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Beyond categorical diagnostics in psychiatry: Scientic and medicolegal implications

Henrik Anckarster
Forensic Psychiatry, University of Gothenburg, Lillhagsparken 3, 422 50 Hisings Backa, Sweden
a b s t r a c t a r t i c l e i n f o
Mental disorder
Conforming to a medical disease model rooted in phenomenology and natural science, psychiatry classies
mental disorders according to signs and symptoms considered to be stable and homogeneous across individuals.
Scientic studies addressing the validity of this classication are scarce. Following a seminal paper by Robins and
Guze in 1970, validity of categories has been sought in specic criteria referring to symptoms and prognosis,
aggregation in families, and markers, preferentially laboratory tests. There is, however, a growing mist
between the model and empirical ndings fromstudies putting it to the test. Diagnostic categories have not been
shown to represent natural groups delineated from the normal variation or from each other. Aetiological factors
(genetic and/or environmental), laboratory aberrations, and treatment effects do not respect categorical
boundaries. A more adequate description of mental problems may be achieved by: 1) a clear denition of the
epistemological frame in which psychiatry operates, 2) a basic rating of the severity of intra- and interpersonal
dysfunctions, and 3) empirical comparisons to complementary rather than exclusive dimensions of inter-
individual differences in context-specic mental functions, treatment effects, and laboratory ndings. Such a
pluralistic understanding of mental health problems would t empirical models in the neurosciences and
postmodern notions of subjectivity alike. It would also clarify the assessment of dysfunction and background
factors in relation to the requisites for penal law exemptions or insurance policies and make them empirically
testablerather thandependent onexpert opiniononissues suchas whether a specic dysfunctionis psychiatric,
medical, or ascribable to personality.
2009 Elsevier Ltd. All rights reserved.
1. Introduction
As a branch of modern medicine, psychiatry has applied models of
disease (usually referred to as disorders) and pathogenesis to
problems of the mind. Categorical diagnoses of disorders are based on
structured evaluations of operational criteria thought to reect
various aspects of mental problems, such as painful inner experi-
ences, reduced cognitive abilities, or maladaptive patterns of beha-
viours (American Psychiatric Association, 2000). The diagnostic
categories are constructed as syndromes with criteria referring to
various situations and time frames and ordered in hierarchies to avoid
overlaps. Diagnoses are assigned by counting and comparing signs and
symptoms to notions of diagnostic cut offs or thresholds and are
understood to entail specic properties, such as aetiology, treatability,
and prognosis. This system has drawn on phenomenological work,
particularly that of Jaspers, its foremost theorist, who provided a
philosophical rationale for focusing on abstract entities considered to
be essential across individuals rather than on other aspects, such as
subjective experiences, personhood, social relatedness, or culture, that
were emphasized by other 20th century strands of thinking.
Categories have also supplied culturally well-dened roles for
mental health experts, their patients, and any others confronted with
persons who have mental health problems. This, essentially medical,
grand theory of disease in psychiatry has brought progress indeed.
Functional inter-rater diagnostic reliability for mental disorders has
been greatly improved, and treatment strategies developed over the
last 60 or so years, pharmacologic and psychotherapeutic alike, have
reduced suffering and improved the quality of life for countless
persons. Epidemiological and longitudinal knowledge about mental
health problems is now easily accessible, not least on the internet.
Criticism of diagnostic practices has become rare within psychiatry,
while external critique tends to be discarded as unscientic or even
But are we really condent that this medical model does not itself
contain fundamental scientic weaknesses, even errors? Widely
recognized problems are that large proportions of psychiatric patients
meet more than one diagnostic denition, that many have incomplete
remission of symptoms and remain severely disadvantaged, and that
longitudinal and cross-cultural inconsistencies are common. In this
paper, the validity of the current diagnostic categories that have come
to structure both psychiatric practice and science will be assessed
against the specic criteria developed since rst proposed by Robins
and Guze (1970). The effects of accepting the medical model as the
grand narrative of mental health problems will be exemplied, and
new strategies for the denition of such problems will be proposed.
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International Journal of Law and Psychiatry
2. Methods
In psychiatry, validity has mostly been an issue when determining
how validly a diagnostic instrument may identify a diagnostic
category. Comparatively less attentionhas beenfocusedonthe validity
of the diagnostic constructs. A few leading psychiatrists have
developed criteria for the validity of disorders (Andreasen, 1995;
Kendell & Jablensky, 2003; Kendler, 1980; Robins & Guze, 1970).
Robins and Guze argued that psychiatric diagnoses should be based on
systematic studies instead of a priori principles and dened ve
areas in which such studies should be carried out: 1) systematic
clinical descriptions, 2) laboratory studies, 3) delineation from other
disorders, 4) follow-up studies, and 5) family studies. Kendler (1980)
added that diagnostic validity should require follow-up studies
showing diagnostic consistency over time, similar rates of relapse
and recovery, and homogeneous response to treatment, while family
studies should show aggregation of similar symptom constellations
among relatives. Andreasen (1995) declared that psychiatry had
reached the stage where it was now founded on diagnoses that are
validated by clinical description and epidemiological criteria and
called for a second structural programfor the validationof psychiatric
diagnosis based on methods that are being applied to track mental
illnesses back to the organ systemfromwhichthey emanate, the brain,
and to the aberrations occurring at a molecular level in DNA. Kendell
and Jablensky (2003) attempted to emphasize the scientic basis for
diagnostic classications by separating validity from utility. They
suggested that diagnostic categories should be regarded as valid only
if shown to be discrete entities with natural boundaries that separate
themfromother disorders or fromnormality by a zone of rarity, or if
dening characteristics, such as chromosome or biochemical abnor-
malities, delineate the diagnosis from other conditions with similar
symptoms, and concluded that most diagnostic concepts have not
been shown to be valid in this sense.
