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The Fall of the House of
Kraepelin ‘The Dialectics of
Schizophrenia’ by Phil Thomas
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The
concept
of schizophrenia is contentious. Although most psychiatrists accept
without question the notion that schizophrenia is a disease - a
psychiatric disorder brought about by changes in brain function,
scepticism reigns outside the profession, especially in many of those
to
whom the label is attached. So-called ‘schizophrenics’ may choose a
variety of non-medical ways to understand and explain the nature of
their
experiences, and this leads us to the heart of a conflict in which
the
subject’s explanation of his or her experiences lies at odds with the
psychiatrists. Inevitably it is the psychiatrist’s account which will
turn
out to be the most powerful, as can be seen in the famous case of
Judge
Daniel Schreber (see, for example Leudar & Thomas 1999). But it
need
not always be this way. In this paper, I shall try to demonstrate
some of
the shortcomings of the way in which psychiatrists interpret the
Kraepelinian concept of schizophrenia, especially the relationship
between
the acute ‘symptoms’ of the condition and outcome. I shall then
challenge
the way this interpretation is used to justify the use of long-term
neuroleptic medication, with the conclusion that psychiatrists must
jettison the medical model when working with people in acute
psychoses, in
favour of humanistic models which recognise the importance of the
relationship between the individual and the experience of psychosis.
But
first, we must consider the origins of the concept of
schizophrenia.
Kraepelin
and Dementia Praecox Morel provided one of the earliest
descriptions of the condition we now call schizophrenia. In 1860 he
described a case of severe intellectual deterioration in an
adolescent
which he called demence precoce (dementia of early onset). There
followed
a series of descriptions in the neurological literature of the day,
the
most influential of which was provided by Kraepelin in the fourth
edition
of his textbook in 1893. Here he described an illnesses called
dementia
praecox, under the heading of ‘Psychic Degenerative Processes’. This
group
of illnesses was characterised by a progressive and irreversible
deterioration of intellectual function, typically in young people. He
gave
the following definition of the illness in the eighth edition of his
book
(Kraepelin, 1913): “Dementia Praecox consists of a series of
clinical
states which have as their common characteristic a peculiar
destruction of
the internal connections of the psychic personality with the most
marked
damage of the emotional life and volition.”
Early
psychiatrists, influenced by Griesinger, believed that medical
science
would reveal the cause of all forms of insanity. But basic clinical
sciences such as pathology, physiology and anatomy, which had been so
successful in revealing the cause of neuro-syphilis, failed to reveal
the
cause of dementia praecox so Kraepelin had to rely on systematic
clinical
observation. Hoenig (1983) has described Kraepelin’s katamnestic
method,
which relied on the detailed description of individual cases, in an
attempt to delineate the specific symptoms and signs of dementia
praecox,
in the hope that such an approach would confirm that dementia praecox
was
a disease entity with a specific anatomical basis and pathology. The
issue
here concerns the extent to which he succeeded in describing a single
disease, dementia praecox with poor outcome?
The
first
point concerns the great variability of symptoms to be found in
schizophrenia. Even Kraepelin (1913) admitted this, going so far as
to say
that: ‘Unfortunately in the field of psychic disturbances there is
not
a single symptom which is pathognomonic for any particular illness.
On the
other hand we can expect that the composition of the individual
characteristics which form the total picture, and in particular the
changes which develop in the course of the illness, will not be
produced
in exactly the same way by any of the other diseases.’ (Vol.II,
p.
945, quoted in Hoenig, 1983; my italics).
Kraepelin
failed to provide a “pathognomonic” symptom for schizophrenia, and,
in
lieu of this, he chose to emphasise the importance of the course of
the
illness. This position has been immensely influential. After
Kraepelin,
psychiatrists believed that a deteriorating course was a cardinal
feature
of schizophrenia. Deterioration here refers to the “changes which
develop
in the course of the illness” in the quotation from Kraepelin above.
It is
this that forms the basis of the belief that schizophrenia is a poor
prognosis illness. Furthermore, there is an implicit assumption that
deterioration is related to the putative disease process.
The
problem
is that Kraepelin not only found it difficult to be prescriptive
about the
symptoms required to diagnose schizophrenia and thus predict outcome,
but
he was also unable to show that all of the 127 cases of schizophrenia
he
studied in detail actually turned out to have poor outcome and
deteriorating course. Kraepelin himself found that complete recovery
was
possible in 12.5% of cases (Vol. II, p. 865, quoted in Hoenig, 1983).
Bleuler remained unconvinced that the condition was a single disease
entity, because of the diversity of symptoms and variation in outcome
(Bleuler, 1911): ‘Kraepelin’s concept continues to be opposed by
many,
who because of the wide diversity of the clinical pictures, cannot
accept
it as a single entity, which originally appeared to be based on the
uniform course of the illness, and yet could include cases with a
good as
well as a bad outcome.’
