Although those who recorded their meetings with Kraepelin usually wrote about him with some affection, it is doubtful whether he was fun to be with. Perhaps the closest he came to his colleagues in his later years was during annual walks in the countryside (nicknamed ‘catatonic walks’ by the junior staff), which it was his custom to take with his assistants. At other times he would browbeat his colleagues with his strongly held views about the dangers of alcohol, having decided in 1895 to live a life of uncompromising abstinence in order to set an example to others.10 An American psychiatrist who knew him remarked on the relationship between Kraepelin’s personality and his approach to his work:
Kraepelin’s personal nature was guarded by a wall of reserve. He held himself sternly to his goals; he devoted himself unremittingly to his work, uncompromisingly following what he believed to be the path of investigation – exact, demonstrable and well established by the assembling of all possible testimony step by step. It was consistent with this nature that only the precision of experimental psychology should seem applicable, that the more elastic boundaries of a subjective psychology of mental disease, like psychoanalysis, should seem forbidden and untrustworthy territory.11
Apparently, Kraepelin’s reserve could cross the boundary into complete insensitivity. One of his assistants, who became seriously ill while accompanying him on a visit to the United States, remarked on his return that: ‘If I had died on the trip, Kraepelin would probably have collected my ashes in a cigar box and brought them home to my wife with the words, “He was a real disappointment to me”.’12
Although Kraepelin is usually remembered for his diagnostic concepts, his research interests were broad ranging. For example, influenced by Wundt he advocated the use of psychological tests in psychiatric research, and carried out simple studies of memory and reaction times with his patients. He wrote an interesting study of the role of speech in dreams based on his own dream diary, although, unlike Freud, he believed dreams to be meaningless phenomena caused by transient neuropathological conditions.13 He was also a pioneer of psychopharmacology (the study of the psychological effects of drugs) and carried out experiments on the mental effects of tea, alcohol and various sedatives. In 1903 he travelled to Java with his brother in order to determine whether the forms of mental illness observed there in both Europeans and natives would correspond to those observed in Germany. He concluded that they did,14 and returned convinced of the importance of the human will, although, as a recent commentator has remarked, ‘He was in no manner consistent in conceiving it as being either free or biologically determined and preferred instead to emphasize the former in describing his own condition and the latter in diagnosing that of his patients.’15
Kraepelin wrote about every major type of psychiatric disorder recognized in his time. However, he was particularly interested in the more severe forms of madness in which the individual appears to lose touch with reality. Today, these disorders are known as the psychoses (although the term was used somewhat differently in Kraepelin’s day). Despite the wide range of information that he was prepared to draw upon, his approach was uncompromisingly medical:
Judging from our experience in internal medicine it is a fair assumption that similar disease processes will produce identical symptom pictures, identical pathological anatomy and an identical aetiology. If, therefore, we possessed a comprehensive knowledge of any of these three fields – pathological anatomy, symptomatology, or aetiology – we would at once have a uniform and standard classification of mental diseases. A similar comprehensive knowledge of either of the other two fields would give us not just as uniform and standard classifications, but all of these classifications would exactly coincide.16
This was Kraepelin’s big idea (see Figure 1.2), announced tentatively in the second edition of the Compendium (renamed the Textbook of Psychiatry), which appeared in 1887, and which he elaborated until just before his death in 1926, soon after which the ninth and last edition was published. Mental illnesses fell into a small number of
Figure 1.2 Emil Kraepelin’s big idea. Kraepelin assumed that there was a discrete and discoverable number of psychiatric disorders. Although he recognized that some symptoms could occur in more than one disorder, he argued that each disorder has a typical symptom-picture. He also believed that the different disorders were associated with different types of brain pathology and with different aetiologies. On this view, the first step towards discovering the causes of mental illness was to identify the different disorders on the basis of their symptoms.
discoverable types, and these could be independently identified by studying symptoms, by direct observation of brain diseases, or by discovering the aetiologies of the illnesses (for example, by finding out whether they ran in families and were therefore determined by heredity). Of course, the only practical method of classification available at the time was by symptoms, as very little was known about the neuropathology or aetiology of psychiatric disorders. However, precisely because individuals with the same illness, defined by symptoms, were assumed to have the same brain disease, it could confidently be assumed that the identification of the illness would lead directly to an understanding of aetiology. On Kraepelin’s analysis, therefore, the correct classification of mental illnesses according to symptoms would provide a kind of Rosetta stone, which would point directly to the biological origins of madness. The Rosetta stone, discovered in 1799 by Napoleon’s soldiers during their invasion of Egypt, contained the same inscription (a decree commemorating the accession of Ptolemy V Epiphanes to the Egyptian throne in 197 bc) in Greek, demotic Egyptian and hieroglyphs, allowing linguists to decipher hieroglyphs for the first time. Similarly, on Kraepelin’s analysis, an understanding of the language of symptoms would allow the researcher to decode both the biological underpinnings of madness and their origins.
