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What is the thickness of the cerebral cortex?
varies from area to area
How many neurons are in the cerebral cortex?
Is the cerebral cortex amitotic?
yes, w/ some exceptions
What are the horizontal layers of the cerebral cortex?
- ext. granular
- ext. pyramidal
- int. granular
- int. pyramidal
- multiform (polymorphous layer)
Where does communication of the cerebral cortex occur?
throughout and in-between 6 layers
If a pt survives a stroke, most will have some degree of natural recovery of:
speech, language, motor funciton, sensory perception
What type of process is brain plasticity?
- brain's ability to change structure (reestablish synapses) and function
- pattern of functional and structural changes in responses to environmental, physiological, or pathological events
- changes that occur in organization of brain and in particular changes that occur to the location of a specific info processing functions, as a result of effect of learning and experience
If a pt survives a stroke, most will have some degree of natural recovery of:
- motor function
- sensory perception
What mechanism may account for the natural recovery and return of function from a stroke?
Immediately following transection of SC in humans and other primates, there is loss of what function?
W/in several weeks or months after transection of SC (and loss of bladder function), there is an
- autonomic bladder (reflex) function present from the medulla
- w/ time the SC reestablishes these reflexes. Neurons in SC make new synapses
- If you didn't have neuroplasticity then this wouldn't take place
Facial stimulation evoked an entire phantom representation of the arm in a pt w/ UE amputation. Modification of peripheral input to the CNS results in:
- reorganization of somatosensory and primary motor cortex in a number of species
- Touching the face induced topographically organized sensations in missing upper limb (somatotopic reorganization)
They induced a cortical infarct destroying the M1 hand representation in adult squirrel monkeys and examined the cortical connections of ventral premotor cortex several months later. These data were compared w/ pattern of connections in uninjured animals. To establish post infarct patterns they used a neuronal tracer (dye).
- The dye ended up in the post central gyrus even though it was injected in premotor cortex. The adjacent neurons took up the dye and made new connections
- Thus there appears to be axonal sprouting near the ischemic injury and the establishment of novel connections to distal targets
Stimulate prefrontal gyrus and it makes the forearms of rat contract. Took out forearms. Stimulated electrode in same part a few hours later, and it:
made the shoulder contract since it couldn't stimulate the forearms anymore
What stimulates neuroplasticity in CNS?
- loss or modified afferent input to CNS
- damage to CNS
- Chemical stimulation
- environmental or training stimulaiton
How does loss of modified afferent input to CNS stimulate neuroplasticity?
if you lose afferent/peripheral input then CNS can't be stimulated
What type of damage to the CNS stimulates neuroplasticity?
- stroke or cancer
- neuroplasticity takes place
What type of chemical stimulation stimulates neuroplasticity?
- drugs, meds
- some drugs can enhance neuroplasticity
What is the environmental or training stimuli that stimulates neuroplasticity in CNS?
- natural stuff - experience in everyday life
- this isn't a pathological thing
What is an example of environmental or training stimuli that stimulates neuroplasticity in CNS?
- learning to play banjo
- motor skill training
- increasing sensory input
- teaching someone how to smell wines
What are some theories for neural plasticity?
- stem cell activation (produce new neurons)
- redundancy of systems
- unmasking secondary areas
- structural (morphological) changes***
What is the sparing theory for neural plasticity?
remaining cells (the ones that are spared) become more active. There's always sparring, b/c you can't just totally wipe out everything. Just like overcompensation
What is the redundancy of systems theory for neural plasticity?
- many parallel systems in CNS. If one portion is damaged, other portion can take over
- damage to spinothalamic tract --pt is told they only live for a certain time frame. Then dorsal column tract takes over and all of a sudden the pt lives longer than thought
What is the unmasking secondary areas theory for neural plasticity?
- association areas become more important and they help compensate for the area that's lost
- association areas take over
Are the listed theories the main reasons for neural plasticity?
What is the most credible research world for neural plasticity?
establishment of new synapses
What is the most important theory for neural plasticity?
structural (morphological changes)
What is the main reason for neural plasticity?
- structural (morphological) changes
- anatomical changes that change function
What do structural changes do for synapses?
- increase in synapses (connectivity) --important if you want any permanent memory or rehab
- modification of synapses --need chemical changes to take place in those synapses to change sensitivity
What structural changes occur in dendrites?
increase in dendrites (dendritic sprouting and spines) --since neuron isn't getting input from a certain area anymore, it needs to become more receptive, so it increases dendrites and spines, which increase surface area, which increases more synapses
What structural changes occur in dendrites and axons?
dendritic and axonal remodeling --the way dendrites and axons reconnect to form synapses
What do all the structural changes account for?
reorganization of cereal mapping for specific functions
What research is available for neural plasticity?
- cellular conditioning studies examine direct induction of plastic changes at intermediate level, document changes in selective responses of single neurons as result of short-term conditioning protocols, memory, and learning
- a decade and a half of research has shown that cortical maps are not static in adults, but in behaviorally important experience throughout life. W/in certain limits, cortex can allocate cortical area in a use-dependent manner
Need to be able to differentiate b/w neuroplasticity mechanisms at work and:
ability of organism to compensate
Motor Ex: picking up a pen
pts will compensate by using other muscle groups, twisting differently, etc. Cognitive figuring out how to do it in another way
W/ neural plasticity, new synapses have been formed...
but maybe neural plasticity is a type of compensation
What influences neuroplasticity?
- environmental stimuli
How does enviromental stimuli influence neuroplasticity?
- constraining the good limb forces use of affected limb
- results in contralateral affects as confirmed w/ PET and fMRI studies as well as neurochemical tracer studies (morphological changes and neurochemical tracer studies)
How does complexity influence neuroplasticity?
- complex is more effective than simple (functional and something they will be using, no pegs in holes!)
- motor, sensory, cognitive
How does age influence neuroplasticity?
- less effective as age increases
- plasticity is age dependent
How does timing influence neuroplasticity?
- most effective immediately following CNS insult (the longer you wait for intervention, the harder it will be to regain functionality)
- windows of opportunity
How do neurotrophins influence neuroplasticity?
- can help increase neuroplasticity
- products of glial cells and neurons
- some are activity dependent
Neuroplasticity Ex: kids in the park. 15 kids playing on the square, 4 kids on rectangle, 5 on triangle, 10 on star. Park manager takes away star, so 10 kids now have to go play on other shapes.
now you have more kids on each shape, they're adapting. In neuroplasticity, when nearby cells die, the one's around it adapt