PART II — часть 1

THE PSYCHOSES

CHAPTER I

THE TRAUMATIC PSYCHOSES

Traumatic affections of the nervous system have been recognized in a general way for centuries, although the psychoses resulting directly from injuries have been given very little consideration or attention in the past. Concussion of the brain, referred to in the writings of Hippocrates, Galen and Celsus, was first studied postmortem in 1705 by Littré. It is now discussed in all textbooks on surgery. Usually milder forms are described with evidences of shock or collapse—a brief period of unconsciousness, partial or complete, with visual and auditory disturbances, dizziness, muscular relaxation or temporary paralysis, respiratory symptoms, dilated pupils, weakness of the pulse, lowered temperature, etc. Delirium and stupor or coma are associated with more severe injuries. If the cortex is lacerated, twitchings or convulsions often occur. Returning consciousness shows various reactions—headache, vomiting, amnesia, etc., and may be succeeded by convulsions, encephalitis or mental disturbances. DaCosta[147] says that some cases are followed by a complete change in the personality, forgetfulness, headache, insomnia, attacks of depression, lassitude and vertigo with increased susceptibility to alcohol, heat and physical exertion. Acute surgical injuries, and compression due to growths, hemorrhages, fractures, etc., have been exhaustively studied. Compression has been differentiated surgically[148] by the later appearance of a gradual unconsciousness, more definite paralysis, usually on the side opposite the injury, slow pulse and stertorous respirations, unequal immobile pupils, choked disc, convulsive movements, etc. Traumatic encephalitis and meningitis have long been recognized but present no definitely characteristic symptoms which distinguish them from simple inflammatory reactions.

One of the earliest accurate descriptions of brain injury associated with mental symptoms was that of the well-known "crowbar" case. It will be recalled that while blasting in Vermont in 1848 a man by the name of Gage had an iron bar driven through the frontal region of his skull, making a complete recovery and living for over twelve years after the accident. An autopsy showed that only the prefrontal cortex was involved. A very interesting report on his mental condition was made by Dr. John M. Harlow:[149] "His contractors, who regarded him as the most efficient and capable foreman in their employ previous to his injury, considered the change in his mind so marked that they could not give him his place again. The equilibrium, or balance, so to speak, between his intellectual faculties and animal propensities seems to have been destroyed. He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate yet capricious and vacillating, devising many plans of future operations, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he had the animal passions of a strong man. Previous to his injury, though untrained in the schools, he possessed a well balanced mind, and was looked upon by those who knew him as a shrewd, smart business man, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and acquaintances said he was 'no longer Gage.'"

Various other cases reported have established the fact that mental deterioration usually follows extensive injuries to the frontal lobes. Witmer[150] summarizes this as consisting of "slight intellectual degradation, moral and emotional perversion, deficiency of attention, and volitional inefficiency."

A work by Ericksen in 1866 on "Railway Injuries to the Nervous System" and Page's book in 1882 on "Injuries of the Spine" pointed the way to an extensive study of the so-called traumatic neuroses. This characterization of the functional disturbances of the nervous system following injuries was apparently the result of a monograph by Oppenheim on that subject in 1889. They had previously been considered as purely organic in origin. Traumatic hysteria was discussed very fully at various times by Charcot, whose work is so well known as to require no comment. In 1892 Friedmann described a vasomotor complex due to concussion. This is accompanied by such symptoms as headache, dizziness, loss of capacity for both physical and mental work with an increased fatigability, irritability, memory defects, and changes in personality, such as sensitiveness and eccentricity with a marked intolerance to alcohol. This condition appears some time after the symptoms of concussion and shock have subsided and may last for some months. Friedmann looked upon this as purely a vasomotor disturbance. It is probably an important factor, in some cases at least, of "shell shock". Traumatic epilepsy may result from foci of softening or other local areas of injury to the brain. Neurasthenia, hysteria and other neuroses are now generally looked upon as being essentially functional and not organic in origin, although they may follow a trauma. The simulation of these conditions has led to a great deal of discussion, notwithstanding the fact that Oppenheim found them in only about four per cent of his cases. Köppen (1897) made a very elaborate study of the postmortem lesions in the "traumatic neuroses". He found that violence to the skull often resulted in small injuries at the base of the frontal area, at the apices of the parietal lobes or in the occipital region. The pathological changes involved represented localized encephalitis with hemorrhagic infiltration. Foci of softening were often found in the cerebral cortex. He noted coma and convulsions with only minute areas of destruction of the basal cortex at autopsy. This would indicate a severe irritation, probably due to circulatory disturbances. The resulting symptoms he thought were very likely to be confused with general paresis. In cases of extreme dementia following traumatism he often found no pathological lesion other than a cicatrix in the cerebral cortex.

One of the most important contributions to the literature of traumatism as associated with psychoses was made by Adolf Meyer[151] in 1903. Notwithstanding the statements of such observers as Savage, appearing as late as 1905, he expressed the opinion that traumatism and general paresis are not directly related except that injuries may rarely act as precipitating factors. He does not expect to find psychoses resulting from small lacerations or other similar lesions in the cortex. As a result of his observations Meyer[152] described the following forms of traumatic disorders:—

1. The direct post-traumatic deliria with the following subdivisions:

a. Preeminently febrile reactions;

b. The delirium nervosum of Dupuytren, not differing from deliria after operations, injuries, etc.;

c. The delirium of slow evolution of coma, with or without alcoholic basis;

d. Forms of protracted deliria, usually with numerous tabulations, etc. (with or without alcoholic or senile basis).

2. The post-traumatic constitution:

a. Types with mere facilitation of reaction to alcohol, grippe, etc.;

b. Types with vasomotor neurosis;

c. Types with explosive diathesis;

d. Types with hysteroid or epileptoid episodes, with or without convulsions (such as most reflex psychoses);

e. Types of paranoic development.

3. The traumatic defect conditions:

a. Primary defects allied to aphasia;

b. Secondary deterioration in connection with epilepsy;

c. Terminal deterioration due to progressive alterations of the primarily injured parts, with or without arteriosclerosis.

