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For decades, psychiatry has been polarised between ‘biological’ and
psychological’ approaches to clinical disorders. The biological approach
gained much ground with the advent of drug therapy for mental illness –
the anti-depressants, and the ‘neuroleptics’ for schizophrenia – and many
therapists have concluded that a medical approach to mental illness is best.
But of others, the treatment of what appears to be a psychological disorder
with pills remains a contradiction in terms. These therapists argue that
physical treatments appear to succeed only because they suppress rather
than resolve underlying problems.

This divide between biological and psychological approaches has widened
since the introduction of antidepressants and neuroleptics in the 1950s,
but its origins lie further back. The intitial breach came in the early
years of the century, as part of the medical establishment’s reaction to
the development of psychoanalysis. This reaction was probably based in part
on the professional concerns of psychiatrists, who are medically qualified,
and who wanted to maintain medical control in the marketplace. The reaction
also sprang from the failure of psychoanalysis to provide evidence that
such therapy actually helps people with specified clinical disorders. But
the primary reason for the divide between the two approaches lay in the
psychiatrists’ conviction that people with disorders such as manic depression
and schizophrenia were in principle no more likely to respond to an interpretative
psychotherapy than a person with a brain tumour is.

Psychiatrists taking a medical approach argue that people with manic
depression or schizophrenia suffer from disorders of ‘form,’ as opposed
to disorders of ‘content.’ The notion of a disorder of content refers to
behaviour or communication that falls outside the range of the normal –
usually, it is argued, because the afflicted individuals have abnormal motives
underlying their behaviour. Neuroses and preversions provide good examples
of this. The central assumption is that the disordered behaviour does not
stem from any organic malfunction of the brain. The various non-medical,
psychological schools of thought disagree as to what the ‘diseased’ motivation
may be, but there is no dispute about the central notion that it is the
psychological software, rather than the brain hardware, that needs sorting
out.

If the idea of a disorder of content is relatively straight forward,
this is far from the case when it comes to disorders of form. How are we
to diagnose a disease of the brain? The problem is that although our behaviour
depends on the functioning of the brain’s hardware, it is also constructed
of motives and reasons. So altered behaviour can stem from either a change
in motives or a failure in the hardware.

In a few cases there is no controversy. Take the strange disorder known
as Gilles de la Tourette syndrome, for example. People afflicted with the
syndrome exhibit episodes of grimaces, tics or swearing. Everyone now agrees
that these symptoms stem from a disorder of hardware rather than any motive
of obscenity.

But disorders of form and content are usually difficult to distinguish,
and judgments have altered over the years. For instance, some psychological
approaches have in the past interpreted the tremor and rigidity of Parkinson’s
disease as manifestations of suppressed hostility – a disorder of content
– whereas psychiatrists have argued that such behaviours should not be interpreted
at all, as they stem form cerebral malfunctioning. The discovery that people
with Parkinson’s disease have a shortage of a particular neurotransmitter
in the brain, dopamine, and that treatment with the drug L-dopa dramatically
reduces the symptoms, appears to have settled this particular issue. But
there are many others that remain unsettled.

This is most notably the case when it comes to the complex behaviours
found in the major psychiatric illnesses, manic depression and schizophrenia.
Psychiatrists point to the gross slowing of mental functions in depression
or to the thought disorders typical of schizophrenia as instances of disordered
form rather than content. There is no motive behind this slowing or disruption
of thought, they say. But most mental health workers and lay people do not
accept this conclusion. This is so even though it is now widely thought
that some disorder or brain neurotransmitters occures in depression and
schizophrenia and that antidepressants and neuroleptics produce dramatic
benefits.

One reason why most people do not accept that depression for instance,
is a straightforward ‘biological’ disorder of form seems to lie in an uncertainty
about what such a conclusion implies. Does it mean that when we are feeling
more guilty or sad than normal, for instance, we have a disorder of the
brain rather than a psychological disorder? This just does not seem right.
Or consider the effects of neuroleptics or schizophrenia. Typically, these
drugs reduce delusions – odd beliefs firmly held – and hallucinations –
seeing and hearing things not really there. But neuroleptic drugs do little
to lessen ‘thought disorder’ – the tendency of a person with schizophrenia
to switch from one topic to another with no apparent link between them,
for instance, or to talk on and on without apparently saying anything. So
if drugs reduce delusions and hallucinations, are these disorders of form,
while thought disorder is not?

