Cognitive Neuropsychiatry: The Normal Mind and Brain Through the Lens of Disorder

1. Cognitive Neuropsychiatry: The Normal Mind and Brain Through the Lens of Disorder Vaughan Bell Departamento de Psiquiatría, Universidad de Antioquia Institute of Psychiatry, King’s College London

2. Outline • Cognitive neuropsychology • Cognitive neuropsychiatry • Delusions • Hysteria • Conclusions

3. Phineas Gage • A railroad worker in Vermont, known for his good character and responsible attitude. • Suffered an injury in 1848 where a tamping iron was shot through his head when setting gunpowder to break rocks. • He did not lose consciousness and he walked home. • He was later seen by Dr Harlow who wrote up his case.

4. Skull and Life Mask

5. Damasio et al (1994) Reconstruction

6. Effect on Gage Dr Harlow reported: “He is fitful, irreverent, indulging at times in the grossest profanity… capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned.”

7. Link to Function • This was some of the first evidence that damage to specific areas of the brain could affect personality and behaviour. • Later Paul Broca’s autopsy on a patient with expressive aphasia found a specific lesion in the left frontal lobe, now known as Broca’s area. • This suggested language was not single function and could be linked to certain brain circuits.

9. Trench Warfare and Scotoma

10. Holmes (1916) Scotoma Lesion Map

11. The Modern Era Begins • Marshall and Newcombe (1966, 1973) ushered in the new era by studying dyslexia after brain injury. • They used dissociations between different impairments to understand the cognitive structure of language. • This approach has continued to the present day, focusing on impairments in relatively easy to measure concepts like memory, attention, language, perception and so on.

13. Unknown Lands • However, cognitive neuropsychology is not so good at dealing with other aspects of human psychology, such as: • Belief • Free will • Intentionality • Body ownership • Self-knowledge • Delusion Passivity phenomena Hysteria Somatoparaphrenia Anosognosia

14. Cognitive Neuropsychiatry • So a new field was developed to: • Study how these functions break down to better understand the normal mind and brain. • To explain mental disorders within models of normal neuropsychological function. • Typically looks at symptoms rather than diagnoses.

16. Freeman et al. (2002) model • A psychological model of persecutory delusions. • Almost entirely based on research with idiopathic psychosis patients. • Using psychometric and cognitive measures.

17. Precipitant Anomalous experiences / arousal Emotion: Beliefs about self, world, others Cognitive biases Search for meaning Selection of explanation DELUSION

18. Anomalous experiences / arousal Emotion: Beliefs about self, world, others Cognitive biases Search for meaning Selection of explanation DELUSION Precipitant

19. Langdon and Coltheart (2000) • A cognitive model of belief formation. • Largely based on patients with monothematic delusions, and often after brain injury. • Using single case and double dissociation method of cognitive neuropsychology.

20. Sensory information Monitoring Web of belief Hypotheses Prioritised list of explanations Evaluation Belief accepted Belief rejected

21. Factor One Anomalous Perceptual Experiences Factor Two Reasoning impairment Sensory information Monitoring Web of belief Hypotheses Prioritised list of explanations Evaluation DELUSION Belief accepted Belief rejected

22. Psychometrics • Standardised questionnaires designed to reliably measure which experiences are typical in patients and the general population • 10% of the general population score above the mean of psychotic inpatients on: • PDI (Peters et al., 2004): a measure of delusional thinking. • CAPS (Bell et al., 2006): a measure of anomalous perceptual experiences.

23. CAPS Frequency Distribution

24. Cognitive Measures • Bell et al. (2006b) reviewed differences between delusional patients, other psychiatric patients and controls: • Probabilistic reasoning (data gathering) • Attributions for causes of events • Attentional bias • Attribution of memory source

25. After Brain Damage • Reviews of psychosis after brain damage also stress the importance of the temporal and frontal lobes. • Psychosis has been found most commonly after damage to these areas in studies of: • Cerebrovascular accident (Starkstein et al., 1992) • Tumour (Lisanby et al., 1998) • Traumatic brain injury (Fujii and Ahmed, 2002)

26. Neuroimaging • Commonly finds frontal / temporal changes. • The DTI literature indicates pathways connecting these areas are most commonly abnormal (Kubicki et al., 2007) • Functional neuroimaging of delusions typically implicates frontal and temporal areas (Blackwood et al., 2001), although results can be task and delusion specific (e.g. Blakemore et al., 2000).

