The Neural Basis for a Theory of Cognitive Rehabilitation

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The Neural Basis for a Theory of Cognitive
Rehabilitation

• Ian RobertsonDept of Psychologyand Institute
  of NeuroscienceTrinity College Dublin

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Rehabilitation can work but how?
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Rehabilitation is in the realm of behaviourbut
the models of recovery are in the realm of
physiology
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Biological models on their own cannot tell us how
to rehabilitate (they inform pharmacological, not
behavioural, treatments)hence rehabilitation
has been to a great extent a theoretical orphan
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Rehabilitation needs a theoretical home but
this cannot lie entirely in the realm of
behaviourwe need a way of theoretically
linking behavioural and physiological levels of
analysis
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Conversely biological treatments of brain
damage must consider behaviourneither
behavioural nor biological treatments of brain
damage can on their own maximise effective
rehabilitation
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This is important because (3 examples)

• Rehabilitation can harm as well as help
• Neural transplants often do not take unless the
  correct behavioural input is given to the new
  tissue.
• Pharmacological treatments can enhance
  rehabilitation effects

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Delaying the onset of Huntington's in
micevan Dellen A, Blakemore C, Deacon R, et
al. NATURE 404 (6779) 721-722 APR 13 2000
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Delaying the onset of Huntington's in mice

• 30 male Huntington's disease (HD) R6/1 mice to
  either a normal or a stimulating environment.
• All mice were in groups in standard cages.
• the 'environmentally enriched' groups also
  contained cardboard, paper and plastic objects,
  changed every two days, from the age of 4 weeks.
• To define the onset of disease, motor
  coordination was tested every week in a 'turning
  task

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• RESULTS
• only one of the environmentally enriched group of
  HD mice (14) had developed disease sign at the
  end of testing at 22 weeks
• This 'peristriatal cerebral volume' was 13
  larger in the environmentally enriched HD mice
  than in the non-enriched HD group

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Restitution versus Compensation

• Restitution may require sparing of a minimum
  proportion of cells/connections (Sabel estimates
  10-20)
• Compensation needed where this level not achieved

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This is critically important..

• Do we tackle the aphasia or teach alternative
  means of communication?
• Do we treat the hemiparesis directly, or teach
  use of alternative strategies
• Do we target disordered executive functions or do
  we re-design the environment?
• Etc etc

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If we cant answer these questions

• we may waste precious therapy on ineffective
  treatments
• damage the patient through harmful therapy
• allow atrophy of brain tissue by failing to
  give correct stimulation

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Hebbian Learning and Plasticity

• A theory that begins to integrate behavioural and
  biological levels of analysis
• Cells that fire together, wire together (Long
  term potentiation LTP)
• When cells fire apart wires depart (Long term
  Depression LTD)

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Somatosensory plasticityMogilmer et al PNAS
1993vol 90 3593-3597
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Cognitive rehabilitation

• Structured, planned experience causing temporary
  or permanent changes in brain function

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Ways in which rehabilitation can work

• General stimulation
• Targeted stimulation
• Release of inhibition
• Arousal/attention

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Stimulation can improve brain function

• Abilities may not be lost completely
• Accessing them may be the problem ..
• or they may be inhibited by other parts of the
  brain
• sometimes they are simply not stimulated enough
  for the connections to re-establish
• .. But improvement not possible in all cases

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Rehabilitation of stroke the case of aphasia
(Musso et al 1999)

• Wernicke's aphasia loss of comprehension
• Assumes the inability to access linguistic
  information rather than loss
• Trained comprehension - meaning of sentences
• sentences required only a yes' or no' response.

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Summary Brain Changes

• the posterior part of the superior temporal gyrus
  in the right hemisphere
• the posterior part of precuneus in the left
  hemisphere

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But the wrong stimulation can sabotage or even
reverse recovery

• by stimulating competitor or interfering
  processes
• .. Or through glutamate-induced neurotoxicity,
  for instance

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Two limbs are worse than one
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Constraint-induced movement therapy (Taub et al)
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Eye patching

• Right hemifield versus right eye patching
• A right half-field patches (n 7)
• B right monocular patch (n 7)
• C control group (n 8).
• 3 months post, significantly better functional
  status for A compared to B and C.
• Beis et al (1999), ARCHIVES OF PHYSICAL MEDICINE
  AND REHABILITATION 80 71-76

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Stimulation of memory systems through rote
learning

• Robertson et al (under review)

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Left hippocampal metabolism before and after rote
learning training left Rote Learning right
Control.
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Targetted stimulation

• Constraint-induced movement therapy
• Limb activation training
• Prism adaptation training
• Neck muscle vibration
• Facilitated movement (harness and treadmill)
• and many others.

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Recanzone, Merzenich et al
Attention required for experience-dependent
plasticity to occur
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Attentional networks gate posterior neural
activity
Does attention have a privileged role in recovery
of function?
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Sustained attention and motor recovery after RH
stroke (9 hole peg test)
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Rehabilitation of executive functions

• Manly, T., Hawkins, K., Evans, J., Woldt, K.,
  Robertson, I. H. (2002a). Neuropsychologia, 40,
  271-281.

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Arousal and neuroplasticity

• Availability of neuromodulators potentiates
  experience-dependent plasticity.
• Walker-Batson et al (2001). A double-blind,
  placebo-controlled study of the use of
  amphetamine in the treatment of aphasia. Stroke,
  32, 2093-2097.

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Clinical Implications - Assessment

• Assess for potential not observable function
• Release inhibition
• Modify attention
• Optimise arousal
• Activate sympathetic circuits
• Maximise awareness

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Clinical Implications - Assessment

• What is the goal compensation or restitution?
• Crude measure - minimal function apparent under
  some circumstances

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Clinical Implications - Rehabilitation

• Rehabilitation given without active attention is
  probably a waste of time.
• Typical attention span is probably seconds or few
  minutes, not hours.
• Must change from massed to spaced practice (18
  ten minute sessions per week rather than 3 one
  hour sessions.

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Clinical Implications Rehabilitation 2

• Arousal must be optimised either behaviourally
  or pharmacologically.
• Awareness is critical
• Timing of rehabilitation may be crucial
  critical period (see Nudo et al, Science, 1995)
  

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Conclusions

• Behaviour changes the brain as much as it is
  determined by it.
• We need all branches of neuroscience,
  particularly cognitive neuroscience, to
  understand how to harness this fact for
  rehabilitation..