Orthodox psychiatric thinking mostly stems from Karl Jaspers, the German
philosopher and psychologist writing in the eary decades of this century.
Jaspers argued that delusions involve a order of form. Similarly, psychiatrists
today argue the odd and intensely held beliefs of lunatics are no more interpretable
than the tic of a patient with Tourett syndrome. But Jaspers saw hullicinations
as interpretable phenomena, whereas, today, most psychiatrists tend to see
these, too as disorders of form, because they ‘respond’ to neuroleptics.

If readers have difficulties in spotting the ball here, they should
not despair. The problem seems to be one of deciding exactly what criteria
make for a verdict of disordered form as opposed to one of disordered content.
On this issue there is no agreement. In part, such difficulties are a direct
consequence of the fact that psychiatric terminology has evolved separately
from that of clinical psychology. Today, however, the psychoanalytic empire
has crumbled and the need for an iron curtain between psychiatry and developments
in clinical psychology has passed. What then are the prospects for a new
mixed therapeutic economy?

Several developments in psychology could profitably be imported into
clinical practice. The first of these developments stems from the growth
of neuropsychology. This branch of psychology began at the end of the 19th
century from observations that strokes and brian tumours could alter behaviour.
Studies of these patients revealed that certain psychological functions,
such as speech and memory, seemed localised to particular areas of the brain.
This research was intitially the province of neurologists who also worked
as psychiatrists. But with the work of A R Luria of Moscow State University
in the 1930s, the research became more psychologically oriented. Neuropsychology
is now not so much concerned with the issue of the localisation of psychological
functions as with their construction. For example, it is now clear that
speaking or remembering are not simple, unitary acts. Rather, each such
psychological function has many aspects, some of which may be lost or compromised
when we suffer a brain injury, without the entire function being lost. Thus,
after a stroke there may be discrete impairments in speech intonation or
in the ability to retrieve certain words but not others.

The subject as researcher

Exploring the fine grain of the construction of psychological faculties
has increasingly focused scientists to enlist the experimental subject as
co-investigator. For example, researchers have recently discovered that
some idividuals with a disorder of the frontal lobe of the brain become
‘environmentally dependent.’ Such people appear to be unable to resist imitating
what others around them are doing. And if standing near a dirty comb that
is not theirs may be unable to resist picking it up and combing their hair
– even if asked not to. There are a number of ways we might explain such
behaviour. But it only becomes clear what is happening if the experiences
of the affected individuals are taken into account. In this case, they report
feeling compelled to do the odd things they do, even though they may recognise
that what they are doing is inapropriate. Normally, the sight of a comb
brings with it an invitation to use it. But this invitation is easily resisted.
In an environmental dependency syndrome, the invitation seems to become
a command. Subjects in this state experience a loss of free will that is
quite unlike the experience of patients with obsessive-compulsive behaviour,
impulsive behaviour, manic disinhibition or any of the other conditions
that might bring about superficially similar symptoms.

Another area where the experimental subject has been enlisted as a co-investigator
has been in the study of internal imagery. This area has been much studied
by neuropsychologists in the past few years. The goal is to establish how
images are put together and under what circumstances they arise. Such work
depends critically on a willingness to take the reports of subjects seriously.
In turn, the fruits of research in this area have indicated that such reports
can be worked with profitably.

In taking this turn, neuropsychologists have strayed into the heartlands
of psychiatry and psychotherapy. However, in contrast to the neuropsychological
approach, neither psychiatrists nor psychotherapists take the experience
of psychiatric patients as they report them at face value. If one is psychologically
oriented, one disregards the manifest content of an individual’s utterances
in favour of a supposed latent content. If one is biologically oriented,
one pays heed to what they say only in order to make a diagnosis, because,
crudely put, the diagnosis implies that their brains are not working right.
In practice, this means that nothing such an individual has to say carries
the normal weight in the clinical context.

In psychiatry, the term disorder of form implies that the form of remembering,
perceiving or thinking has changed, because some part of the brain is malfunctioning.
This, however, is exactly what neuropsychologists investigate. Why then
are disorders of form not just seen as neuropsychological deficits? One
reason is simply that at the time when the term disorder of form was coined,
neuropsychology had not yet been established. In 1900 the brain disorders
known to impair psychological faculties – strokes and tumours – involved
almost compete and permanent losses of function, such as the loss of speech
or the inability to recognise objects. These disorders seemed totally different
from psychiatric ones. In addition to being relatively permanent, such severe
deficits prevented subjects from being able to express what was happening
to them.