To assess whether the diagnostic categories used today meet these
extended Robins and Guze criteria, a systematic MEDLINE search
made in 2008 used the following search terms: dimension, broader
phenotype, overlap AND schizophrenia, psychosis, bipolar, depres-
sion, mania, autism, Asperger, AD/HD, attention disorder, OCD,
substance abuse, personality disorder, personality, antisocial, crimi-
nal, and psychopathy. Neurobiological markers and treatment effects
were studied through recent meta-analyses and review papers. A
second literature search was performed for longitudinal development
(with the search terms age, onset, prodrome, AND disorders as
above), and a third for familial aggregation (using relative, family,
adoption, twin, AND disorders as above, selecting only studies aimed
at assessing specicity/overlap).
3. Results
3.1. Clinical validity (Robins and Guze criteria 1 and 3)
Considering what we nowknowabout the epidemiology of mental
health problems, it is obvious that what Andreasen expected in 1995
has not come about. First, no mental disorder (besides mental
symptoms induced by medical diseases, such as Huntington's chorea)
has yet been statistically distinguished fromthe normal variation by a
zone of rarity or shown to constitute a taxon among other
problem types in the population variance (Cloninger, 1999). Instead,
the notions of broader phenotypes or sub-threshold disorders
(initially described in relatives of probands in genetic research) and
spectra of overlapping or comorbid disorders, have gained wider
acceptance. A literature search for overlaps between mental
disorders yielded over 1600 publications during the rst four years
of the new millennium (Clark, 2005). Studies on the nature of this
phenomenon have found that there is more to these overlaps
between disorders than just that several disorders happen to occur in
a given individual. Continua have, for example, been demonstrated by
item response analyses between alcohol abuse and dependence
(Gelhorn et al., 2008; Saha, Chou, &Grant, 2006), and between various
forms of anxiety and depression (Watson, 2005).
3.2. Laboratory markers (Robins and Guze criterion 2)
Findings from the laboratory have provided no further support for
the categorical system. Andreasen (1995) noted that the markers
required by Robins and Guze had not emerged and that they had
rather risen and fallen (e.g. the dexamethasone suppression test for
depression), but her condence in the development of new methods,
such as brain imaging and molecular genetics, remained unbroken.
Findings from studies using these increasingly sophisticated techni-
ques, however, have been at least as difcult to replicate and/or as
unspecic in relation to diagnostic categories as those produced by
the older models. Molecular genetic linkage or associations to mental
disorders have been of minute effect size, inconsistently replicated,
and often involved in more than one diagnostic category (Kendler,
2005). Instead, polygenetic causation in the forms of rare mutations
or more common variants, sometimes in vast numbers and with
endless possibilities for allelic and/or epistatic interactions, and
various types of phylogenetic epigenetic shifts, have been proposed
to formthe basis for different disorders, such as schizophrenia, bipolar
disorder, and autism (Francks et al., in press; Moskvina et al., 2008;
Rzhetsky, Wajngurt, Park, & Zheng, 2007).
This lack of specicity seems difcult to reconcile with the disease
model unless we imagine that the mind has but a few nal common
pathways through which it reacts to unspecic adversity in genes,
neurobiology, and interactions with the environment, forming a limited
number of higher-order types of mental dysfunctions. Brain imaging
studies, however, have demonstrated similar reductions and other
deviations in regional circulation, metabolism, or transmitter-specic
molecular expression across diagnostic categories (e.g. Pinkham,
Hopnger, Pelphrey, Piven, & Penn, 2008). Cognitive tests thought to
reect various aspects of executive or socio-communicative dysfunc-
tions have not been more disorder-specic.
3.3. Longitudinal follow-up (Robins and Guze criterion 4)
Research on longitudinal diagnostic stability is impeded by the
artefactual hiatuses caused by the division in child- and adolescent
psychiatry vs. adult psychiatry at about age 18, or in adult general
psychiatry vs. neuropsychiatry or personality psychology. Child
psychiatric conditions are often interpreted in terms of cognitive
disabilities rather thandiseases, even whenmedicationis the standard
treatment. With increasing age, denitions subsequently become
more inuenced by adult designations of symptoms, introducing
concepts such as paediatric mania or prodrome schizophrenia. To
what extent these clinical conditions really correspond to similar
conditions in adulthood has not been established, but differences in
symptom presentation and treatment response have been noted (e.g.
SSRI treatment of depression in adolescents, Weller, Tucker, & Weller,
2005), and heterotypical progressions of problems from childhood
into adulthood seem to be the rule rather than the exception
(Hofvander, Ossowski, Lundstrm, & Anckarster, 2009).
This separation of child and adult psychiatry has probably
obscured developmental clues of value for meaningful denitions of
life-long susceptibilities and led to over-emphasis on symptom
progression during adulthood. The Kraepelinian distinction between
deteriorating or intermittent course in psychoses is challenged by
descriptions of affective episodes in the schizophrenic conditions and
of cognitive problems between episodes in manic depression
(Craddock & Owen, 2005; Hafner, 2007), and could possibly be
resolved by empirical analyses of independent assessments of child-
hood antecedents and neurocognitive functioning, providing more
60 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965
meaningful clinical descriptions of the background to the dysfunc-
tional reality assessment. A waxing and waning course is also a
common feature of mental problems (e.g. Biederman, Mick, Faraone,
& Burback, 2001). Situational factors, rather than the biological or
cognitive diathesis for the condition, may inuence the actual
symptom expression and lead to oscillations around the cut-off for a
categorical diagnosis, with subjects moving in and out of the category
by small changes in severity or general functioning.
Nor do longitudinal treatment effects seem to respect diagnostic
categories. Pharmacological remedies alleviate symptoms across
diagnostic divisions, no matter if their target is specic or wide.