4. Psychoses in which trauma is merely a contributing factor:

a. General paralysis, with or without traumatic stigmata;

b. Manic-depressive and other transitory psychoses, catatonic deterioration and paranoic conditions, with or without traumatic stigmata.

5. Traumatic psychoses from injury not directly affecting the head.

The most interesting feature perhaps of this classification is the post-traumatic constitution. Meyer[153] quotes Köppen's excellent description of this condition as follows:—"Men who have suffered from a cranial lesion in which there has been a severe damage of the brain, with or without an injury to the cranial bones, on their recovery from the immediate results complain especially of all kinds of sensations in the head, which they describe either as pain or as pressure with feeling of crawling or dullness of the head, more or less definitely located at the point where they were hit. They frequently become dizzy, and at times even faint for a short time without any epileptic attack. Although slight attacks of dizziness may recur frequently, epilepsy with typical attacks need not develop. There is further in our patients a great irritability and nervosity. The formerly good-natured or even-tempered persons become irascible, hard to get along with; formerly conscientious fathers cease to care for their family. The irritability at times increases to excessive violence in which actions occur of which they have no remembrance; the nervous system is not only under the influence of psychic irritation but especially susceptible to the influence of alcohol or tobacco, in even small quantities. The working capacity of our patients is very poor. It suffers variously, although such individuals often give an impression of perfect capacity; and since the morbid symptoms are essentially subjective, they always arouse doubts whether they could not do something at least, even if they are unable to work in a noisy shop or on a high scaffolding. It is, however, certain that the patients are very forgetful; in giving orders or doing errands they make the most incredible blunders; frequently everything must be written down. Their capacity for thought has suffered, as is sometimes shown, especially in the great slowness of thought. These patients are unable to concentrate their attention, not even in occupations which serve for mere entertainment, such as reading or playing cards. They like best to brood unoccupied; even conversation is rather obnoxious. This point is so characteristic that it gives a certain means of distinction from simulation, which as a rule does not interfere with taking part in the conversations and pleasures of the ward and playing at cards, which means as a rule too much of an effort for the brain of actual sufferers. The patients are usually advised to take light physical work, but even there they are perfectly useless. Excessive sensitiveness of their head obliges them to avoid all work which is connected with sudden jerks, bending over is especially troublesome; and there is hardly any physical work in which this can be avoided; the blood rushes to the head, headache increases, dizziness sets in and the work stops. Patients feel best when in the open air, inactive and undisturbed. There are but few objective signs, such as increase of pulse, flushing of the face, dermatographia, trembling and uncertainty in the Romberg position, such as is shown in all general nervosity. But the complaints are so exceedingly uniform that the uniformity of the subjective complaints justifies the conclusion that they are well founded. The picture thus is briefly that of a mental weakness shown by easy fatigue, slowness of thought, inability to keep impressions, irritability, and a great number of unpleasant sensations, before all headaches and dizziness."

It is exceedingly interesting to note that Schläger in discussing disorders resulting from concussion of the brain, in 1857, as quoted by Griesinger,[154] makes the following comment on these cases:—"Very often the character and disposition changes; in 20 cases great irascibility, an angry, passionate manner even to the most violent outbursts of temper was remarked—less frequently over-estimation of self, prodigality, restlessness, disquietude; in 14 cases there were attempts at suicide, frequently weakness of memory, confusion." Meyer found, furthermore, in his analysis "all the possible degrees of episodes of more or less dazing and dream states; from a temporary dazed feeling to episodes of hysteriform or epileptoid absences. Apart from the subjective feeling of haziness, the characteristic trait is the occurrence of complete dream interpretations and peculiar fabrications, which color the primary traumatic insanity as well as the subacute and episodic types, and even the paranoic type."

Kraepelin[155] describes concussion and compression, traumatic delirium, traumatic epilepsy and traumatic mental enfeeblement. He finds these conditions due to concussion, compression or injury to the brain substance either at the site of traumatism or at some point opposite. There may be contusions, lacerations of the brain tissue or hemorrhages, usually in the frontal, occipital or parietal regions. Injuries to the cortex are not demonstrable in all cases. The circulatory disturbances he considers an important factor and thinks that they account for smaller lesions of the cerebral tissue in many instances where no gross changes are apparent. More or less disturbance of consciousness is to be expected in these conditions. The patient is somewhat dull, drowsy, clumsy, forgetful and absentminded. Memory is sometimes much affected. In more severe cases there is a complete loss of consciousness which may last a few minutes only or be a matter of hours or days. On waking, the patient is bewildered and confused, with a marked disturbance of apprehension. Perception is involved as in the recognition of complicated pictures or the understanding of long and detailed statements. A clear comprehension of events and surroundings is lacking. The patients may know that they are in a hospital without knowing what hospital it is or why they are there and are unable to recognize persons around them. Occasionally hallucinations of sight or of hearing occur. At times delusional ideas are expressed, usually of a depressive type. They have no realization whatever of their own condition. The memory disturbance may take the form of a Korsakow's complex. Memory gaps appear sometimes for events just before the accident and in other cases cover long periods of time. While as a rule events of the remote past are retained, recent impressions are quickly lost. They cannot repeat what is read to them, do not remember the names of persons about them, and sometimes show evidence of falsification of memory with fabrication. All idea as to time is usually lost. Mental reactions become noticeably difficult. The patient is distractible, cannot count accurately, has difficulty in repeating dates and numbers and forms no correct judgment as to his own personal affairs. Many express themselves, however, on the other hand, with great facility and readiness. Some show considerable fatigability. The mood is often elated with a tendency to facetiousness, although frequently tearful and anxious, particularly at night. Irritable, faultfinding trends usually appear later. As a rule they are talkative, restless, sensitive, abusive or even insolent. Bonhöffer has reported stereotypies as well as stuporous and other catatonic types. In speech the patients often become incoherent, make mistakes, forget words or coin new ones. Similar mistakes appear in reading and writing. Asymbolism and parapraxia are observed. Residual symptoms of the brain injury are headaches, dizziness, fainting attacks and convulsions. The pupils are contracted and do not react properly to light. The pulse is frequently very slow.

