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Optimising Brain and Behaviour - Short Summary

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Optimising Brain and Behaviour

Institution
Maastricht University (UM)

This document contains a short summary of PBL tasks. It contains everything you need to know for the exam! If you would like a broader overview, have a look at my other document that contains all my notes of the PBL sessions.

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neuropsychology
optimising brain and behaviour

Institution
Maastricht University (UM)
Education
Master Neuropsychology
Course
Optimising Brain and Behaviour

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Optimising Brain and
Behaviour
Short Summary
Period 2
Maastricht University
Emma Leibbrand

Table of content
Task 1 – Is It All About the Brain? (page 1)
Task 2 – The Memory Palace (page 7)
Task 3 – Slow Down (page 14)
Task 4 – Just A Young Gun With A Quick Fuse (page 21)
Task 5 – It’s All Between the Ears (page 27)
Task 6 – I Fell in Love with Someone Else (page 34)
Task 7 – Promises for the Future? (page 38)

, [ Task 1 – Is It All About the Brain? ]
(1) HAN: NEUROPLASTICITY OF COGNITIVE CONTROL NETWORKS FOLLOWING COGNITIVE
TRAINING FOR CHRONIC TRAUMATIC BRAIN INJURY

Introduction
 Cognitive control => the ability to coordinate thoughts and actions to achieve goals.
 This study identified neural plasticity induced by cognitive control training for TBI using resting state
functional connectivity (rsFC).
 Resting state functional connectivity (rsFC) => technique measuring the BOLD signal from anatomically
separated brain regions acquired at rest.
o RsFC increasingly popular => they do not require subject performing a specific task.
o Identifies both injury pattern + association between injury and behavioural impairments.
o It also measures neuroplasticity within the injured brain.
 Diffuse axonal injury (DAI) is one of the primary mechanisms of TBI.
o Injuries to axons which provide the structural basis of spatially distributed networks.
o THUS => DAI leads to breakdown of a brain network connectivity.
 Strategy-based cognitive training for chronic TBI => program to improve cognitive control by exerting
more efficient thinking strategies for selective attention + abstract reasoning.
 There are 2 distinct resting-state networks related to cognitive control:
o Cingulo-opercular network (salience network) => during cognitive control processes, this
network is associated with the ability to maintain relevant goals.
o Fronto-parietal network (executive network) => during cognitive control processes, this network
is associated with the ability to adjust goals.
 TBI decreases white matter integrity of the cingulo-opercular network + functional connectivity between
the cingulo-opercular and default networks during a cognitive control task.
 Individuals with mild TBI showed increases and decreases in the cingulo-opercular and frontoparietal
networks across brain regions, relative to healthy individuals.

Methods
 RsfMRI was used to identify effects of a strategy-based cognitive training for chronic TBI on the cognitive
control networks (i.e. cingulo-opercular and fronto-parietal networks) compared to a knowledge-based
comparison condition.
 Participants randomly assigned to one of the two training groups:
o A strategy-based reasoning training called Strategic Memory Advanced Reasoning Training
(SMART) group (experimental condition; blocking distractors (internal strategies)).
o The knowledge-based training called Brain Health Workshop (BHW) group (control; only
psychoeducation).

Results
 There were statistically significant increases in rsFC following the SMART program and these changes
occurred primarily within the SMART group relative to the comparison BHW group.
 Connectivity changes after SMART primarily at the level of between-network connectivity.
o Cingulo-opercular network changes =>primarily occurred between the connectivity with the
default mode network.
o Fronto-parietal network connectivity changes => primarily occurred in association with the visual,
somatomotor, and default mode networks.
o Interactions between brain networks are critical for successful cognitive control => due to diverse
nature of cognitive control processes drawing from neural resources across the brain.
 Network analyses => showed increased between-network connectivity when more cognitive components
were engaged in a task.
o Indicates importance of between-network connectivity for assessing higher-order cognitive
function.

1

, o TBI patients => show deficits in ‘higher order’ cognitive functions that require integration of
information across the brain + TBI disrupts between-network connectivity leading to reduced
efficiency of information processing.
 Taken together, increased between-network connectivity with the cingulo-opercular and fronto-parietal
networks following SMART for TBI may indicate improved integration of information processing for higher-
level cognitive functions.
 Trail-making test scores were correlated with fronto-parietal network connectivity within the SMART
group => this test involves a combination of working memory, task-switching, and visuoperceptual
abilities, indicating that cognitive control is an essential element in successfully coordinating abilities to
achieve better performance.
 Lastly, findings demonstrate the sensitivity and specificity of rsFC in assessing neuroplasticity. Something
that was harder to capture with conventional neuropsychological assessment.
 RsFC => neuroimaging biomarker for evaluating of the effectiveness of SMART program.

(2) NASIOS: COGNITIVE IMPAIRMENT AND BRAIN REORGANISATION IN MS

Introduction
 Multiple Sclerosis => a de-myelinating disease of the central nervous system (CNS) that affects both white
and grey matter (includes the brain + spinal cord).
 Various mechanisms throughout its course (i.e. grey matter lesions + atrophy) result in cognitive network
dysfunction => results in cognitive impairment in half of the persons with MS.
 Why only half of the patients? => dynamic balance between brain destruction and brain reorganisation.
o This balance acts in favour of keeping brain systems functioning effectively.
o Not the case in all patients, and the effect does not last forever.
 Eventually, the system collapses, and reorganisation is not effective anymore => impairments evident.
 4 types of MS => RRMS, SPMS, PPMS, PRMS.
 People living with MS commonly exhibit cognitive deficits => negatively affects them multidimensionally.
o Deficits can be present at all stages and across different clinical subtypes.
o Deficits more frequent and widespread in the progressive rather than the relapsing variant.
o Deficits may even appear before an MS diagnosis => explanation: the loss of synapses can occur
early in the disease course, before demyelination.
 Causes of cognitive impairment relate to tissue damage, tissue repair, and brain reorganisation.
 Functional brain reorganisation (neuroplasticity) can help counter disease progression.

