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What is plasticity?

The ability of the brain to change
- changes in the brain = changes in our abilities
- gray matter thickening or shrinking
- neural connections being forged and refined or weakened and severed


Brain and plasticity

The brain - a highly plastic organ
- previously - thought to be quite static
- actually - there is a lot of rapid on-going changes
- certain windows for plasticity
- e.g. childhood and language learning
- has important implications for therapeutic approaches


Sperry - Brain Plasticity

Split brain patients
- fully severed corpus callosum connection between two hemispheres
- P's were still able to complete tasks etc
Argue that there is some form of brain plasticity going on here?


Brain Plasticity and learning things

Draganski et al (2004)

Juggling training
- whole brain magnetic resonance imaging
- visualised learning-induced plasticity in brains
- transient and selective structural changes in brain areas that are associated with the processing and storage of complex visual motion

Changes in gray matter
- even after the training stopped - there was still an increase in volume

Behaviour training - direct / immediate correlate


Brain Plasticity and learning things

Maguire (2000)

London taxi cab drivers
Learning the 'knowledge'
DV - volume of the hippocampi - anterior, body & posterior regions
Taxi drivers - significantly increases GM volume in the L and R posterior hippocampi compared to controls

Learning something - the 'Knowledge' etc - has an impact on your brain connections etc???


Brain Plasticity - Nudo et al (2001)

Stroke patients

Stroke / other sources of injury
- looked at the role of adaptive plasticity in recovery of functions after damage to motor cortex - review article!
- stroke / other source of injury to motor cortex often result in movement deficits
- recovery - initially thought to be not very good BUT recent neuroimaging studies have provided substantial evidence that adult cerebral cortex is capable of significant functional plasticity

Found that motor cortex of adult mammals can undergo widespread changes in functional organisation as a result of behavioural experience and central or peripheral injury

New motor skills - alters motor cortex
- muscles and movements get represented over greater cortical territories
- this is accompanied by anatomic alterations (e.g. increase in synaptic numbers)


What is the rationale for conducting neuroimaging research into the effects of psychological interventions?

(1) Investigate the effects they have on brain functioning

(2) Identify the mechanisms of action

(3) Define appropriate biomarkers for treatment selection and response


What is Cognitive Behavioural Therapy (CBT)?

- therapist and client work together as a team to identity and solve problems
- helping clients overcome their difficulties by changing their thinking, behaviour and emotional responses
- effective in more than 1,000 outcome studies
- used for a wide range of psychiatric disorders
- has also been adapted for a wide range of individuals (children, adolescents etc)


CBT and Neuroimaging

- the psychological intervention which has been most closely investigated in Neuroimaging

- there is a sizeable literature as these interventions have lasting and memorable changes on brain functioning


CBT and Neuroimaging

Porto et al (2009)

- does CBT change the brain?
- review of neuroimaging in anxiety disorders
- essentially looking at the neurobiological consequences of psychological treatment


CBT and Neuroimaging

Porto et al (2009) - SPECIFIC PHOBIAS

Spider phobias

- CBT was shown to be effective in reducing symptoms

Before treatment - significant activation in dorsolateral PFC and para-hippocampal gyrus
- after CBT - no significant activation in these structures

CBT reduces phobic avoidance through:
- the extinction of contextual fear which is learned in the hippocampal/parahippocampal region
- reduces the dysfunctional and catastrophic thoughts in the PFC


CBT and Neuroimaging

Porto et al (2009) - SOCIAL PHOBIAS

Looked at a PET study

- significant reduction of regional blood flow bilaterally in amygdala, hippocampus and medial and anterior temporal cortex

- hippocampus and amygdala - structures related to the conditioning of aversive stimuli in P's with social phobia

- finding this out - implications for future treatments????


Functional Neuroimaging of Anxiety

Etkin & Wager (2007)

Meta-analysis of emotional processing in PTSD, social anxiety disorder and specific phobias

Study of human anxiety disorders - benefitted greatly from functional imaging approaches

BUT individual studies have varied greatly in their findings

Looked at fMRI and PET studies - PTSD, social anxiety disorder, specific phobia and fear conditioning

- looking at neuroimaging results of these disorders
- can find regions of interest / vulnerable areas
- target them for future treatment
- understand how these disorders work


Functional Neuroimaging of Anxiety

Etkin & Wager (2007) - RESULTS

PTSD - hypo- and hyperactivity
Other two - just found hyperactivity

Each disorder had a range of areas demonstrating hyperactivity
- BUT hyperactivity was common in all 3 in 2 structures
- Amygdala and Insula

Amygdala - exaggerated activity in clinical anxiety
- this meta-analysis provided / revealed consistent amygdala hyperactivity in all 3 disorders
- ALSO saw consistent amygdala activation during fear conditioning in healthy subjects
- SO the hyper-activation seen in the 3 disorders reflects a common exaggerated engagement of fear circuitry which results in shared symptoms


What is exposure therapy?