In fractures at the base of the brain there is likely to be a hemorrhage from the ears and deafness from injuries to the labyrinth. Involvement of the pyramidal tracts may cause unilateral weakness or even paralysis, with increased knee-jerks and occasionally a Babinski reflex. Usually the mental symptoms appear promptly after the injury. Sometimes, however, there is for a while only a slight dulness. The patients are unable to go about the house unassisted, and act peculiarly, becoming clouded or delirious after a few hours or days. Improvement begins to show itself in a few weeks as a rule unless some intercurrent affection intervenes, but the symptoms may persist for several months. Meningitis or abscess formation often causes death. These developments are usually indicated by a marked delirium or coma. There may also be paralysis, convulsions, disturbances of speech, rise of temperature, etc. The subsidence of active delirious symptoms is sometimes succeeded by Kraepelin's traumatic neurosis. Following the traumatic delirium or concussion psychosis described, mental enfeeblement sometimes appears. Clouding of consciousness is not a factor in this condition. There is usually a complete change in the psychic personality. The patients tire easily, are incapable of sustained mental efforts, forgetful, absentminded, complain of dizziness, dulness, noises in the ears, pressure in the head, migraine, palpitation, etc. Or they may be irritable, with outbursts of anger often alternating with apathy. Some are depressed, anxious or hypochondriacal. There is a greatly increased susceptibility to alcohol and intoxication often induces excitements, epileptiform attacks, stupors or rarely actual dreamstates.

Wildermuth found a history of traumatism in 3.8 per cent of his cases of epilepsy. The statistics of the German Army show 4.2 per cent. When the convulsive manifestations are in the foreground and the picture is one of traumatic epilepsy, advanced mental deterioration may be exhibited, with impairment of mental capacity and disturbance of memory. These cases remain apathetic, forgetful, dull, irritable and childish. At autopsy there are often no evidences of any great injury to the brain. Occasionally extensive areas of softening may, however, be found. Usually there is a widespread destruction of the nerve cells and their associated fibres. There is often a proliferation of the glia, with changes in the vessel walls which may be thickened and dilated, with capillary hemorrhages and softenings. Extensive areas of the cortex may be involved. Bleuler's description of the traumatic psychoses is not essentially different from that of Kraepelin.

The differentiation of these conditions as suggested in the statistical manual of the American Psychiatric Association is as follows:—

"The diagnosis should be restricted to mental disorders arising as a direct or obvious consequence of a brain (or head) injury producing psychotic symptoms of a fairly characteristic kind. The amount of damage to the brain may vary from an extensive destruction of tissue to simple concussion or physical shock with or without fracture of the skull.

"Manic-depressive psychoses, general paralysis, dementia praecox, and other mental disorders in which trauma may act as a contributory or precipitating cause, should not be included in this group.

"The following are the most common clinical types of traumatic psychosis and should be specified in the statistical record of the hospital:—

"(a) Traumatic delirium: This may take the form of an acute delirium (concussion delirium), or a more protracted delirium resembling the Korsakow mental complex.

"(b) Traumatic constitution: Characterized by a gradual post-traumatic change in disposition with vasomotor instability, headaches, fatigability, irritability or explosive emotional reactions; usually hyper-sensitiveness to alcohol, and in some cases development of paranoid, hysteroid, or epileptoid symptoms.

"(c) Post-traumatic mental enfeeblement (dementia): Varying degrees of mental reduction with or without aphasic symptoms, epileptiform attacks or development of a cerebral arteriosclerosis.

"(d) Other types."

We have not as yet, unfortunately, sufficient data at our disposal to warrant intelligent conclusions as to the frequency of the various forms of traumatic psychoses. One hundred and twenty-seven cases reported from the New York state hospitals during a period of six years were classified as follows:—

Undoubtedly with a more definite understanding as to the delimitation of these different conditions more complete information will be available later. We are nevertheless justified in feeling that the frequency of the traumatic psychoses considered as a group can be determined with a fair degree of accuracy. Of 49,640 first admissions to the New York hospitals during a period of eight years, 161, or .32 per cent, were definitely ascribed to traumatism. Twenty-one other hospitals in fourteen different states reported forty-five cases of traumatic psychoses (.24 per cent) in 18,336 admissions. Two hundred and seventeen cases (.3 per cent) have therefore been reported in a total of 70,987 first admissions to forty-eight state hospitals for mental diseases in this country.

CHAPTER II

THE SENILE PSYCHOSES

Never until very recently has any great importance been attached to the psychoses due solely to age or much interest manifested in them. These forms of insanity in the majority of our textbooks have appeared only under the designation of senile dementia. This is true of the earlier editions of Krafft-Ebing and many other writers. Clouston referred to senile dementia as one of four varieties of mental enfeeblement. "Most cases,"[156] he says, "fall under three varieties. The first has as its chief characteristics depression and lethargy. The second consists chiefly of excitement, sometimes with a certain exaltation, but always with irritability, restlessness, unreason, suspicion, and change of affection. The third variety consists chiefly of the abolition of mind in all its forms, or senile dementia, and of complete dotage. In some cases those three varieties form three different stages in the same case. In others they do not change." Régis, in a work on mental medicine covering 668 pages in all, devoted two and one-half pages to a consideration of the insanity of old age. Ziehen[157] in 1894 included "dementia senilis" with general paralysis, epileptic, alcoholic and terminal deteriorations in his group of "acquired defect psychoses" and characterized it as "a chronic organic psychosis of advanced years, the principal symptom of which is a progressive intelligence defect." Excitements, depressions, confusional states, deliria, deteriorations, mental mechanisms of any and all kinds, occurring late in life, were usually disposed of without any effort at differentiation by the very convenient method of relegating them to the obscure domain of senile dementia. This is a field which on exploration has been found to be one of considerable interest. It has been pointed out that manic-depressive insanity not infrequently occurs in persons of advanced age. Uncomplicated alcoholic psychoses are not at all rare. Bleuler has advanced the theory that dementia praecox and certain of the senile conditions are similar if not identical processes. General paresis has been demonstrated in the later periods of life by modern laboratory methods and the diagnosis confirmed at autopsy. Cerebral syphilis certainly cannot be left out of consideration. Toxic deliria are encountered now and then. Even the psychoneuroses are possibilities.