How Many Psychoses are There?
Once Kraepelin had decided that the psychoses fell into a small number of discoverable types, the next step was to establish exactly how many different types there were. To achieve this, he collected information about his patients’ symptoms and also data on the long-term course and outcome of their illnesses.17 It was the recognition that symptoms changed with time, and therefore that patients should be observed throughout their lifetimes, that led Kraepelin to collect the thousand and more case studies which, in 1896, still seemed inadequate for his purposes. And it was on the basis of these case studies that he began to conclude that different groups of symptoms followed characteristically different courses.
Between 1893, when he published the fourth edition of the Textbook, and 1915, when the eighth edition was published, Kraepelin began to group together illnesses described by other researchers that apparently had a poor outcome. He included catatonia, a disorder characterized by stupor and abnormal postures. Also included was hebephrenia, a disease that struck during adolescence and which led to a rapid deterioration of mental functions. Finally, there was dementia paranoides, a disease which again led to rapid deterioration, but which was characterized by bizarre fears of persecution. This focus on illnesses with poor outcome reflected a preoccupation with psychological degeneration that was common among psychiatrists of his time, and that had been stimulated by the writings of Augustin Morel, a French psychiatrist who had died in 1873. Morel had suggested that mental illness (like sin) is passed on and exacerbated by heredity, weakening successive generations. (Many years later, this theory would have disastrous implications for the practice of psychiatry in the Third Reich.) It was therefore striking that Kraepelin, on deciding that catatonia, hebephrenia and dementia paranoides were manifestations of the same illness, chose to name the illness dementia praecox, a term originally proposed by Morel as an alternative name for hebephrenia.
The Latin term ‘dementia praecox’ means senility of the young, and that was exactly how Kraepelin saw the disorder. Its various subtypes – ten according to the eighth edition of the Textbook – were reflected in a variety of symptoms which usually
first appeared in adolescence or early adulthood. Patients might experience an absence of emotion, or their emotional responses might be highly inappropriate (for example, a patient might laugh at a funeral). They might display stereotyped behaviour (for example, clapping five times before entering a room) or adopt catatonic postures. Problems of attention were also common, so that patients became distractible and easily confused. They might suffer from strange perceptions, particularly auditory (hearing imaginary voices) and tactile (feeling something touching them in the absence of an actual stimulus) hallucinations. Irrational beliefs were also frequently observed, particularly delusions of persecution (for example, patients might believe that they were being persecuted by the German royal family) or of grandiosity (believing that they had improbable powers). However, the common underlying feature that was always present was an irreversible deterioration of the intellectual functions. Dementia praecox patients became mentally disabled, unable to lead productive lives, and they never recovered. It was for this reason that Kraepelin could confidently assert that:
Although there still are in many details far reaching differences of opinion, the conviction is gaining ground more and more, that dementia praecox is by and large a distinct disease entity; and that we are justified in regarding at least the main group of often very diverse clinical pictures brought here together as the expression of a uniform morbid process.18
During the years in which he was developing the concept of dementia praecox, Kraepelin came to believe that he could recognize a second major type of mental illness, characterized by a periodic course and a good prognosis. As was the case for dementia praecox, this second type emerged gradually over successive editions of the Textbook, in which he collapsed a number of previously described disorders into a single category. The common feature of these disorders was a recurrent or ‘circular’ disorder of mood in which episodes of illness were followed by periods of normal functioning. By the eighth edition of the Textbook, Kraepelin had grouped all mood disorders into the single category of manic depressive illness.19 His use of this term was broad by modern standards. He included disorders in which there are episodes of depression but no episodes of mania, which would now be described as unipolar depression. He also included illnesses in which the individual experienced only one episode followed by a complete recovery.20
A final category of illness described by Kraepelin, but given less attention by later historians of psychiatry, was paranoia. From the fifth edition of the Textbook onwards, this term was used to refer to a chronic illness characterized by delusional beliefs in the absence of significant changes to the patient’s personality. It was differentiated from dementia praecox – in which delusions were also observed – because more general deficits of thinking or will were absent. Until the eighth edition of the Textbook, Kraepelin believed that paranoia had a similar unremitting course to dementia praecox. However, he eventually came to the view that paranoia included cases of low severity, in which at least a partial recovery was possible.
