Philosophical discussions of mental illness fall into three families.
there are topics that arise when we treat PSYCGUATRY as a special science and
deal with it using the methods and concepts of philosophy of science.
includes discussion of such issues as explanation, reduction and classification.
Second, there are conceptual issues that arise when we try to understand the
very idea of mental illness and its ethical and experiential dimensions.
there are interactions between psychopathology and the philosophy of mind and language (How a schizophrenic understands an implicature seeing that a stereotype of a schizophrenic is his literalness).
Philosophers have used clinical phenomena to illuminate issues in the philosophy
of mind, and philosophical findings to try to understand mental illness.
We shall discuss issues in the philosophy of science and philosophy of mind
that pertain to psychiatry.
textbooks alike agree (though they might not like it) that psychiatry now
adheres to the “medical model”, which advocates “the consistent application, in
psychiatry, of modern medical thinking and methods” (Black 2005, 3) because
psychopathology “represents the manifestations of disturbed function within a
part of the body” (Guze 1992, 44) to wit, the brain.
But what does it mean to
adopt this view of psychiatry, and what difference does it make?
think that the medical model merely commits us to a brain-based view of mental
illness with few implications for science, and it is true that clinical or
scientific differences across practitioners seldom seem to have much to do with
divergent interpretations of the medical model.
However, many theorists have
argued that our current diagnostic categories, as compiled into DSM-IV-T-R
(American Psychiatric Association 2000: I refer to different editions of this
work by its abbreviated title), are faulty because they are derived from
observable variables rather than underlying physical pathologies.
theorists are sceptical about many existing psychiatric diagnoses, and not just
on empirical grounds.
They see DSM diagnoses as collections of symptoms rather
seeing them as medicine understands diseases — in terms of destructive processes
realized in bodily tissues.
Genuine mental illnesses, on this view, are not just
sets of co-occurring symptoms but destructive processes taking place in
Following Murphy, this may be termed the strong
interpretation of the medical model.
In contrast, a minimal interpretation of
the medical model thinks of mental disorders as collections of symptoms that
occur together and unfold in characteristic ways, but it makes no commitments
about the underlying causes of mental illness.
These two interpretations
correspond to different ways of cashing out the medical model.
The strong interpretation
naturally suggests that psychiatry should embrace the practices of medical
If disease is a pathological process in bodily systems, then there
must be a way of understanding how such processes occur in the brain, and how
they explain the clinically observable facts about mental illness.
But it seems
that the logic of the medical model does not force us to privilege any one level
of explanation—notably, it does not commit us to explanations restricted to the
resources of molecular biology.
Psychiatry, then, is a multi-level science.
we often know very little about the mental illnesses that psychiatrists study,
and much explanation in psychiatry involves case studies or narrative accounts
that cite the characteristics of a disorder, rather than underlying systems.
Theorists disagree over whether these should be seen as different kinds of
explanation, or as rudimentary forms of a full causal explanation.
idea that psychiatry is a branch of medicine is not universal, but even if we
stick to professed believers in the medical model with the same broad view of
the subject, we find disagreements about how its core commitments should be
It may be helpful to distinguish minimal and strong interpretations.
A minimal interpretation makes no commitments about the underlying physical
structure that causes mental illness.
The strong interpretation of the medical
model, in contrast, dissents on just this issue.
It says that the proper medical
understanding of disease is in terms of morbid anatomy.
It is committed to
specific causal hypotheses in terms of abnormalities in underlying
Minimalists treat diagnostic labels as useful
heuristics rather than natural kind terms, whereas a strong interpretation
commits psychiatry to a view of mental illness as a medical disease in the
strongest sense, that of a pathogenic process unfolding in bodily
Minimalists employ a concept of
disease as the observable, regular unfolding of a suite of symptoms.
applied it to psychiatry as the basis for differential diagnosis, for example
between "dementia praecox" (Bleuler's "schizophrenia") and other forms of insanity (1899,
It is a familiar idea that the DSM's syndrome based conception of
mental illnesses stands in the tradition of Kraepelin, who argued that “only the
overall picture of a medical case from the beginning to the end of its
development can provide justification for its being linked with other
observations of the same kind” (1899, 3).
This familiar neo-Krapelinian picture
is that mental illnesses are regularly co-occurring clusters of signs and
symptoms that doubtless depend on physical processes but are not defined or
classified in terms of those physical processes.
Guze, for example, is
When he advocates seeing psychiatry as a part of medicine what he
means is that we can classify disorders in terms of their characteristic
symptoms and courses.
McHugh and Slavney seem to agree.
They say that a
disease “is a construct that conceptualizes a constellation of signs and
symptoms as due to an underlying biological pathology, mechanism and cause
To diagnose a patient as suffering from a mental disorder, for McHugh
and Slavney (48), is to label them in a way that we judge helpful as a starting
point for investigating physical processes.
McHugh and Slavney deny that a
disease is a physical process—“its essence is conceptual and inferential” (48).
As a precursor of this view, they cite Thomas Sydenham, the great seventeenth
century English physician who distinguished varieties of pox based on their
characteristic courses and outcomes.
This way of thinking about diseases
prescinds from theorizing about underlying causes of a disease entity in favor
of a concentration on observable phenomena, not hidden causes.
However, it is
diseases understood as destructive processes that make up the taxa of medicine.
Similarly, the successive editions of the DSM have sought to classify mental
illnesses based on course and symptoms but not specific causes.
Sydenham has been dead for over three hundred years, and medicine moves on.
psychiatry adheres to a conception of disease that looks like Sydenham's it may
depart from the rest of medicine.
Many scholars have argued (e.g. Bynum 1994,
Carter 2003, Whitbeck 1977) that in the nineteenth century medicine changed in
many ways, including a shift in thinking about disease.
Instead of seeing
disease as the identification of symptoms, it was the linkage of symptoms to
distinct pathologies, understood as departures from normal function, that came
to define disease. Heinrichs (2001, 271), for example, insists that psychiatry
needs to employ this basic medical outlook, and therefore needs a developed
theory of how the mind/brain works that can be used to identify psychological
abnormalities and explain how they arise. Andreasen (2001, 172–76) embraces the
strong interpretation. She argues that psychiatry now emerging as a form of
cognitive neuroscience, is for the first time able to identify the specific
pathophysiologies that underpin the symptoms of mental illness. This development
fits the pattern suggested by Hempel (1965), who expected psychiatry, as it
matured, to develop a theory-driven classification scheme based on an
understanding of the objective nature of mental illness rather than just
pragmatic factors (Hempel 1965; See Fulford et. al 2006: 324–341: Thornton 2008:
treats mental disorders as syndromes along the lines of the minimal medical
model. Individuals who share a DSM diagnosis have a subset of symptoms in
common, often drawn from a larger list so that although some people may have all
their symptoms in common, there may be no overlap at all in other cases. These
collections of symptoms are also supposed to unfold over time in more or less
the same way, once we make due allowances for some individual variation. They
are also expected to respond to treatment in the same way. The previous version
of the DSM assumed that each diagnosis represented malfunction in some mental,
physical or behavioural trait or capacity (DSM-IV-TR, xxi). However, the
diagnoses were listed without worrying about what that underlying malfunction
might be, and in most cases there was (and remains) no agreement about what
causes what. DSM-5 (American Psychiatric Association 2013) defines mental
disorders (p. 20) as syndromes comprising clinically significant disturbances of
cognition, emotion or behaviour that reflect underlying dysfunctions. These are
normally associated with distress or social disability, but cannot be diagnosed
if the behaviour is culturally normal or merely socially deviant, unless it
reflects a dysfunction.
DSM diagnoses are usually taken to reflect a
conventional concept of disease, despite the talk of underlying malfunction,
because of their emphasis on syndromes and their lack of any causal hypotheses.
In the manner of the minimal medical model, they let us make use of descriptive
and statistical reasoning and offer the hope of accurate prediction and
effective control. In the opinion of some philosophers, that is all science ever
aspires to. I began by citing a textbook declaration that psychiatry uses normal
medical methods, and there is certainly nothing within McHugh and Slavney's
discussion of mental illness that makes scientific methods
Other philosophers, though, will tell you that the job of
science is to discover the causal structure of the world. Furthermore, there are
plenty of students of psychopathology who argue that the neglect of causal
structure in psychopathology is getting in the way of science (Poland, Von
Eckardt and Spaulding 1994, Murphy 2006, Gerrans 2014). They worry that we are
lumping together different groups of people based on behavioral evidence alone,
when in fact their observable similarities mask important underlying
differences, including differences between normal people who are troubled but
basically healthy, and their pathological counterparts. From this
philosophical-cum-clinical perspective it looks like dereliction of duty when
any scientific discipline, but especially psychiatry, decides to isolate itself
from inquiry into causes. Suppose we ask why the conventional view of diseases
is successful in organizing prediction and control (what psychiatrists sometimes
call “predictively valid”). The obvious answer is that successful predictive
categories are actually tracking the causal structure in the world that accounts
for the shared nature of the different instances, so we should aim for a
stronger validation of the diagnosis than mere predictive validity. Whilst the
reliability of a diagnosis is a gauge of agreement across measurements and
observers, validity is supposed to be about what is really there.
obvious that even the most expert observers could all agree but nonetheless be
wrong, whereas proper validation reassures us that we are measuring something
that is really there. (Psychiatrists employ the concept of validity in several
ways; for help in sorting them out, see Fulford et al. (2006: 318–19), Schaffner
(2012) and the essays in Zachar et al. 2014.)
Someone committed to a strong
version of the medical model sees validating a diagnosis as understanding its
underlying causal structure: a diagnosis is valid if it rests on a biological
process that can be identified by experiment and observation using the methods
of the biological and cognitive sciences. Any approach to psychiatry that looks
to science to validate its categories in this way must meet at least two
conceptual challenges. First, there is a metaphysical challenge, which is that a
concept of validity tied to the uncovering of neurobiological processes
seemingly adopts a realist philosophical position, thinking that science can
tell us how the world is really put together. Many philosophers think that
realism is a wholly unnecessary and unwarranted metaphysical commitment, and
that all science can really tell us about is a set of relationships among the
data. These relationships let us make predictions and exert some control over
nature, but do not tell us what is really out there. Philosophical disputes over
realism have often centred on the notion of the unobservable. Electrons are a
paradigm example, but other posits of fundamental physics play the same role. In
psychiatry the situation is different; theories and constructs employ latent
variables rather than reference to unobservables. Schizophrenia, as a construct,
is not a further type of stuff that lies behind the appearances and explains
them: it is constituted by visible phenomena. We are not looking for an
unobservable, but asking which observable phenomena (neurological, genetic,
developmental, social) explain the symptoms. If the strong conception of the
medical model is philosophically realist, it is so in light of its commitment to
causes, not to unobservables. We may look for a hidden variable that explains
the observable phenomena, or for some other hypothetical underlying cause. Gold
and Gold (2014, p.163-66) for example, suggest that many delusions and other
psychotic symptoms may reflect a malfunctioning “Suspicion System” that has
evolved to detect and monitor social threats. If such a system exists it is not
directly observable, but its components should be open to observation and
manipulation via the standard methods of the cognitive sciences. Psychiatry,
like many sciences, deals in hidden variables or hypothetical causal structures,
but it is not helpful to think of these as unobservable in the traditional
The second conceptual challenge to the realist interpretation of
validity is normative. The challenge is that there is an important sense in
which diagnoses cannot be validated at all, if by “validation” we mean “shown to
be a real disorder”. All validation can do is show that a pattern of behaviour
deemed to be clinically significant depends on a physical process. Whether that
pattern of behaviour is really pathological - rather than immoral or harmlessly
odd- is another matter. The second challenge probably is very hard to meet. It
requires that judgements of pathology be like findings of positive charge, i.e.
scientifically grounded, rather than judgements of ugliness, i.e human
responses. If so, there has to be some natural fact of the matter about whether
some physical system is dysfunctional. If this cannot be done, then predictions
about physical states can be validated, but disorders cannot be.
above that the DSM approach is often called “neo-Kraepelinian”.
did not adopt it as a first choice. He saw classification by clinical
description as an interim measure. It satisfies the practical requirements of
physicians and establishes a productive heuristic for subsequent pathological
and etiological inquiry, since “the value of every diagnosis is thus rated
essentially by the extent to which it opens up reliable prospects for the
future” (1899, 4).