Kraepelin first established the importance of involution melancholia as a form of depression warranting separate consideration. The anxiety psychoses occurring late in life have since been made the subject of exhaustive study by various observers. It was discovered that many of the mental disturbances of the aged could be attributed directly to arteriosclerosis alone. Korsakow's syndrome has been found to be as frequently due to senility as it is to alcoholism. Some of our more modern works on psychiatry have included very elaborate chapters on purely "presenile" conditions. Kraepelin[158] in his last edition devotes twenty pages to a review of this subject.

He divides the presenile psychoses into melancholia, anxieties, late katatonia, depressive delusional conditions, anxious delusional types terminating in advanced deterioration, depressive states with deterioration, excitements and paranoid forms. The development of Kraepelin's conception of melancholia has been fully discussed in another chapter. He speaks also of the occasional occurrence of anxious conditions in late life with excitements or an exalted mood with grandiose ideas or even paranoid manifestations. These may present a catatonic picture with more or less inaccessibility, stereotypies, peculiar attitudes and movements, absurd resistance, impulsiveness, desultoriness and disconnected speech. Our knowledge as to the exact causation and nature of katatonia still being far from complete, he knows of no reason why a process of that kind should not be recognized as one of the presenile conditions. Thalbitzer suggested the name, depressive delusional insanity (depressiven Wahnsinn), for the conditions exhibiting numerous delusions and active hallucinations with an emotional reaction "determined by the course of the disease." Rehm also described a similar form associated with arteriosclerotic changes and characterized by hallucinations of hearing, together with mannerisms and sterotypies.

Kraepelin[159] describes first a group of presenile cases showing the development of depressive ideas and anxious states with a progressive mental enfeeblement. Delusions of self-accusation and persecution present themselves early in the course of the disease. Symptoms of a more decidedly hypochondriacal type may occur later. Hallucinations and somatic delusions also develop, often with nihilistic trends. Everyone is dead, the patient is the only one left in the world, has no legs, cannot go out of the house, has entirely disappeared, does not exist any more, etc. The consciousness is usually fairly clear, orientation is well preserved and there is no marked disturbance of thought. Anxious excitement is often an important feature. The termination is in mental enfeeblement invariably. This condition manifests itself usually at about the fortieth year. He is of the opinion that this symptom complex cannot be considered either as belonging to manic-depressive insanity or attributable to arteriosclerosis, nor is it catatonic in its origin.

He finds another group of cases occurring in women between forty-five and fifty years of age, characterized pathologically by striking anatomical changes and clinically by a very unfavorable course. A depression first appears, followed by anxiety with thoughts of suicide. Hallucinations do not occur as a rule. Restless and agitated excitement is a prominent symptom leading finally to confusion, clouding of consciousness, and disorientation. This is followed by a condition of mental enfeeblement terminating in early death. Well-defined postmortem changes have been found, such as the "grave alteration" described by Nissl, proliferation of the glia, swelling of the protoplasmic bodies with cell enclosures, etc., but no fibril formation. Large quantities of lipoid material are found in the surrounding vessels and in the vascular sheaths. This condition, also observed by Nitsche and Döblin, Kraepelin looks upon as probably a presenile process of autotoxic origin, there being no other cause demonstrable. He does not consider this disease process as being related to "late katatonia," genuine katatonia or manic-depressive insanity.

He would also separate out another smaller group as probably belonging to the presenile forms—cases with excitements of long duration, terminating in a marked deterioration. This condition is likely to be of sudden onset, with depressive ideas of self-accusation, later showing an active restlessness. These patients soon become clouded and confused, often with grandiose ideas suggesting general paresis. They may show memory falsifications. Stuporous states occasionally intervene, followed by an active excitement. Echolalia is common. The excitement may last for months or even for a year or more and often stops suddenly, always with deterioration later. In the cases which have come to autopsy Alzheimer has reported severe and widespread cell alterations, fibre loss, glia reactions, and changes in the vessel walls, somewhat suggesting the pathological findings in general paresis. The cases in this group usually have been of the male sex between sixty and seventy years of age. Kraepelin speaks of the clinical picture as a mixture of the symptoms of general paresis, katatonia and manic-depressive psychoses and it is usually diagnosed as one or the other of these conditions.

The paranoid presenile forms occur usually in women. Consciousness is clear, although there may be a mild anxiety or hypochondriasis. The persecutory ideas are variable and changeable. Delusions of jealousy are common although hallucinations are infrequent. Memory is often somewhat impaired and retrospective falsifications are occasionally observed. The mood is as a rule anxious and suspicious. Suicidal tendencies often appear. Restlessness, excitement, impulsive actions and outbursts of anger are noted at times. Rarely a more cheerful mood develops. The disease may become stationary and show no marked changes for years.

Kraepelin himself seems to be very uncertain as to the significance and the delimitation of these various presenile forms. It must be confessed that some of the types described very strongly suggest the condition formerly looked upon by him as involutional melancholia. It will be noted that he considers as possible etiological factors the disturbance of metabolism which may result from regressive or involutional processes. The differentiation from manic-depressive forms, from arteriosclerotic disorders and from senile psychoses must also be looked upon as presenting some difficulties which cannot be entirely disregarded. Many possibilities suggest themselves.

In the senile deteriorations Kraepelin notes particularly a loss in the capacity of apprehension and perception, with a sluggishness of the train of thought, a dulling of the emotions, a reduction of energy and the development of conduct disorders. Ranschburg in psychological tests noticed a lengthening of the reaction time, with a delay in the choice of action, the reading of words, the performance of addition, and the formation of judgment. The retardation was shown particularly in psychic processes and the association time. The reactions were, moreover, much more monotonous, irregular and unreliable than in the young. Memory tests also showed poor associations.

