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The mind-brain gap and the neuroscience-psychiatry gap

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DOI: 10.1111/jep.12891

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DOI: 10.1111/jep.12891

PERSONAL VIEW

The mind‐brain gap and the neuroscience‐psychiatry gap

Diogo Telles‐Correia MD PhD, Professor

1
Psychiatry Department, Faculty of Medicine,
University of Lisbon, Lisboa, Portugal
Correspondence
Diogo Telles‐Correia, Faculty of Medicine,
Psychiatry Department, University of Lisbon,
Av Egas Moniz, Lisboa, Portugal.
Email: tellesdiogo@gmail.com
Abstract
A problem underlying the mind brain gap is the complex integration among the disciplines
involved in it: neurosciences, clinical psychiatry and psychology, and philosophy of science.
Research in neurosciences and clinical psychiatry requires a positioning in relation to some
conceptual/philosophical aspects. These are related to the models of interrelationship of the
brain and the mind, to explanatory approaches in psychiatry, and to conceptual issues such as
dimensionality versus categories, symptoms versus disorders, and neurobiological correlates
versus clinical determination of mental disorder. In this article, we try to address some of these
issues that, if taken into account, could reduce the gap between psychiatrists and neuroscientists
and turn the research in this area more profitable.

KEY W ORDS

causality in psychiatry, mind‐brain gap, mind‐brain models, neurosciences, philosophy of psychiatry,

psychiatry

1 | I N T RO D U CT I O N empirical research, such as translational psychiatry that seeks to find

The mind‐brain problem, which Shopenhauer referred to as the “world
knot,”1 is 1 of the most complex enigmas in mankind.
A problem underlying the mind brain gap is the complex integra-
tion among the disciplines involved in it: neurosciences (biological
domain), clinical psychiatry and psychology (clinical domain), and phi-
losophy of science (domain of concepts).
The area of psychiatry in general escapes the ideal of science
described by Kuhn because it obligatorily integrates different para-
digms. Thus, unlike most sciences in which research deals with solving
problems within a single paradigm, in psychiatry, any research requires
an integration of paradigms.2
Research in neurosciences and clinical psychiatry requires a posi-
tioning in relation to some conceptual/philosophical aspects, although
this often goes unnoticed. These are related to the models of interre-
lationship of the brain and the mind and to explanatory approaches
in psychiatry, for example.
On the other hand, recent conceptual analysis carried out by psy-
chiatrists and psychologists has drawn attention to some issues, such
as the importance of dimensionality rather than categories and symp-
tom assessment rather than disorders, to obtain a more valid picture
3
of what is going on in the minds of people with mental disorders.
These conclusions are mainly the result of conceptual analysis and
not empirical research. However, they can and should be used by
the neurobiological correlates of mental symptoms. One of the weak-
nesses of the research in translational psychiatry is that it sometimes
lack a conceptual analysis that can guide it ontological and epistemo-
logically. Before research in this area is initiated, a deep conceptual
reflection is needed for the emergence of innovative objectives and
research topics, and for selecting the most appropriate research
methods.4
In this article, we try to address some (because it is an infinite area)
issues that, if taken into account, could reduce the gap between psy-
chiatrists and neuroscientists and turn the research in this area more
profitable.
1. Models of interrelationship of the brain and the mind
There are different models that seek to establish a relationship
between the brain and the mind.
Among them are dualism, identity theory, and functionalism.
Dualism argues that the mind is constituted by something very
different from the physical and material components and that the
mental events are governed by other than the laws that guide the
natural sciences.5-7
Two types of dualism can be considered: (1) substance dualism
that holds that mind and brain are composed of different substances
and (2) property dualism, which holds that, although they are made