Network-connectivity brain reorganisation
 Brain reorganisation in MS mainly studied with functional neuro-imaging methods.
o Functional connectivity (FC) => can detect hyper-connectivity and hypo-connectivity in brain
networks, which can compensate for tissue damage, allowing pwMS to cope.
o Even from early disease phases, dynamic changes in functional brain networks are observed.
 Patients with MS => exhibit greater network connectivity at baseline than people without MS + they have
strengthening of local network properties.
o These are adaptive mechanisms to maintain brain function in response to neuroinflammation.
 Inverted U-shape => hyperconnectivity as compensation for tissue damage; in the late stage is hypo-
connectivity => the compensation doesn’t last forever.
 THUS => clinical expression of MS is limited by enhancement of interactions between brain regions
normally recruited + recruitment of alternative areas + use of complementary cognitive strategies.

Regional tissue damage and atrophy
 GM lesions and atrophy play important role in CI in MS => white matter atrophy remains stable, but grey
matter atrophy dramatically increases + it mainly involves the deep structures and cortical regions.
 Biomarkers for MS => structural damage (cortical atrophy), thalamic volume, altered functional
connectivity, amygdala atrophy (impairment of social cognition), hippocampus atrophy (predictor of CI).

Synaptopathy in MS
 MS initially recognised as myelin-targeting autoimmune disease of CNS, GM pathology’s influence was
recognised later, with synaptic dysfunction playing a key role.

2

,  Inflammation leads to imbalances in neurotransmitters and excitotoxic effects => causing synaptic
degeneration, independent of GM demyelination and neuronal loss.
o Increased glutamate-mediated and decreased GABA-mediated signalling
o Increased glutamate => excitotoxic effects => leads to synaptic degeneration.
 Synaptopathy, rather than axonal loss, may lead to disability accumulation early in the disease.
 Long-term potentiation and long-term depression are core mechanisms of synaptic plasticity.
 Because synaptic function is present in MS, it is important to preserve the synaptic function => targeting
synapses therapeutically becomes important.
o Loss of synapses is reversible => reversing disease progression.
o Therapeutic targeting synapses is possible => disease-modifying therapies (DMTs); pass the BBB.
o Neurorehabilitation and neuromodulation => enhance plasticity + promote brain reorganisation.

SUMMARY

Synaptic dysfunction, particularly involving LTP and LTD, plays a significant role in MS. This dysfunction is
linked to inflammation, neurotransmitter imbalances, and excitotoxic effects, leading to synaptic
degeneration. Importantly, early in the disease course, it is synaptopathy, rather than axonal loss, that
contributes to disability accumulation in MS. However, the loss of synapses is reversible, and targeting
synapses therapeutically, along with neurorehabilitation and neuromodulation, may offer strategies to delay
disease progression and promote brain reorganisation, primarily at the synaptic level.

Neurorehabilitation and neuromodulation for MS-related CI
 Cognitive dysfunction negatively affects lives of pwMS => must be targeted by neurorehabilitation.
 Cognitive rehabilitation of MS is complicated => heterogeneous nature of CNS lesions => unique patterns
of cognitive difficulties for each MS person.
 Mechanism of action of rehabilitation for MS => enhancement of neuroplasticity.
 Neuromodulation => technology directly acting upon the nervous system .
o Non-invasive stimulation (NIBS) = application on scalp of a changing magnetic field (TMS).
o tDCS => low intensity electrical current over short period of time; can be self-administered at
home with online supervision during a task, relatively cheap.
o rTMS => must be carried out in the presence of a skilled clinician and during rest.
 Depending on volume and topography of lesions in each patient => different electrical current flow.
 MAIN MESSAGE => emphasis on the importance of early diagnosis, treatment, and ongoing research to
improve the management of MS and address cognitive impairment.

(3) WADE: WHAT IS REHABILITATION?

Introduction
 There is no agreement about or understanding of what rehabilitation is => different interpretations.
 This paper tried to discover the main characteristics of effective rehabilitation + to develop a definition.
 The results are presented in three domains: context, process, and interventions.

Context => are the benefits of rehabilitation restricted to specific patient groups, or to delivery in
specific locations?

 What conditions are associated with benefit? => Rehabilitation, whatever it is, is likely to
benefit anyone with persistent disability associated with an illness, regardless of the
underlying disease or disorder.
 Is rehabilitation effective everywhere? => Rehabilitation has been found to be effective in
most settings (rehab out of hospital after discharge is especially effective). But, note that
direct comparisons between different settings have rarely been studied.
 Does stage of prognosis of disease affect effectiveness? => Categorisation of disabling
disorders by stage and prognosis is difficult. But evidence that rehab is effective in:
o Acute phase of sudden onset disorders, e.g. stroke, hip fracture, and TBI
(including those with no natural recovery; rehab transforms e.g. social funct.).

3

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