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Affective neuroscience and psychiatry

  • Neil A. Harrison (a1) and Hugo D. Critchley (a2)

Summary

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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Copyright

Corresponding author

Professor Hugo Critchley, Department of Psychiatry, Brighton and Sussex Medical School, Univeristy of Sussex Campus, Falmer, Brighton BNI 3AR, UK. Email: h.critchley@bsms.ac.uk

Footnotes

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Declaration of interest

None.

Funding detailed in Acknowledgements.

Footnotes

References

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Adolphs, R., Tranel, D., Damasio, H., et al (1994) Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala. Nature, 372, 669672.
Dalgleish, T. (2004) The emotional brain. Nature Reviews Neuroscience, 5, 582589.
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Harrison, N. A., Singer, T., Rotshtein, P., et al (2006) Pupillary contagion: central mechanisms engaged in sadness processing. Social Cognitive and Affective Neuroscience, 1, 517.
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Singer, T., Seymour, B., O'Doherty, J., et al (2004) Empathy for pain involves the affective but not sensory components of pain. Science, 303, 11571162.
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Affective neuroscience and psychiatry

  • Neil A. Harrison (a1) and Hugo D. Critchley (a2)
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eLetters

Caution required while implying causal relationship between organic and psychological phenomena

Channapatna Shamasundar, Consultant Psychiatrist
28 November 2007

In their scholarly editorial, Harrison and Critchley (2007) have highlighted the landmarks in the field of investigative neuroscience that studies clinical phenomena in psychiatry. Facts like the capturing of theorganic component of such an elusive subjective phenomenon as empathy are truly remarkable.

However, I was a little concerned at the implication of such a statement in the summary as “ …affective neuroscience addresses the brain mechanisms underlying emotional behaviour.” The reason for my concern is that the word ‘underlying’ implies a causal primacy to brain mechanisms over psychological counterparts.

I suspect that this word ‘underlying’ in the quoted statement accidentally found its way during the fluent flow of expression and that the authors do not really believe its implications.

Such a causal primacy is true for certain genetically and organicallydetermined conditions. But, this causal relationship cannot be generalised. In large majority of instances, what has so far been established is the correlation or concomitance between psychological, brain, and chemical mechanisms, and not the causal relationship between them. My concern is that such implications may eventually cascade over a period of time into an established paradigm (or, myth?) well ahead of its proof.

Neil A. Harrison and Hugo D. Critchley (2007), Affective neuroscienceand Psychiatry, British Journal of Psychiatry, 191, 192-194

Declaration of interest: Nil
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Conflict of interest: None Declared

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Affective neuroscience and the brainstem

Frank M Corrigan, Consultant Psychiatrist
07 September 2007

Affective neuroscience and the brainstem: a letter to the editor

While it is refreshing to see an editorial on affective neuroscience and clinical psychiatry (Harrison and Critchley 2007), the focus on cortexand amygdala excludes the huge body of work by Jaak Panksepp on the hypothalamic and mesencephalic generation of core mammalian affects such as fear, rage, separation distress, sexual urges and pain. Both he and Watt (2000) have stressed the importance of the hypothalamus and the midbrain periaqueductal gray (PAG) for spontaneous emotional behaviour andspeculated on the role of the PAG in distributed brain networks for self-awareness and other functions of consciousness. It is through inputs to the PAG that amygdala activation, when a threat is identified, leads to the physiological changes of fear and the appropriate active or passive defence responses. Therefore, while certain clinical conditions may be found to have enhanced amygdala sensitivity for specific triggers, it is also quite possible that the midbrain areas of superior colliculi and PAG contribute to hypervigilance and exaggerated defence responses in disorders such as PTSD (which could then be re-defined as at least partly a mesencephalic fear disorder rather than as an entirely cortical anxiety disorder). Now that a paradigm has been developed for the study of the ventromedial prefrontal cortex (VMPFC) and PAG in response to threat in humans (Mobbs et al 2007) it will be possible to test such speculation by study of the VMPFC-PAG axis in clinical populations. Alcohol, cannabis, and opiates are likely to be popular and effective agents for distress tolerance in humans because they act on different components of the PAG, with opioid-mediated analgesia induced by activation of ventrolateral columns (Bandler & Shipley 1994) and cannabinoid-mediated analgesia (Hohmann et al 2005) by activation of lateral columns.