J Eval Clin Pract. 2018;1–6. wileyonlinelibrary.com/journal/jep © 2018 John Wiley & Sons, Ltd. 1
2 TELLES‐CORREIA
of the same substance, mind and brain have different properties. While
substance dualism was advocated by Descartes, property dualism is
6
that most defended nowadays.
The identity theory opposes the previous one. It defends that
“mind is brain” and nothing more than this. According to this line of
thought, it would be expected with the evolution of science that all
mental states could be “observed” in neuroimaging exams. An example
of this view would be to interpret that the sensation of pain was
equivalent to the physical and natural properties of the neurons
(not having to consider any other aspect as, for example, the personal
meaning of pain), and the same would happen regarding all different
mental states.5,6
Monism is a special doctrine of the identity theory that accepts
that the same substance may seem different kinds of things or acquire
different atributes.8,9
There are several kinds of monism such as neutral monism and
anomalous monism.
According to neutral monism, nature consists of 1 kind of
substance (itself neither mental or physical) but capable of mental or
physical attributes. Grouped 1 way, the neutral entities that constitute
our brain are thoughts and feelings; grouped another way, they are
neurons. But the entities themselves are free of mental or physical
properties (therefore, their neutrality).10-12
A theory very related to this one is the double aspect theory
according to which a subject can be described equally in mental or
physical terms, which then denote different aspects of the same
entity.11,13
Another kind of monism, the anomalous monism, described by
6,11
Donald Davidson, argues that all mental states are also physical
and biological states but that the laws that regulate mental states are
different from the laws that regulate physics and natural sciences
(therefore, the term anomalous). It can be defined as a metaphysical
6
reductionism but not an epistemological reductionism. According to
Davidson, “anomalous monism resembles materialism in its claim that
all events are physical, but rejects the thesis, usually considered
essential to materialism, that mental phenomena can be given purely
11
physical explanations” (p. 214). Thus, this integrative line of thought
denies that there are psychophysical laws but defends that mental
characteristics are in some sense dependent, or supervenient, on
physical characteristics.
Functionalism is an approach closely linked to cognitive science,
computer science, and artificial intelligence, which argues that men-
tal states should be functionally characterized in relation to their
sensory inputs, behavioural outputs, and links with other mental
states.5,12 Functionalists consider the mind as software that runs in
the hardware of the brain. Thus, mental disorders can be due to
problems in the software of the mind or in the hardware of the
brain, exactly as it occurs when the computer programmes stops
working (due to software or hardware problems). Functionalists
do not care about knowing what the mind is made of, but only
how it works.5,12
In recent years, several proposals for new mind‐brain models
have emerged. Among them stands Thomas Fuchs model, which sees
the mind as a complex process (activity) where brain, body, and
environment participate. The brain serves to mediate this interaction
between a whole organism and the environment, functioning as
a mediator and not a causal factor.13
2. Explanatory approaches to psychiatric disorders
The search for causality in psychiatry may also follow different
paths. Reductionism is opposed to explanatory pluralism.
Biological reductionism argues that mental illness can be
completely defined and understood through neuroscience. There were
2 major moments in history when reductionism was most pronounced
in psychiatry: at the end of the 19th century (Griesinger and his
disciples) and at the end of the 20th century (following the onset of
psychotropic drugs). At the beginning of the 21st century, this reduc-
tionist model started to be criticized because its results (in discovering
the neurobiological mechanisms of mental illnesses as well as in psy-
chopharmacological advancement) fell short of expectations. Contrary
to what is often claimed, reductionism is not a scientific attitude but a
metaphysical one. There is no scientific method that proves that the
mind can be reduced to the brain and that the laws that govern the
mind are the same that govern the nervous system.14 Reductionism
can be openly assumed, but it can also manifest indirectly through
the way the research methodology is planned as well as through how
the results are interpreted.14
As an alternative to the reductionist explanatory model emerges
the explanatory pluralism, which argues that psychiatric diseases are
influenced by different causal mechanisms that act at different levels
of abstraction.4 There are several reasons why explanatory pluralism
(involving multiple causes at different levels of explanation) is a more
realistic and fruitful attitude in scientific research:
(i) The importance of environmental factors can manifest itself in
different ways. There is strong enough evidence that traumatic