An effusive clinical intervention that is based on progressive confrontation with the pathologically feared stimuli

Approximately 95% of patients treated for phobias in one several hour sessions maintain significant improvements in symptoms for 1 year


Different forms of exposure therapies

Exposure therapy can be placed in different ways

Flooding - expose P's to the highest rated fear immediately

Systematic Desensitisation - combine exposure with relaxation exercise to make them more manageable and to associate the feared 'item/object/situation' with relaxation


Systematic Desensitisation - McGrath et al (1990)

- successful treatment of a 9 year old girl with noise phobia
- used systematic desensitisation
- Lucy - was able to control the presentation of loud noises
- taught relaxation techniques
- constructed a hierarchy of feared noises - gave them scores out of 10
- over the sessions, was able to do more tasks associated with the loud noises
- eg allowing a balloon to be popped, being able to pop the balloon, party poppers, cap gun etc


Problems with Exposure Therapy?

- lots of evidence supporting the efficacy of the treatment
- neuropsychological mechanisms underlying the fear reduction have not yet been discovered
- single sessions present a valuable opportunity
- can identify the immediate changes in neural processing of feared stimuli and then compare them with the LT changes


Exposure Therapy - Hauner et al (2012)

Monitored changes in brain activity ass a result of successful treatment for specific phobia of spiders

Before treatment:
- brain activity for phobogenic vs neutral images was greater in limbic, paralimbic & related regions
- included R amygdala, bilateral insula & cingulate cortex

All P's treated successfully within 3 hours or less

Treatment involved a progressive series of tasks to approach a live tarantula


Exposure Therapy - Hauner et al (2012)


Increased activity in R dorsolateral PFC in post therapy scan for phobogenic vs neutral images (opposite pattern from baseline)
- involvement emotion regulation?
- result of therapy?

Other areas (initially fear-responsive regions) showed activity decreases
- no longer exhibited activity for phobogenic vs neutral images
- specifically involves areas known to be involved in fear generation


Neurobiology - Depression

Depp. symptoms - depressive mood, negative cognitive biases, behavioural withdrawal

Negative cognitive biases
- negative thinking patterns, memory biases
- these serve to sustain negative emotional processing

Beck - depressed P's frequently have negative thoughts about themselves
- self-referential bias - this is a key dysfunctional cognition
- maintains and intensifies the depression


Neurobiology - Depression

Disner et al (2011)


- hyperactivity in amygdala and hippocampus
- correlates with increased activation in subgenual cingulate cortex
- this integrates limbic feedback & relays to the PFC

Activity in subgenual cingulate cortex:
- corresponds with increased activity in medial PFC
- this region shows default mode activity that is associated with internal representations of self

Associations with PFC - emotional regulation
- more focus on negative thoughts etc with depressed P's
- hyperactivity which is relayed to PFC - more negative thoughts???


CBT & Neurobiology - Depression

Yoshimura et al (2013)

CBT - targets self-referential processing of emotional stimuli

- examined the effects of CBT on S-R processing in depressed P's using fMRI
- visually presented words
- self-reference, other reference, semantic processing or letter processing

Before CBT in depressed P's:
- hyperactivity in medial PFC during self-referential processing of negative words


CBT & Neurobiology - Depression

Yoshimura et al (2013) - RESULTS

After CBT:
- MPFC and ventral anterior cingulate cortex activity during S-R processing in depressed P's
> increased for positive stimuli
> decreased for negative stimuli

These findings highlight the importance of prefrontal regions in the maintenance of depressive ruminative thoughts and the effects of CBT on these regions



SO, can neuroimaging be used to predict treatment response?

Can we use EEG/fMRI/PET as bio markers for stratifying or classifying treatments?

Unipolar depression:
- activity in subgenual anterior cingulate cortex
- significant down signature??
- BUT these results have not been prospectively replicated!!