The most advanced form Kraepelin describes as senile dementia, a progressive mental enfeeblement in which the loss of apprehension and memory becomes a conspicuous feature. The perception of external impressions is diminished and delayed and there is a profound disorder of attention. Memory of the remote past is much better than it is for current events. Retrospective falsification is a common symptom. The patient is, moreover, unable to change old viewpoints or acquire new ones. Delusional manifestations such as childish egotism, foolish suspicions or notions of impending illness develop. Grandiose ideas often occur, delusions of great wealth being common. These symptoms are transitory and come and go without apparent reason. In some cases the hallucinations resemble those found in the alcoholic psychoses. Sooner or later there is a disturbance of consciousness leading to a dreamlike existence suggesting a delirium. There is a noticeable dulling of the emotional feelings. The patients become indifferent and apathetic, losing interest in their surroundings, and are often irritable and excitable. In a certain number of cases depressive states develop, sometimes with suicidal tendencies. The delusions may be hypochondriacal or nihilistic in character. Complaints of persecution are common. Some of the patients show a simple, childish deterioration with seclusive tendencies. Stuporous or cataleptic states may develop. Others become uneasy, wander in the streets, remove their clothes, collect rubbish, or show sexual excitement. Restlessness at night is especially suggestive.

Delirious excited states ("Senile Delirium") characterized a certain number of Kraepelin's cases. In these, clouding of consciousness is marked. The presbyophrenic complex described by Kahlbaum often occurs. These cases are fairly clear mentally at first, as far as their surroundings are concerned, but show memory disturbances, particularly for recent events. Orientation is lost very soon and they fail to recognize old friends and relatives. Fabrications are resorted to for the purpose of remedying these defects of memory and delusions are very common. Nevertheless, judgment about many things is well retained. In some instances, however, orientation for time, place and person is completely lost. Kraepelin is in doubt as to whether presbyophrenia should be looked upon as constituting a definite entity or only a form of senile insanity. It may last for years or terminate in a marked deterioration. In some of the senile cases arteriosclerotic changes in the cortex are very pronounced. This is more noticeable in the depressive and anxious forms and in the incoherent varieties. These individuals become clouded, incoherent, and deteriorate rapidly.

There is also a characteristic paranoid form of senile psychosis. Delusions of suspicion and jealousy are common in these cases. They usually develop persecutory trends and often exhibit hallucinations of hearing. They sometimes show partial disorientation and gaps in the memory. The mood is usually irritable and often anxious. There is very likely to be a disturbance of sleep and often signs of physical enfeeblement. There may be neurological symptoms caused by the arteriosclerotic complications, such as headache, pupillary changes, tremors of the tongue and disturbance of the reflexes. Tremors are also shown in the writing. Paraphasia occurs and there may be sensory aphasia or apraxia.

In severe cases of senile dementia Kraepelin expects to find definite lesions at autopsy. The brain weight is always decreased, sometimes to a very striking degree. The volume of the brain is reduced and the ventricles enlarged. The cortex is diminished in thickness, the frontal region being most affected. The parietal region may be involved, but not to any such extent as in general paresis. There may be localized areas of atrophy. Pachymeningitis and hemorrhagic membranes are often found. The microscope shows a proliferation of the glia cells and there is often some disturbance of the layering of the cortex. Cell alterations appear, with fatty degeneration, some neurones showing little more than a darkly colored nucleus. The glia cells are enlarged. There should be no marked changes in the vessels. Fatty changes in the ganglion cells are very noticeable. There is also some loss in the tangential fibres.

Quite characteristic of the senile brain is the occurrence of the miliary plaques or "drusen" described by Redlich in 1898. Fischer in 1907 reached the conclusion that these "drusen" were pathognomonic of presbyophrenia, as he did not find them in senile dementia, in other psychoses or in normal brains. Hübner, however, noted them in alcoholics and "circular" cases as well as in normal individuals. Oppenheim also found them in the brains of the aged when no psychoses were observed. The interior of the plaque is a homogeneous, dark-staining, structureless mass. Sometimes there is a clear space around this center, with club- or spindle-shaped bodies in the periphery, representing remnants probably of neurones, glia cells or axis cylinders. The whole structure is encapsulated in glia fibres. These so-called plaques were spoken of by Fischer as "miliare Nekrosen" and by Redlich as "miliare Sclerosen." Kraepelin is of the opinion that they are associated either with senile cases showing arteriosclerotic changes or presbyophrenia. Alzheimer has described a senile atrophy of the brain with wedgeshaped areas showing cell loss. This is due to a gradual occlusion of the smaller vessels extending down from the meninges into the cortex, and may result in a hemorrhage, a softening or merely an atrophic area characterized by an absence of ganglion cells. He has also described another group of cases showing characteristic cell changes.

This condition has been given the name "Alzheimer's disease" by Kraepelin.[160] It is marked clinically by a gradual senile deterioration with organic brain changes. These eases show some thought defect, loss of memory, confusion, and clouding. Later they become restless, talkative, sing and laugh, etc. Aphasic disturbances develop early, with paraphasia or apraxia. There are speech disturbances ending in a senseless jargon and writing becomes impossible. An advanced deterioration ensues. Physically there is a general weakness and uncertain gait, sometimes with epileptiform attacks. The pupillary reaction may be lost and evidences of arteriosclerosis usually appear. The disease may last for many years. At autopsy "drusen" are common in the cortex and almost a third of the nerve cells are found to be destroyed. These are replaced by darkly-staining fibril bundles. There is marked neuroglia reaction, particularly around the "drusen" and retrogressive changes are found in the vessel walls. This disease usually appears about the fortieth year and may be looked upon, Kraepelin says, as a "senium praecox," although its significance is not clear.