Kraepelin's preferred basis for classification and inquiry
actually rested on his less well-remembered belief that “pathological anatomy
promises to provide the safest foundation” for classification of mental illness
in a mature psychiatry (1899, 2). He considered the correct taxonomy would be
one in which clinical description, etiology and pathophysiology coincided:
“cases arising from the same causes would always have to present the same
symptoms and the same post-mortem result” (3).
There is a substantial
difference between thinking of clinically-based, syndromic classification in
this way and thinking of it as the DSM does. The DSM classification has been
designed (DSM-IV-TR, xxiii) to improve communication between psychiatrists and
across disciplines and provide a basis for education. But it is not advertised
as the jumping-off point for a mature system of causally organised
classification and practice. This reflects a minimal interpretation of the
medical model; it can guide empirical research but not uncover causal
DSM leaves itself open to the charge that a classification which
groups together observable phenomena can sort entities into heterogeneous
classes, with underlying diversity masked by surface similarities. We already
know from other areas of medicine that what looks like the same phenomenon—a
cough, say, or a sore throat, or chest pain—can reflect different biological
processes and hence may really signify different conditions. A taxonomy that
relies content with surface features risks lumping different conditions together
and keeping related ones apart.
Here are some examples of this charge in the
recent literature (for others, see Murphy 2006 (chapters 1–3) and McNally,
forthcoming). Ross et al. (2008, 33–34, 200–01) suggest some revisions to the
current diagnostic category of Pathological Gambling (PG) (see DSM-IV-TR,
671–74). The category of pathological gambling is designed to operationalize a
concept whose content is, roughly, gambling that causes problems for the
gambler. But Ross et al. reason as follows: the existing category “maps
relatively smoothly onto the class of people who exhibit classic patterns of
addictive behaviour as a result of a specific kind of dysfunction in their
dopaminergic reward system and consequent neuroadaptation impairing frontal
control circuits. We therefore believe that clarity would be served … by
replacing the behaviourally derived concept of PG with the neuroscientifically
anchored concept of addictive gambling (200)”.
A judgment that the DSM-5
categories have insufficient validity has led the National Institute of Mental
Health to introduce the Research Domain Criteria (RDoC) in grant proposals
(Insel et al. 2010). The originators of the RDoC acknowledge that the system
entrenched by previous versions of the DSM has increased diagnostic reliability.
But they worry that it is too detached from the nature of mental illness, which
they conceive of as disorders of brain circuits: though the domains of inquiry
themselves are to be identified in psychological terms. For example, rather than
existing categories such as depression, the RDoC envisages a domain of negative
valence which will include symptoms of anxiety or depression that might come to
be seen as expressions of an underlying disorder of specific brain circuits
(Sanislow et al 2010) . These disorders could be studied at many levels and need
not be identified with simple lesions. But future models of mental illness are
expected, on this vision, to draw on psychological, neurological, and genetic
mechanisms, as well as information about the wider cultural context. It is
expected that current research and future diagnosis will have to be based on
these models in order to be properly warranted by the underlying facts about the
causal structure of mental illness, rather than on clinical signs and symptoms.
Clearly, in this case, validating a diagnosis is thought of as understanding its
underlying causal structure: a diagnosis is valid if it rests on a biological
process that can be identified by experiment and observation using the methods
of the biological and cognitive sciences.
Ross and his colleagues argued
along similar lines in their discussion of gambling, which may be seen as an
example of the sort of work the RDoC foresees. They think there are two benefits
to the conceptual change that they advocate. First, it would provide a clearer
and principled demarcation of the addicted gambler from the “problem gambler”
which is currently somewhat arbitrary (201). They also show the way to a better
understanding of the nature of the addictive disorders more generally via the
use of their preferred approach, which combines neuroscience and behavioural
economics. They draw on prior research (ch. 6.2) to suggest that addictive
gambling resembles dependence on stimulants (like cocaine) more than it does
alcoholism, and hence enlarges our understanding of addiction more fully than
purely behavioural criteria would do. The worry is that a behavioural approach
misses the similarities and differences between forms of addiction by treating
all as more or less the same, based on shared behavioural and phenomenological
To make these arguments we have to distinguish the truly
pathological gambler, whose life is dominated (and typically wrecked) by
gambling, from merely habitual gamblers. Habitual gamblers might engage in
gambling more than they feel they should, or periodically lose more than they
can afford, but there is a qualitative difference between this population and
the population of genuinely addicted gamblers. This qualitative difference is
detected by observing behaviour and rating the results of questionnaires.
However, if we classify gamblers according to quantitative measures alone, we
miss the reason why different groups behave differently. The reason is a causal
process. The brains of the real addicts don't work like the brains of the merely
troubled; thinking of addiction merely in terms of habitual behaviours will not
let us make the discriminations among gamblers that neuroscientific evidence
A stronger but similar argument was made by Horwitz and Wakefield
(2007). They claim that only a hypothesis about causes distinguishes a normal
population from a disordered one. They begin with the DSM criteria for
diagnosing major depression. To receive a diagnosis of Major Depressive Episode,
a subject must suffer from five of the following nine symptoms in a two week
period (including either or both of depressed mood or diminished interest or
pleasure in almost all activities): depressed mood; diminished interest; weight
gain or loss (without dieting) or change in appetite; insomnia or excessive
sleep; observable psychomotor agitation or retardation; fatigue or loss of
energy; feeling worthless or excessively guilty; diminished ability to think or
concentrate, or indecisiveness; recurrent thoughts of death or suicide or a
planned or attempted suicide.
Obviously many ordinary episodes in a person's
life can cause behaviors or feelings from this list, such as losing one's job.
The traditional concept of melancholy or depression, which has a continuous
history going back to classical antiquity (Radden 2000), allowed that life's
tragedies cause melancholy with perfect reason. That traditional view of
melancholy sees pathology only where one's circumstances do not justify a normal
melancholy response: “pathological depression is an exaggerated form of a normal
human emotional response” (Horwitz and Wakefield 2007, 71).
The DSM, however,
ignores this tradition. Anyone who fits the syndrome receives the diagnosis
regardless of how their life is going. The sole exception stipulates that grief
following bereavement does not count towards diagnosis of Major Depressive
Disorder until two months have elapsed, after which one may diagnose major
But not even that qualification is made if you show depressive
symptoms after your intended jilts you at the altar or you fail all your exams
or get your legs blown off. In subsequent work Horwitz and Wakefield (2012) have
extended their analysis to the anxiety disorders. They argue both that normal
human anxieties are being pathologized and that the diagnostic criteria for
anxiety and depression have been much too sharply distinguished from those for
depression, leading to an inability to explain why depression and anxiety so
During the run-up to DSM-5 the Mood Disorders Work Group
proposed eliminating the bereavement exclusion. This met considerable
professional opposition and attracted much adverse public comment (see Zachar
2014, ch. 10 for a summary of the debate and a discussion of the issues). From
the standpoint of Horwitz and Wakefield, the proposal appeared to be
pathologizing a normal human reaction. However, it was never suggested that
grieving itself was pathological. Rather, the proposal was based on the idea
that stressful life events often precipitate episodes that meet the criteria for
a major depressive episode, and there was no reason to exempt bereavement. Many
people, after the death of a loved one, exhibit symptoms very like those of
major depression, and are at risk for subsequent episodes. From this
perspective, the elimination of the bereavement exclusion is justified by
science, regardless of common sense (Kendler et al 2007; Lamb et al 2010). Why
should bereavement alone be exempted from the general claim that depression is
caused by stressful life events?
Horwitz and Wakefield suggest that genuine
depression is caused by a dysfunction on the part of a loss-response system that
evolved to respond to losses that threaten to deprive us of reproductive
resources. In depression the system misfires. It causes a loss-response in
situations where it should not. Whether or not that is convincing, the argument
that Horwitz and Wakefield make about the conflation of depression and sadness
stands on its own merits. They make the case that the DSM conception of
depression respects neither folk psychological common sense nor previous
psychiatric consensus about depression. They conclude that the concept of
depression defined by this diagnostic syndrome represents a major conceptual
break. Our use of the new concept, they suggest, means that many people who are
just normally miserable for understandable and ordinary reasons are being
diagnosed as depressed. This leads to unnecessary alarm about an epidemic of
depression as well as carrying unfortunate consequences for many people who are
wrongly diagnosed. However, it is certainly open to those theorists opposed to
the bereavement exclusion to insist that if depression is the result of an
underlying system that misfires, it could misfire in response to bereavement.
The proposal is not that everyone who grieves should be called depressed, but
that there are reactions to bereavement that are severe enough to meet the
criteria for major depression and should be classed as such. (For a more
detailed guide to the debate see Zachar 2014, Ch. 10.)
The DSM concept of
depression, on the face of it, lumps together different psychological and
behavioral types in the same category. It does this because it neglects the
diverse etiologies that may produce similar signs and symptoms. There is no way
to answer this charge, or to arrive at a satisfactory taxonomy that mirrors that
of general medicine, unless we adopt a causal foundation for nosology as
suggested by psychiatrists who urge the adoption of what I have called the
strong medical model. Indeed, without an account of underlying causal structure,
it becomes difficult to give a principled answer to the question why some
conditions should be seen as pathological to begin with. Merely saying that
members of a class have certain properties does not tell us whether, let alone
why, they are mentally ill. To answer that question we need some basis for
making the judgment. The DSM, as we have seen, states that we have such a basis;
mental disorder is an outward sign of dysfunction. But to make that argument, we
need a commitment to finding dysfunction somewhere on the basis of the outward,
observable phenomena. No amount of observation alone will uncover the
dysfunction without a commitment to the idea that there is a destructive
neuropsychological process at work that causes an underlying dysfunction. In
other words, the minimal model can only answer questions about the relationship
between membership in a taxon and some other variable: it will not explain why
the taxon has the nature that it has, or why it should be seen as a kind of
Doing that involves not just the empirical study of mental
disorder, but a strong interpretation of the medical model, with its commitment
to a view of disease as not just a syndrome but a destructive process. It is
certainly possible to collect data using the DSM concept of depression,
especially information about epidemiology and natural history. In that sense
normal medical reasoning can indeed be employed, but there much medical
reasoning is directed at trying to understand causes. It is here that we come to
the strong interpretation, with its commitment to the idea that a mental
disorder, like any other disease, is not just a construct to guide inquiry, but
a genuine part of the causal structure of the biological world—a destructive
entity with a distinctive pathophysiology which explains the observable
phenomena that the minimal model is content with.