The
Course
of Schizophrenia There have been two ways of investigating
this.
The first depends upon long-term studies of large numbers of patients
over
many years. The second involves smaller studies over shorter periods
of
time, but has the advantage that standardised diagnostic and outcome
criteria are used. In the first approach Huber et al (1979) in Bonn
studied the outcome of over 500 people diagnosed with schizophrenia
over
21 years. In 57% of cases outcome was favourable, although there was
great
complexity in the patterns of the condition over time. In Zurich,
Bleuler(1978) followed up over 200 patients for 22 years. He found
good
outcome in 53% of subjects. Ciompi (1980) identified nearly three
hundred
people admitted to a psychiatric hospital in Lausanne whose histories
were
documented until the age of 65. The average follow-up period was
almost 37
years. Like Huber, he found considerable variation in the pattern of
the
symptoms with time. Overall, 49% of patients had a favourable
outcome, and
in comparison with the situation on admission, in two thirds of cases
mental health was completely or partially improved. These studies
show
remarkably similar outcomes for schizophrenia, with approximately 50%
having good outcome, but there are weaknesses relating to the
retrospective design of these studies, and the reliability of the
diagnoses. Ciompi used Bleuler’s criteria, which may include some
people
who are not suffering from schizophrenia and who are destined to have
a
good outcome, thus artificially improving the apparent outcome in
schizophrenia. The best way around this is to use a prospective
design.
Carpenter et al (1978) followed up over 130 patients in the American
IPSS
research centre after five years, and split their sample into two
groups,
based on the twenty patients with the best and twenty patients with
the
worst outcome scores. Only restricted affect discriminated between
the two
groups of subjects on initial assessment. The authors concluded that
the
diagnosis of schizophrenia, when based on the presence of acute
(positive)
symptoms was of little value in predicting the course and outcome of
the
condition. This study indicates the difficulties in predicting
outcome
when people present with acute symptoms of schizophrenia. The main
purpose
of diagnosis and recognising diseases is to enable us to make such
predictions. Hays (1984) has pointed out that despite the efforts of
thousands of researchers over many years and the development of many
different sets of diagnostic criteria, the cause of schizophrenia
remains
unknown. Psychiatrists must, he argues, face up to the unpalatable
fact
that schizophrenia as a disease entity conceived of by Kraepelin does
not
exist.
“...
(Kraepelin) is the sole, flawed, authority for this extraordinary but
influential theory.” (Hays, 1984)
This
forces
us to the conclusion that there is little evidence to support the
Kraepelinian model of schizophrenia. There is neither the evidence to
support biological models of the condition, nor the evidence to
justify
the existence of the condition as a diagnostic category,
characterised by
specific acute symptoms which predict outcome. I want to make one
final
point concerning poor outcome. Ciompi found that in two thirds of
cases
social outcome was either intermediate or poor. His figures suggest
that
the main field of impairment in schizophrenia is not symptoms, but
social
functioning. But in view of the fact that all the patients studied
had
been institutionalised for decades, this is hardly surprising, and
may
have little to do with the progress of an illness. Zubin et al (1983;
see
chapter two, p. 38) have suggested that over the last fifty years
schizophrenia has become a less severe condition with a better
outcome.
Over this period the management of the condition has changed
profoundly.
People who have the condition are no longer incarcerated in
institutions
for years as was the case when Kraepelin wrote about dementia
praecox.
This raises the possibility that the poor outcome described by
Kraepelin
was an artefact of institutionalisation.
Medication
and Outcome Research indicates that between 60 to 80 percent
of
subjects whose symptoms are controlled by depot neuroleptics
experience a
relapse and hospitalisation if medication is discontinued. Such
evidence
provides strong support for the role of neuroleptics in the long-term
management of schizophrenia. The difficulty is that there is also
much
evidence that medication fails to help many people diagnosed with
schizophrenia. There are four issues at stake here. The first
concerns the
efficacy of neuroleptics in controlling positive symptoms of
schizophrenia. The second concerns their claimed effect in favourably
changing the long-term outcome of schizophrenia. The third concerns
the
validity of this evidence, much of it drawn from specially designed
research protocols (drug trials), in relation to the reality of the
day to
day practice of psychiatry. Finally, and most worrying of all, there
is
evidence that relapse, should it occur, arises through a
supersensitivity
reaction similar to that thought to be responsible for
TD.
1.
Efficacy of neuroleptics Davis and Caspar (1977) noticed that
25
percent of people continued to have psychotic symptoms despite taking
neuroleptics. The persistence of their symptoms was not explained by
the
presence of physical health problems that might cause them to be
suffering
from organic brain disorders. Davies et al (1980) reviewed a
large
data base of clinical trial data from the 1960’s generated by the
National
Institute of Mental Health Psychopharmacology Research Branch in the
USA.