Since then, however, we have come to realise that many other brain disorders
may produce milder, reversible, neuropsychological impairments. Moreover,
for the most part, subjects are aware of what is happening to them and can
comment on it. For example, subjects with Parkinson’s disease or Tourette’s
syndrome can describe clearly their abnormal experiences. The parallel with
someone suffering from inluenza is instuctive. A person with flu notices
a temporary drop in the ability to think clearly. Could depression and schizophrenia
similarly bring about specific reversible neuropsycho-logical changes? More
particularly, could these disorders bring about disorders about which the
subject may be quite aware and able to comment on?

Perhaps the best known attempt in psychiatry to describe a set of clinical
features specific to a particular malfunctioning of the brain is by Kurt
Schneider with his ‘first rank’ symptoms of schizophrenia. You have a first
rank symptom if you say that you feel that your thoughts or emotions are
not your own and must have been put in from outside, or that your body is
functioning independently of your will. If you make such statements, psychiatrists
invaribaly see them as signs of delusion – errors of judgment or false beliefs.
Yet paradoxically, we insist on treating these beliefs with physical treatments.

But when Schneider formulated his first rank symptoms, he saw them as
abnormal experiences. In this view, what the subject reports is the subjective
experience of a neuropsychological impairment – one that arguably has close
affinities with the environmental dependency syndrome mentioned earlier.
In schizophrenia, however, individuals atempt to interpret their experience
and it is their interpretations that lead to difficulties.

The success of neuropsychology has offered a new legitimacy to the notion
that our internal mental life can be investigated scientifically. There
are, however, two important implications of seeing disorders of form as
neuropsychological deficits. One is that not all internal events should
be interpreted in terms of motives. Some will arise as experiences, and
to investigate these we need to describe them in a detailed and accurate
fashion, rather than try to ‘interpret’ them.

The second point concerns the question of who does the describing. Detailed
and accurate describing is not something one expects of the ‘insane.’ But
subjects with environmental dependence syndrome, Tourette syndrome and other
neuropsychological syndromes are not seen as insane, even though the experiences
they describe may be highly unusual. The implication of this is that patients
with psychiatric disorders of form need to be more ‘insane’ than other subjects
with neuropsycholgical impairments. And just as neuropsychologists have
begun to enlist the subject as co-investigator, psychiatrists might also
profitably do so. What their patients say should not merely provide the
basis for a diagnosis. Their statements can also tell us subtle things about
the way psychological functions are constructed. These statements might
ultimately provide useful guides to appropriate care and import leads for
research.

The principal difficulty with this position would be if any alterations
of brain functioning produced delusions. This would compromise the value
to be put on the patients’ own reports. But at the moment this does not
seem to be the case. Interfering with brain function can disrupt memory,
perception, sleep or appetite, but it does not produce delusions. Why, then,
do individuals with manic depression or schizophrenia become deluded?

Here again a new branch of psychology would seem to have something to
offer. This concerns the study of judgments made in conditions of uncertainty.
Our normal rationality, it turns out, is not strictly logical. Individuals
forced to make judgments in uncertain circumstances tend to behave like
gamblers – we generate hunches based on stereotypes and biased towards recent
events, which we stick to even though the evidence may not support us. We
seem biased towards bending the evidence to fit the hunch rather than towards
switching hunches as we accumulate more evidence.

Illnesses typically put all of us into situations of uncertainty. We
must attempt to account for what is happening, and we do so in the manner
of gamblers at a roulette wheel. People who have schizophrenia have to account
for some quite bizarre experiences. Similarly, people who become depressed
have to account for changes in performance so subtle that it is often impossible
for them to decide whether there is anything physically wrong or not.

In the case of depression, not having an obvious fever to blame for
our lethargy and poor concentration, we look for other possibilities that
would account for a decline in performance and an inability to pull our
weight. One possibility is that we might be useless and worthless. Once
we entertain this explanation, we can always find evidence from our past
that might support this conclusion. Or the subtle physical changes associated
with depression may lead us to conclude that we have a tumour or AIDS perhaps,
that we are being poisoned or that we have sinned greviously and our symptoms
derive from being abandoned spiritually.