Proponents of the strong interpretation,
then, can agree with Guze that there are distinct mental illnesses with
characteristic symptoms and natural histories. But they go further. If
psychiatry is really a branch of medicine, they suspect, we should see the
specific causal hypotheses emerge about mechanisms that cause the symptoms of
mental illness. Both Andreasen and Guze assume that to find the specific causes
of disease we need a background theory of normal function. Psychopathology is to
be identified as the departure of a psychological system from its proper state.
(We should note what counts as a malfunction is often contested in psychology
and neuroscience. Furthermore, the presence of a malfunction does not suffice
for mental illness. Most scholars agree that our thoughts about the nature of
disease are sensitive to biological abnormalities but are also guided by
judgments that such abnormalities impede human flourishing (See Cooper 2007,
Murphy 2006, Sadler 2004, Wakefield 1992). The medical model also sees
abnormalities or dysfunctions as necessary but not sufficient for mental
illness. The broader issues involved will be put aside here. Our question is:
how far can psychiatry adopt medical reasoning about pathogenic neurobiological
The strong interpretation seeks explanations that cite
pathogenic processes in brain systems, just as bodily diseases are explained by
processes in other organs. The process at issue need not be destructive, in the
sense that it makes the system collapse. Bolton and Hill (2004, 252) note that
many mental illnesses seem to be the outcome of systems in a poorly regulated
state that is stable, albeit suboptimal. But, as they say, the same is true of
hypertension and Cushing's disease; the idea of a specific pathogenic process in
medicine includes dysregulation.
Heinrich and Andreasen assume that since the
brain is an information processing organ the obvious background theory is
cognitive neuroscience. Other thinkers have argued that the correct background
theory for psychiatry is molecular biology (Kandel 2005, ch.2).
Hill worry that whatever background theory the medical model employs, it will
require explanations in terms of biological rather than intentional phenomena.
They conclude that biological psychiatry can only accommodate disorders in which
“intentionality has run out” (2004, 256). If true, this rules out using the
medical model to explain the many psychopathologies that appear to involve
irreducibly intentional or meaningful processes (cf. Thornton 2007, ch 4). The
worry is founded on the assumption that there is an unbridgeable distinction
between understanding a phenomenon in intentional terms and providing a causal
explanation of it. But the brain is a cognitive organ—and, indeed, a social one.
Many disciplines study the effects of healthy cognition on behaviour, and there
is no reason to expect that cognition will suddenly become irrelevant to the
explanation of behaviour when we study mental illness. For instance, Kendler and
Prescott (2006, 148ff) found that “stressful life events” are among the chief
causes of depression, that they are especially depressogenic if they involve
experiences of humiliation (160), and that humiliation cannot be given a
molecular reduction (350). Kendler and Prescott call Major Depression one of the
oldest diagnoses in medicine (52) and they are committed to finding specific
etiologies. Yet they are happy to employ “classically mental constructs” (350)
as parts of their causal models of mental illness.
As presented so far, the
strong interpretation of the medical model includes a demand for understanding
biological systems in terms of their normal function if we are to understand why
they become abnormal. Kincaid (2008, 375) has argued that a demand like that is
unreasonable, because we can conduct research on depression (his example), as we
do medical research more generally, based on “partial and unsystematic” causal
understanding. Kincaid identifies the demand for a background theory with the
search for a “complete wiring diagram of the organism from fertilization to
maturity” (377) and he identifies that search with a conception of science as a
search for laws of nature and natural kinds. But these seem to be separable: a
background theory could comprise a number of partial wiring diagrams arrived at
by piecemeal investigation, nor does it have to be driven by a desire for
explanation in terms of kinds participating in laws. The questions are, what
sort of general orientation toward mental phenomena does the medical model
permit, and what sorts of explanations can it encompass? We do not need a
complete theory of how biological systems work in order to conduct fruitful
research. The issue is whether, at a minimum, there need to be some rough
theoretical frameworks and shared empirical claims within which otherwise
abnormalities can be identified and outcomes assessed.
First, nothing in the
strong interpretation of the medical model rules out explanations that cite
cognitive processes in brains: Andreasen (1997) argues that schizophrenia and
depression are cognitive pathologies and sees psychiatry as both a form of
medicine and “the discipline within cognitive neuroscience that integrates
information from all these related disciplines in order to develop models that
explain the cognitive dysfunctions of psychiatric patients based on knowledge of
normal mind/brain function” (1586). This conception of psychiatry is fully
biological but not committed to a particular metaphysical interpretation of what
biological explanation must look like. It sees mental illness as the result of
pathogenic processes taking place in brain systems but does not force us to
choose reductive explanations as a matter of logic. So Bolton and Hill's worry
about the compatibility of the medical with their “neural encoding” theory
(2005, ch.2) seems overstated. They are right to stress that the brain can be
seen as a socially situated, cognitive organ, but there are advocates of a
strong medical model who are equally attuned to this conception of neuroscience.
Existing medical and biological practice already cites processes that cross
levels of explanation (Schaffner 1993, 1994) and incorporate environmental
information about stress or other risk factors. There is in principle no
objection to adding an intentional level to the mix. Any conception of normal
neurological functioning must take information-processing into account, because
processing information is what brains are for.
Most mental illnesses are
caused by diverse environmental and genetic factors. We have little reason to
think that all the relevant causes can be given a reductive analysis, for as
Schaffner dryly points out, to specify and measure environmental variables in
purely molecular terms “would be a very long-term project” (1994, 287). But one
might still think that molecular processes are the root causes of mental illness
even if many other contributory factors exist and define the context within
which genes work. Kandel (2005) offers a very stringent version of this view,
which assigns all explanatory significance to proximal genetic causes on the
grounds that “all of ‘nurture’ is ultimately expressed as ‘nature’ (39)” He
means that behavioral and cultural factors influence gene expression, but he
also seems to think that this implies that psychiatric explanations need only
mention gene expression, which will screen off everything else.
genetic reductionism is a metaphysical position aimed at identifying a
privileged level in nature and a general explanatory strategy that unifies the
phenomena and offers lawlike explanations. However, in medicine the goal of
causal explanation is instrumental. We seek the factors that make a difference
in a given case, not a metaphysically privileged level or a general unifying
account. There is little reason so far to believe that the reductonistic
approach Kandel urges has been more fruitful.
In studying eating disorders,
for example, we find that social factors may explain particular epidemiological
patterns, like different levels of eating disorder across populations. But
social factors don't tell us why only one girl in a family gets bulimia. To
explain that we can look at a particular brain chemistry that puts her at risk
(Steiger et al 2001). But that does not establish that neurobiology really is
fundamental. Rather, nothing is fundamental. Culture or trauma may require
biological mediation to have its pathological effect, and vice-versa. Neither
one should be considered fundamental, but seen rather as the best way to answer
a specific question about what makes a difference in a context.
identification of a cause of a disease often depends on what we want to control.
The reason for this, as Whitbeck (1977) and Kincaid (2008) have convincingly
argued, is that physicians care about causes for instrumental reasons. The goal
is to understand why a biological system has departed from a functional state
and identify components and processes within the system that can be manipulated
so as to understand the abnormal character of the system, and, ideally, mitigate
it. In looking for the relevant factors we do not seek a final description of
the system or look for the ultimate sources of an abnormal or disvalued outcome.
Rather, we hope to identify the variables that made a difference to the
That is why alternative etiologies can complement, rather than
compete with, each other, as in Meehl's (1977) example of an elderly man,
genetically somewhat at risk for depression, who develops it after his spouse
dies. It seems wrong to call this a genetically caused episode of depression:
the genes needed an unusual environment, so that in most other circumstances the
man would not be depressed. But he would not have developed clinical depression
had his genes been different. Both factors are causally relevant.
this stress on figuring out what makes a difference in a context, medicine is a
natural home to manipulationist accounts of causation, as Whitbeck also saw
(1977, 627–28). The basic idea behind the manipulationist approach is that it
puts us in a position to begin explaining a phenomenon “when we have identified
factors or conditions such that manipulations or changes in those factors or
conditions will produce changes in the outcome being explained” (Woodward 2003,
10). We may have a correlation—say that between smoking and heart disease. We
get from there to a causal explanation if we can intervene so as to manipulate
the value of the causal variable by itself—by stopping one group from smoking
and letting an otherwise identical group smoke, for example. If smoking causes
heart disease, we will see an effect on the cancer variable that reflects our
meddling with the smokers. If smoking doesn't cause heart disease then there
will not be a correlation between the two variables. (This view is compatible
with many proposals about the underlying metaphysics. There will be more on this
account of causation in section 3.1. For the technical details see Spirtes et al
2000, Pearl 2009).
Kandel's avowed molecular reductionism dissents from the
goal-driven, manipulationist view. Kandel bets that molecular explanation picks
out nature's own preferred level. He assumes that as we learn more we will be
able to supply fundamental explanations at such a level. Kandel invites us to
give up a fruitful approach in favor of a promissory note, on which we have
scant reason to expect payment. Molecular explanations do not appear to be
flourishing alone among all possible approaches to mental illness. (Schaffner
(1998) points out how hard it is to supply reductive explanations even for
simple model organisms.)
Things may turn out as Kandel expects, but it is not
clear that they will, based on the current fortunes of different kinds of
psychiatric explanation. In any event, it seems that the medical model does not
require any particular level of explanation. Rather, it seems to be marked, in
its strong interpretation, by a search for explanations of a particular form
that can involve many different levels. These are explanations that show how
symptoms of mental illness systematically depend on disruptions to the normal
functioning of biological and cognitive processes. The strong interpretation of
the medical model bets on such explanations being available and—which is a
further claim—being clinically useful when they are finally uncovered. Whether
the ensuing explanations privilege one form of explanation over others is an
empirical question to be answered case by case. However, psychiatry currently
recognizes many different causal factors and we should expect that to continue.
One way of cashing out this idea is to say that psychiatry must pay attention to
different levels of explanation. The next section, on explanation, will begin
with a discussion of this point.
We may begin with a picture that is familiar to philosophers of
psychology, Marr's (1982, 24–5) distinction between three levels of explanation
in cognitive science.
The highest specifies the computational task accomplished
by the system of interest. It tells us what the goal of the system is, specified
in terms of what it computes. The middle level describes the actual
representations and algorithms that carry out the goal. The lowest level tells
us how brain tissue or other material substrate, such as the parts of a machine,
can implement the algorithm. Note that the levels of description are different
perspectives on the same mental process - Marr thinks of vision as the
construction of a 3D representation from a 2D input, and the three levels are
three different ways to understand that construction. Other cognitive phenomena
can also be understood in these three ways.
