Lecture 8: Brain Plasticity

Clinical and Experimental NeuropsychologyLecture 8: Brain PlasticityDevelopmental Plasticitysticity is any change in neuronal nction

tal brains contain 30-60% more n adult primate brains. Corpus 400% more axons

station there are widespreadn type and location of cells and rconnections

tion largely ends at birth but n local cortical connectivity

xposure to particular stimuli (i.e.ct of brain lesions

re age 1 greatest impairment

-5 reorganisation of brain function

+ - little or no sparing of functionDevelopmental PlasticityThe brain was constructed to change (Merzenich, 2003)ck of plasticity once the sensitive periods of development ssed

assumption that the mature brain is hardwired

vances in cognitive ability were ascribed to alterations in ty between existing neurons

realisation that plasticity still occurs to some degree rom injury, learning, memory

hood onwards the brain modifies its machinery in a more way, refinement.

representation of behaviorally relevant inputExploring Neuroplasticityects of Practice

covery from Brain InjurySensory and Motor Maps can be modified with experiencenich et al (1980s) Primate StudiesPascual-Leone et als (1993) Braille readersed motor cortex for representations of g finger in Braille readers and controls rallyFindingsrepresentation of reading finger significantly at the expense of representation of othern Braille readers only

n observe changes within a day when Braille ced for 4-6 hours (Pascual-Leone et al.,

ed with piano players & other learning ntsPascual-Leone et al (1995)ng on a specific piano exercise with one 2 hr/day.

sed motor output maps after 5 days compared rained hand.

rol group played piano at will for 5 days rmediate mapEnhanced Representational Fidelityd, goal-directed practice is key Experiment asked Ss to practice piano exercises stead of physicallyis doing!Uncovers a fundamental link between d actionsticity changes are inherently mpetitive

a result, they are not always positiveaneous stimulation of 5 fingers d differentiation in cortical mapsPhantom Limbsanisation in somatosensory cortex following ation / denervation

erented cortex becomes functionally ted by surrounding cortex

m limbs: awareness of a nonexistent body mentally competent individuals

hs post-op: 90% experience phantom limb ons, 67% phantom limb pain (Jensen et al,d sensations on the phantom limb when nt sites are stimulated

raphical effect: when moving a stimulus adjacent area, speed, distance & directionvement are felt in phantom limbExamples of labile body imagea car extension of body boundaries of balance following lengthy bus or urneymage illusionser hand illusionChanging the body image with illusionssed on the Pinocchio illusion ckner, 1988) sensation that body s change size & shapese illusions make use of the fact that ration of the skin over the tendon of aextensor muscle elicits a vivid esthetic illusion that the joint isssively flexing:Neural Substrate of Body Size: Illusory Feeling of Shrinking of the Waist(1988) if vibrated body part touches another body sensation arises that the touched part changese:Resultsvity in the cortices lining the leftcentral sulcus and the anterior part of the parietal sulcus reflected the illusion ofst shrinking, and this activity was lated with the reported degree of king

gests that altered body images are mputed by higher-order somatosensorytal areas, through integration of more mentary somatic signalsMechanisms underlying neuroplasticityChange in balance of excitation inhibition - can happen very quicklyibition is removed, regions of functional ence are increased

Strengthening of exisiting ses,e.g. through long-term ation (LTP)change in neuronal membrane xcitability

anatomical changes, e.g. sprouting newaxonal terminals & formation of new synapses

omical changes take longertraditionally considered as feasible mechanisms of icitychanisms are not mutually exclusiveic changes occur on multiple time scalesHebbian learningnt framework for bridging neural and oural levels of analysis

nciple: two neurons or groups of neurons disconnected may become connected ifre repeatedly activated at the same timeCells which fire together wire togetherrsely, if the firing pattern between neurons atedly nonsynchronous then thection may become inhibitedCells which fire apart wire apartMaladaptive connectionsin clinical/rehab settings, not all experience od

me type of stimulation may exaggerate ts in a vulnerable circuit

mpetitor network may be activated which er inhibits an already malfunctioning ork (Kapur, 1996)

during rehab lecture.Promotion of Adaptive connectionscase scenario: to foster adaptive ections within a lesioned network and mise the possiblity of accidently fostering y connections with other networks.b et al (1993).Patients suffer unilateral kes leading to poor function of one upper

t is the best way to activate the unctional limb in view of HebbianTaubs approach:scourage patients from using their good limb, ep hand at rest in pocket.courage use of dysfunctional limb

ndings: significant improvement in motor nction after 2 weeks lasting up to two years

, postive effects resulting from a specific pattern stimulation; activation of one limb combinedth deactivation of the otherNeurogenesis in the adult human brain?et al (1998): new cells emerging in caudate and hippocampus

xperience-dependent: more cell genesis inn enriched environments than impoverished t al, 1999)

may reduce occurrence of neurogenesis (e.g. et al 1999, Vietnam Veterans)Evidence of Structural Plasticity in Adulthoode et al. (1997) Experienced taxi drivers found to larger right hippocampi than novices androls.Negative Plasticity and Cognitive Decline?

point the flipside of this plasticity is that cells connections may atrophy and die due to lack ofnegative plasticity

to keep the mind active into old-age to prevent tive deterioration like Alzheimers Disease and ntia

dons Nuns Studies (1996, 1997, 2000)

arch on plasticity shows we remain amenable to degree of change throughout the lifespanCoq and Xerri (2001) NeuroscienceCognitive Enrichment offsets Cognitive DeclineOpen questions remainre the mechanisms and precise principles functional & structural neuroplasticity ? versus harmful stimulation?parts of cortex equally flexible ? What about ical structures ?t extent are higher cognitive functions to experience dependent plasticity? lisation?Predictors of recovery?AgeSparing of frontal lobes Awareness of deficitesion sizeExtent of rehabilitation High IQReferencesd Whishaw, Gazzaniga et al: Plasticity rl Merzenich,mis.com/brainsciencepodcast/2009/02/54-merzenich/son IH, Murre JJ (1999) Rehabilitation of amage: Brain Plasticity and Principles of Recovery. Psychological Bulletin4-575.and Cummins (2009). Chapter on Pascual- studychandran Phantoms in the brain - youtube