Lithiumstabilizes mood in a subgroup of patients diagnosed as bipolar
but not in all (thus the category of lithium responders). Regardless
of diagnostics, neuroleptics tranquilize and serotonin reuptake
inhibitors reduce depressed mood and anxiety (Kramer, 1997).
Boundaries created by exclusion criteria may also form an obstacle
to meaningful treatment. One example of this is mental retardation,
which excludes the diagnosis of attention decit/hyperactivity
disorder (AD/HD), thus precluding adequate treatment of inattention
among subjects with a concomitant learning disability (Gillberg &
Soderstrom, 2003).
3.4. Familial aggregation (Robins and Guze criterion 5)
Familial aggregations of disorders have been studied by epidemio-
logical methods to assess the overall importance of heritable factors
for the variance in psychiatric phenomena. Family and adoption
studies, not least twin studies, have provided ample support for the
notion that hereditary factors play important causative roles in the
variation of all mental health problems and associated features
(Rutter & Silberg, 2002). This strand of research has used categorical
as well as dimensional denitions (Levy, Hay, McStephen, Wood, &
Waldman, 1997). More recent twin studies also collect data on co-
existing and interacting problem constellations (Lichtenstein et al.,
2009) and follow developmental trajectories from adolescence
(Silberg, Rutter, Neale, & Eaves, 2001) into the adulthood disorders
(Cardno, Rijsdijk, Sham, Murray, & McGufn, 2002; Kendler, Gardner,
Annas, & Lichtenstein, 2008; Kendler, Gardner, & Prescott, 2003).
Separate aetiologies have been reported for features previously linked
into syndromes (Ronald, Happe, Price, Baron-Cohen, & Plomin, 2006),
and conceptually different facets of clinical problem constellations
have been found to have aetiological factors in common (Larsson,
Andershed, & Lichtenstein, 2006).
3.5. The example of autism
Let us now use autism as an example of how the meaning of a
nosological term may change within the medical reference system.
Initially described by Bleuler as one of the core schizophrenia
symptoms, childhood autism used to be synonymous with childhood
psychosis but came to evolve into a denition thought to reect
specic neurocognitive developmental disabilities. No more than a
couple of decades ago, autism was known as an extremely rare
condition characterized by severe restrictions in social interaction,
communication, and exibility (Wing, 1981). Today, it is instead
generally regarded as the core of a broad clinical spectrum (the
autism spectrum disorders), encompassing more than one percent
of all humans (Gillberg, Cederlund, Lamberg, & Zeijlon, 2006), that
extends into the normal population over a broader phenotype
(Constantino & Todd, 2003) (also referred to as a shadowsyndrome,
Ratey &Johnson, 1997) rst reported among non-affected siblings and
relatives in twin or family studies who displayed some autism-like
features but did not reach the threshold for a formal autism diagnosis
(Folstein & Rutter, 1977).
The autismspectrumdisorders have been reported to overlap with
other problem denitions, such as tics (Baron-Cohen, Mortimore,
Moriarty, Izaguirre, & Robertson, 1999), mood disorders, and social
phobia (Bolton, Pickles, Murphy, & Rutter, 1998; Piven & Palmer,
1999), anorexia nervosa (Nilsson, Gillberg, Gillberg, & Rastam, 1999),
attention decit/hyperactivity disorder (Constantino et al., 2006;
Gadow, DeVincent, & Pomeroy, 2006), psychotic disorders (Stahlberg,
Soderstrom, Rastam, & Gillberg, 2004), and personality problems,
including disorders in all major clusters and categories (Anckarster
et al., 2006). No delineation (zone of rarity) has ever been demon-
strated between autism, the spectrum, and the normal variation,
between the various diagnostic categories proposed within the
spectrum (such as Asperger's disorder or high-functioning autism),
or between the spectrum and any disorders that overlap with it
(Anckarster et al., 2008). The autism spectrum is often said to
represent one extreme of normally distributed abilities in social
interaction and communication (Constantino & Todd, 2003), with the
broader phenotype in the lowermost end of the normal variation
(Ronald et al., 2006).
Despite criteria worded to reect distinct behaviour problems, the
convergence between parent-, teacher-, and self-ratings is surpris-
ingly low (Ronald, Happe, & Plomin, 2008). Yet, the follow-up
consistency is high for classical autism, but lower for high-functioning
variants such as Asperger's disorder (Cederlund, Hagberg, Billstedt,
Gillberg, & Gillberg, 2008). There is evidence for overrepresentations
of brain damage or dysfunction, such as epilepsy, not only among the
most impaired subjects but also among cases with normal general
intelligence (Gillberg, 1995). Autistic-like functional impairments
have been shown in connection with a panoply of brain pathologies
(genetic syndromes such as fragile X or tuberous sclerosis, rare
mutations, foetal injuries, and early infections, but also herpes
simplex encephalitis and other limbic damages later in life, Durand
et al., 2007; Gillberg & Coleman, 2000; Jamain et al., 2003). There is
consistent evidence that the autism spectrum phenotype is one of the
most heritable in psychiatry, with around 80% of the variance
ascribable to genetic factors (Lichtenstein, Carlstrm, Rstam, Gill-
berg, & Anckarster, submitted for publication; Ronald et al., 2006),
but the specicity of these genetic effects has not been demonstrated.
Instead, important overlaps between genetic effects for autism
spectrum disorders and AD/HD have recently been reported (Ronald,
Simonoff, Kuntsi, Asherson, & Plomin, 2008). Nor has it been possible
to associate the population variance in autism or its broader
phenotype with any specic molecular genetic variants or chromo-
somal regions in a way that would indicate a larger than marginal
effect size, in addition to overlaps with other phenotypical denitions
(Melke, 2008). While it seems obvious that interactive genetic
networks or epigenetic modications must play a major role, the
specic mechanisms involved remain to be identied. To stress the
aetiological heterogeneity, the condition has been referred to as
autisms in the plural. Complicating the conceptualization of autism
even further, specic advantages have been emphasized as parts of
the syndrome, such as excellence in engineering and science or
absolute pitch (Baron-Cohen, 2000; Baron-Cohen et al., 1998). The
range of functional effects of diagnostics, frombeing labelled autistic
in socially disadvantaged or powerless situations, to being nerdy in
the sense of intelligent, creative, and special, is so wide that one
wonders whether any one diagnostic concept could match these
different uses.