He finds the senile psychoses occurring usually between the ages of sixty-five and eighty, although they occasionally appear before sixty. Seven and sixty-seven hundredths per cent of his cases were between sixty and sixty-five years of age; ten per cent between sixty-five and seventy; thirty-five per cent between seventy and seventy-five; 27.8 per cent between seventy-five and eighty; 22.2 per cent between eighty and eighty-five; 10.5 per cent between eighty-five and ninety; and 2.78 per cent were over ninety years of age. Of 183 cases studied, twenty-three per cent were cases of presbyophrenia; sixty-three per cent of simple deterioration; eight per cent of arteriosclerotic origin; and the remainder, of delusional forms. More than half of the cases of presbyophrenia occurred in persons over seventy-five. The paranoid and arteriosclerotic forms occurred in younger individuals. In the alcoholic cases the Korsakow complex was common. The analysis of presenile psychoses made by Kraepelin is, to say the least, exceedingly interesting. Such clear-cut differentiations as he describes are, however, not always possible or necessary. Very few other writers have gone into the question so exhaustively, nor is his classification of these conditions generally accepted. Bleuler[161] in 1918 in discussing the presenile psychoses quotes Kraepelin's classification and also refers to Gaupp's anxious depressive forms. Under the senile deteriorations he describes "dementia senilis" and presbyophrenia. He also calls attention to the fact that Binswanger spoke of a "pre-senile dementia" occurring between the fortieth and fiftieth years of age and characterized by an emotional dulness and a diminished capacity for work. Bleuler speaks of the affective disturbances in advanced years as senile mania and melancholia, which he says may recover, the former frequently, the latter more rarely.

The American Psychiatric Association has only attempted to cover the principal groupings of the characteristic senile forms. The differentiation of these conditions as suggested in the statistical manual is as follows:—

"A well defined type of psychosis which as a rule develops gradually and is characterized by the following symptoms: Impairment of retention (forgetfulness) and general failure of memory more marked for recent experiences; defects in orientation and a general reduction of mental capacity; the attention, concentration and thinking processes are interfered with; there is self-centering of interests, often irritability and stubborn opposition; a tendency to reminiscences and fabrications. Accompanying this deterioration there may occur paranoid trends, depressions, confused states, etc. Certain clinical types should therefore be specified, but these often overlap:

"(a) Simple deterioration: Retention and memory defects, reduction in intellectual capacity and narrowing of interests; usually also suspiciousness, irritability and restlessness, the latter particularly at night.

"(b) Presbyophrenic type: Severe memory and retention defects with complete disorientation; but at the same time preservation of mental alertness and attentiveness with ability to grasp immediate impressions and conversation quite well. Forgetfulness leads to absurd contradictions and repetitions; suggestibility and free fabrication are prominent symptoms. (The general picture resembles the Korsakow mental complex.)

"(c) Delirious and confused types: Often in the early stages of the psychoses and for a long period the picture is one of deep confusion or of a delirious condition. "(d) Depressed and agitated types: In addition to the underlying deterioration there may be a pronounced depression and persistent agitation.

"(e) Paranoid types: Well marked delusional trends, chiefly persecutory or expansive ideas, often accompany the deterioration and in the early stages may make the diagnosis difficult if the defect symptoms are mild.

"(f) Pre-senile types: The so-called 'Alzheimer's disease.' An early senile deterioration which usually leads rapidly to a deep dementia. Reported to occur as early as the fortieth year. Most cases show an irritable or anxious depressive mood with aphasic or apractic symptoms. There is apt to be general resistiveness and sometimes spasticity.

"(g) Other types."

The frequency of senile cases is shown by the fact that of 84,143 admissions to the New York hospitals during a period of sixteen years, 12,017, or 14.2 per cent, were over sixty years of age, while 8.4 per cent were between sixty and seventy years old, and 4.5 per cent between seventy and eighty. Of 49,640 first admissions to the New York state hospitals during eight years 4,724 cases, or 9.52 per cent, were diagnosed as senile psychoses. They constituted 9.63 per cent of the admissions in Massachusetts during 1919 and 10.61 per cent of the 18,336 admissions to twenty-one hospitals in fourteen other states. Of 70,987 admissions to all of the institutions referred to, 6,961, or 9.8 per cent, were senile psychoses.

During a period of eight years in the New York state hospitals, when the present classification was not adhered to absolutely, 4,724 senile psychoses were divided into types as follows:—Simple deterioration, 52.01 per cent; presbyophrenia, 5.75 per cent; delirious and confused states, 12.99 per cent; depressed and agitated forms, 8.25 per cent; and paranoid varieties, 16.23 per cent. During the same period less than one per cent of presenile psychoses were reported. Since the Association's classification has been in use the same institutions show the following distribution of 1,351 senile psychoses during 1918 and 1919:—Simple deterioration, 56.24 per cent; presbyophrenia, 4.14 per cent; delirious and confused states, 13.53 per cent; depressed and agitated forms, 18.65 per cent; and paranoid varieties and presenile forms, less than one per cent. The senile psychoses in the Massachusetts hospitals during 1919 were divided as follows:—Simple deterioration, 56.94 per cent; presbyophrenia, 7.79 per cent; delirious and confused states, 7.45 per cent; depressed and agitated forms, 7.11 per cent; paranoid conditions, 18.64 per cent; and presenile forms, 2.03 per cent. In nineteen hospitals in other states 1,823 cases were classified as follows:—Simple deterioration, 64.39 per cent; presbyophrenia, 11.62 per cent; delirious and confused states, 9.59 per cent; depressed and agitated forms, 4.71 per cent; paranoid conditions, 6.91 per cent; and presenile forms, .27 per cent. The total of 6,842 cases referred to above were, therefore, distributed as to type as follows:—

Four hundred and nineteen cases reported by the Ohio state hospitals in 1920 and not included in the above summary were shown as follows:—

These constituted in all 14.4 per cent of the 2,895 first admissions during the year, a much higher rate than that shown in other states. In analyzing these findings it should be borne in mind that the American classifications do not take into consideration presenile conditions as such, they being all reported with the senile psychoses, with the exception of involutional melancholia, which is, of course, shown separately.

Southard[162] has called attention to the margin of error in the diagnosis of senile psychoses. Forty-two cases unanimously diagnosed as "senile dementia" were "reviewed clinically and anatomically, with a surprisingly low general percentage of accuracy (sixty-six per cent) where either cerebral atrophy or cortical arteriosclerosis or both were regarded as confirmatory, and with still lower percentages: (48 per cent) where cortical arteriosclerosis was considered essential and (38 per cent) where cerebral atrophy was considered essential for a correct diagnosis." It is significant that exactly one-third of the cases studied were found by Southard to more properly "belong in a group of acute psychoses or other mental diseases occurring in old age but not dependent on recognizable senile changes."