Marr sought to understand
psychological capacities in the abstract without worrying about biology:
although he certainly assumed that capacities could be realised in a physical
set up, he thought that the details of the particular set up would not make a
difference to the way the psychology was understood. But as the sciences of the
mind have become more interested in the brain we are learning that this idea may
need to be amended. Cognitive neuroscience is learning to look for physical
structures in the brain that carry out information-processing jobs, or what
Glymour (1992) calls “cognitive parts”. Our understanding of biological
realization feeds back into and constrains our understanding of the abstract
processes of cognition (Bechtel and Richardson 1993). Rather than relating
abstract psychological capacities to each other, higher level descriptions of
the mind/brain in cognitive neuroscience relate capacities understood as
functional descriptions of fairly coarse-grained brain areas, not purely
abstract computational task specifications. Theories of the normal system
specify the nature and interrelation of cognitive parts. Armed with these
assumptions about cognitive parts, psychiatrists can see a disorder as a
breakdown in normal functioning within and between cognitive parts. Marr's first
level might seems to be useful as a source of background theory for doing
psychiatry, because it asks “what is it for?” and much of psychiatry is about
finding out psychological systems fail to do what they are for.
still face the question of how psychological deficits are related to other
levels of explanation, and here Marr's picture comes under real stress. Marr's
three levels are different representations of the same process. But in
psychiatry different levels typically represent distinct causal processes. For
example, the causes of many mental illnesses include a mix of genes and
environmental factors, as in Meehl's example, cited above, of genetics and
bereavement conspiring to cause depression. The genes and environmental effects
are different kinds of processes, not different levels of one process. If we
were dealing with one process, describable in different ways, then we could
anticipate a reductive account, in which higher-level variables are mapped on to
lower-level ones. But even though it is hard enough to imagine a molecular or
neurological reduction of a psychological construct like humiliation (which, we
saw above, is depressogenic), it is even harder to imagine a reductive analysis
of socio-cultural factors like unemployment or childhood sexual abuse. They have
brain effects, but the brain effects vary across classes of individuals in ways
that depend on other environmental and genetic contexts (see Kendler and
Prescott 2006 for a comprehensive review.)
Schaffner (1993, 1994) suggests
this structure is the norm throughout biology, and sees it as relating causes
and effects at different levels of explanation. Appealing to levels of
explanation is unobjectionable if it just involves a reminder that we need to
relate variables of many sorts. But it is not clear that we have any principled
grounds for sorting phenomena into levels. Marr did, because he imagined levels
as descriptions of the same process (the construction of a 3D image from 2D
retinal impacts) couched in the vocabularies of different sciences. But when we
move outside the skull and begin introducing environmental factors and other
kinds of cause, the Marrian picture looks less plausible.
Another way in
which levels talk has featured in recent philosophy of psychiatry is as a
constraint on permissible kinds of explanation. Chris Frith (1992, 26) for
example, imagines what we would say if we found a strong correlation between a
spike in dopamine levels and delusions of thought insertion (in which, for
example, one has the experience of another person's thoughts in one's own mind).
He argues that such a correlation is “simply not admissible” as an explanation
because we would remain in the dark about why a sudden upsurge in dopamine
causes thought insertion rather than something else. To show why thought
insertion comes about, Frith thinks, we need a cognitive story which shows us
how it is caused by failures of normal subpersonal processing.
is that a causal explanation of a psychotic phenomenon, or some other mental
symptom, must cite properly cognitive variables to be explanatory. That is,
explanations should relate variables from the same level. The relationship
between dopamine and thought is just opaque to reason, and we want variables
that are related in ways that are transparent to reason. There is a constraint
here; the idea that explanations of psychological phenomena should relate cause
and effect in ways that we find intelligible. Campbell (2008) in attacking this
picture, notes that talk of levels of explanation is often wheeled in at this
point, as it is by Frith, to supply relations that are transparent to reason in
the right way. The idea is that only processes at a level let us grasp
explananda at that level. Explanantia at a different level are not intelligible
in the right way, so although lower-level processes may realise the higher ones
they cannot explain them. This amounts to a constraint on acceptable
explanation. Should we accept it?
The debate here quickly gets into technical
arguments about the concept of causation. Campbell argues against Frith in
favour of the Humean idea that we simply cannot tell in advance of inquiry what
causal relations obtain in nature. Anything can cause anything and it is just as
unwarranted to suppose that the relevant explanatory variables for psychotic or
affective phenomena must be cognitive as it is to adopt a simple reductionism
and insist on their being biological. Decades of research have revealed that
mental illness is caused by, and causes in turn, many different physical,
psychological and social factors. We simply have to take our causal relations
where we find them, including interlevel ones. Craver and Bechtel (2007, 554) on
the other hand, argue that it stretches the concept of causation to breaking
point to admit interlevel causes: they say that “to accept interlevel
relationships as causal violates many of the central ideas associated with the
concept of causation”. Craver and Bechtel argue from the perspective of
mechanistic explanation. Mechanisms explain effects in terms of interlocking
parts, and the relation across levels, they affirm, is one of constitution, not
causation; causation can only be intra-level. Interlevel causation, on this
view, amounts to something causing itself, because different levels are
different ways of talking about the same thing. However, talk of levels in
psychiatry often involves relating different parts of the world, as in Meehl's
example: genetics and bereavement may be seen as requiring different levels, but
they are not different ways of describing the same process. Causal models must
interrelate phenomena of very different types.
In part because of these
issues, that levels in psychiatry are not Marrian, Campbell (2006) argues for an
interventionist approach to causation. This is the view that when we say X is a
cause of Y we are saying that intervening on X is a way of intervening on Y
(Woodward and Hitchcock 2003, Woodward 2003, Pearl 2000): manipulating one
variable makes a difference to another. This is not a reductive analysis of
causation, since it makes use of causal ideas—it just states that questions
about whether X causes Y are questions about what would happen to Y if there
were an intervention on X. Kendler and Campbell (2009) have argued that an
interventionist model provides a rigorous way of articulating the idea that any
combination of variables might characterize the causes of a disorder, whilst at
the same time providing a clear test of what variables are actually involved,
thus avoiding a simple-minded holism that just says that lots of things are
relevant. They further note (2009, 997) that interventionism “permits the clear
separation of causal effects from the mechanistic instantiations of those
effects”, thus directly confuting the approach favored by Bechtel and
Appealing to levels of explanation in psychiatry, then, might just be
a reminder that we need to relate variables of many sorts in explaining the
causes of disorder. But it may also be connected with particular perspectives on
reduction, explanation and causation. We won't go into these debates here;
rather, we will move on to discuss a further problem. As well as great diversity
in causal factors, psychiatry also confronts the problem of diverse symptoms;
many mental illnesses take a different form in different people. Although two
people might both be diagnosed with major depression, they need share few
symptoms. Both are very likely to feel miserable and lose interest in activities
they normally enjoy. However, one might lose weight, sleep less and becomes
physically agitated while the other sleeps more and becomes lethargic and
tormented by feelings of guilt and thought of suicide. The philosophical problem
arises from the confrontation between the great variation in clinical reality
and the need to simplify in order to render that reality scientifically
tractable. In summary form, the problem is; what are we trying to explain when
we explain a mental illness? Is it a diverse set of real-world phenomena, or
some simplified representation of those phenomena?
One way to start thinking about what we have to explain
in psychiatry is to borrow from Thagard's (1999, 114–5) account of diseases as
networks of “statistically based causal relations” which are discovered using
epidemiological and experimental methods. This fits the picture that Kendler and
Prescott present for depression quite neatly (although their models are designed
to incorporate both causal relations between variables and correlations).
Thagard's causal-statistical networks, like Kendler and Prescott's path models,
provide “a kind of narrative explanation of why a person becomes sick” (p15).
They incorporate information about the typical course of a disease as it unfolds
over time, including information about typical risk factors for the disease—such
as the finding that heavy use of aspirin increases acid secretion which makes a
duodenal ulcer more likely. The causal network does not specify how each causal
factor produces its effects, though. It is really a descriptive model that lets
us ask the question; what facts make it true that people get sick in these
In effect we have a set of exception-prone generalizations about the
pathways a disorder takes: people in this situation are likely to become
depressed unless such and such intervenes. And when they are depressed they will
probably have the following experiences, unless they have these other ones.
Thagard's idea of a narrative is helpful here; path models represent typical
stories about characteristic ways of getting sick. But a narrative by itself
might not explain anything; if it is explanatory, it is because earlier events
mentioned in the narrative pick out the causes of later events.
(2007) presents a way of thinking about psychiatric explanation that fits well
with the idea that a diagnosis lets us tell a story. We often find ourselves
with narratives that tell us how someone gets sick, and it might be that a
useful narrative is one which isolates the temporally prior variables and lets
us see how later phenomena depend on them. One way to think about this is that a
good narrative is one that talks about a natural kind. If we have a natural
kind, with some causal structure underpinning it, the systematic dependence of
later states on earlier ones is easy to grasp. Several theorists have defended a
view of psychiatric disorders as natural kinds. Influential recent philosophical
treatments have rejected the idea that mental disorders have essences, but have
defended the idea that mental disorder are natural kinds in Boyd's sense of
homeostatic property clusters (Beebee and Sabbarton-Leary 2010; Kendler et al.
2010; Parnas et al. 2010; Samuels 2009, Zachar 2014), in which properties occur
together often enough, and reliably enough, to support ampliative inferences,
even if the mechanisms responsible for the kind do not make every member of it
the same as every other member. When inductive reasoning works, thinks Boyd, it
works because we have have latched onto these underlying causal mechanisms that
bring about the clustering. Successful inductions track the observable
manifestations of the causal mechanisms responsible for the characteristics of
the kind. The mechanisms, we might say, leave an identifiable causal signature
in the world. The HPC account seems to suit mental disorders. They often vary
across cases, with characteristic symptoms sometimes absent even when the
patient presents a typical cluster of signs and symptoms. So it is
understandable that theorists who are sympathetic to the medical model in
psychiatry should be drawn to the homeostatic property cluster idea.
Cooper distinguishes natural-history based explanations
from case studies. She presents them as distinct kinds of psychiatric
explanation, but she doesn't go into detail about what the other types might be,
so her overall position is hard to grasp. But one idea is very clear; at least
some mental illnesses are natural kinds, and natural history explanations work
by “invoking natural kinds” (2007, 47). Once we know which kind an object
belongs to, we can explain and predict its behaviour based on its kind
membership: we can say why a substance has expanded upon being heated by
invoking the fact that it's a bit of metal, and metals expand when heated. Or we
can predict that if Rex is in the kitchen then leaving the roast beef there
unattended is a bad idea, since Rex is a dog and dog-meat interactions take a
predictable form. And, it is hoped, we can explain why Laura hears voices by
appealing to the fact that she has schizophrenia. And our confidence that she is
schizophrenic warrants (pessimistic) predictions about her future.
also talks about case histories and argues that they explain another person's
unique situation by drawing on our capacities for simulation of other people's
states of mind. This claim involves commitments in the explanation of theory of
mind that would take this essay too far astray. The relation of folk psychology
to case histories is unexplored, as is the nature of reasoning from cases more
generally: we lack a good general account of what a case history explains or is
otherwise good for, in psychiatry or in any other field. (Forrester (1996)
points out that reasoning with cases seems to be a distinctive and ubiquitous
style of thought in science and elsewhere, and we have no good account of it.)
So for now, we must put case histories aside.