Inter alia, cognitive behavioural therapy (CBT) is a neurobiological hybrid in which cognitive restructuring recruits areas of prefrontal cortex for down-regulating activity in the amygdala (e.g. Ochsner et al 2002) thus facilitating the changes within the amygdala (Harrison and Critchley 2007) which occur with behavioural exposure. Rapid reversal of stimulus –reinforcement evaluation occurs in orbitofrontal cortex rather than amygdala (Rolls 2005) so behavioural experiments and clinical exposure paradigms which depend only on reversal within the amygdala wouldbe predicted to be slow and painful and have a high drop-out rate.

Corticocentricity is also seen in the section on social biology. There is no doubt of the importance of mirror neurons for motor behavioursand the VMPFC is critical for empathy (Shamay-Tsoory et al 2003). However,mammalian systems for care, nurturance, attachment, play and sexuality areall dependent on brainstem structures and the PAG is crucial for separation distress. Perhaps psychiatry will come to see panic in the Panksepp sense as the acute distress associated with sudden loss and isolation rather than as a synonym for terror, an intense response in the fear system.

We need affective neuroscience to inform clinical neurobiology but itneeds to include affective systems defined in all mammals if it is to helpus to understand and reduce the angry hypersensitivity to social threats seen in some paranoid personalities, the profound shame and self-loathing often residual from severe childhood trauma, the hypersensitivity to potential separation and loss in insecure attachments, the catastrophic and unrelenting pain of unresolved bereavements, the changes in the hedonic valence of the core self with significant life events, the fear ofdisgusting contaminants which rules life in certain obsessive-compulsive disorders, the somatization of unbearable distress, to select but a few examples. On the positive side, understanding laughter and social joy (Panksepp 2007) may help us to build resilience and define new coping strategies. It will then be possible to be clearer about those disorders which have arisen specifically from the evolution of the human brain (e.g.Horrobin 2001) and to determine how individual phenomenology is given shape and complexity by responses of networks with their core generators in the mammalian brainstem.

References

Bandler, R. & Shipley, M.T. (1994) Columnar organization in the midbrain periaqueductal gray: modules for emotional expression? Trends in NeuroScience, 17: 379-389

Harrison, N.A., Critchley, H.D. (2007) Affective neuroscience and psychiatry. British Journal of Psychiatry, 191: 192-194

Horrobin, D.F. (2001) The madness of Adam and Eve: how schizophrenia shaped humanity. Bantam Press, London

Mobbs, D., Petrovic, P., Marchant, J.L. Hassabis, D., Weiskopf, N., Seymour, B., Dolan, R.J., Frith, C.D. (2007) When fear is near: threat imminence elicits prefrontal-periaqueductal gray shifts in humans. Science, 317: 1079-1083

Ochsner, K.N., Bunge, S.A., Gross, J.J., Gabrieli, J.D.E. (2002) Rethinking feelings: an fMRI study of the cognitive regulation of emotion.Journal of Cognitive Neuroscience, 14: 1215-1229

Panksepp, J. (1998) Affective neuroscience. Oxford University Press

Panksepp, J. (2007) Neuroevolutionary sources of laughter and social joy: modelling primal human laughter in laboratory rats. Behavioural BrainResearch, 182:231-244

Rolls, E.T. (2005) Emotion explained. Oxford University Press

Shamay-Tsoory, S.G., Tomer, R., Berger, B.D., Aharon-Peretz, J. (2003) Characterization of empathy deficits following prefrontal brain damage: The role of the right ventromedial prefrontal cortex. Journal of Cognitive Neuroscience,15, 324-337.

Watt, D.F. (2000) The centrencephalon and thalamocortical integration: neglected contributions of periaqueductal gray. Consciousness& Emotion, 1:91-114

Author: Dr F M Corrigan MBChB, MD, FRCPsych, Consultant Psychiatri
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