Having read this far, any psychiatrist will probably have recog-
nized analogies in his or her own special eld of interest among the
major mental disorders, be it schizophrenia, bipolar disorder,
hyperactivity, impulsive/compulsive disorders, alcoholism, or any
other of the symptom-dened mental disorders.
4. Discussion
Despite the obvious lack of empirical support for today's diagnostic
models, it is not without a sense of heresy one has to conclude that
61 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965
most, if not all, of the mental disorders known today, i.e. the categories
that have structured both the psychiatric praxis and the research into
their prevalences, patterns of distributions, comorbidities, and
aetiologies, simply do not exist as such. The artefactual boundaries
between syndromal categoriesand between disorders and nor-
malitymay indeed be the main reason behind the relative failure of
psychiatry to identify molecular genetic susceptibility factors, patho-
physiological mechanisms, biological markers and paradigmatically
new treatment strategies for suffering and decits related to mental
Every reasonable description of mental health problems has to
start with a clear delineation of the knowledge that can actually be
derived fromthe psychiatric scientic endeavour. As a natural science,
psychiatry identies law-bound, caused, and to some extent predict-
able, patterns of mental phenomena that should be generalizable to
other persons or groups than those under study. Therefore, psychiatry
cannot capture aspects of the human that express randomness, free
will, transcendence, or meaning. In spite of the modernist term
psych-iatry, a derivative of the Greek word for soul, psyche, the
aspects of the human actually dealt with in psychiatry are mental
functions (a derivative from the Latin word mens, which does not
carry the spiritual connotations of the word soul) and do not refer to
aspects described by, for instance, a word like soulful.
The medical
grand narrative generated the idea that doctors could understand and
heal even the sufferings of the human soul, in line with the
Enlightenment trend to spread the light of modern science into
areas where superstition used to reign. By posing as doctors of the
soul (psych-iatrists), doctors have extrapolated research on mental
functions, such as mood stability, reality testing, and aggression, into
expertise on disaster, the rationality of political opinions, and
criminality in general. People are still expecting psychiatry to heal
their grief after losses and traumas, explain evil or provide clues to the
meaning of life. The ensuing disappointment could have been
prevented by a clear notion of the epistemological preconditions of
natural sciences and what they can inform us on among the various
facets of the human. A rigorous demarcation of the eld of explanation
based on considerations of the methodology applied is as crucial for
science as correct interpretations of ndings within the epistemolog-
ical frame thus delineated.
Butonce its premises are accepted, what can be achieved through
empirical positivistic psychiatry is good enough. The next step
towards describing mental problems in a way that is useful for both
research and clinical treatment is an overall assessment of the basic
mental functioning in terms of intra- and interpersonal stability,
behavioural control, and relatedness over time. Subjective distress or
reduced functioning would then indicate mental health problems that
can be quantied accordingly. In today's systems, quantication is
most often based on the number of problem types (criteria)
encountered, although this is a measure of severity that has seldom
been validated against actual health impact, and it is obvious that a
single mental symptom may carry a greater functional impairment
than several symptoms that are less severe or more easily compen-
sated for.
The medical model has served to provide a cut-off point to
distinguish the ill from the healthy in, for example, courts of law,
military psychiatry, and general health insurance policies. Such
partitions have generally been made by experts who have not had to
provideanyscientic data tosupport their notions of whois accountable
or t and of who is not. Generally, vague references to clinical
experiences and professional consensus have supplanted facts based
onepidemiological studies or tests of causative relations to, for example,
crimes (Anckarster et al., 2009) or reduced capacity for work. No
matter how useful this practice has been for a number of societal
institutions, it will, if based on false assumptions, invariably have led to
arbitrariness and inequality in the application of the law. Especially, the
requirement that the mental dysfunction should be of a medical or
psychiatric kind, which is often included for example in denitions of
reduced accountability in the penal law, has to be acknowledged as
unfounded in science. The current attempts to separate mental
impairments caused by illness from those speculated to be caused
by trauma, personality, or simply a lack of constructive will in, for
example, insurance medicine, have lost ground as pharmacological and
psychotherapeutic responses and genetic susceptibilities have been
reported in personality disorders and traits just as in the DSM post-
traumatic stress disorder and other Axis I disorders (e.g. Sadock,
Sadock, Ruiz, & Kaplan, 2009). Traits previously thought of as indicating
a lack of upbringing are now conceptualized as medical disorders with
clear evidence both for a partly genetic aetiology and manipulability by
treatment measures, whichultimately means that inthe individual case,
it will beimpossible totell whether a specic behaviour is due to the one
or the other. If this means that society to a lesser extent will be
dependent on (or able to use) medical doctors as expert advisors in
cases of jurisdiction, it may be seen as negative by some of the parties
involved but would also offer a range of positive effects. Doctors might
go on working according to their age-old ethics, while politicians,
lawyers and societal decision-makers could speak clearly of the
conditions that should be required for exemptions in the penal law or
for insurance benets without being intimidated by professional jargon
or obscurities.