Cooper argues that a natural
history explanation needs to cite natural kinds if it is to be helpful. But in
order to work the explanations do not need to cite the actual causal mechanisms
responsible for the behaviour of the members of the kind in question. We know
that Rex will devour the roast if we leave him in the kitchen with it, and we
can safely make this prediction despite total ignorance of canine physiology.
The history of psychiatry offers a number of instances in which pharmacology has
led to the recognition of new kinds even in the absence of detailed causal
knowledge. For example Cade's (1949) discovery that lithium greatly inhibited
the startle reflex and other forms of anxiety in guinea pigs was useful even
without good information about their underlying cognitive neurobiology, since it
led him to predict that whatever was going on might also apply in
Invoking kinds give us power over the world, by making it easier to
predict, control or mitigate the outcomes we care about. One philosophical
question we can ask, of course, is whether science wants anything more. If you
think science just aims for empirical adequacy, then it may seem that sorting
patients into kinds is enough, provided that we can understand the course of the
In particular, natural history explanations fit a conception of
diseases as syndromes unfolding over time that is enshrined in both DSM-IV-TR
and the minimal construal of the medical model. It does not deny that there are
causal processes, but sees mental illnesses as collections of signs and symptoms
with characteristic histories. They doubtless depend on physical processes but
are not defined or classified in physical terms. This picture of disease
naturally goes along with the employment of natural history explanations, since
they too invoke natural kinds without worrying about the mechanisms that explain
the behaviour of members of the kind. It's enough to be able to identify kind
membership, thereby giving us a degree of explanatory and predictive
Natural history explanations fit Thagard's disease network nicely;
if a disease network provides a narrative account of why people get ill, and
predicts some outcomes, we can see it as a graphical representation of the
historical pathway typical of a kind. Much epidemiological work in psychiatry
fits the pattern here; we try to isolate the causal factors that define a
disease history that is met with regularly. These histories display relations
between variables that show how later phenomena, like the symptoms of depression
or substance abuse, depend on earlier phenomena, like the genes you were born
with, or the parental abuse you endured.
Unlike some of the more homespun
examples, the natural histories uncovered by systematic longitudinal research
can be quite surprising and genuinely explanatory. But (as Cooper and Thagard
both suggest) they leave us with a lot to do; whatever the philosophers of
science may say about how empirical adequacy is good enough, physicians have
spent a century and a half looking for causal explanations of pathological
phenomena (Carter 2003).
Cooper suggests that natural history explanations provide us with what Murphy (2006)
calls causal discrimination, as opposed to causal understanding. We can know two
kinds are causally different even if we don't why they are different, because
the details of the underlying causal structure evade us. Different types of
plant may need to be put in the ground at different times, or in different
seasons, in order to maximize crop yield, for instance, and we may be able to
predict accurately that different patients will respond to different drugs even
if the basis for these differences remain unknown. But we assume that these
differences rest on an underlying causal structure. In psychiatry, differential
diagnosis follows a similar logic, but sceptics wonder if the degree of
variation makes the predictions too unreliable for this approach to really
An explanation of this type places entities in kinds, thereby tracking
the as yet unknown causal factors that regularly make the same kind of
difference in patients of the same type. Rather than identifying the causal
factors, then, the natural history approach tracks the operation of hitherto
unknown causes, by sorting patients into kinds with a presumed common nature,
based on the natural history of their conditions, or on other grounds that I
have not talked about, like differential responses to drugs.
explanatory job is to explain the observed causal-statistical network by
identifying the mechanisms and other forces that give rise to it, viz. the
causal structure of disorders. The problem, of course, is the sheer variety of
the phenomena, which does not give us the degree of epistemic security we get
when we sort phenomena into kinds in other sciences. One way to make this
variety tractable, suggested by the natural history approach, is to look for
some stable phenomena that do not vary. These are not likely to be found at the
level of diagnoses, because in many cases two people with the same diagnosis
will exhibit different behaviours and other symptoms depending on their personal
lives, cultural background, other mental illnesses, and so on. There is too much
variety at the level of diagnosis. So we must search for smaller units of
We can think of this first approach as zooming-in on one small
portion of the overall network, looking for a unit that has enough stability
across histories to allow for an explanation in which there are cause-effect
regularities; if the underlying causal structure is too diverse, look for causal
units that stably replicate across patients, explain them, and then put these
well-understood parts together to explain individuals. Another advantage of this
approach is that it promises to treat patients as individuals rather than
clumping together into kinds that they only approximately fit.
approach is exemplified by Bentall (2005) and Spaulding et al (2003). They both
look for the smallest unit of reliable explanation or manipulation.
al. argue from a clinical perspective for seeing patients as collections of
“problems”, with the problems in each case drawn from a repertoire of clinically
significant phenomena that different patients exemplify in different ways.
Bentall argues that diagnoses like depression or schizophrenia have proved
helpless in the face of all the variation that patients exhibit. He sees
individual cases as mosaics made up of recurring symptoms like hallucinations,
which can be separated out and studied in isolation. According to this view,
there is no such thing as schizophrenia. That's not because there is nothing
wrong with schizophrenics, but because schizophrenia is not a natural kind. The
natural kinds of psychiatry are specific pathologies that schizophrenics display
in shifting conjunctions. These are distinct psychotic phenomena that should be
approached separately and treated as distinct symptoms or complaints.
thinks “we should abandon psychiatric diagnoses altogether and instead try to
understand and explain the actual experiences and behaviours of psychotic
people” (2005, 141). But in fact he tries to relocate diagnosis at a more
reliable level. For example, Bentall (ch. 15) objects to the old model of
inferring thought disorder on the basis of disordered speech. His sees
disordered speech as a failure of communication, which is especially likely when
subjects are emotionally aroused. In Bentall's tentative model, initial deficits
in working memory caused by emotional arousal interact with other deficits in
semantic memory, theory of mind and introspective monitoring. The result is a
failure to communicate and a lack of self-awareness of one's failure to
communicate (which distinguishes psychotic patients from normal subjects in the
grip of powerful emotions who are struggling to get their ideas across). This is
a stable phenomenon, in the sense that we can give the same causal story in all
cases of thought disorder, thus giving us a robust account that transfers across
patients. A general theory of schizophrenia would have too many qualifications
and varieties to transfer in this way.
Zooming-in faces two problems. First,
where do we stop when looking for smaller units? There is always the chance that
some finer causal discrimination will uncover an even more stable
A proponent of zooming-in can always argue that the idea, as in
any science, is to develop the descriptive apparatus empirically in a way that
ultimately fits one's theory of the domain. Bentall and Spaulding et al. are
betting that any clustering of problems or symptoms will not line up neatly with
the DSM categories, and this is probably a good bet for any approach. Bentall's
chosen approach stresses the cognitive science of psychotic phenomena, whereas
Spaulding et al. tend to look for correlations between clinically significant
problems and a wider variety of underlying phenomena; for Spaulding et al, the
relevant sciences for identifying problems span many levels of analysis from the
intra-cellular to the socio-cultural. Their examples include low levels of
cortisol and learning deficits (127–130).
Nonetheless, there will always be
differences across patients in the phenomena that we ultimately zoom in to. This
is likely to be especially problematic when these independently characterised
lower-level phenomena start to combine in actual patients. Zooming in should
not, therefore, be thought as an alternative to idealization, since any search
for commonalities across patients will involve some degree of idealization. The
rival approach is another form of idealization, but zooms out to think in terms
if idealized patients, rather than idealized problems.
Zooming out begins by
accepting that mental illness almost always depends on complex interactions
between diverse lower-level phenomena and tries to deal with this variety by
treating disease networks as idealizations that are more or less similar to
actual histories. It is a recurring theme in the history of psychiatry that the
textbook expression of a disorder can be realized in individuals in different
ways. Charcot (1887–88) distinguished archetypes, which are ideal types of
disorder, from formes frustes, which are the imperfect forms the ideal type
manifests in individual subjects. Birnbaum's (1923) distinction between the
pathogenic features of a psychosis and itspathoplastic features is similar. The
former define its essential structure, and the latter express the personal
circumstances of the patient.
Murphy (2006) argues that the variety in mental
illness requires us to explain psychiatric phenomena not by looking for stable
regularities but by constructing exemplars. Murphy sees the exemplar as an
imaginary patient who has the ideal textbook form—something like Thagard's
network, and the narrative it provides—of a disorder, and only that disorder,
although the textbook needs to thought of as a statement of the final theory,
and not any current work in psychiatry. As with zooming-in, the approach assumes
that commonalities across patients will be revealed by inquiry. The idea is to
model all the causes that contribute to a natural history so as to explore how
they work together in different contexts to produce the various outcomes of
interest, and then understand patients as idiosyncratic instances of the
exemplar. When we explain a disease, we construct an exemplar and model it. But
the causal structure that explains the exemplar resembles real world patients to
varying degrees. So when we talk about individuals we explain their symptoms by
identifying processes in the patient and showing how they resemble some part of
the model. Godfrey-Smith (2006), following Giere, suggests that there may not be
a helpful general treatment of these resemblance relations. They are not formal
relations but the sort of comparisons between imaginary and real states of
affairs that we all perform effortlessly. If there is a general theory, then, it
is likely to be found not by philosophers but by cognitive scientists studying
analogical thought (e.g. Hummel and Holyoak 2005). And because it is
instrumental concerns that drive our search for explanations in psychiatry, as
in medicine more generally, the clinically significant relations between
disease, model and patient are likely to be highly context-specific; they will
be determined in part by whether they offer opportunities for successful
therapeutic interventions, which depend not just on how the world is arranged,
but also on what our resources and opportunities are.
The exemplar lets us
identify robust processes (Sterelny 2003, 131–2, 207–8) that are repeatable or
systematic in various ways, rather than the actual processes that occur as a
disorder unfolds in one person. But we do not stop there: the ultimate goal is
causal understanding of a disease. We build a model to serve this end. It aims
to represent the pathogenic process that accounts for the observed phenomena in
the exemplar. To explain an actual history in a patient is to show how the
processes unfolding in the patient resemble those that are assumed to occur in
the exemplar. Exemplars provide an idealized form of the disorder that aims to
identify the factors that remain constant despite all the individual variation.
Not every patient instantiates every feature of an exemplar, and so not every
part of a model will apply to a given patient. Once we understand the
resemblance relations that exist between parts of the model and the exemplar, we
can try to manipulate the model so as to change or forestall selected outcomes
in the real world.
In commenting on this approach, Mitchell (2009) points out
that her own work (2003) contains an alternative approach to model-based
explanation in complex sciences. Her “integrative pluralism” aims to isolate
individual causes and model them individually, seeing how each makes a causal
contribution on its own. Theorists then put together a collection of models of
individual phenomena and try to integrate them by applying multiple models as
seems necessary to explain a particular case. Mitchell's approach resembles the
zoom-in in its search for decomposing, but it tries to isolate causes that can
recombine—such as genes or interpersonal difficulties—rather than searching for
explanations of particular clinical phenomena like thought disorder (see also
Tabery 2009). This is similar to the way Spaulding et al. seek the development
and integration of causal models in the service of developing a comprehensive
clinical understanding of people and their problems.