events can have a causal influence on the onset of psychiatric ill-
ness. For example, a traumatic event in childhood (eg, death of a
relative) may have a causal influence on the onset of depression
in adulthood. Although the traumatic event in childhood may have
a translation at the level of brain biology, it does not mean that it is
through neurosciences that these traumatic events can be best
described and explored. Here, we will need another level of
abstraction other than neurosciences to assess causality in
psychiatry.4,15
On the other hand, sociocultural factors can also have a major
influence on the emergence or resurgence of certain mental ill-
nesses,16 for example, not only in eating disorders17 but also in anxiety
and depression,18 among others.
(ii) Biological factors do not act directly predisposing to mental ill-
ness but rather interact with environmental factors. For example,
the impact of genetic risk factors on the onset of psychiatric dis-
eases can be modified by the surrounding environment,19,20 by
stressful life experiences,21,22 and by sociocultural factors.23 On
the other hand, it is important to know not only the biological
components (genetic, molecular, and neuronal) that may predis-
pose to the emergence of psychiatric symptoms but also those
TELLES‐CORREIA
that are associated with the influence that environmental factors
have on the whole process that leads to these symptoms.24 Also,
the association between genes and the clinical manifestation of
a mental disorder may not be linear and direct. For example, cer-
tain genes may influence the onset of depression because they
predispose to certain behaviours that favour instability
in interpersonal relationships, which, in turn, can lead to
depression.25
Further, it is known that the influence of genes on the onset of
mental illness does not follow a one‐to‐one pattern. But a gene may
predispose to different mental illnesses, depending on environmental
circumstances, so there are many different ways to get to the same
syndrome.24
(iii) First‐person mental phenomena also have causal effects over the
brain, in the outside the world, and also on other mental states.4
This fact complicates the causal relations at this level because
mental states themselves can alter the functioning of the brain,
influence the environment (these, also causally related to mental
states), and directly induce other mental states.
(iv) In psychology and psychiatry, we have to talk about different
types of causality that coexist. One is the causality related to
the world of meanings and intentionality, which explains that
certain experiences associated with a certain symbolism may be
the basis of some mental states. This intentional or meaningful
causality, with its own rules, can only exist through the brain
but cannot be reduced to the brain (which contradicts the mind
brain reductionism). The other unintentional causality is free of
meaning and follows the universal physical laws.26
3. Other epistemological issues
There are several other conceptual factors that can hinder the
epistemology of clinical and translational research in psychiatry.
(i) Neurobiological correlates versus clinical determination of mental
disorder
A factor of great confusion, especially in the field of transla-
tional psychiatry, has been the idea that psychiatric disorders are
natural kinds and can be directly visualized and discriminated by
neuroimaging tests. Psychiatric disorders are “social constructs”;
they are not natural kinds that exist independently of any human
16,27
effort. The evaluation of what is or is not pathological in
psychiatry is related to (1) comprehensibility (whether or not the
mental state/behaviour is comprehensible given the sociocultural
context of the patient), (2) adaptability (adaptive or nonadaptive
in the context of the patient), and (3) connection to distress and
disability (whether or not they cause distress or disability). The
latter is the most universal criteria.28,29 These clinical criteria are
those that determine whether a symptom or a mental disorder is
present, which is primary or even secondary to a physical illness.
For example, if there is a brain tumour that secondarily determines
a depression, clinical depression is evaluated by the clinical criteria
3
(comprehensibility, adaptability, and harm criteria). Mental illness
(and symptom) only assumes itself as such at the time of its clinical
manifestation and the determination of what is considered inade-
quate, disadapted, or cause of harm (taking into account the socio-
cultural context of the patient), regardless of its neurobiological
basis. In neurosciences, what we can find are the neurobiological
correlates of these clinical situations (which cause distress/disability
to the patients). This does not mean that the distinction between
normal and pathological in psychiatry is made through neurobiolog-
ical markers. So, in this context, the clinical concepts precede the
biological ones.16
(ii) Dimensionality of the mental symptom
On the other hand, it has not been possible to demonstrate the
presence of natural borders between mental illness and normality nor
points of rarity between the different syndromes. Thus, the latest evi-