Kraepelin’s Legacy
In the final decade of his life, Kraepelin wrote a number of papers that attempted to draw together his conclusions about mental disorders and the methods by which they could be studied. The most important, published in 1920, was entitled ‘Clinical manifestations of mental illness’,21 and has sometimes been mistaken for a retraction of his previous ideas. To be sure, the tone adopted in the paper was less certain than in many of his earlier publications. Indeed, he began by conceding that progress in understanding the aetiology of most disorders had been painfully slow:
In the past, when tissue was first examined microscopically, new discoveries were made daily. Today we can only make significant progress by using very refined methods. In the case of some diseases many questions have already been answered. It is difficult to broaden our knowledge in such instances. The more we scratch below the surface, the more obvious the problems become and the more refined our tools must be. In spite of all this our successes are becoming more modest. We shall have to resign ourselves to this state of affairs, which after all corresponds to that found in other branches of scientific inquiry.
In passages that anticipated debates that would haunt psychiatry for the remaining years of the twentieth century, he acknowledged the difficulty of distinguishing between disease entities:
No experienced physician would deny that cases occur with unwelcome frequency in which, despite the most assiduous observation, it is impossible to reach a diagnosis. The experience that we cannot significantly reduce the number of misdiagnoses has a crippling effect on one’s job satisfaction.
And:
We shall have to get accustomed to the fact that our much used clinical checklist does not permit us to differentiate reliably manic depressive insanity from [dementia praecox] in all circumstances; and that there is an overlap between the two, which depends on the fact that the clinical signs have arisen from certain antecedent conditions.
However, this did not mean that manic depression and dementia prae-cox were no longer to be regarded as separate diseases. On the contrary:
We cannot help but maintain that the two disease processes themselves are distinct. On the one hand we find those patients with irreversible dementia and severe cortical lesions. On the other are those patients whose personality remains intact. This distinction is too overwhelming for us to accept much overlap between the two groups, particularly as we can often predict the course of the two from the clinical signs.
The problem, as Kraepelin now saw it, was that the patient’s symptoms are not uniquely determined by the disease process. Rather, the symptoms brought out by the disease depend on the individual nature of the patient. Therefore:
It seems absurd to propose that neurosyphilis [damage to the brain that occurs in the final stages of a syphilitic infection] causes patients to believe that they are the proud possessors of cars,* mansions or millions of pounds, and that cocaine causes visual hallucinations of mites and lice. Rather, the general desires of such people are reflected in their delusions of grandeur.
These kinds of influences, Kraepelin believed, could be revealed by the methods of comparative psychiatry, which allowed the varying manifestations of a disorder to be studied in different people and different circumstances. Studies of this kind revealed that symptoms were affected by personal and social factors such as sex (‘women show a greater propensity to erotic delusions and are less flamboyant in the presentation of delusions of grandeur’), age (‘the clinical form of juvenile dementia praecox is… characterized by occasional excitement on a background of apathy and obtuseness’) and culture (‘it goes without saying that [in Java] no one suffered from delusions of guilt because these have their origins in religion’).
These subtle qualifications were all but ignored by the majority of Kraepelin’s followers. To many readers of the successive editions of the Textbook, his work appeared to bring order to a field that had previously lacked an agreed language. However, his system was not adopted immediately or uncritically, partly because alternative models of psychiatric classification were available from his academic rivals. In France, Kraepelin was attacked because of the ‘woolliness of his suggested clinical pictures’,22 and the concept of dementia praecox was accepted only grudgingly. In Germany, Great Britain and the United States his system of diagnosis was vigorously debated before finally being embraced by most clinicians. This ultimate triumph partly reflected the simplifying effect that Kraepelin’s ideas had on the theory and practice of psychiatry. He had asked himself how many different types of psychosis there actually were and had come up with a surprising answer: only three.
2
After Kraepelin
Every great man nowadays has his disciples, and it is always Judas who writes the biography.
Oscar Wilde1
Unlike Freud, Kraepelin never encouraged the formation of a group of disciples who would revere his case studies and proselytize his theories for the benefit of later g
enerations of clinicians. Nevertheless, those who have followed him have by and large regarded his diagnostic system as the foundation stone around which a scientific psychiatry could be built. Indeed, Kraepelin’s success is evident from the fact that his diagnostic concepts have survived until the present time. Two of the names he selected to describe major classes of mental illness – manic depression and paranoia – are in use today. The third – dementia praecox – was discarded in the first important revision of his system, which was brought about by a Swiss psychiatrist, Eugen Bleuler.
Madness Explained Page 3