Neuroimaging - Depression - Treatment response

Siegle et al (2013)

Seeing whether subgenual cingulate activity is a reliable and robust prognostic outcome marker for CT for depression and whether it's activity changes in treatment

- fMRI task
- this was sensitive to sustained emotional information processing before and after 16-20 sessions of CT

P's with lowest pre-treatment sgACC activity displayed the most improvement in response to negative words

sgACC activity may:
- reflect processes which interfere with treatment (eg emotion generation)
- alternatively, it's absence may facilitate treatment response


Neuroimaging - Depression - Treatment response

McGrath et al (2013)

Toward a neuroimaging treatment selection biomarker for MDD

Identifying a biomarker - may improve remission rates for MDD?
- to predict differential outcome to medication or psychotherapy

- PET - measured brain glucose metabolism
- drugs vs CBT therapy (drug = escitalopram)
- six limbic and cortical regions were identified

- showed the most robust discriminant properties across groups
- Insula hypermetabolism - remission to CBT, not drugs
- Insula hypometabolism - remission to drugs, not CBT

NEEDS to be verified with prospective testing

BUT - the insula metabolism-based treatment-specific biomarker defined there is the first objective biomarker to guide initial treatment selection


CT vs Drugs for Depression?

Beck et al (1977)

Compared efficacy of CT and Pharmacology (imipramine)

- both groups showed statistically significant decreases in depressive symptomatology

- better on self-adminsitered measures of depp and clinical ratings
- 78.9% showed marked improvement or complete remission of symptoms compared to 22.7% of drug P's

Higher dropout in drugs!
- 68% of drugs - re-entered treatment for depression
- only 16% of psychotherapy P's re-entered treatment


CT vs Drugs for Depression?

Hollon et al (2005)

AD medication - prevents the return of depressive symptoms but only as treatment is continued

Wanted to determine whether CT has an enduring effect and to compare this effect against the effect produced by continued AD medication

- P's who responded to CT were withdrawn from treatment and compared during a 12 month period with medication responders
- medication responders - randomly assigned to either continuation medication or placebo control

Relapse = a return of symptoms for at least 2 weeks

P's withdrawn from CT were significantly less likely to relapse during continuation than P's withdrawn from medications
- no more likely to relapse than P's who kept taking continuation medication

CT - has enduring effect that extends beyond the end of treatments --> as effective as keeping P's on medication!!!!


CT vs Drugs for Depression - Neurobiology

Goldapple et al (2004)

Studied neural responses to CT in 14 unmedicated depressed P's who received CBT

Compared the results with a previously collected sample of paroxetine-treated depressed P's

- PET glucose metabolic rate was measured in CBT P's within one week prior TO and AFTER treatment
- had to avoid ruminating on one topic

Frontal & parietal decreases, hippocampal increases
--> seen with CBT P's, the reverse seen in paroxetine P's

Common in both treatments - decreases in ventral lateral PFC

- target different brain regions
- reasons for differences in efficacy


CT vs Drugs for Depression - Neurobiology

DeRubeis et al (2008)

- probably affect limbic and prefrontal circuitry
- proximal mechanisms may differ

- replace automatic emotional reactivity with more-controlled processing
- function of the PFC that are impaired in depression such as task-related direction of attention, wilful regulation of emotional responses an reappraisal are the focus of therapeutic activity of CT

- might target limbic regions directly rather than relaying on inhibition through the PFC
- SSRI's increase the availability of serotonin at the synapse which could lead to inhibition of the amygdala as well as of other ventral limbic regions


CT vs Drugs for Depression - Neurobiology

DeRubeis et al (2008)


Before ADM & CT - amygdala hyper-activity leads to decreases PFC function of efficiency

CT - increases PFC functioning
ADM - decreases amygdala hyperactivity directly

After ADM or CT - increased PFC function leads to decreased amygdala activity


What about the effects of long-term psychodynamic interventions?

Never been assessed!


Psychodynamic and CBT therapies

Leichsenring (2001)

Meta-analysis of CBT and short-term psychodynamic psychotherapy

- six studies
- no significant difference could be detected in 97% of the comparisons made
- this was concerning the effects on depressive symptoms, general psychiatric symptomatology and social functioning

ONLY preliminary results though
- equally effective methods in the treatment of depression

Problem - not many studies fitted in inclusion criteria
- only 13 session - what about 16-20 sessions?
- specific forms of STPP - sometimes can't be generalised to other forms of STPP


Psychodynamic Psychotherapy

Bucheim et al (2012)

Examined the effects of LT psychodynamic psychotherapy

- investigated recurrently depressed (DSM-IV) unmedicated outpatients and control P's before and after 15 months of treatment
- trying to detect any underlying brain processes from this treatment