Once an overall measure of functional outcome is established, a
theoretically endless number of complementary, systematic, and
replicable inter-personal differences in mental reactions, expressions,
and functions may be assessed and statistically evaluated in relation to
overall functioning. In order to increase clarity, these should be
empirical, distinct, and narrow. Whereas the current classication has
demanded pervasive symptoms across situations, assessments of
interpersonal differences in relation to specic situations, demands,
and challenges, including response to psychoactive substances, hold
greater promise as endophenotypes. Context-specic dimensional
assessments could then replace the diagnostic labels presumed to be
valid across situations, demands, and life-spans, and their possible
inter-relations and interactions creating the impact on functioning
could be a matter for empirical study. In view of the recent ndings of
common genetic and environmental effects across wide categories, it
seems to be a reasonable hypothesis that some molecular and
biological factors will be directly associated with overarching dimen-
sions of functioning, while others will be more strongly associated
with specic inter-individual differences or with a compensatory
force, which may mediate the risk inherent from another factor.
This proposal carries the implication that artefactual dichotomies,
such as child vs. adult psychiatry, personality disorders vs. major
mental disorders, disordered vs. normal, or neuropsychiatry vs.
other forms of psychiatry, would no longer structure psychiatric
research and practice.
To concretize these proposed principles, let us rst go back to the
autism example. Instead of trying to rene the current classication
we might begin to let our clinical evaluations focus on the restriction
of functioning, thereby avoiding the difcult discussion whether some
almost normal persons with odd social interaction and perhaps
nerdy interests are autistic or not. Persons who function well and
feel comfortable with who they are may then discuss whether they
recognize this or that peculiarity without the implication that they
have a mental disorder. Another advantage would be in relation to
persons who met diagnostic criteria at some time during childhood
and adolescence but no longer do so at a later date or even display
Let us try the following analogy to describe what can be known by psychiatry. Just
as other mental functions, a sexual attraction towards a fellow human being may to
some extent be studied and predicted by quantitative methods. In contrast, love, even
if it integrates the sexual attraction, is thought of as a voluntary generosity from one
human being to another, and therefore cannot be predicted or generalized based on
earlier studies of similar phenomena.
62 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965
signs consistent with another diagnosis, such as AD/HD or social
phobia. In these cases, the proposed focus on functioning would spare
the clinician and everyone else the complicated explanations of why
one diagnosis has disappeared and been replaced by another.
Instead of labelling patients, focus in clinical work will be on
functioning and well-being, with a door open to possible amelioration
or cure by treatment, education, and acceptance ofor even
adaptation tothe life situation. The researcher, on the other hand,
may rst include as predictors of dysfunction the domains that
today constitute the diagnostic criteria for autism, neuropsychological
test assessments, neurobiological measures, environmental factors
and genes in complex models that may be tested empirically rather
than based on expert opinions.
Another example of special relevance for penal law is that of
childhood hyperactivity, impulsivity, inattention, conduct problems,
adulthood criminality, aggressive antisociality, and interpersonal
destructive attitudes. Today, we use about ten diagnostic categories
to capture various facets of these problem behaviours and combine
them into syndromes, such as psychopathy or antisocial person-
ality disorder. Torrents of ink and computer bites have been used on
issues such as the degrees of overlap between the two domains of AD/
HD, oppositional deant disorder, and conduct disorder, and on how
many aspects to consider for a diagnosis of psychopathy. An
alternative approach may proceed as outlined below.
1. Conceptual analyses demonstrate what psychiatry can inform us
about in the eld of norm-breaking behaviours. For example, moral
evaluations (notions of evil or retributional justice) require the
assumption of a free will, which, since it is incompatible with the
determinist basic assumption of psychiatry (that mental and
behavioural manifestations are caused), should be omitted from
psychiatric diagnostics, while it is stressed that psychiatry can
neither prove nor disprove, or increase our understanding of, these
aspects (in spite of frequent claims to the contrary from leading
forensic psychiatric or psychological experts in the popular media).
2. The overall intra- and interpersonal functioning should then be
assessed by real-life achievements in a longitudinal perspective
according to the GAF-like scale just proposed. The absence of
aggressive antisocial behaviours and attitudes and the ability to
conform to ethic and societal norms are key characteristics of
mental functioning.
3. Instead of the denitions used today, which are focused on
behavioural shortcomings across heterogenous situations, inter-
personal differences in problem behaviours should then be assessed
in specic social situations or in relation to demands (such as
learning, peer interactions, adult family interaction, societal norm
compliance and anger), in cognitive abilities (such as attention,
impulse control, cognitive theory of mind), and in behavioural or
cognitive response to drugs such as methylphenidate or lithium.
The degree of convergence between these dimensions, various
types of susceptibility factors (e.g. genes, brain imaging results or
stress reactions in relation to emotions) and the overall functioning
will then be an empirical issue.
A vast number of psychiatric research projects already contain
data that might be re-analyzedstatistically as well as theoretically
in accordance with a multi-dimensional rather than the categorical
model. An example of the prospect of reconsidering previously
assembled data is a recent report that established previous criminal
behaviour as the aspect most predictive of criminal recidivismacross a
range of earlier studies on psychopathy (Walters, Knight, Grann, &
Dahle, 2008).
A similar model is easily envisaged for psychoses. Epistemological
analyses have long addressed the question of what to regard as
psychotic representations of reality and rejected the early modernist
notions that political opinions or nonconformist behaviours couldcount
as psychotic. We can therefore proceed to the next stepmeasuring
functioning, suchas abilitytointeract withothers, tocontrol behaviours,
to maintain a stable identity and personal hygiene and nances, and to
judge the reality of perceptions. Finally, inter-personal differences in
delineated signs and symptoms, such as hearing voices, bizarre
representations of reality (delusions), motor inhibition, incoherence of
thoughts, and ideas of worthlessness, should be assessed together with
psychometric dysfunctions, such as poor theory of mind, verbal
incoherence and hostility. Then, if the wish to establish disease-like
categories canbe resisted, the convergence of overall dysfunction, inter-
personal differences, psychometric ndings, neurobiological differ-
ences, pharmacological responses, and prognostics can be calculated
in a given population, thereby clarifying, for example, the important
commonalities betweenthe types of psychoses demonstratedingenetic
causes (e.g. Lichtenstein et al., 2009; Moskvina et al., 2008), neuro-
physiological test results (Thaker, 2008), and neurocognition (Smith,
Barch, & Csernansky, 2009). The rationale for considering similar
complex models for depression and anxiety, or for the various degrees
and types of alcohol-related dysfunctions, has been presented earlier in
this paper together with key references to, for example, Watson (2005)
and Saha et al. (2006).
