The British Journal of Psychiatry (2007) 191: 192-194. doi: 10.1192/bjp.bp.107.037077
© 2007 The Royal College of Psychiatrists
Affective neuroscience and psychiatry
Neil A. Harrison, MRCP, MRCPsych
UCL Institute of Cognitive Neuroscience, London
Hugo D. Critchley, DPhil, MRCPsych
Brighton and Sussex Medical School, University of Sussex Campus,
Brighton, UK
Correspondence:
Professor Hugo Critchley, Department of Psychiatry, Brighton and Sussex
Medical School, Univeristy of Sussex Campus, Falmer, Brighton BN1 3AR, UK.
Email:
h.critchley{at}bsms.ac.uk
Declaration of interest None.
Funding detailed in Acknowledgements.
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ABSTRACT
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Affective neuroscience addresses the brain mechanisms underlying emotional
behaviour. In psychiatry, affective neuroscience finds application not only in
understanding the neurobiology of mood disorders, but also by providing a
framework for understanding the neural control of interpersonal and social
behaviour and processes that underlie psychopathology. By providing a coherent
conceptual framework, affective neuroscience is increasingly able to provide a
mechanistic explanatory understanding of current therapies and is driving the
development of novel therapeutic approaches.
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INTRODUCTION
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Over the past 25 years there has been a revolution within neuroscience,
characterised by recognition of the importance of emotion to behaviour and
subjective experience (Dalgleish,
2004). This revolution and the consequent snowballing of studies,
now subsumed within affective neuroscience, was initiated and led by a key
group of experimental, cognitive and social psychologists, anatomists,
neuroscientists, clinical neurologists and psychiatrists. Affective
neuroscience has challenged `standard' cognitive models to account for
empirical and clinical evidence of `emotion' influencing, processes such as
attention, perception, learning and memory at every level. Affective
neuroscience focuses on brain function and how emotions are ultimately linked
to genetic imperatives, primary motivations and reinforcement learning. More
recently, affective neuroscience has extended its reach beyond the individual
to address dynamic influences on social and economic behaviour.
Well-being and psychiatric dysfunction are necessarily measured against
subjective emotional experience. Neurophysiological understanding of emotional
disorders, including depression and bipolar disorder, provides a broad
framework that may then usefully be applied to other psychiatric conditions,
to address biological determinants of stress responses, disorders of
personality and even prognosis across mental illness. This has contributed to
a systematic integration of previously disparate genetic, neurochemical and
psychodynamic models. This process continues to enrich the conceptual language
empowering both clinician and patient and driving the development of novel
diagnostic tools and therapeutic interventions. Neurobiological accounts of
emotional behaviour, interpersonal and social interactions are increasingly
plausible and no longer represent merely `retreats into organicity'
irreconcilable with psychosocial formulations. Affective neuroscience does not
aim for a fully reductionist account of emotional social mechanisms, but
rather to provide insights into control and influence of emotion without the
constraints of established disciplinary boundaries. This may be illustrated in
our increasing understanding of the neural processes mediating the effect of
social and psychological stress on mood disturbance, memory impairments and
enhanced risk of mortality. These cross-disciplinary approaches open exciting
new treatment options.
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EMOTIONAL LEARNING
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To illustrate how advances within affective neuroscience have the potential
to influence psychiatry, we have predictably chosen to focus our discussion
around the `most limbic of brain regions', the amygdala. The contribution of
the amygdala to affective behaviour was recognised within MacLean's concepts
of the visceral/limbic/mammalian brain
(MacLean, 1990). Weiskrantz
(1956), following observations
by Klüver & Bucy
(1937) on behavioural effects
of temporal lobectomy, showed that focal bilateral amygdala lesions had a
detrimental impact on the social and emotional behaviour of monkeys. More
recent studies of patients with bilateral amygdala lesions reveal impairments
in processing of social and emotional cues, notably the recognition of facial
or auditory expressions of fear (Adolphs
et al, 1994). As a consequence, amygdala dysfunction is
linked both theoretically and empirically to psychiatric disorders in which
social behaviour is compromised. These include autism, schizophrenia and
psychopathy. Practitioners can now conceptualise `biological' impairments in
emotional understanding/behaviour as originating in focal dysfunction of
regions such as the amygdala.
The amygdala supports the detection and learning of motivational
significance. In animal experiments, this is typically illustrated in fear
conditioning studies (i.e. the learning of threat). Fear conditioning
represents a basic model for understanding the pathogenesis and maintenance of
anxiety disorders, including post-traumatic stress disorder and panic. The
role of amygdala in fear conditioning has been extensively described in
rodents (LeDoux, 1996). In
humans, the contribution of the amygdala to processing threat is evident in
studies of patients with lesions and from neuroimaging, where amygdala
activity is now almost treated as a biomarker of functional integrity within
neural systems concerned with emotion. Findings such as these are now
beginning to inform psychiatric treatment. Cognitive–behavioural therapy
(CBT) remains a gold standard therapy for anxiety disorders by engendering
`unlearning' of fear responses through exposure and habituation. Animal
studies indicate that both learning and unlearning (extinction) of threat are
dependent on glutamine/N-methyl-D-aspartic acid (NMDA)
receptors within the amygdala dependent, a pharmacological mechanism that
neuroscientists have stimulated to enhance this behavioural extinction
process. Early trials suggest that boosting glutamine/NMDA receptor function
with cycloserine, a partial agonist at the NMDA receptor, enhances
exposure-based CBT, with promising results in the treatment of acrophobia
(fear of heights) and social anxiety
(Hofmann et al, 2006).