Mitchell (2009, 131)
suggests that we might need both her models and Murphy's as circumstances
dictate. And there might be room for zoom-in models as well. There seems no
reason why psychiatric research could not aim to be pluralist about explanation
and combine elements drawn from all these explanatory styles as we learn more
about what works when we try to figure out mental illness.
Ghaemi (2003. ch
12) offers a different defense of zooming-out. He argues that current DSM
diagnoses function as ideal types in Weber's sense. One way to understand
Weber's idea is just as a forerunner of modelling, in which essential variables
are isolated and inessential ones put aside. Ghaemi, though, locates it in a
tradition of hermeneutic understanding that is most closely associated in
psychiatry with Karl Jaspers (1997). This approach looks for meaningful
psychological connections between phenomena and is contrasted with causal,
scientific explanation. In Ghaemi's view the DSM categories are designed to
foster understanding of this type by directing clinical attention to aspects of
the patient's life that are relevant to the disorder at hand. He sees this as an
application of the methods of the humanities, rather than those of the
One argument that might be made against zooming-out is that it
assumes that mental disorders are categorical, rather than dimensional.
neo-Kraepelinian approach is often faulted for assuming that disorder is an all
or nothing affair, whereas it might mark an extreme point on a dimension that is
present to a greater or lesser degree throughout the population (Kendell 1975,
McHugh and Slavney 1998, Poland et. al 1994, Widiger and Sankis 2000). So
schizophrenia might be seen either as condition that is present or not—just as
one either is of voting age or not. But we might also see it as like having high
blood pressure—marking a point on one or more dimensions where normal
psychological traits become aggravated enough to constitute a population of
clinical concern. Some psychiatrists have supported one approach or the other.
Others, like Ghaemi (203), have argued that some conditions, like the major
psychoses and mood disorders, are probably categorical, whereas other
conditions, especially the personality disorders, are dimensional.
clearly an empirical issue in the end, so if the zooming-out approach is
committed to a categorical approach it is a cause for concern. However, a
zooming out approach could treat its models as end points on a spectrum that
usefully capture differences between populations (Ghaemi, 199); this is
compatible with looking for causal stories that explain the model. Furthermore,
in so far as the zooming-in approach relies on idealizations too, it faces the
same problem. Bentall's approach, for instance, faces the issue of what degree
of language difficulties counts as pathological, and Spaulding et al. need to
find a way of distinguishing a clinical problem from a phenomenon that is normal
Successive editions of the DSM
have been published in North America, and questions have always arisen about the
applicability of its categories outside the West. DSM-5 follows its predecessor
in coping with cross-cultural variety in two ways. First, some conditions, such
as depression and anxiety, are treated as universal – found in every culture,
despite local differences in character. We may term this the unificationist
project. The DSM-IV-TR averred that major DSM categories occur all around the
world but with symptoms and courses that are influenced by local cultural
factors. Second, DSM-IV-TR employed the concept of culture-bound syndromes,
which were defined as “recurrent, locality-specific patterns of aberrant
behavior and troubling experience that may or may not be linked to a particular
DSM-IV diagnostic category” (p. 898). Culture-bound syndromes occur in a limited
number of specific societies or cultural areas. They are local, often
traditional, diagnostic categories that make sense of patterns of thought and
behaviour that are treated as deviant or troubling in that context.
theory, culture-bound syndromes are those folk illnesses in which alterations of
behaviour and experience figure prominently, relative to local norms. Standard
DSM diagnoses are not thought of in this way, even if they are culturally
limited. Multiple Personality Disorder/ Dissociative Identity Disorder, for
example, was widely diagnosed in the USA in the 1980s, but seldom found
elsewhere. That did not lead psychiatrists to treat it as a culture-bound
syndrome, even though it seems to fit the definition. The assumption in
mainstream psychiatry is that Western conditions are not culture-bound; they
represent abnormalities in a universal human endowment. This is the case even
for conditions (such as some kinds of body dysmorphia) for which prevalence data
only exists in a few western nations.
DSM-5 has moved away from concept of a
culture-bound syndrome and adopted that of “cultural concepts of distress”
(p.758). These are ways in which “cultural groups experience, understand and
communicate suffering, behavioural problems or troublesome thoughts and
emotions”. DSM-5 distinguishes three main types of cultural concepts: syndromes,
idioms (ways of expressing distress), and local explanations. The last is
particularly interesting: a standard picture of mental illness in both
non-Western and premodern societies represents it as explained by supernatural
forces like ghost possession. But Edgerton (1966) reported that the East African
tribes he studied were divided over the explanation of psychosis. Some tribes
did understand it in terms of ghost possession, but others thought of it as
having an organic cause (“brain worms”). DSM-5 makes room for such findings as
part of the integration of local explanations into a theory of mental
DSM-5 supplements this conceptual reform with a thorough overhaul of
the “Outline for Cultural Formulation”. This is an interview outline introduced
in DSM-IV-TR, in part in response to pleas from cross-cultural psychiatrists
dissatisfied with the old ways (e.g. Canino and Alegria 2008). It reflects an
unprecedented investment in applying anthropology to psychiatry by the DSM-5
Cultural Issues Subgroup, who ran field trials of the new Cultural Formulation
Interview (CFI) in 6 sites around the world (Aggarwal 2013). The CFI is designed
to assess both the cultural or ethnic groups that the subject belongs to and the
ways in which those groups understand the problem and affect the subject’s
experience of it. It comprises a series of questions designed to gather
information from the point of view of the patient and his or her cultural peers,
including specific questions that tell the patient not to repeat what the doctor
has told them but to express their problems as they see them and describe which
aspects of their identity are most important to them. It could be used with any
subject anywhere, and the manual acknowledges that all mental illness, including
the DSM diagnoses, is shaped by the surrounding culture. On the other hand, the
CFI and its associated conceptual material are poorly integrated into the DSM-5
– many diagnoses pay no attention to cultural formulation at all – and the
culture-bound syndromes do in fact survive. They have been renamed “Cultural
Concepts of Distress” but the appendix listing them survives, so one may wonder
how thorough the overhaul has been.
The other approach to cultural variation,
as mentioned, is to treat different diagnoses as manifestations of the same
underlying DSM condition. The issue is how different a diagnosis needs to be
before it stops being a form of a DSM condition and becomes a culture-bound
syndrome. It has been suggested that anxiety disorders, for example, should have
their "worry domains" expanded because people from other cultures may worry
about things that Euro-Americans don’t fret over (Lewis-Fernandez et al 2010).
The assumption here is that anxiety disorders are common enough in all human
cultures to merit treating as a universal, but that this can be missed if
clinicians do not appreciate the different triggers, reactions and conceptions
that distinguish the anxiety disorders in different populations. We need to
recognise the greater variety of symptoms among sufferers from anxiety who live
in Western cultures but don’t show the typical symptoms of a Westerner.
Lewis-Fernandez and his team (2010) argue that a majority of Latino sufferers
from ataque de nervios would meet panic disorder criteria, for example, if the
DSM amended the requirement that a panic attack lasts only a few minutes. Ataque
de nervios was listed as a culture-bound syndrome in DSM-IV-TR. Its symptoms
commonly include a mix of classic panic attack symptoms like palpitations and
sensations of bodily heat and loss of control. But it may also involve
uncontrollable shouting and threats of violence, together with other symptoms
less often found in panic attacks, and it may last much loner. Lewis-Fernandez
is interested in the idea that ataque de nervios can be assimilated to existing
anxiety diagnoses provided we take the variation in symptomatology more
This unificationist approach may be used to argue that the
diagnostic entity itself is the same in all cases – some shared underlying
process that adapts or responds to different cultural settings to produce
different behaviors. Some scholars argue that the underlying abnormality, even
if it exists, is beside the point. Our response to the condition should be
determined by its expression, even if there is an underlying psychological kind.
Kleinman argued that depression in the West and in East Asia are different
enough in their expression and course that they should be seen as different
conditions (1987, 450): “Depression experienced entirely as low back pain and
depression experienced entirely as guilt-ridden existential despair are such
substantially different forms of illness behavior with different symptoms,
patterns of help-seeking, course and treatment responses that though the disease
in each instance may be the same, the illness rather than the disease is the
Horwitz and Wakefield (2007, p. 199) opt for
universality in response: “we agree with Kleinman’s distinction between disease
as a universal underlying dysfunction and illness as the culturally shaped
expression of a given dysfunction … [but] if there are indeed underlying common
dysfunctions, then treatment presumably depends in large part on the science of
identifying and intervening in such dysfunctions irrespective of their cultural
The unificationist project is an empirical bet that is based
on the assumption that human psychology is enough alike to treat at least some
culturally distinctive forms of mental disorder as expressions of a shared human
nature that is differently shaped by local culture. The appeal to culture bound
syndromes is also a perfectly good bet, reflecting the idea that some forms of
behaviour are entirely local and not assimilable to a universal model. Both
unificationism and recognition of culture-bound syndromes could be pursued at
the same time. Given the boring but probably correct observation that people
around the world are both alike and different, that may be the obvious course.
However, pursuit of these strategies should be freed from the apparent
assumption in DSM-5 that western minds are the blueprint for the world. The
western form of a condition may be unusual: the more we look, the more it seems
as though the cognitive aspects of depression – the complex psychology of
self-blame and immiserating introspection – may be distinctively Western. There
may be conditions that DSM treats as universal but which in fact are
culture-bound syndromes that only exist in NATO countries.
Psychiatric models explain idealization of some sort. The point
of it all, though, comes when that understanding lets us help patients. Guze
(1992) calls this the move from the biological perspective to the clinical one.
In making the move we shift from a general description of a disease process to a
specific description of the biology of an individual. The clinician takes the
imaginary ideal patient and specifies more real-world detail, so as to produce a
description of a smaller set of patients, perhaps even a single case. The
scientific project idealises, whereas the clinical one uses the resources of the
science to help individuals. In displaying causal relations that give rise to
features of the model we present opportunities for therapeutic action, whether
we have zoomed in or out. The model defines a set of relations that differ from
those present in a real patient along various dimensions. One is precision: the
causal relations the model represents may need to be made more precise when we
look at real patients. The degree to which a symptom is present, for example,
might need to be specified precisely in a clinical setting, whereas in the
exemplar the symptom can be defined as inhabiting some range of values, any one
of which might apply in nature. Or we can supply a determinate story that
embraces the details of the beliefs and other intentional states of the patient,
instead of just citing the fact that a particular information-processing pathway
is implicated in patients of that type.
surveyed so far in this entry mostly counts as philosophy of science, where
psychiatry is the science in question, and the philosophy is concerned with
topics familiar to philosophers of science, such as explanation. Another
tradition in philosophy of psychiatry belongs to what Graham and Stephens (1994,
6) call applied philosophy of mind, which is one of the approaches they
distinguish in their rough taxonomy of approaches to philosophical
psychopathology. The remaining category or work Graham and Stephens recognises
looks at the ethical and experiential aspects of mental disorder. This section
surveys some recent work in applied philosophy of mind. It does not aim to be
comprehensive, since this area has probably seen the most intense flowering of
recent philosophical work. We will look at some representative work to get a
sense of the varieties of topics and projects under philosophical
Philosophers writing in this vein (exemplified by Graham, 2010)
look to incorporate empirical results into philosophical reflection on topics
like personal identity, rationality or voluntary action. They may also seek
distinctively philosophical explanations of psychopathologies, which try to
understand them in terms borrowed from the philosophy of mind. Whereas Murphy
(2006), for example, sees the scope of the mental as defined by the sciences of
the mind, Graham thinks of the mental as possessing the twin hallmarks of
intentionality and consciousness. Disturbances of intentionality and
consciousness are what count as mental illnesses, therefore, and philosophical
theories that treat of intentional or conscious states can help us to understand
mental disorders better.