27. Cognitive Modelling • Computer models of delusions have existed since Colby’s (1975) natural language simulation PARRY. • Recent simulations tend to be based on connectionist models (Rolls et al., 2008). • These are designed to perform a particular cognitive task… • …and are then ‘damaged’ to simulate the proposed neurobiological dysfunction. • To see if they produce ‘delusion-like’ behaviour.

28. Neurocognitive Modelling • We wanted to look at the causative role of the temporal cortices in anomalous experience. • Used a paradigm from Brugger et al. (1993) • [ Demo Here ]

29. Bell et al. (2007) • In reality, all patterns were completely random. • Brugger et al. (1993) found that healthy participants who believe in telepathy were more likely to ‘see’ meaningful information in visual noise. • We did the same experiment, but controlled for anomalous experience in the 12 participants.

30. Bell et al. (2007) • Used transcranial magnetic stimulation on the vertex, left and right lateral temporal cortices before stimulus. • TMS caused no significant effect on reaction time.

31. Effect on ‘detect’ responses * Sig main effect p< 0.05; * Sig diff from left at p < 0.05

32. Hysteria • Now diagnosed as ‘conversion disorder’ or ‘dissociative disorder’ and typically based on three main assumptions (Miller, 1999) • Symptoms are not adequately explained by tissue damage. • The patient has no voluntary control over the symptom. • They can be caused by the ‘conversion’ of psychological distress into physical symptoms.

33. Hysteria • Can involve: • Paralysis • Amnesia (psychogenic amnesia) • Blindness / deafness • Walking / gait problems (atasia-abasia) • Loss of voice (psychogenic aphonia) • Seizures (psychogenic non-epileptic seizures) • and many others…

34. Hysteria and Dissociation • The ‘conversion’ hypothesis was originally an idea from Ferriar, popularised by Freud, but lacks evidence. • There is more evidence for ‘dissociation’. • Defined as the unconscious compartmentalisation of normally integrated mental functions (Janet, 1887; Aybek et al., 2008). • Recent evidence suggests that this ‘compartmentalisation’ works by top-down attentional modulation.

35. Neuropsychology of Dissociation • EEG studies find that early sensory pathways are intact in hysterical sensory impairment… • …but signals from higher level perception areas are abnormal (e.g. Xu et al., 2001). • TMS studies of hysterical paralysis show that primary motor pathways are intact (e.g. Cantello et al., 2001). • Neuroimaging typically shows functional decreases in areas linked to impairment with increases in prefrontal cortex activity (review in Bell et al., forthcoming) • Suggesting inhibition at the cognitive level.

36. [ Demo Here ]

37. Distribution of Hypnotisability

38. Hypnosis and Dissociation • 19th century French neurologist Jean-Martin Charcot noted the similarities between the effects of hypnosis and hysteria. • He noted that hypnosis could simulate and treat hysteria. • He argued that hysteria occurred due to functional inhibitions of the motor cortex that were produced by a form of autosuggestion.

39. Hypnosis and Hysteria • Marshall et al. (1997) increases in frontal activity with motor cortex decrease in hysterical paralysis. • Halligan et al. (2000) repeated the study but with someone with hypnotic paralysis and found remarkably similar pattern. • Our research group is continuing to investigate hypnosis as a model of hysteria.

40. Hypnosis and Hysteria • As well as the functional similarities, it seems people with hysteria are more hypnotisable than the general population (review in Bell et al., forthcoming) • So we can use hypnosis to model hysteria… • …and studying high hypnotisable people might give us a clue to susceptibility to dissociation.

41. Imaging State Related Changes Perfusion imaging using arterial spin labelling High hypnotisables, hypnotised, absorption correlation

42. In Psychopathology Research • There is now an increasing interest in hypnosis as a psychopathology research tool (Oakley, 2006) • For example, used to simulate: • Hysterical paralysis (Halligan et al., 2000) • Peri-traumatic dissociation (Holmes et al., 2006) • Delusions of alien control (Blakemore et al., 2003) • ‘Functional’ pain (Derbyshire et al., 2004)

43. Conclusions • Cognitive neuropsychiatry aims to understand mental disorder in terms of models of normal neuropsychological function. • It also aims to study disorder as a window on to the normal mind and brain. • This helps us understand the less easily accessible concepts like belief, free will, intentionality etc. • We need to integrate phenomenology, psychology, cognitive science and neuroscience.