This proposed reconsideration of psychiatry would now, in the new
millennium, free the discipline from the imperative to make reality
conform to a notion of diseases and diagnostics developed for bacterial
and neoplastic diseases during the 19th century. The multi-layered
assessments suggested here would allow more rigorous empirical
research on mental problems than any other approach so far and
demand a more specic delineation of what is understood as mental,
physical, or contextual. This shift in theory and practice frommodernist
psychiatry would also align itself with the pluralistic notions of
subjectivity inthepostmodernera,
andopenupfor problemdenitions
that would empower rather than stigmatize those seeking psychiatry's
help. The mysticism of diagnostic categories and their markers has
acted as a power structure both in clinical psychiatry and in the societal
coercion exercised with the aid of psychiatry. This kind of service to
society has so far resulted in a number of well-known ethical
catastrophes and the less conspicuous erosion of condence in
psychiatrists. The straightforward assessment of function in relation to
behavioural and cognitive interpersonal differences would also form a
rational basis for changes in line with the postpsychiatry proposed by
BrackenandThomas (2001). The idea that psychiatryshouldfocus more
on context than on technology and coercion is more consistent with
empiricismthanthe current, modernist psychiatric model, includingthe
suggested return to the models of Kraepelin and Jasper in the hope of
conrmation from new laboratory or technological methods recently
proposed by Andreasen (2007).
4.1. Implications
Dimensional, multi-layered, and complementary problem descrip-
tions including both overall functioning and context-specic interper-
sonal differences stand a better chance than any disease model of
identifying mental correlates to new discoveries within the neuros-
ciences and of identifying effects of new pharmacological or other
treatment strategies. The stigma associated with diagnostic designa-
tions wouldbe alleviated, as mental problems couldbe namedandmore
easily discussed in everyday language. The dialogue with the large
number of patients in whomtreatment ameliorates but does not cure
would be facilitated. Ways to reach personal maturity and adaptive
strategies could be developed for persons with mental health problems
Postmodernism is used here as a provisional description of cultural and scientic
efforts to deal with the questions arising in the aftermath of what is commonly
referred to as modernity. In no way does it mean the profession of a senseless
relativism but instead a sharper notion about the epistemological frames of different
ways of acquiring knowledge. It is somewhat difcult to understand the scarcity of
such endeavors in the areas of psychiatry and psychology.
63 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965
and others alike (Cloninger, 1999). Humans strive for meaning,
experience dreams, have ambitions, and choose their actions. We
interpret our experiences in a language-dependent web of cultural and
meaning-creating connotations. Modernist psychiatry has tried to
replace these frame-works of experience by psychosexual, biological,
evolutionary, and other unifying reasoning. Instead, psychiatry could
nd its place as part of complementary epistemological frame-works
that do not exclude each other but describe different aspects of the
human experience by specic principles for the acquisition of
knowledge. Rigorous empiricism rather than overarching models
could thus dene a psychiatry freed from trying to be what it is not.
4.2. Limitations
This is an idea-based review and thus the expression of a
subjective and possibly idiosyncratic approach. Despite the attempt
to structure the literature review on the Robins and Guze model, a
proper meta-analysis of the literature on clinical validity proved to be
unfeasible, and was replaced by a structured probing of the literature.
My co-workers in the Forensic Psychiatric research group in
Malm and Gothenburg and all the colleagues who have attended to
my many questions over the last year are gratefully acknowledged for
their valuable advice and practical help during the work on this paper,
which has been proposed at a number of professional meetings since
the rst rawsketch presented at the Sjgren Day at the University of
Lund in December 2005. Several anonymous referees and the editor of
this journal are also gratefully acknowledged for the work they put
into the nalization of the manuscript. The project was funded by the
University of Lund and the Malm University Hospital and nalized
within the chair of forensic psychiatry created by the University of
American Psychiatric Association. (2000). Diagnostic criteria from DSM-IV-TR. American
Psychiatric Association: Washington D.C.
Anckarster, H., Larson, T., Hansson, S. L., Carlstrom, E., Stahlberg, O., Gillberg, C., et al.
(2008). Child neurodevelopmental and behavioural problems are intercorrelated
and dimensionally distributed in the general population. The Open Psychiatry
Journal, 2, 511.
Anckarster, H., Stahlberg, O., Larson, T., Hakansson, C., Jutblad, S. B., Niklasson, L., et al.
(2006). The impact of ADHD and autism spectrum disorders on temperament,
character, and personality development. American Journal of Psychiatry, 163(7),
Anckarster, H., Radovic, S., Svennerlind, C., Hglund, P., & Radovic, F. (2009). Mental
disorder as a cause of crime: The cornerstone of forensic psychiatry. International
Journal of Law and Psychiatry, 32(6), 342347.
Andreasen, N. C. (1995). The validation of psychiatric diagnosis: New models and
approaches. American Journal of Psychiatry, 152(2), 161162.
Andreasen, N. C. (2007). DSMand the death of phenomenology in America: An example
of unintended consequences. Schizophrenia Bulletin, 33(1), 108112.
Baron-Cohen, S. (2000). Is Asperger syndrome/high-functioning autism necessarily a
disability? Development and Psychopathology, 12, 489500.
Baron-Cohen, S., Bolton, P. F., Wheelwright, S., Short, L., Mead, G., Smith, A., et al. (1998).
Does autism occurs more often in families of physicists, engineers, and mathemati-
cians? Autism, 2, 296301.
