Description

Neurological injury can be compared to a traffic accident - disruption of messages/pathways, re-routing.

Neuroplasticity occurs throughout life, with every experience had not just injuries, E.g. learning instrument, driving etc.

Plasticity = moldable or adaptable word first used by William James in the book 'the principles of psychology.'

This was initially ignored as ramon-y-Cajal discovered brain localisation, i.e. Broca, Wernicke, Penfield – homunculus.

Led people into believing neuroplasticity was not possible in adults.

Neuroplasticity mechanisms:

synaptic remodelling/reshaping/synaptogenesis:

Unmasking of pre-existing/silent synapses (fast – hours)
Alterations of synaptic strength/efficiency (fast – hours/days)

Increase in number of synapses and their dendric arborisation (slow – day/weeks)

regenerative synaptosis and reactive synaptosis
synaptic stabilisation
synaptic turnover/elimination

angiogenesis – formation of new blood vessels
neurogenesis – formation of new neurons
glycogenesis' – glial cell hypertrophy/formation
needs to be appropriate as having more synapses is not necessarily better
bot grey and white matter changes are required in order to support behavioural change

Neuroplasticity in adults is still poorly understood.

In adults, changes are less related to structural change and more pertaining to functional change (although vice versa can still occur)

the rewiring, axonal growth, apoptosis and dendric arborisation occurs but not at the same level as infancy
more likely to involve accessing and strengthening silent synapses
compared to plasticity in infancy, plasticity in adults involves the reshaping of well-established connections/pathways - more limited/restraint to change than the newly established pathways of early childhood.

Functional plasticity:

Involves changes in some physiological aspects of the nerve cell function, such as:

The frequency of nervous impulses
the probability of release of a chemical signal – both of which make synaptic connections stronger or weaker

Changes to the degree of synchronicity among populations of cells

Structural plasticity:

Volumetric changes in discrete brain regions
formation of new neural pathways, brought about either by the:

formation of new nerve fibre branches and synapses

growth and addition of new cells

Long term potentiation (disc 1973) - physiological mechanism that increases the efficiency of synaptic transmission, in which synapses can be lengthened for prolonged periods of time.

LPT is now widely believed to be the neural basis of most, if not all, forms of learning and memory. (constandi, 2016)

Hebbian principle: "cells that fire together, wire together." - repetitive activation of a presynaptic neuron together with simultaneous activation of a neighboring postsynaptic neuron leads to an increase in synaptic strength between them.

Substantiated by experimental evidence and underpins LTP and LTD; If this happens once then it is short term potentiation.

Once LTP has been induced, the post synaptic cell sends a signal back to its presynaptic partner.
Once it enters the presynaptic cell, this back-propagated signal activates genes that synthesise the many cellular proteins needed to maintain LTP.
The gaseous neurotransmitter nitric oxide has been implicated as this so-called retro grade messenger.
learning and memory also involve structural changes that can significantly alter neuronal architecture. As well as modifying the strength of existing synaptic connections, experience and learning lead to the creating of entirely new synapses.

collateral sprouting – if an axon is injured and degenerates, postsynaptic cell needs more charge to reach action potential. This means neighbouring axons can sprout to fill vacant synapses.
Cortical maps "use it or lose it"
Topology (general anatomy) of the sensory and motor cortex is not fixed but flexible and adapts to learning and experience (Donoghue., 1996)
areas with more connections – fine motor control or more acute sensation – have a larger representation

Factors that promote change:

Enriched environment

Lack of sensory input (e.g. amputation)

Immobilising a limb

increase in size relates to increased skill

Implications for rehabilitation:

Areas can adapt their function – rather than acquiring new functions.
Intensive training of one cortical area may be at the expense of other surrounding areas.
Rapid changes in cortical activity – intensive vs extensive training
Identify damaged regions and targeted therapy.

Pascual-leone et al (1995) - piano players – muscle plasticity.

A control group of people who rehearsed piano without playing it had an increase in cortical representation in finger flexor and extensors.
The group who rehearsed piano and trained had a larger increase in cortical representation in finger flexor and extensors.

Leipert et al 1998(stroke-induced movement therapy)

Before treatment, the affected hemisphere had a significantly smaller cortical representation of hand muscle. After treatment, the muscle representation significantly enlarges, corresponding to improved motor performance of the paretic limb.

Wolf et al 2006 (constraint-induced movement therapy)

Constraint-induced movement therapy: constraining the unaffected Upper limb with a sling or mittens etc, to 'force' the patient to use their affected arm.
a 2-week program of constraint-induced movement therapy (CIMT) for patients more than 1 year after stroke who maintain some hand and wrist movement can improve upper extremity function that persists for at least 1 year

Ward et al 2003 (influence of other cortical motor areas)

Patients with poor recovery recruited more motor-related brain regions than the control group.
Patients with a complete recovery are more likely to have 'normal' task-related brain activation.
Those with poor recovery must compensate by accessing other motor networks to achieve motor tasks.
Initially, after stroke, attempts to move associated with widespread activity in motor areas of both hemispheres -? functional benefit.

Principles of neuroplasticity

Use it or lose it – Neural connections lose strength when they are not being used.
Use it and improve it – Neural pathways grow stronger the more they are used.
Specificity – Your brain forms a specific circuitry in response to particular activities
Salience matters – Brain exercises must be meaningful to you to yield lasting change.
Transference – Improving one skill may transfer its benefits to enhancing others.
Interference – Neuroplastic changes that result from maintaining a lousy habit can interfere with learning and adopting a new good habit
Time matters – It takes varying amounts of time for the brain to change depending on how complex or foreign the new behaviour or skill is to you
Age matters, but not as much as you'd think – Younger brains are more plastic, but neurogenesis and plasticity continue at any age and phase of life.
Repetition matters – Consistency is the key to building new synapses and solidifying new skills.
Intensity matters – Neuroplastic changes result from incremental progressive challenges to elicit a positive growth response.

(Kleim and jones 2008)

References

Kleim JA, Jones TA. (2008) Principles of experience-dependent neural plasticity: implications for rehabilitation after brain damage. J Speech Lang Hear Res. Feb;51(1):S225-39.

Kolb B, Gibb R. (2014) Searching for the principles of brain plasticity and behavior. Cortex. Sep;58:251-60.

Liepert J, Miltner WH, Bauder H, Sommer M, Dettmers C, Taub E, Weiller C.(1998) Motor cortex plasticity during constraint-induced movement therapy in stroke patients. Neurosci Lett. Jun 26;250(1):5-8.

Nudo RJ, Milliken GW. (1996) Reorganisation of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys. J Neurophysiol. May;75(5):2144-9.

Pascual-Leone A, Nguyet D, Cohen LG, Brasil-Neto JP, Cammarota A, Hallett M. (1995) Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills. J Neurophysiol. Sep;74(3):1037-45.

Ward NS, Brown MM, Thompson AJ, Frackowiak RS. (2003) Neural correlates of outcome after stroke: a cross-sectional fMRI study. Brain. Jun;126 (Pt 6):1430-48.

Wolf SL, Winstein CJ, Miller JP, Taub E, Uswatte G, Morris D, Giuliani C, Light KE, Nichols-Larsen D; EXCITE Investigators. (2006) Effect of constraint-induced movement therapy on upper extremity function 3 to 9 months after stroke: the EXCITE randomised clinical trial. JAMA. Nov 1;296(17):2095-104.

personal Research and Summary of Neuroplasticity made during my stroke placement This page is part of the collection 'Ed's Portfolio'.

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