Unit 25 Flashcards
Chronic traumatic encephalopathy
A progressive degenerative disease following multiple concussions
Levels of analysis of plasticity
Behavior, neural imaging, cortical maps, physiology, synaptic organization, mitotic activity, molecular structure
Focal hand dystonia
Loss of motor control of one or more digits due to fusion of digit motor maps. After repetitive, synchronous movements
Two methods of studying plasticity through physiology
Long term potentiation and kindling
Kindling
Development of persistent seizure activity after repeated exposure to a sub convulsant stimulus. Like LTP. Involves production of neurotrophic growth factors
Studying plasticity through synaptic organization
Using Golgi type stains to show dendritic arborization and using electron microscope’s to inspect synapse number and size. Requires post Mortem tissue.
Mitotic activity of olfactory bulbs cells
Stem cell mitosis along walls of lateral ventricles in sub ventricular zone. Migrate along rostral migratory Stream
Location of precursor cells in the hippocampus
Located between granule cell layer and the hilus
Gene chip arrays
Miniature grid exposed to neural tissue. Particular genes present in the tissue react with a substance at various locations on the chip. Detect epigenetic changes following life experiences
Experience expectant plasticity
Occurs during development. Certain brain systems require specific types of experience to develop. E.g. ocular dominance columns
Experience dependent plasticity
Brain changes in response to experiences throughout the lifetime. E.g. problem-solving, response to drugs,
Meta-plasticity
The attempt to determine how the experiences of a lifetime interact
Series of events following ischaemia
Changes in pH and properties of cell membrane. Causes massive release of glutamate an opening of calcium channels. Influx of calcium instigates second messenger pathways, resulting in mRNA stimulation, protein production. Inflammation, swelling, diaschisis
Neuroprotectant drugs
Can block calcium channels, prevent ionic imbalance, reduce swelling, or enhance metabolic activity.
Stages of recovery from motor cortex damage
Return of reflexes, development of rigidity, grasping facilitated by other movements, development of voluntary grasping. Sequential from shoulder to hand. First flexor, then extensor.
Trends in aphasia recovery
Head injury patients recover better than stroke patients. Most recovery occurs in first three months some in following six months little after
Language components most resistant to brain damage
Naming, oral imitation, noun comprehension, and yes no responses. Maybe mediated by right hemisphere
People most likely to recover from brain injury
Young, left-handed females. Highly intelligent, optimistic, extroverted, and easy-going people. People with less functional lateralization
Constraint induced movement therapy
Forcing the patient to perform daily activities with the impaired limb, finding the healthy limb for hour long sessions over weeks.
Mechanism of tactile stimulation
Skin may release neurotrophic factors which travel to the brain. Correlated with changes in dendritic length and spine density.
Sensecam
Small camera on a lanyard that automatically takes photos at fix time periods. The where can later review them. For memory impairment
Nogo-A
An endogenous compound that inhibits axon sprouting and regeneration. Administering an antibody stimulates axon generation in cortical pyramidal neurons.
Posterior cortex
Can prompt relatively automatic movements, specifies movement goals and send sensory information to frontal regions.
Prefrontal cortex
Gets instructions from posterior cortex, generates plans for movements that are passed on to pre-motor and motor cortex
Premotor cortex
Has a movement repertoire/lexicon. Recognizes others movements and select similar or different actions. Just anterior to M1
Primary motor cortex
Consists of more elementary movements than the promoter lexicon
Lenneberg and Kimuras left for language theory version
Says that the left hemisphere is actually specialized for certain voluntary motor functions, both verbal and nonverbal. Left lesions disturb voluntary movement, lead to aphasia and apraxia. Speech started as motor signing.
Splenium
Posterior part of corpus callosum, which is larger in women
Chimpanzee brain asymmetries
In both Broca’s area and the planum temporale