This philosophical project involves, but is not
limited to, conceptual clarification. Philosophers have made useful
contributions by interrogating the details of psychiatric concepts. This way of
doing philosophical psychopathology is exemplified by Part One of Potter (2009).
She looks at key concepts in the current understanding of Borderline Personality
Disorder, which is characterized by feelings of emptiness or loss of self,
impulsive or self-destructive behaviour, bursts of anger and unstable
relationships. A staple of the literature on the condition is the idea that
borderline patients are manipulative. Potter (ch.6) usefully asks what this
A therapist may often feel outmanoeuvred by a patient who has managed to
bring about an outcome that the therapist did not prefer—for instance, a patient
who still wishes to be admitted to hospital despite her therapist's judgement to
the contrary may deliberately injure herself to force the hospital to admit her.
In this case, the patient has certainly taken extreme measures to get her way,
but it is not clear that it counts as manipulation. The patient has defied
medical opinion, but she has not changed the therapist's mind or been
deceptive—we might prefer to think of manipulation as deliberately changing
someone else's mind through charm, trickery or some other psychological process.
That kind of ability to get your own way is often ascribed to psychopaths, but
in her work Potter makes us wonder if the same idea really applies to borderline
patients. Perhaps they should just be seen as desperate people who are trying to
cope with their distress, or socially inept (115–16) rather than agents setting
out to bend others to their will. And even if they are trying to get their own
way, well, why shouldn't they? The concern Potter raises is that the concept of
manipulativeness is being used by clinicians to just mean something like
‘behaviour that makes my job harder’.
set out by Graham and similar theorists has a different agenda that goes beyond
It involves both using concepts from psychiatry to
shed light on philosophical problems and using existing philosophical positions
to explain, or at least make clearer, some of the issues that daunt
psychiatrists. Take, for example, delusions of thought insertion. Subjects with
this condition say that they have thoughts inside their minds that have been put
their by someone else or are actually being thought by someone else, as in the
following famous case reported by Mellor (1970): “I look out the window and I
think that the garden looks nice and the grass looks cool, but the thoughts of
Eamonn Andrews come into my mind. There are no other thoughts there, only his …
He treats my mind like a screen and flashes thoughts onto it like you flash a
picture.” (Eamonn Andrews was a British TV personality.)
It is very hard to
imagine what thought insertion could be like: how can I be introspectively aware
of something as an episode in my mind, yet at the same time experience it as
someone else's thought? Graham and Stephens (2000) suggest that thought
insertion should be seen as alienated self-consciousness. They draw on
Frankfurt's (1988, 59) idea that only some of things I do actually express my
agency. Some bodily movements can be movements of my limbs without counting as
actions of mine—perhaps because someone else is controlling my movements. The
same can be true of mental events. If a tune runs through my mind unbidden, it
is an episode in my mental history. But it does not count as my mental activity
in the same way as the mental arithmetic I do to balance my checkbook counts as
mine. The latter, but not the former, comprises intentional thought that
expresses my agency. Graham and Stephens (2000, 152) call these properties of
thought the sense of subjectivity and the sense of agency. They propose that the
two properties can come apart, so that in thought disorder the sense of
subjectivity occurs without the sense of agency. On this picture, attributing
the thought to someone else makes sense, because it is the kind of mental
activity that must be produced by something, carrying as it does the hallmarks
of agency (just notmy agency).
Such a theory does not explain where the
abnormal experiences come from. Rather, it tries to use philosophical resources
to make the experience somewhat less unfathomable, and perhaps clear some ground
for an explanation by pointing the way towards the sort of mental processes that
would need to be involved. A different approach to philosophical psychopathology
looks to the science to illuminate a philosophical debate.
The debate over psychopathy seems to be a case where
empirical findings have a clear philosophical contribution to make.
about psychopathy have been appealed to in two debates. First, they are involved
in the debate over whether moral judgments are intrinsically motivating, or
whether it is possible to know what morality requires yet remain unmoved. Jesse
Prinz (2007, 42) has called psychopathy a “test case”, which helps us to
discriminate between the claim that moral judgments are intrinsically motivating
and the contrary claim that you could form a moral judgment without being
motivated to act on it. A second, albeit related issue in moral psychology is
the extent to which moral judgments are the product of reason or of affective
Hume (1751, section IX) imagined the “sensible knave”, who, “in
particular incidents, may think, that an act of iniquity or infidelity will make
a considerable addition to his fortune, without causing any considerable breach
in the social union and confederacy. That honesty is the best policy, may be a
good general rule; but is liable to many exceptions: And he, it may, perhaps, be
thought, conducts himself with most wisdom, who observes the general rule, and
takes advantage of all the exceptions.” Hume's sensible knave knows what virtue
requires but does not care, because he lacks the sentiment of benevolence that
normally counteracts self interest. The sensible knave cannot be argued into
morality but not because of any intellectual deficiency; he just does not feel
the pull of morality at all. Shaun Nichols (2004) has argued that psychopaths
are actual cases of sensible knavery, since they seem to fit Hume's
According to Nichols, psychopaths are sensible knaves—amoral
but fully rational agents.
They lack prosocial emotions (especially empathy),
and this lack leads them to disregard the claims of morality because they do not
respond normally to the sufferings of others. Nichols argues that because the
moral flaws of psychopaths are traceable to their emotional deficits, rather
than any shortcomings of reason, psychopaths refute what he calls “empirical
rationalism”. Empirical rationalism is the idea that ethics is based on, or is
just a province of, practical reason. Our moral judgments are explicable in
terms of the same rational standards that apply to ordinary thought and action.
Simply put, being moral is just indistinguishable from being rational. If
psychopaths refute this view, thinks Nichols, they count as evidence in favour
of a broadly Humean approach to morality
Nichols distinguishes empirical
rationalism from moral rationalism. Empirical rationalism claims that it is an
empirical fact that moral judgment in humans is a kind of rational judgment;
i.e. our moral judgments derive from our rational faculties or capacities.
Conceptual Rationalism states that it is a conceptual truth that people who make
moral judgments are motivated by them. That is, if you understand what morality
requires you will want to do it (because it is the rational thing to do).
Nichols concentrates on the empirical case—the extent to which moral psychology
is a form of practical reason.
Heidi Maibom (2005) has challenged Nichols'
treatment on several grounds. Most directly, Maibom points to literature showing
that psychopaths do in fact suffer from rational impairments. Psychopaths seem
to have trouble learning from experience, lack a grasp of means-end reasoning,
and lack an ability to plan for the longer term or formulate and pursue
longer-term goals. Maibom argues that because of these deficits psychopaths fail
to meet the rational constraints on practical reason, such as coherence and
consistency. Maibom also argues that to support a Humean position, it is not
enough to tie these blemishes in the reasoning of psychopaths to ultimate
abnormalities in their emotional lives. For a Humean, she argues, emotional
deficits should have a direct effect on morality via an absence of empathy, not
an indirect one via reasoning failures caused by a general lack of
It does seem to be correct that psychopaths suffer from various
rational deficits. But nobody is perfectly rational, and the case has to be made
that psychopaths are different enough from normal subjects. For Maibom to make
her case, the rational shortcomings of psychopaths need to make them a different
class of subject, since Nichols' argument depends on their being as rational as
the average subject. We remain unsure about the nature of the rational deficits
in psychopathy, but also about the significance of the various models of
psychopathic irrationality. Perhaps it is wrong to think of practical reason as
a unitary phenomenon or faculty. Psychopaths seem to be perfectly normal when it
comes to theory of mind and general intelligence, so maybe their reasoning
deficits are circumscribed in ways that leave them rationally in the same class
as normal subjects when it comes to the reasoning systems that matter for
morality. It may be in the end that psychopathy involves a combination of
emotional and rational shortcomings that reflect a failure of normal
neuropsychological development. If that were the case, then they would be less
suitable to adjudicate between Humean approaches and Kantian approaches that see
morality in terms of practical reason, rather than emotional
Controversy also exists over the extent to which psychopaths
really understand moral concepts, which they would have to do in order to count
as amoralists, rather than as people who do not understand morality. Although
psychopaths can employ moral language and use emotion terms, some theorists
(e.g. Hare 1993, ch 3) have argued that they seem incapable of attaching the
same sense as the rest of us to the moral concepts they use. This may suggest
that they do not really grasp moral concepts. However, it may still be that
their failure to grasp moral concepts is due to their emotional stuntedness
rather than some deficit in reasoning (Prinz 2007, 46–47).
Philosophers have also sought scientific support for their
theories by appealing to Multiple Personality Disorder, or Dissociative Identity
Disorder as it was called in DSM-IV. This has been a very controversial
diagnosis. Some philosophers have thought that it shows something very
interesting about the development of the self in normal subjects. Other theorist
have been more sceptical, both about the philosophical claims and about the very
reality of the condition itself.
The basic picture of MPD/DID is that a
sufferer has several distinct personality states, known as “alters”. At various
times, one of the alters is in charge of the subject's behaviour. Each alter has
a peculiar, enduring pattern of perceiving, thinking about and relating to the
environment and self, as well as different patterns of speech and physical
comportment. The “alters” emerge spontaneously and involuntarily to control
behaviour, and function more or less independently of each other. Not all alters
are known to the patient. This results in significant amnesia (not ordinary
forgetting) on the patient's part for those periods of time when an alter was in
Scepticism about MPD in the clinical community was fostered by the
circumstances under which it became prominent in the 1970s and 1980s. The
existence of dissociation is not controversial. DSM-IV (477) defines it as
“disruption in the usually integrated functions of consciousness, memory,
identity or perception of the environment. The disturbance may be sudden or
gradual, transient or chronic”. Dissociation does not have to be pathological:
it can occur in normal life when, for example, one becomes absorbed in a task to
the exclusion of other aspects of the environment. And the idea of an alter
personality assuming control of behaviour emerged in the nineteenth century. But
the sceptics point out that fewer than a dozen cases had been reported before
the early 1970s, when a sudden epidemic flowered up in North America, featuring
subjects who had several, sometimes dozens, of alters. Proponents of the
diagnosis pointed to greater awareness of child abuse as the key factor that
made widespread diagnosis possible, since it took great efforts to overcome
public reticence on that key causal factor.
By the mid-nineties, the epidemic
was waning, as more and more psychiatrists began to conclude that the symptoms
of MPD/DID were being produced in the clinic by hypnosis and suggestion, in
concert with portrayals of the condition in the media. Questions were also
raised in retrospect about the validity of the diagnosis in some of the key
cases that inspired the great take-off in the diagnosis (McNally, forthcoming ch
5). But there is no doubting the reality of the symptoms that are displayed by
people who receive the diagnosis. A tendency has been to ask whether multiple
personality is a real disorder or the product of social circumstances, a
culturally permissible way to express distress? We should reject the
presupposition that there is an important contrast between being a real disorder
and being a product of social circumstances. The fact that a certain suite of
mental symptoms appear together only in specific historical or geographical
contexts does not imply that it is not real (See Hacking 1998 on transient
mental disorders). Philosophical discussion of dissociation is not imperilled if
the sceptics about MPD carry the day. However, philosophical theories which are
tied strongly to the more controversial claims about the nature and etiology of
MPD do look less plausible.