CHAPTER III

THE PSYCHOSES WITH CEREBRAL ARTERIOSCLEROSIS

Sufficient weight has not been attached heretofore to the important influence of cerebral arteriosclerosis in the production of mental diseases. Unquestionably it has been a complicating factor in many of the generally recognized psychoses which has not been given adequate consideration. Its relation to involution melancholia as well as the presenile and senile disorders has been given a great deal of attention, but cannot as yet be clearly defined. Only in its syphilitic forms can it be looked upon as contributing to the clinical picture in general paresis. It is, however, productive of late deterioration in the chronic alcoholic conditions and in the manic-depressive psychoses occurring in advanced years. It plays a part frequently in the terminal stages of dementia praecox. In paranoia and the paranoid conditions of long standing it often becomes a factor to be reckoned with. Certainly in the differentiation of the epilepsies of the aged it must be taken into definite account.

The importance of arteriosclerosis, a term used first by Lobstein some seventy-five years ago, has long been recognized. Osler in referring to this subject made the following interesting comment:—"To a majority of men death comes primarily or secondarily through this portal. The onset of what may be called physiological arteriosclerosis depends, in the first place, upon the quality of arterial tissue (vital rubber) which the individual has inherited and secondarily upon the amount of wear and tear to which he has subjected it. That the former plays the most important rôle is shown in the cases in which arteriosclerosis sets in early in life in individuals in whom none of the recognized etiological factors can be found. Entire families sometimes show this tendency to early arteriosclerosis, a tendency which cannot be explained in any other way than that in the make-up of the machine bad material was used for the tubing."

Our present knowledge as to the relation of syphilis to this disease has not changed the significance of the observations made by Osler in any way. Heredity more than any other one factor undoubtedly determines the development of both senility and arteriosclerosis. "When," as Lambert[163] expresses it, "physiological involution anticipates in time or exceeds in direction, extent and severity normal senescence, the various senile and arteriosclerotic disorders are the result." It is as a rule only in the later stages of the disease when focal symptoms occur or a psychosis develops that hospital care becomes necessary. Practically any of the vessels of the brain may be involved and it frequently happens that more than one is affected either directly or indirectly. The neurological symptoms resulting depend entirely on the location and extent of the lesion. Lambert[164] has made the following excellent anatomical classification of the more common arteriosclerotic processes:—

I. Incipient type.

II. Focal types.

(a) Trunk disorders.

1. Basilar-carotids.

(b) Branch disorders.

1. Inferior cerebellar.

2. Superior cerebellar.

3. Posterior cerebral.

4. Middle cerebral.

5. Anterior cerebral.

(c) Twig disorders.

1. Medullary.

2. Cortical.

Some reference should be made, perhaps, to the focal symptoms resulting from more or less sharply circumscribed lesions which are productive of certain fairly well known complexes, whether due to arteriosclerotic softenings, hemorrhages, or growths. These have been concisely summarized by Barker[165] somewhat as follows:—

Frontal Lobes—Lesions of the left inferior frontal in righthanded persons cause motor aphasia. Subcortical involvements cause word dumbness. Disturbances in the anterior part of the frontal region are sometimes associated with the Witzelsucht of the German writers—a tendency towards joking and witticisms.

Central and Paracentral Lobules—Contralateral sensory, motor symptoms or a combination of the two. Monoplegias, anesthesias and Jacksonian epilepsies are characteristic. Contralateral tactile agnosia and apraxia occur, especially in lesions of the left hemisphere. An involvement of the left side may also cause a homolateral apraxia, dyspraxia or a tactile agnosia.

Parietal Lobes—Lesions in the anterior part cause contralateral somesthetic disturbances, tactile agnosia or apraxia. Involvement of the left angular gyrus may cause optic aphasia or alexia; if deep enough, hemianopsia results. The voluntary movement of the eye may be interfered with.

Temporal Lobe—Lesions in the posterior half of the first temporal may cause Wernicke's sensory aphasia and a subcortical involvement, word deafness. Bilateral destruction of the first and transverse temporals causes cortical deafness. Extensive bilateral lesions in the lower part of these lobes result in mind deafness. Irritative lesions in the uncinate gyrus lead to hallucinations of taste and smell, with smacking of the lips and tongue movements.

Island of Reil—Lesions of the anterior part cause symptoms resembling Broca's motor aphasia. Lesions of the posterior part result in symptoms suggesting Wernicke's sensory aphasia. Transcortical motor and sensory aphasia may result.

Occipital Lobes—Lesions of the calcarine area give rise to hemianopsia, and bicortical involvements lead to cortical blindness. Bilateral lesions of the lateral surface may cause mind blindness.

Disturbances in the centrum ovale may cause monoplegias or monoanesthesias, and lesions in the corpus callosum, apraxic symptoms. Characteristic of cerebellar lesions are ataxias and disturbances of equilibrium, often with vertigo and paroxysmal vomiting.

An involvement of the corpora quadrigemina may cause pupillary changes, unilateral or bilateral paralysis of eye muscles, nystagmus, visual disturbances, deafness and ataxia or anesthesia.

Lesions of the cerebral peduncles may give rise to very characteristic syndromes. If the tegmentum and pes pedunculi (basis pedunculi) are both involved, there may be a complete hemiplegia of the opposite side with an oculomotor paralysis on the same side (Weber-Gubler syndrome). Or there may be in addition to this a marked tremor in the limbs of the paralyzed side (Benedikt's syndrome). A unilateral oculomotor paralysis may be combined with a cerebellar ataxia (Nothnagel's syndrome). The thalmic syndrome of Déjerine and Roussy shows a contralateral hemianesthesia, violent and persistent pains on the anesthetic side, hemiataxia, hemichorea or hemiathetosis, slight temporary hemiparesis and sometimes hyperesthesia. Lesions further back, possibly involving the internal capsule, may cause hemianesthesia of touch, pain and temperature senses.