dence demonstrates that the symptoms and mental disorders must
have a dimensional structure.3,30-32 Thus, we should not look in neuro-
sciences for models of cleavage between normal and pathological, but
rather correlations between neurobiology and psychiatric symptoms
that are believed to be dimensional without a rigid boundary between
normal and pathological.
(iii) Symptoms versus disorders
Much of the research that has been done both neurobiologically
and clinically has been based on syndromes or disorders rather than
symptoms.3 At the moment, it is advocated that it is based on the
observation and description of the psychiatric symptoms that maybe
one day will reach the mental axioms that correspond to the biological
correlates we are looking for.3 Most of the current psychiatric
disorders are constructs (probabilistic groups) grouped in certain previ-
ous historical periods and therefore carry with them contemporary
presuppositions and bias.33
The current diagnostic categories have been shown to have many
limitations, and for new possibly more valid perspectives to emerge,
we have to look at the purest manifestation of mental illness, ie, the
symptom. Unfortunately, in the post‐third generation of Diagnostic
and Statistical Manual of Mental Disorders (DSM‐III) era, descriptive
psychopathology was abandoned and replaced by diagnostic catego-
ries.3 This situation has not only impoverished clinical practice but also
blocked advances in research.34
According to several authors, the pursuit of the biological corre-
lates of psychiatric diseases can only be based on symptoms and not
in disorders.34,35
(iv) Terminological issues
The problem of terminological issues has long been a problem in
psychiatry. Since 1980 with DSM‐III, the designations of the disorders
were generalized by all countries, as well as their diagnostic criteria
(increasing reliability). However, the terms used to define the various
symptoms in psychopathological semiology (and that according to
the new models must guide research by neurobiological correlates)
4 TELLES‐CORREIA
vary between countries and even between researchers with different
backgrounds.
The concern with the reliability ensured by the nosological catego-
ries of the DSM came to bring a gradual disregard for the terms and
34
concepts associated to descriptive psychopathology. Today, there
has been an attempt to recover these concepts and ways of evaluating
them so that they can also be used in all kinds of psychiatry research.
Moreover, according to some authors, often, neuroscientists mis-
use psychological/psychiatric terms, without knowing exactly to which
36
concepts they correspond. Sometimes, there is no concern to clarify
the expressions, words, and concepts that are used, and this can
jeopardize all the steps of the investigation from the definition of
objectives to the implementation of appropriate methodology and
the interpretation of results.36 Terms corresponding to complex
concepts such as depression, for example, are often used in ways that
do not correspond to their original meaning. For instance, some
concepts are sometimes used as synonyms of depression but
correspond only to phenomena often associated with states of depres-
sion (such as lack of energy, cognitive distortions, and hopelessness).
4. An example of a translational research on depression
Transposing some of these considerations to a particular case such
as the translational research on depression, we could mention some
suggestions.
In research projects where we seek to investigate the cause of
depression, it is essential that we accept an explanatory pluralism: (a)
symbolic meaningful‐traumatic events in childhood and adulthood
(which follow a meaningful causality that obeys to its own rules and
cannot be reduced to neurobiology) and (b) genes and neurobiological
characteristics (which also interact with the environment and meaning-
ful‐traumatic events).
It is also important to accept that the neurobiological dimension
can influence the onset of depression through different ways that
may each be studied by translational neuroscience: (a) neurobiological
dysfunctions that are directly associated with the emergence of the
symptoms of depression, (b)other neurobiological characteristics that
can predispose to certain forms of personality that in turn can trigger
the emergence of traumatic events that cause depression, and (c) neu-
robiological characteristics that may interfere with the way an individ-
ual responds to traumatic events and can determine whether or not
depression emerges.
On the other hand, it is essential to study the manifestations of
depression as dimensional symptoms, without a rigid boundary
between normal and pathological. And so a research on the neurobio-
logical correlates of some of the depression symptoms (such as depres-
sive mood) could include persons with and without a nosological
disorder, respecting the natural continuity of symptoms.
According to our considerations, it will also be determinant to
search for the neurobiological correlates of symptoms rather than for
those of nosological disorders (which follow the criteria of nosological
classifications). In the case of depression, depressive mood, anhedonia,