About 30% of subjects in these studies were rated as either minimally
improved or clinically worse, following treatment with neuroleptics.
Kane
et al (1988) suggested that a conservative estimate indicates that
the
symptoms of a fifth of all patients suffering from schizophrenia fail
to
respond to neuroleptic drugs. The most striking evidence of a group
of
people whose psychotic symptoms failed to respond to neuroleptic
medication came from a British study. Curson et al (1988) found that
46%
of their sample of over 200 long-stay patients had persistent
delusions,
and 32% had persistent auditory hallucinations. The point here is
this
group of people had been exposed to what the authors described as
“energetic pharmacological ... treatments”. These studies indicate
clearly
that some people diagnosed as suffering from schizophrenia do not
respond
to neuroleptic medicationand continue to experience so-called
positive
symptoms. But what about the effects of neuroleptics on the course of
schizophrenia?
2.
Neuroleptics and long-term course Psychiatrists, prompted by
the
pharmacological industry, have believed that maintenance medication
taken
for many years not only controls positive symptoms, but also improves
social function. Ciompi (1980) was also interested in the extent to
which
neuroleptic medication influenced the course of schizophrenia. He
divided
his subjects into three groups by date of first admission,
corresponding
to the period prior to the introduction of electro-convulsive therapy
(pre
1933), the period prior to the introduction of the neuroleptics (1933
to
1953), and the period following the introduction of neuroleptics
(post
1953). If neuroleptics have a beneficial effect on outcome, then we
would
expect the latter group of people to fare better. Ciompi was
surprised and
disappointed to find that over very long periods of observation, no
statistically significant differences could be found in outcomes of
people
admitted in these different therapeutic eras. He concluded that
people
admitted with schizophrenia in the nineteen fifties, following the
introduction of the neuroleptics did no better in terms of social
adjustment than those admitted in the first three decades of the
century.
Kane and
Freeman (1994) have reviewed the advantages and drawbacks of
neuroleptic
treatment. First, they make the point that a number of authorities
have
doubted whether neuroleptics have a beneficial effect on
outcome. “...it remains debatable whether or not long-term
neuroleptic
treatment substantially alters the course and outcome of this
disorder...” (Kane & Freeman, 1994, p.22)
Karl
Leonhard
(1980) argued that psychiatrists should only consider using long term
therapy once it was established without doubt that the condition from
which the individual was suffering was a phasic disorder, that is a
condition characterised by recurrent episodes of positive, or other
acute
psychotic symptoms. This was based on his view that such a symptom
pattern
tended to respond to neuroleptics, whereas the defect state did not.
Schooler (1991) in her study of dose reduction commented that the
results
of naturalistic long-term follow up studies in schizophrenia show
clearly
the great diversity of outcomes of the condition. Despite long term
medication, some people appear to have a very poor outcome. On the
other
hand some people do very well with little or no medication. The word
naturalistic is very important here. Most of the accepted evidence in
support of the value of neuroleptics in the short-term and long-term
management of schizophrenia comes from drug trials, which are special
studies resourced and supported by the pharmacological industry. Such
studies can hardly be described as independent. In addition, they are
performed under ideal conditions which are hardly representative of
the
circumstances under which these drugs are used by psychiatrists in
the
daily work. In this sense, the ecological validity of these studies
must
be called into question.
The most
naturalistic study in this sense was undertaken by Johnstone et al
(1986)
working at Northwick Park in London. Patients were under the care of
forty
psychiatrists working within a thirty five mile radius of Harrow.
Over 460
patients met the criteria for inclusion in the study over a period of
almost two and a half years, yet 14% of these patients could not be
assessed for a number of reasons. These included refusal of either
patient
or consultant to consent to study, self-discharge before assessment
could
be made, administrative problems such as patient not admitted, or
‘conversation’ barriers. These problems are typical of those commonly
encountered by psychiatrists in their day to day work. Of the
patients who
could be assessed, only 120 could be entered into a randomised
placebo-controlled drug trial of maintenance neuroleptic medication
(Crow
et al, 1986). They found surprisingly high rates of relapse in the
two
years following discharge both in the placebo group and,
surprisingly, the
group who received active medication. Although 70 percent of patients
on
placebo relapsed, 58 percent of those taking active medication did so
over
the same period. Overall these results suggest that at best, the
benefits
of neuroleptic medication in preventing relapse are marginal.
The
situation
is summarised well by another quote from Kane and Freeman
(1994): ‘Thus, current neuroleptics, despite their great value in
controlling schizophrenic symptoms, have a number of major drawbacks.
They
are far from consistently effective, and a substantial subgroup of
patients derive little if any benefit from them. They remain
ineffective
against negative symptoms. They cause adverse neurological effects
which
may interfere with psychosocial and vocational rehabilitation and are
associated with major problems of drug compliance.’ (p.29)
3.