S. A. K. Wilson in 1912 called attention to a particularly important syndrome, designated by him as "progressive lenticular degeneration" and characterized by dysarthria, dysphagia, general tremors of the extremities, forced laughing and crying, muscular rigidities and contractures, with a slight intellectual impairment. Interesting features of this disease complex are that it is familial in type, but not hereditary, comes on early in life, usually progressing to a fatal termination, and is associated with a cirrhosis of the liver which is not alcoholic in origin. At autopsy degenerations of the nucleus lentiformis have been found. J. Ramsey Hunt in 1916 called attention to the association of both paralysis agitans and Huntington's chorea with lesions in the globus pallidus. Oppenheim has recently differentiated a striatum syndrome to which he gave the name "dystonia musculorum." Difficulties in writing, tremors, disturbance of the gait, rigidities, tonic and clonic movements of the muscles and other neurological symptoms are present. Several cases reported by Abrahamson in 1920 showed definite emotional disturbances. Cecile and Oskar Vogt have recently (1919) studied the striatum lesions from a standpoint of both pathology and symptomatology. As summarized by Lhermitte[166] their work shows that athetosis, paralysis agitans, Huntington's chorea, dystonia musculorum, probably paralysis agitans and various other neurological syndromes are to be attributed directly to conditions involving the striate bodies. Prominent among these are softenings and hemorrhages which may result from arteriosclerosis. In view of these facts a careful study of the focal lesions associated with the arteriosclerotic disorders is exceedingly important.

The pathological processes involved have been carefully studied by Heubner and others. He was originally of the opinion that cerebral arteriosclerosis was always of specific origin. Baumgarten, however, subsequently showed that this was not the case. The more characteristic changes in the larger vessels manifest themselves in the form of patches of atheromatous thickening so common at autopsy. As a result of degenerative changes in the elastica and media, and a consequent weakening of the vessel wall, intimal thickening takes place. This is not the circular, uniform, concentric involvement found in syphilitic processes but a localized proliferation of the intima at some one point. There may be an infiltration of colloid and calcareous material in the media. This leads to further intimal thickening. In the smaller vessels arteriocapillary fibrosis has been described—a uniform thickening of the vessel walls with a connective tissue formation. Endarteritis obliterans, first described by Friedländer in 1876, is probably always of syphilitic origin.

In addition to the vascular changes in the cerebral vessels Kraepelin[167] finds usually atheromatous changes in the aorta and its branches, particularly the coronaries, with ulcerations or calcareous plates, hypertrophy and dilatation of the heart, myocarditis, interstitial nephritis and infarctions of various organs. At autopsy the dura and pia are usually thickened and adherent, with a general atrophy of the cerebral convolutions. There are often fresh hemorrhages under the membranes as well as cyst formations and dilatation of the brain ventricles. He particularly emphasizes a splitting of the elastica in the larger cerebral vessels with a thickening and tortuosity, fatty infiltration and calcareous deposits. Hyaline degeneration is common in the elastica and muscularis with fatty granular cells in the adventitia. Capillary aneurysms are often found. Glia proliferation is to be expected in the surrounding area. A condition described by Alzheimer as perivascular gliosis often occurs. There is a disappearance of the perivascular nervous elements with consequent proliferation of the neuroglia. In a general way Kraepelin differentiates several distinct pathological groups—a diffuse cortical involvement, circumscribed processes in the neighborhood of vessels, hemorrhages and softenings. There is also a loss of nerve fibres which are replaced by neuroglia. Binswanger has described a "chronic subcortical encephalitis" due to arteriosclerosis. This consists of an atrophy of the white matter due to an involvement of the deeper marrow vessels. Large gaps and lacunae are found in the course of the vessels. There is an extensive atrophy of the fibres and there may be occasional foci of softening. As a general rule involvement of the large vessels is liable to affect the medullary substance while sclerosis of the smaller vessels leads to cortical disturbances. It is also possible to have extensive lesions without mental symptoms and well developed psychoses with only a slight physical basis. The site of the damage to the vessels determines this. On the other hand, the mental condition may be due to cardiovascular complications resulting usually in anxiety psychoses. The symptomatology may be complicated by senility, alcoholism or syphilis.

Clinically Kraepelin [168] divides the arteriosclerotic psychoses into deteriorations, or milder forms of mental enfeeblement, dementias, depressions, excitements, late epilepsies, and apoplectic dementia. In the milder forms there is a gradual change in the entire psychic personality, with a later development of more marked changes, either physical, mental or both. The early symptoms are a general reduction of the mental capacity and an impairment of memory. The patient tires easily and loses all evidences of energy, with no inclination to undertake anything new. Familiar names and dates are forgotten. Recent occurrences are particularly lost to memory. The real is confused with the false. In business the patient becomes careless and unreliable, overlooks important transactions and forgets appointments. There are often subjective feelings of impending illness. The mood becomes depressed, whining and tearful. Irritability and outbursts of anger occasionally appear, characterized by a marked emotional instability, varying rapidly from tears to laughter. Suicidal tendencies are sometimes noted. Mild confusional states may be induced by alcoholic indulgences. Early physical symptoms are headache, sensations of fulness and pressure in the head, followed by a feeling of dizziness, fatigue, exhaustion, debility, etc. Sooner or later, following a seizure of some kind, neurological signs appear—drooping of the mouth, lateral deviation of the tongue, weakness of an arm, dragging of one leg, loss of sensation on one side, ankle clonus, an increase, decrease or inequality of the patellar reflexes, and sometimes a Babinski reflex. The pupils are very likely to be unequal and sluggish in reaction. The features present a tired, sleepy expression and speech becomes tremulous and monotonous. There may be a difficulty in finding words, or the misuse of words. There are usually tremors of the fingers and movements are uncertain, the gait being unsteady. Romberg's symptom may be present. Dizzy spells and fainting attacks also occur, sometimes followed by genuine convulsions. Apoplectiform seizures may be observed, with unconsciousness for hours or days. These may be followed by sensory or motor aphasia, unilateral paralysis with or without disturbances of sensation, hemianopsia, alexia, agraphia, asymbolism or apraxia. Cardiac disturbances with anxieties are often complications. These apoplectiform and other severe attacks sometimes occur a long time after mental symptoms have appeared. They are likely to recur, mental deterioration progressing rapidly with the repetition of the seizures.