Stimuli - derived from the Adult Attachment Projective Picture System
- established method of assessing attachment patterns
- describe scene in the picture - what the characters were thinking, feeling, what they think might happen next
- trigger for looking at mentalising processes

BEFORE treatment
- P's showed a higher activation in the left anterior hippocampus / amygdala, subgenus cingulate cortex and medical PFC


Psychodynamic Psychotherapy

Bucheim et al (2012) - RESULTS

BDI - was significantly reduced as a result of treatment

Reduction of activity in the areas previously seen to show higher activity after 15 months
- this reduction was associated with improvement in depressiveness specifically and in the medial PFC with symptom improvement more generally

FIRST STUDY to document neurobiological changes in circuits implicated in emotional reactivity and control after long-term psychodynamic psychotherapy


Transference Based Psychotherapy

Zanarini (2009)

Based on Kernberg's conceptualisation of the core problem of BPD

Early aggression has led the young child to split his/her positive and negative images of themselves and their mother

Excess aggression may be inborn or it may have been caused by real frustration
- unable to merge the positive/negative images and attendant affects to achieve a more realistic and ambivalent view of themselves and others

Primary goal of the therapy - reduced symptomatology and self-destrictuve behaviour through modification of representations of the self and others as they are enacted in the here and now transference

Clarifications, confrontations and transference interpretations are the primary techniques of this twice-weekly therapy


Transference Based Psychotherapy

Zanarini (2009) - CLARKIN ET AL

TFP, Dialectical Behaviour Therapy and psychdynamically oriented supportive group

- all 3 showed showed positive changes in depression, anxiety, global functioning and social functioning during one year of treatment

TFP and DBT - associated with improvements in suicidality
TFP & supportive - associated in anger & facets of impulsivity

ONLY TFP associated with improvement in irritability, verbal and direct assault



Perez et al (2016)

Examined the neural association with, and predictive of, clinical improvement in emotion and behavioural regulation in BPD following TFP

- scanned pre- and post-TFP treatment (within subjects)
- disorder specific emotional linguistic go/no-go task
- used to probe the interaction between negative emotional processing and inhibitory control

Significant treatment related effects with relative dorsal PFC activation and relative decreased ventrolateral PFC and hippocampal activation following treatment

Preliminary findings!
- potential TFP associated alterations in front-limbic circuitry
- biomarkers remain to be identified though!!!


Cognitive Remediation Therapy

Behavioural based training intervention

- aims to improve cognitive processes
(attention, memory, executive function, social cognition or meta cognition) with the goal of durability and generalisation

CR approaches:
- applied to a wide range of disorders - mainly ScZ!
- also applicable to ageing and in the modification of cognition in general


Neural Correlates of Cognitive Remediation

There is evidence to suggest that dysfunctions in higher cognitive processes are related to more basic impairments in sensory processing

- loss of gray matter
- loss of dysfunction in higher areas related to more basic processing in sensory processing?
- eg delusions or hallucinations


Neural Correlates of Cognitive Remediation

Subramanian et al (2013)

ScZ P's suffer from severe cognitive deficits such as impaired reality monitoring
- RM = the ability to distinguish the source of internal experiences from outside reality

During these tasks:
- ScZ P's make errors identifying 'I made it up' items
- even during accurate performance, they show abnormally low activation of the medial PFC
(a region that supports self-referential cognition)

80 hours of computerised training of cognitive processes - emotional states, determining mental states of others


Neural Correlates of Cognitive Remediation

Subramanian et al (2013) - RESULTS

ScZ P's who received the computerised training of component auditory/verbal, visual and social cognitive processing showed:

1. Significant improvement in their accuracy preforming a complex reality monitoring task that wasn't part of the training exercise

2. Significant increase in medial PFC activation during performance on this task

3. A significant association between the level of medial PFC activation and task performance

4. A significant relationship between in medial PFC activation after training and better social functioning six months later

FINDINGS - consistent with prior work indicating that medial PFC dysfunction is associated with poor self-reflection processes, social cognition and social functional states in ScZ


Neural Correlates of Cognitive Remediation

Wykes et al (2002)

ScZ P's

- looking at the effects of a psychological rehabilitation programme aimed at information processing strategies
- those receiving CRT - did show improvements post-treatment
- showed an increase in activation over time in regions associated with working memory, particularly fronto-cortical areas


What are the implications of CRT?

