurd. However within the past decade, we have learned that the pineal gland synthe
sizes powerful neurohormones and that these "animal spirits" do move through the
third ventricle to affect the pituitary gland and probably vital nuclei in the hypothalamus
and medulla as well. And Descartes did it all with deductive reasoning and lyric prose.
The first investigator to localize consciousness to the cortex was Joseph Gall (Acker
knecht, 1958). By 1810, he had formalized a new concept of brain function that was
based mainly on 12 proofs he derived from comparative anatomy of the brain. His initial
conclusions were fourfold:
1. Faculties are innate.
2. Faculties depend on organic structures.
3. The brain is the organ of all faculties, tendencies, and feelings.
4. The brain is composed of as many organs as the individual has faculties, tendencies,
and feelings.
Gall observed that the development of these faculties paralleled the evolution of the
neocortex, so he localized these organs in the cortex but, while his anatomy was revolu
tionary, his physiology was his downfall. He believed whenever a certain faculty like
memory was highly developed, an appropriate part of the cortex was enlarged. This in
turn led to certain protuberances of the skull. Finally he conceived that he could palpate
and influence these organs through an intact skull. This was the beginning of phrenology
and the ending of science.
The real impact of evolution occurred in the last half of the nineteenth century, in
large measure this was inspired by Darwin. At this time the neocortex was precisely
defined anatomically and Sherrington was the unquestioned leader in localizing different
levels of brain function. However, his methodology was not well suited for a study of
consciousness; this remained a task for Hughlings Jackson, using human disease as the
experimental model. Jackson related consciousness to his highest centers, which he iden
tified in various parts of the cortex but in which he recognizes several levels (Taylor,
1931). In epilepsy, he says:
There are three degrees of negative affection of consciousness; in ciinicallanguage they are
mental confusion, insensibility and coma.
His conception of insanity was even more important for he believed this to be the
result of a dissolution of the various levels of consciousness:
In every insanity, with one obvious exception (complete dementia), there is a double symptomatic
condition, a condition of two opposite mental elements, one negative and one positive (or superposi
tive). Repeating what has just been said, there is in every insanity (1) negatively, defect of conscious
ness (loss of some consciousness) and there is (2) the consciousness remaining.
In complete dementia, the situation becomes quite different:
Here the negative mental affection is greatest, is indeed total; there is dementia. There are no
positive symptoms; there is no mind or consciousness. There is complete dissolution, and thus no
4
lower range of evolution remains. Here is what I called "the obvious exception" to the statement
that the mental condition in insanities is a double condition, one of a negative and a positive element.
In this depth there is no person but only a living creature. (Hughlings Jackson, 1834-1911.)
Following the stimulus of Jackson's ideas, insanity was recognized as brain disease
and not the result of an indwelling evil spirit, or a just tribute exacted by an intemperate
and dissolute life. This was an abnormality of the neocortex and the primary brain
change was cortical atrophy.
During this same interval the clinical manifestations of dementia were being re-evalu
ated and reclassified. Prior to this time mental illness was distinguished on the basis of
activity (mania, melancholia) and on the time of life (adolescence, menopause, senium,
etc.). Now Maudsley (1868) and Clouston (1874) in England, Charcot (1868) in France,
and Kraepelin (1883) in Germany were furiously characterizing the various forms of
insanity. Probably the best example of this new psychiatry is the evolution of dementia
praecox (schizophrenia), which occurred in the eight editions of Kraepelin's textbook
Psychiatrie that appeared between 1883 and 1910.
A major advance occurred when it became clear that only certain forms of insanity
were associated with cortical atrophy. These chiefly occurred after age 65 and, because
this was believed to be due to brain aging, the entity was called senile dementia. Conver
sely most of the insanities occurring at an earlier age had no change in the brain organ.
We must appreciate that although the new entities were considered to represent abnor
mal brain function, no one had any idea of the basis of the problem or of a rational
form of treatment. Indeed the situation had been unchanged since Pinel took the chains
off the mental patients in the Bicetre in 1793.
The insanity related to degeneration of the brain was chronic, progressive, and fatal.
By 1868 Maudsley was able to characterize several categories of chronic insanity:
They represent in undistinguishable varieties the shattered wrecks of the mental organization.
Three main groups of them may perhaps be made. The first will consist of those who exhibit a few
striking delusions which seem to be automatically expressed.
In a second group of cases there is a more general incoherence or craziness, without any parti
cular delusion, but with greater external activity.
Lastly, there is a group of demented patients in whom the mind is almost extinguished: who have
to be fed, moved, clothed, and cared for; who evince little or no sensibility; whose only utterance is
a grunt, a whine, or a cry; and whose only movements are to rub their heads or hands.
These chronic progressive disorders were even less treatable than the functional prob
lems but some idea of cause was derived from the brain changes. In 1874, Clouston
could write about the cause of senile insanity on the basis of 203 cases occurring in sub
jects over the age of 60:
The three great dangers to normal mental senility are hereditary brain weakness, a diseased vas
cular system, and the effects of over exertion or toxic irritations of brain structures either at the
time or at former periods of life which have left the convolutions weakened.
It is impossible to fix an age at which physiological senility begins, and therefore we cannot fix
an age for senile insanity.
Premature age in look characterizes many of those who become insane after 4S.
By the end of the century, sophistication but no fundamental change in Maudley's
concept had occurred. Senile dementia had become a disease entity comprising two
forms. Simple senile dementia appeared to be the comparatively benign form, beginning
with episodes of confusion that gradually became complicated by loss of memory and