These findings result from a growing awareness of the important effects of
emotional processes on basic cognitive functions and could not have resulted
from models of memory based on standard cognitive neuroscience.
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SOCIAL BIOLOGY
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Recent widespread clinical recognition that pervasive neurodevelopmental
disorders, including Asperger syndrome, place demands on clinical services for
adults of working age have forced a reappraisal of conventional psychiatric
practice. In parallel, neuroscience has explored the neural mechanisms through
which we understand other people (i.e. the cognitive component of
interpersonal interaction, which was previously a preserve of psychodynamic
psychotherapy). Theoretically, we can understand the experience or intentions
of other people by `simulation'. Mirror neurons represent a convincing
biological instantiation of simulation. Mirror neurons are located within
premotor and motor cortex and in primates respond both when performing a
specific action and when viewing another monkey performing that specific
action (Rizzolatti et al,
1996). Many studies now show activity in the human brain,
mimicking or mirroring the performance of perceived actions, which is
consistent with a testable neural model for perspective taking, intentional
stance and theory of mind. Emotional empathy has been related to co-activation
of the same brain regions when experiencing actual physical pain and observing
one's partner in pain (Singer et
al, 2004). Similarly, brain responses to the distress of
others engage unconscious autonomic bodily responses that mimic, in sympathy,
the observed emotional cues (Harrison
et al, 2006). Together these studies expand
perception–action principles beyond classical `mirror' regions and
suggest that a correspondence between observed and experienced sensations,
actions and feelings may be a more general feature of the human brain.
Behavioural and neural evidence for robust simulatory systems actually
predicts individual differences in emotional empathy. Conversely, individuals
with autistic-spectrum disorders and developmental psychopathy show attenuated
activation of brain `mirror regions' when observing emotion in others. Such
findings can have implications for the future diagnosis and monitoring of
disorders of empathy.
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INTEGRATION
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The capacity for affective neuroscience to cross disciplines is illustrated
within psychosomatic medicine, a field as relevant to primary care as liaison
psychiatry. Broadly speaking, advances are being made in unpicking the
mechanisms through which emotional trauma and stress impair cognitive,
emotional and physical well-being. Adaptive physiological responses to acute
physical and psychological trauma may have pathological effects on the brain
and body if the challenges are extreme or prolonged. Stress hormones such as
cortisol represent one mechanism. Lifelong stress (even within a general
healthy population) is associated with reductions in hippocampal volume that
reflect diminished cognitive (especially memory) and behavioural resources.
Such findings offer a perspective on clinical psychiatry, as they address core
processes underlying vulnerability to psychopathology. Psychosomatic medicine,
within affective neuroscience, examines the health consequences of
mind–body interactions. This has particular relevance to psychiatry
where high rates of physical morbidity require appraisal in the context of
potentially cardiotoxic and metabolic effects of medication.
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BROADENING THE NET
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Advances in methods for human brain imaging have assisted the affective
neuroscience revolution. The capacity to observe the `brain in action' at
fairly high spatiotemporal resolution increasingly informs our understanding
of physiological mechanisms underpinning human experience. In the clinical
context, identification of functional and structural biomarkers contributes to
the characterisation of psychiatric conditions and may enhance the monitoring
of clinical course, and even targeting of treatments. Functional signatures in
brain activity associated with depression and obsessive–compulsive
disorder (OCD) were recognised relatively early. Subsequent studies of both
healthy people and patients, using positron emission tomography and functional
magnetic resonance imaging (Drevets et
al, 1997), support the proposal that abnormalities in
subgenual cingulate function in depression may relate to low mood and can
predict treatment responsiveness. Animal studies had already linked this
region closely with vegetative homoeostatic control. These findings, coupled
with the observation of abnormalities of subgenual structure in individuals
with unipolar depression, led to neurosurgical targeting of this region in
treatment-resistant depression using deep brain stimulation resulting in a
marked and sustained symptomatic improvement
(Mayberg et al, 2005).
Likewise, findings from neuroimaging studies are contributing to targeting of
selective fronto-striato-thalamic circuits for the control of severe OCD and
Tourette syndrome.
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PROSPECTS
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Biological psychiatry, particularly in relation to emotional disorder, is
recovering from a position of low status within the hierarchy of scientific
priorities. Affective neuroscience embodies a resurgence of interest in
emotional behaviour within biological and social sciences. Recognition that
emotion influences a broad spectrum of human functioning suggests that much of
biological psychiatry could be rebranded clinical affective neuroscience.
Integration of knowledge across disciplines represents an exciting future for
psychiatry research and the examples emerging from affective neuroscience are
promising. Molecular science already contributes to this integrative process
(e.g. in studies of gene–environment interactions which underpin
emotional development, behaviour and psychiatric vulnerability). Consideration
of biological, psychological and social aspects of psychiatric disorder is
fundamental to clinical practice, and it is encouraging that these
interactions are becoming central to both basic and clinical research.
Finally, affective neuroscience provides a robust investigative framework
for exploring the fundamentals of adaptive emotional behavioural and
psychiatric morbidity.
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ACKNOWLEDGMENTS
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We thank Marcus Gray for helpful comments. N.A.H. and H.D.C. are funded by
a Wellcome Trust programme grant to H.D.C.
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Received for publication February 16, 2007.
Revision received April 26, 2007.
Accepted for publication May 3, 2007.
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ABSTRACT
INTRODUCTION