It is with such conclusions that ‘cognitive’ therapy takes issue by
asking for the evidence and challenging the person to offer other possible
explanations. This newly developed therapy works even for the kind of depression
that normally responds to antidepressants and it may also work for delusions.
Apart from efficacy, however, the point here is that the operations of normal
rationality on uncertain experiences may produce quite odd and firmly held
conclusions. This happens in an illnesses, from diabets to multiple sclerosis.
So such ‘irrational’ conclusions should not be taken as evidence that someone
with depression or schizophrenia has lost their sanity or is not accessible
to a psychotherapy.

Therapies to explore experience

The crux of the matter is, which therapy? Any therapy that believes
all there is to manic depression or schizophrenia is a set of disordered
motives, is all too likely to compound the mistake the affected individual
is making. On the other hand, there is no a priori reason that what is appropriate
therapy cannot help even though what is involved is a physical illness –
as the example of the successful management of stomach ulcers without drugs
indicates.

Some indication of the potential power of the methods I advocate here
comes from considering what is lacking in modern psychopharmacology. At
present, this enterprise is almost exclusively concerned with the study
of brain biochemistry – in particular, levels of neurotransmitters and the
specific receptors for them on brain cells. This approach in effect treats
the brain as more complex than, but essentially similarto, organs such as
the heart or liver. This is a far cry from the original scope of the discipline,
which was begun by Emil Kraepelin working in Munich just before the treatment
of mental disorders split into distinguishably medical and psychological
camps in 1892. Kraepelin called his new science ‘pharmacopsychology,’ and
saw its role as one of exploring the psyche – or mental life – by means
of drugs. This approach would make pharmacopsychology a sister discipline
to neuropsychology and something quite different to the current discipline
which has little use for the reports of the people who take the drugs.

What would happen if psychopharmacologists regarded patients who were
given drugs as potentially rational co-investigators of their own internal
workings? The impact on current research on neuroleptics and antidepressants
would be enormous. Ignoring what patients say now leads to bizarre distortions
of the evidence. For instance, we know that neuroleptics act through so-called
D2 receptors in the brain. This has led to the ‘dopamine’ hypothesis of
schizophrenia – that the disorder is caused by a disturbance of the neurotransmitter
dopamine, which binds to D2 receptors in the brain. However, neuroleptics
induce a feeling of indefference in the face of stress – an ‘antiagitation’
effect. This they do in anyone who has them, whether schizophrenic or not.
They take the same amount of time to induce this effect as they take to
bind to D2 receptors. If one accepts the reports of both patients and volunteers
who take these drugs, the D2 receptors are apparently working in the same
way in both groups – and so the dopamine theory of schizophrenia cannot
be right.

In the case of the antidepressants, the ‘monoamine’ hypothesis proposed
that these drugs act by increasing other neurotransmitters, called amines.
The pscychostimulant drugs, cocaine and amphetamines, also work on brain
amines and within a few minutes produce a rewarding and arousing affect.
Yet depressed patients who take antidepressants do not find that these drugs
produce a cocaine-like stimulant effect. Furthermore, the effect which they
do produce, of normalising mood, takes several weeks to appear – even though
antidepressants, like cocaine, act immediately on brain amines. The reports
of subjects taking antidepressants, then, if taken seriously, would suggest
that we should diversify our research efforts from an exclusive focus on
brain amine systems.

These examples illustrate the importance of enlisting the efforts of
individuals with psychiatric disorders in the investigation of their own
disorders. They also illustrate that the insights of patients may be important
not just in the investigation of the psychological aspects of such disorders.
All too often the idea that there may be a biological malfunction involved
in the major mental disorders has been used to justify the exclusion of
affected subjects from the management of their own illnesses, even to the
extent of detaining and treating people under mental health act orders.

In contrast, I argue that disorders such as manic depression and schizophrenia
are not solely constituted by disorders of neurotransmitters. Rather, core
biological disturbances may result from social events. These may in turn
set up a variety of experiences, depending on the differing social circumstances
and personality styles of individuals. A scientific neuropsychotherapy may
hope to intervene in this process by providing clear and detailed descriptions
of abnormal core experiences. It can also unravel the ways in which our
everyday common sense can lead us to interpret these experiences in damaging
ways. At the very least, such a therapy would greatly reduce the amount
of distress engendered by manic-depression and schizophrenia. Depending
on the natural history of the underlying disorder, it may also powerfully
assist its resolution.

Dr David Healy is deputy director of the academic sub-department of
psychological medicine, University of Wales College of Medicine, North Wales
Hospital, Denbigh, Clwyd. He is author of The Suspended Revolution; Psychiatry
and Psychotherapy Re-examined, published by Faber and Faber earlier this
year.