etc could be the target of a translational research and not the nosolog-
ical types of depression (eg, bipolar depression, unipolar depression,
and dysthymia).
2 | CO NC LUSIO NS
Some of the models of interrelationship of the brain and the mind
were explained, such as dualism, identity theory, and functionalism.
It has not been demonstrated through any kind of research that either
of these models is true or false. For example, the fact that neurosci-
ences have found biological correlates of some mental phenomena
does not prove that the identity theory is true or that the dualistic
theory is false.6
In relation to explanatory approaches, there are a number of evi-
dences that demonstrate that these should be pluralistic. Thus, it is
not profitable in this area to defend “causal monologues,” by obses-
sively seeking the relation between a particular factor and a psychiatric
illness, but it will be more useful to accept multiple causality. On the
other hand, one should not only think of the type of causes but of
the interaction between them (interaction models). This can be a key
element in the discovery of the explanation of many of the psychiatric
diseases.37 The interaction of environmental and biological causal fac-
tors occurs at all levels. Most of the causal relations that psychiatry will
need to understand will be these organism‐environment interactions
that cross levels.37
Methodological reductionism may emerge as a possible practice‐
oriented solution but with no ambitions of explanatory theory. Accord-
ing to this view, given that mental phenomena result from multifacto-
rial causality (biological, social, etc), the attempts to reduce them will
always be partial (considering some of their possible causes), but they
may be useful, in particular, for designing interventions that could alle-
viate the suffering caused by these situations.6 Kendler introduces the
concept “patchy reductions,” which corresponds to the possibility of
clarifying the causal complexity of some phenomena through partial
explanations that arise from interlevel causal models. In other words,
instead of immediately pursuing a “grand theory,” it could be possible
to phase out some partial evidence at different levels of causality that
may later be integrated.4
In the last decades, many attempts have been carried out to find
the neurobiological correlates of mental states. In this area, a dualistic
view is not profitable.38 To find the brain‐mind correlations, it is neces-
sary to establish “bridge laws bettween psychiatry and neuroscience”
that should be “underpinned with factual connections based on real
findings of clinical sciences and neurobiology in health and disorder”
(p. 74).38 It is essential to develop in this area specific methodologies
that can lead to the establishment of correlations between different
subject matters (from different paradigms, eg, neuroscience and clinical
psychiatry). This interdisciplinary science, with its epistemological
specificities, must include researchers that are not limited to an area
of knowledge but integrate different disciplines (clinical psychiatry,
neurosciences, and philosophy of science).
However, regardless of the research models we choose, we can
never fail to believe that psychiatry's fundamental goal as a medical
discipline is to alleviate the suffering/disability of patients, associated
to psychiatric symptoms that are accessed in a clinical context (through
the first‐person reports of patients).4 To reduce the symptomatology,
we can use the knowledge born from neuroscience research, in partic-
ular the biological correlates of psychiatric symptoms, and we can even
try methdological reductions in some research. But we cannot mistake
TELLES‐CORREIA
the main focus of psychiatry (human suffering associated with symp-
toms) with one of the means of trying to find some evidence that could
help us to relieve these symptoms and suffering. Nor can we restrict
the focus of psychiatry research to the evidence that has been found
so far in neurosciences and which, as we know, only partially reflects
the reality of mental illness.
In essence, not to distance ourselves from what is really going
on in patients' minds, it is always essential to integrate different
disciplines that focus on different types of causality and models to
evaluate these causalities. It is also crucial that concepts are always
well defined so that research is embedded in a good conceptual
basis. Only this way, one can ask the right questions and design
the best methodology to find the answers. Thus, it is imperative that
research groups in this area should include not only neuroscientists
but also researchers who are familiar with clinical and conceptual
issues (such as clinical psychiatrists and philosophers of science), so
that the results are more fruitful and useful. As Kendler highlighted:
“Psychiatric disorders are by their nature, complex multilevel
phenomena. We need to keep our heads clear about their stunnung
complexity and realize, with humility, that their full understanding
will require the rigorous integration of multiple disciplines and
4
perspectives” (p. 439).
ORCID
Diogo Telles‐Correia http://orcid.org/0000-0003-4217-2823
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