Baron-Cohen, S., Mortimore, C., Moriarty, J., Izaguirre, J., & Robertson, M. (1999). The
prevalence of Gilles de la Tourette's syndrome in children and adolescents with
autism. Journal of Child Psychology and Psychiatry, 40(2), 213218.
Biederman, J., Mick, E., Faraone, S. V., & Burback, M. (2001). Patterns of remission and
symptom decline in conduct disorder: A four-year prospective study of an ADHD
sample. Journal of the American Academy of Child and Adolescent Psychiatry, 40(3),
Bolton, P. F., Pickles, A., Murphy, M., & Rutter, M. (1998). Autism, affective and other
psychiatric disorders: Patterns of familial aggregation. Psychological Medicine, 28(2),
Bracken, P., & Thomas, P. (2001). Postpsychiatry: A new direction for mental health.
BMJ, 322(7288), 724727.
Cardno, A. G., Rijsdijk, F. V., Sham, P. C., Murray, R. M., & McGufn, P. (2002). A twin
study of genetic relationships between psychotic symptoms. American Journal of
Psychiatry, 159(4), 539545.
Cederlund, M., Hagberg, B., Billstedt, E., Gillberg, I. C., & Gillberg, C. (2008). Asperger
syndrome and autism: A comparative longitudinal follow-up study more than
5 years after original diagnosis. Journal of Autism and Developmental Disorders, 38
(1), 7285.
Clark, L. A. (2005). Temperament as a unifying basis for personality and psychopa-
thology. Journal of Abnormal Psychology, 114(4), 505521.
Cloninger, C. R. (1999). A new conceptual paradigm from genetics and psychobiology
for the science of mental health. Australian and New Zealand Journal of Psychiatry,
33(2), 174186.
Constantino, J. N., Lajonchere, C., Lutz, M., Gray, T., Abbacchi, A., McKenna, K., et al.
(2006). Autistic social impairment in the siblings of children with pervasive
developmental disorders. American Journal of Psychiatry, 163(2), 294296.
Constantino, J. N., & Todd, R. D. (2003). Autistic traits in the general population: A twin
study. Archives of General Psychiatry, 60(5), 524530.
Craddock, N., & Owen, M. J. (2005). The beginning of the end for the Kraepelinian
dichotomy. British Journal of Psychiatry, 186, 364366.
Durand, C. M., Betancur, C., Boeckers, T. M., Bockmann, J., Chaste, P., Fauchereau, F.,
et al. (2007). Mutations in the gene encoding the synaptic scaffolding protein
SHANK3 are associated with autism spectrum disorders. Nature Genetics, 39(1),
Folstein, S., & Rutter, M. (1977). Infantile autism: A genetic study of 21 twin pairs.
Journal of Child Psychology and Psychiatry, 18(4), 297321.
Francks, C., Tozzi, F., Farmer, A., Vincent, J. B., Rujescu, D., St Clair, D., et al. (in press).
Population-based linkage analysis of schizophrenia and bipolar case-control
cohorts identies a potential susceptibility locus on 19q13. Molecular Psychiatry.
Gadow, K. D., DeVincent, C. J., & Pomeroy, J. (2006). ADHD symptom subtypes in
children with pervasive developmental disorder. Journal of Autism and Develop-
mental Disorders, 36(2), 271283.
Gelhorn, H., Hartman, C., Sakai, J., Stallings, M., Young, S., Rhee, S. H., et al. (2008).
Toward DSM-V: An item response theory analysis of the diagnostic process for
DSM-IV alcohol abuse and dependence in adolescents. Journal of the American
Academy of Child and Adolescent Psychiatry, 47(11), 13291339.
Gillberg, C. (1995). Clinical child neuropsychiatry. Cambridge: Cambridge University Press.
Gillberg, C., Cederlund, M., Lamberg, K., & Zeijlon, L. (2006). Brief report: The autism
epidemic. The registered prevalence of autism in a Swedish urban area. Journal of
Autism and Developmental Disorders, 36(3), 429435.
Gillberg, C., & Coleman, M. (2000). The biology of the autistic syndromes, 3 ed. London:
Mac Keith.
Gillberg, C., & Soderstrom, H. (2003). Learning disability. Lancet, 362(9386), 811821.
Hafner, H. (2007). On the track of initial symptoms of depression, anxiety disorders and
schizophrenia. Timely treatment saves much suffering. MMW Fortschritte der
Medizin, 149(13), 2627.
Hofvander, B., Ossowski, D., Lundstrm, S., & Anckarster, H. (2009). Childhood-onset
disruptive behaviours as the core phenotype denition of aggressive antisociality.
International Journal of Law and Psychiatry, 32(4), 224234.
Jamain, S., Quach, H., Betancur, C., Rastam, M., Colineaux, C., Gillberg, I. C., et al. (2003).
Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are
associated with autism. Nature Genetics, 34(1), 2729.
Kendell, R., & Jablensky, A. (2003). Distinguishing between the validity and utility of
psychiatric diagnoses. American Journal of Psychiatry, 160(1), 412.
Kendler, K. S. (1980). The nosologic validity of paranoia (simple delusional disorder). A
review. Archives of General Psychiatry, 37(6), 699706.
Kendler, K. S. (2005). A gene for...: The nature of gene action in psychiatric disorders.
American Journal of Psychiatry, 162(7), 12431252.
Kendler, K. S., Gardner, C. O., Annas, P., & Lichtenstein, P. (2008). The development of
fears from early adolescence to young adulthood: A multivariate study. Psycholo-
gical Medicine, 38(12), 17591769.
Kendler, K. S., Gardner, C. O., & Prescott, C. A. (2003). Personality and the experience of
environmental adversity. Psychological Medicine, 33(7), 11931202.
Kramer, P. D. (1997). Listening to Prozac. New York: Penguin Books.