- are these effects limited to when P's train?
- or are they durable effects?
- or are they specific, don't really generalise to other tasks


Cognitive Enhancement Theory

Integrated approach to the remediation of cognitive impairments in ScZ that utilises computer-associated neuro-cognitive training and group-based social-cognitive exercises


Cognitive Enhancement Theory

Eack et al (2013)

Scz P's - characterised by marked impairment in cognition which place profound limitations of function recovery

- 53 P's in the early course of ScZ or schizoaffective disorder participating in a 2 year randomised controlled trail

CET - neuro-cognitive training in attention, memory and problem-solving

Compared with P's receiving enriched supportive therapy

Broad areas of frontal and temporal gray matter change were analysed


Cognitive Enhancement Theory

Eack et al (2013) - RESULTS

P's receiving CET

- demonstrated significantly greater preservation of gray matter volume over the course of 2 years in L hippocampus, parahippocampal gyrus and fusiform gyrus
- significantly greater gray matter increases in L amygdala compared to enriched therapy
- these results are significantly related to improved cognition and mediated the beneficial cognitive effects of CET

CET - offers neurobiologic protective and enhancing effects in early ScZ that are associated with LT cognitive outcomes


Cognitive Training

Lee et al (2013) - BACKGROUND

Brain abnormalities acquired early in life - may cause ScZ?

- characterised by adult onset of psychosis, affective fattening and cognitive impairments
- cognitive training during the adolescent period or neuro-plastic development can tune compromised neural circuits to develop in the service of adult cognition and attenuate schizophrenia-realted cognitive impairment that manifests in adults

Early intervention also normalised brain function, enhancing cognition-associated synchrony of neural oscillations between the hippocampi - measure of brain function that indexed cognitive ability

Adolescence appears to be a critical window during which prophylactic cognitive therapy may benefit people at risk of ScZ


Cognitive Training

Lee et al (2013) - STUDY

Premorbid motor and cognitive impairments in ScZ have been reported in children and young adults who later developed ScZ

- found that cognitive training in adolescence prevents the onset of adult cognition deficits in neonatal ventral hippocampal lesion (NVHL) rats - an established neurodevelopment animal model of rats

Despite the persistence of the brain lesion into adulthood, the early intervention:
- prevented cognitive control deficits when NVHL rats are adults
- extended the precognitive effects beyond the training task
- improved brain function assessed by inter-hippocampal synchrony of cognition-related neural oscillations

Preventing psychosis of ScZ?????


Cognitive deficits - what other disorders are affected?

NOT just Schizophrenia but also AGEING!


Cognitive Deficits - Ageing

Kirchoff et al (2012)

Cognitive training can improve older adults recollection

- investigated whether CT-related increases in older adults recollection are associated with changes in their hippocampal activity during memory retrieval
- examined it before and after they were trained to use semantic encoding strategies to intentionally encode words
- training-related changes in recollection were positively correlated with training-related changes in activity for old words in the hippocampus bilaterally

These results suggest that CT related improvements in older adults recollection CAN be supported by changes in their hippocampal activity during retrieval



Summarises a range of behavioural techniques aimed at increasing self-control through continuous exercises

Various forms of meditation - have been shown to have positive effects on mental health and information processing

Recent years - there has been growing interests in the effects of meditation on cognition and brain functioning


Studying Monks

- changes in their meditative states - high frequency oscillations
- characterise this unique state of the brain
- different degrees of meditative states
- did show patterns BUT instead correlated with facial muscle expressions
- muscle artefacts rather than actual brain states


Meditation and Neurobiology

Luders et al (2012) - BACKGROUND

Unique brain anatomy of meditation practitioners - alterations in cortical gyrifcation

Various brain regions have been reported to be anatomically different between meditators and controls
- amount of meditation practice, changes as a consequence of meditation exercises

Evident across the lateral and medial surfaces of the cortex as well as buried beneath (e.g. insula) suggesting that cerebral cortex is associated with meditation


Meditation and Neurobiology

Luders et al (2012) - STUDY

50 meditators and 50 controls
- years of meditation practice ranged between 4 and 46 years

Cortical gyrification in LT meditators - larger in numerous regions across the lateral and medial cortices
- CG appears to increase as the number of meditation years increases

Gyrification larger in both groups in numerous areas across the cortex

Meditators showed larger gyrification in regions where previous analyses have revealed thicker cortices in meditators vs controls
- right anterior insula, left inferior temporal gyrus, left central sulcus & its vicinity and right parietal operculum

- positive correlation with CG and intelligence?
- controlling for IQ in future studies - ensure that individual intelligence is not a significant modulator when comparing meditators and controls with respect to gyrification