Dennett and Humphreys draw on MPD/DID to support
a philosophical proposal about the nature of the self. They do seem to tie their
interpretation of MPD/DID to the specifics of the causal story, since they treat
the condition as evidence for a particular theory about the development of the
self in normal cases. Different alters, as they put it, express exaggerated
moods but retain memories of their periods of control that host personalities
lack. These memories become aggregated into a distinct self (or
self-representation). The causal story they favour (49–51) is borrowed from the
MPD community, and asserts that children endure abuse by dissociating and
leaving an alter behind to deal with the abuse. Then the alter splits into
pieces that express different emotional relations to what is going on (including
conflicting feelings towards the parent who is also the abuser).
alters different selves? Dennett and Humphreys distinguish two theories of the
The “Proper Self”: a ghostly supervisor who lives inside the head. The
seat of thought and consciousness.
The “Fictive Self”: a “center of narrative
gravity” of a biography, but with no real causal power. This is a representation
of what you are like that does not correspond to anything inside the
Dennett and Humphreys dislike the “proper Self” idea because they think
that it is untrue to the way the human mind is organized. They argue that the
mind is a collection of unintelligent subcomponents, with no overall executive
control center. Like a termite colony, a human being is made up of a set of
independent systems: different functional units responsible for (e.g.) vision,
language processing, theory of mind, working memory, emotional appraisal,
spatial cognition and so on. All these simple systems give rise to intelligent
behaviour. But unlike a termite colony, a human being has a figurehead: each of
us “first creates—unconsciously—one or more ideal fictive selves and then elects
the best supported of these into office as her head of mind” (1998, 41)
this view, normal development of the self is a matter of finding the
representation that makes the most sense. The representation that makes the most
sense does not have to be accurate. It reflects a desire for coherence (and a
role in social relations) rather than accuracy. In MPD, Dennett and Humphreys
argue that this process fragments into lots of competing systems, since there
are too many inconsistent pictures of the “real you”: so the alters persist as
different representations that make partial sense of different aspects of the
self. The normal integration of different representations into a coherent one is
prevented by the strains of development.
Owen Flanagan (1994) has developed a
version of this view that is slightly different. He argues that the self is a
narrative: an unfolding rationale for what in fact happens to you. Normally we
assume that there is one self per person, and that the self permits continuity
across change as we develop. But in the normal case, Flanagan thinks, the self
is multiplex—it permits some differentiation across situations. The notion of a
complete, well-integrated personality is a normative concept—a way we think
people ought to be—rather than anything that is usual in psychology. It is a
goal we work towards that can be achieved in different ways.
treat MPD as evidence for a particular theory of how the self comes into being
via developmental work at integrating different aspects of the person. Ian
Hacking (1995a, chs 16–18), on the other hand, is sceptical of any claims that
MPD/DID is evidence for positions in the philosophy of mind. It may illustrate
positions—if you believe Dennett and Humphreys' theory of the self then you can
see how their view makes sense of the phenomenon of MPD/DID. But the
philosophical theory has to be confirmed elsewhere. This is partly because the
understanding of the syndrome the theory rests on is so recent: Hacking argues
that people “have been diagnosed with double consciousness or multiple
personality for two centuries `now. But they began to talk the way they do
now—using the symptom language described by Dennett—only very recently. Today
they all say such things, or at least suspect that they ought to say them. That
is how they learn to describe themselves in therapy” (226). Dissociation may be
a genuine psychological condition, but the details of dissociative identity
disturbances are too contentious to bear much philosophical weight. Hacking
doubts that there is any stable condition to have knowledge about, because the
very act of being classified alters human behaviour via what he calls the
“looping effect” (1995b, 2007. For discussion, see Cooper 2004, Murphy 2001,
2006 (ch 7), Tsou 2007). The looping effect comes about when individuals change
their behaviour in response to classification. Such a feedback loop could, in
principle, keep behaviour stable, but Hacking is interested in those cases in
which the behaviour is rendered unstable. He has also (1998) examined the case
of transient mental illnesses, which appear to flare up and then go out of
Of all psychiatric concepts, it is probably
delusions that have received the most extensive recent treatment from
Here the issues straddle philosophy of mind and philosophy of
science. Some theorists have raised conceptual difficulties for accounts of
delusions, others have sought to frame scientific hypotheses that can explain
delusions in terms of information-processing deficits or other subpersonal
problems. And some philosophers have looked for a distinctively philosophical
explanation of delusions, which draws on concepts previously formulated in the
philosophy of mind.
Like many other psychological concepts, the concept of
delusion has a fairly explicit and self-conscious scientific use and a variety
of commonsense uses. There is considerable overlap between some psychiatric uses
and some casual employments of “delusion”. But there are clearly everyday
occasions when “delusion” merely refers to a belief that seems obviously false
or unwarranted to the speaker. I might call you delusional when you announce
that you expect to buy a four bedroom house in your neighbourhood for what you
can afford to pay, without meaning that your reasoning is symptomatic of a
psychotic illness; it is just wishful thinking. But delusions in a technical
sense are manifestations of psychosis. DSM-IV-TR (819) defines a delusion as ‘A
false belief based on incorrect inference about external reality that is firmly
sustained despite what almost everyone else believes and despite what
constitutes incontrovertible and obvious proof or evidence to the contrary ….’.
Furthermore, the delusion must be inexplicable in cultural terms, so that
religious beliefs are not counted as delusional, no matter how bizarre. The fact
that the patient belongs to a culture or community in which the relevant belief
is treated as a religious claim means that it does not count as a delusion. This
proviso has seemed odd to many people. It may just testify to the disinclination
of psychiatrists to take sides in religious disputes, but perhaps the best way
to view it is as an acknowledgment of the importance of testimony or social
context in the normal acquisition of our beliefs. We expect people to acquire
religious, or otherwise culturally specific, beliefs that might strike outsiders
to the culture as odd. But the weirdness of the belief does not impugn the
normality of the process of culturally specific belief transmission, so the
products of such cultural transmission should not be treated as pathological, no
matter how strange we may think they are.
Other aspects of the definition of
delusion have also come under attack. Gipps and Fulford 2004 ably summarize some
standard objections. These include the idea that a delusion has to be false.
Jaspers (1997, 106), for instance, argues that someone who is pathologically
jealous and suffers from delusional beliefs about their partner's infidelity
(“the Othello Syndrome”) might in fact be correct. The partner could actually be
unfaithful. In this case the truthfulness of the belief is beside the point,
since we can recognise pathological jealousy without regard to truth. Ryan
(2009, 24) notes that someone with Ekbom's syndrome (the belief that one is
infested with bugs) might coincidentally suffer scabies. Fulford (1989, 204–5)
also mentions a patient whose only symptom of psychopathology was the delusion
that he was mentally ill—if he really was mentally ill, then that couldn't have
been a delusion. On the other hand, as Graham and Stephens (2007, 194) note,
many theorists have doubted that delusions are really beliefs at all. Delusions
often lack properties that beliefs have been thought to possess. In particular,
delusions often seem poorly integrated with the rest of the subject's beliefs,
and they can lack the affect associated with firmly-held beliefs. These
objections are rebutted by Bortolotti (2009). The boundaries between delusion
and other states, like self-deception, have also been discussed (Bayne and
Fernandez 2009. For general philosophical accounts of delusion see Bortolotti
2009, Radden 2010.)
Analyses of delusion can look like inversions of the
attempts made by analytic epistemologists to define knowledge. We may agree that
a delusion is a false belief, just as knowledge is true belief, but, as with
knowledge, we do not rest there. Knowledge is true belief plus something that
ties the true belief to the world in the right way. So too, we try to find that
extra property of the false belief that converts it from a false belief into a
delusion. This conceptual program is seen as the prelude to the development of
empirical theories of delusion, in which philosophers work alongside cognitive
scientists (Davies and Coltheart 2000).
These theories have tended to assume
that when ‘delusion’ is used in the technical sense it denotes a psychological
natural kind (Samuels 2009) whose basic psychological structure can be worked
out via attention to paradigmatic cases. Call this the explanatory project. We
can distinguish two versions; one involves explaining delusions as caused by
failures of normal relations among components of our cognitive architecture, or
at least those parts of it that have to do with the fixation of belief. Another
way of proceeding is more philosophical. It is less bothered with causal
theories of cognitive architecture and more concerned to find resources in the
philosophy of mind that characterise delusions in an illuminating
Neuropsychological theories of the origin of monothematic delusions
(Those characterised by one dominant delusional belief about one specific
matter) have come to fall into two camps: one factor and two factor theories.
According to one familiar version of the two-factor theory (Davies and Coltheart
2000), an unusual experience is the first factor in the aetiology of a delusion,
but there must also be a second factor. The first factor can be seen as an
impairment that effects the reception of information about the world. The
delusion belief explains that input—your spouse seems odd, so you conclude that
he has been replaced by a robot. That explains the oddness, but in order for you
to form that belief there has to be a second impairment, in some system that
forms or evaluates beliefs. This will typically be some neurocognitive deficit
that interacts with the experience. The impairment in your reasoning system
prevents you from rejecting the explanatory belief, despite its lack of warrant.
The disagreement with one factor theories (Davies et al. 2005) turns on whether
the first deficit suffices to cause the delusion.
The more purely
philosophical approach to explaining delusions concentrates on the role the
delusion plays in the subject's mental life, as understood in terms of some
theories in philosophy of mind. Arguably, these attempts at philosophical
understanding of delusions originate with Jaspers' (1997) concept of a primary
delusion, which is a subjectively meaningful transformation in the patient's
experience of the world. Recent work in this tradition includes the delusional
stance idea of Graham and Stephens (2007). In a similar vein to their
explanation of thought disorder in terms of identifying with one's own thoughts
or being alienated from them, they suggest (194) that delusions are constituted
by a higher-order stance towards lower- order intentional states. This stance
involves an identification with the lower order states, which become seen as an
expression of one's own agency or mental nature. As in Jaspers' treatment, it is
the role of the delusion in the subjective mental life of the deluded person
that is critical.
These two approaches represent two ways of doing
philosophical psychopathology, as a foundational contribution to a scientific
inquiry or as a piece of philosophy of mind. They are not incompatible; the
philosophical projects may help us to better describe the phenomena
psychiatrists care about and make the explanatory project easier. On the other
hand a two-factor explanation, or some other neuropsychological account, does
not have to falsify a philosophical description of delusions. It may be that
philosophical accounts make unwarranted empirical assumptions, but they may
simply illuminate the condition as it is experienced by those who suffer from
it, or guide us towards a philosophical account of the mind that is informed by
real cases rather than armchair ones. The last decade has seen a great increase
in work on the epistemology and philosophical significance of psychiatry, which
is becoming a recognisable philosophical field. The full implications of this
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