Larsson, H., Andershed, H., & Lichtenstein, P. (2006). A genetic factor explains most of
the variation in the psychopathic personality. Journal of Abnormal Psychology, 115
(2), 221230.
Levy, F., Hay, D. A., McStephen, M., Wood, C., & Waldman, I. (1997). Attention-decit
hyperactivity disorder: A category or a continuum? Genetic analysis of a large-scale
twin study. Journal of the American Academy of Child and Adolescent Psychiatry, 36
(6), 737744.
Lichtenstein, P., Carlstrm, E., Rstam, M., Gillberg, C., & Anckarster, H. (submitted for
publication). The genetics of autism spectrum disorders and related neuropsychi-
atric disorders in childhood.
Lichtenstein, P., Yip, B. H., Bjork, C., Pawitan, Y., Cannon, T. D., Sullivan, P. F., et al. (2009).
Common genetic determinants of schizophrenia and bipolar disorder in Swedish
families: A population-based study. Lancet, 373(9659), 234239.
Melke, J. (2008). Autism: Which genes are involved? The Clinical Neuropsychologist, 5
(1), 6269.
Moskvina, V., Craddock, N., Holmans, P., Nikolov, I., Pahwa, J. S., Green, E., et al. (2008).
Gene-wide analyses of genome-wide association data sets: Evidence for multiple
common risk alleles for schizophrenia and bipolar disorder and for overlap in
genetic risk. Molecular Psychiatry, 14(3), 252260.
Nilsson, E. W., Gillberg, C., Gillberg, I. C., & Rastam, M. (1999). Ten-year follow-up of
adolescent-onset anorexia nervosa: Personality disorders. Journal of the American
Academy of Child and Adolescent Psychiatry, 38(11), 13891395.
Pinkham, A. E., Hopnger, J. B., Pelphrey, K. A., Piven, J., &Penn, D. L. (2008). Neural bases
for impaired social cognition in schizophrenia and autism spectrum disorders.
Schizophrenia Research, 99(13), 164175.
64 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965
Piven, J., & Palmer, P. (1999). Psychiatric disorder and the broad autism phenotype:
Evidence from a family study of multiple-incidence autism families. American
Journal of Psychiatry, 156(4), 557563.
Ratey, J. J., & Johnson, C. (1997). Shadow syndromes, 1st ed. New York: Pantheon Books.
Robins, E., &Guze, S. B. (1970). Establishment of diagnostic validity inpsychiatric illness:
Its application to schizophrenia. American Journal of Psychiatry, 126(7), 983987.
Ronald, A., Happe, F., & Plomin, R. (2008). A twin study investigating the genetic and
environmental aetiologies of parent, teacher and child ratings of autistic-like traits
and their overlap. European Child and Adolescent Psychiatry, 17(8), 473483.
Ronald, A., Happe, F., Price, T. S., Baron-Cohen, S., & Plomin, R. (2006). Phenotypic and
genetic overlap between autistic traits at the extremes of the general population.
Journal of the AmericanAcademy of ChildandAdolescent Psychiatry, 45(10), 12061214.
Ronald, A., Simonoff, E., Kuntsi, J., Asherson, P., & Plomin, R. (2008). Evidence for
overlapping genetic inuences on autistic and ADHD behaviours in a community
twin sample. Journal of Child Psychology and Psychiatry, 49(5), 535542.
Rutter, M., & Silberg, J. (2002). Geneenvironment interplay in relation to emotional
and behavioral disturbance. Annual Review of Psychology, 53, 463490.
Rzhetsky, A., Wajngurt, D., Park, N., & Zheng, T. (2007). Probing genetic overlap among
complex human phenotypes. Proceedings of the National Academy of Sciences of the
United States of America, 104(28), 1169411699.
Sadock, B. J., Sadock, V. A., Ruiz, P., & Kaplan, H. I. (2009). Kaplan & Sadock's comprehensive
textbook of psychiatry, 9th ed. Philadelphia: Wolters Kluwer/Lippincott Williams &
Saha, T. D., Chou, S. P., & Grant, B. F. (2006). Toward an alcohol use disorder continuum
using item response theory: Results from the National Epidemiologic Survey on
Alcohol and Related Conditions. Psychological Medicine, 36(7), 931941.
Silberg, J., Rutter, M., Neale, M., & Eaves, L. (2001). Genetic moderation of
environmental risk for depression and anxiety in adolescent girls. British Journal
of Psychiatry, 179, 116121.
Smith, M. J., Barch, D. M., & Csernansky, J. G. (2009). Bridging the gap between
schizophrenia and psychotic mood disorders: Relating neurocognitive decits to
psychopathology. Schizophrenia Research, 107(1), 6975.
Stahlberg, O., Soderstrom, H., Rastam, M., & Gillberg, C. (2004). Bipolar disorder,
schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD
and/or autism spectrum disorders. Journal of Neural Transmission, 111(7), 891902.
Thaker, G. K. (2008). Neurophysiological endophenotypes across bipolar and
schizophrenia psychosis. Schizophrenia Bulletin, 34(4), 760773.
Walters, G. D., Knight, R. A., Grann, M., & Dahle, K. P. (2008). Incremental validity of the
Psychopathy Checklist facet scores: Predicting release outcome in six samples.
Journal of Abnormal Psychology, 117(2), 396405.
Watson, D. (2005). Rethinking the mood and anxiety disorders: A quantitative
hierarchical model for DSM-V. Journal of Abnormal Psychology, 114(4), 522536.
Weller, E. B., Tucker, S., & Weller, R. A. (2005). The selective serotonin reuptake
inhibitors controversy in the treatment of depression in children. Current Psychiatry
Reports, 7(2), 8790.
Wing, L. (1981). Asperger's syndrome: A clinical account. Psychological Medicine, 11(1),
65 H. Anckarster / International Journal of Law and Psychiatry 33 (2010) 5965