Relapse
- drug discontinuation or illness? It is worth pausing at this
point to consider an important assumption present in much of the
research
that we have considered here. When psychiatrists talk about the
relationship between relapse and discontinuation of neuroleptic
medication, the relapse has always been viewed as a function of the
illness process which, in some way or another, was being damped down
or
held at bay by medication. Nobody has ever produced a satisfactory
explanation of how this might happen. But there are
psychopharmacological
models that can explain the appearance of abnormal mental states
following
discontinuation of drugs. Most people are familiar with the minor
withdrawal symptoms such as anxiety, insomnia and mild depression
which
occur when someone stops minor tranquillisers after taking them for
any
length of time. Could the ‘relapse’ of schizophrenic symptoms on
stopping
neuroleptics in reality be a neuroleptic withdrawal syndrome rather
than a
true relapse of the illness? The model of Tardive Dyskinesia is
relevant
here. This condition is thought to arise because of an increased
number
and sensitivity of dopamine receptors in the striatum. Presumably
there is
no reason why such a mechanism should not occur in the meso-limbic
system,
the pathway thought to be important in relation to the symptoms of
acute
schizophrenia. If this is so, then reduction or cessation of
neuroleptic
medication in the presence of increased receptor sensitivity in this
area
should result in a relative increase in dopaminergic transmission in
this
system with the appearance of acute psychotic symptoms. In these
circumstances the occurrence of ‘relapse’ is hardly an intrinsic
feature
of the disease process, but an iatrogenic (brought about by medical
intervention) phenomenon arising as a consequence of the effects of
dopaminergic blocking agents on the brain.
There is
evidence that this indeed may be the case. A few years ago, Chouinard
and
Jones (1980) published a paper in the American Journal of Psychiatry,
which, in its day, was widely quoted as evidence in support of the
dopamine theory of schizophrenia. In it, they described in detail the
drug
treatment histories of ten patients treated with neuroleptic drugs.
In
each case a recurrence of psychotic symptoms was noticed almost
immediately following reduction or discontinuation of medication.
This
runs contrary to expectation. There is nothing in our knowledge of
the
course of schizophrenia that would lead us to expect a sudden
reappearance
of symptoms on discontinuing medication. All the subjects had had
lengthy
periods of exposure to neuroleptic, and in addition, most had
evidence of
tardive dyskinesia. The dyskinesia became more apparent on
discontinuation
of medication, and with the appearance of psychotic symptoms. The
authors
note that:
‘An
implication of neuroleptic-induced mesolimbic supersensitivity is
that the
tendency toward psychotic relapse in such patients is determined by
more
than just the normal course of the illness.’ (Chouinard &
Jones,
1980: p. 16)
Further
evidence in support of the supersensitivity psychosis comes from one
of
the most thorough reviews of neuroleptic withdrawal ever made.
Gilbert et
al (1995) reviewed 66 studies of neuroleptic withdrawal in
schizophrenia
involving over 4,000 patients. She found that amongst other things
‘relapse’ was more likely to occur in people who had been taking
higher
doses of neuroleptic medication prior to discontinuation, or in
people who
had experienced rapid discontinuation (over two weeks) as opposed to
gradual discontinuation (over eight weeks). These are exactly the
features
we might expect to find in a disturbance that occurs simply as part
of a
drug withdrawal state.
Of
course, no
research study has seriously addressed the possibility that symptom
recurrence in schizophrenia on stopping neuroleptics is effectively a
drug
withdrawal syndrome. To examine this possibility you would have to
examine
the symptoms of a large number of people in their first episodes of
schizophrenia, and then compare these symptoms in great detail with
those
seen in the same people after discontinuing neuroleptics. Such a
study has
yet to be performed. It is interesting to note how the drug
withdrawal
explanation for ‘relapse’ has been overwhelmingly neglected in the
psychiatric literature. Descriptions of drug withdrawal states
dominate
clinical accounts of the effects of psychoactive drugs and
substances. All
doctors are familiar with the phenomenon of drug withdrawal syndrome,
and
although Chouinard’s work has been in the literature for 16 years,
this
explanation for the link between relapse and medication has been
glossed
over. The implications of this are too frightening for psychiatry to
contemplate. It means that for many patients ‘relapse’ may be
iatrogenic,
a consequence of drug treatment and not an inevitable part of the
process
of a disease.
References Leudar, I. & Thomas, P. (1999)
Conversations with Voices. Forthcoming, Routledge: London.
There
are
enormous difficulties in undertaking a study such as this. For
example,
there are different ways of defining relapse. For some people relapse
is
defined simply as the reappearance of psychotic symptoms. For others
it is
necessary for you to be readmitted to hospital. This makes it very
difficult to compare the outcome in different studies.
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