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151 Cards in this Set

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Posterior parietal association cortex

- Integrates information about body part location and external objects
- Receives visual, auditory, and somatosensory information
- Outputs to motor cortex, including dorsolateral prefrontal association cortex, secondary motor cortex, and frontal eye field
Dorsolateral posterior association cortex
- Input from posterior parietal cortex
- Output to secondary motor cortex, primary motor cortex, and frontal eye field
- Evaluates external stimuli and initiates voluntary reactions - supported by neuronal responses
Apraxia
- Damage to posterior parietal cortex
- Disorder of voluntary movement - problem only evident when instructed to perform an action - usually a consequence of damage to the area on the left
Contralateral neglect
- Damage to the posterior parietal cortex
- Unable to respond to stimuli contralateral to the side of the lesion - usually seen with large lesions on the right so that patient "ignores" the left
- Sometimes manifested in terms of gravitational or egocentric coordinates, sometimes in terms of object-based coordinates
Secondary motor cortex
- Input mainly from association cortex
- Output mainly to primary motor cortex
- May be involved in programming movements in response to input from dorsolateral prefrontal cortex
- Active during imagining and planning of movements
Areas of secondary motor cortex
- Supplementary motor areas (including supplementary eye field)
- Two premotor areas (dorsal and ventral)
- At least 2 cingulate motor areas
Mirror neurons
- About 10% of neurons in inferior frontal/parietal areas have "mirror" qualities
- Active when a subject is performing an action or watching another perform the same action
- Fire when there are enough clues to imagine what will happen next
- Possible neural basis of social cognition (knowledge of others' mental processes - e.g. intentions, or theory of mind)
- Currently known to exist in higher primates --> indirect evidence from functional brain-imaging studies, found in secondary areas
Studies of mirror neurons
- Mirror neurons fired in a monkey --> grasping or watching another grasp a particular object but not others, grasping or watching another grasp an object for a specific purpose but not for another purpose
Primary motor cortex
- Precentral gyrus of the frontal lobe
- Major point of convergence of cortical sensorimotor signals
- Major point of departure of signals from cortex to the rest of the body
Conventional view of primary motor cortex function
- Somatotopic - more cortex devoted to body parts that make complex movements
- Motor homoculus
Current view of primary motor cortex function
- Regions of primary motor cortex support initiation of species-typical movements
- Neurons direct movement to a target of the movement rather than simply a pre-coded direction
Other brain regions involved in motor processing
- Cerebellum: 10% of brain mass but 50% of its neurons, input from primary/secondary motor cortexes, input from brainstem motor nuclei, feedback from motor responses, involved in timing, fine-tuning, and motor learning, may also do the same for cognitive responses
- Basal ganglia: a heterogeneous collection of interconnected nuclei, neural loops that receive cortical input and send output back via the thalamus, modulate motor output and cognitive functions including learnings
Descending motor pathways
- Two dorsolateral pathways
- Two ventromedial pathways
- Both corticospinal tracts are direct
Dorsolateral tracts
- Synapse on areas of spinal gray matter
- Two kinds: corticospinal and corticorubrospinal
Dorsolateral corticospinal tract
- Descends through the medullary pyramids, then cross over --> synapse on motor neurons projecting to leg muscles, control of wrist, hands, fingers, toes
Dorsolateral corticorubrospinal tract (Dorsolateral)
- Synapse at red nucleus and cross before the medulla --> some control muscles of the face, distal muscles of arms and legs
Ventromedial tracts
- Corticospinal
- Cortico-brainstem-spinal tracts
Ventromedial corticospinal tract
- Descends ipsilaterally
- Axons branch and innervate interneuron circuits bilaterally in multiple spinal segments
Ventromedial cortico-brainstem-spinal tract
- Interacts with various brainstem structures and descends bilaterally carrying information from both hemispheres
- Synapse on interneurons of multiple spinal segments controlling proximal trunk and limb muscles
Comparison of the two dorsolateral motor pathways and the two ventromedial motor pathways
- Dorsolateral: one direct tract, one that synapses in the brain stem, terminate in one contralateral spinal segment --> distal muscles and limb movements
- Ventromedial: one direct tract, one that synapses in the brain stem, more diffuse, bilateral innervation --> proximal muscles, posture and whole body movement
Sensorimotor spinal circuits
- Motor circuits of the spinal cord show considerable complexity
- Formerly thought that the spinal circuits were dependent on the brain --> now known that these circuits are independent of brain signals
- Animals who have had the connection to the brain severed can walk once the motion has been initiated
Muscles: Organization
- Motor units: a motor neuron plus muscle fibers; all fibers contract when motor neuron fires
- Acetylcholine: released by motor neurons at neuromuscular junction causes contraction
- Number of fibers per unit varies: units with the least number of fibers have the finest control
- Muscle: muscle fibers (mix of slow and fast) bound together by a tendon
Sarcolemma
Cell membrane of striated muscle cell, muscle fiber is made up of chains of myofibrils
Muscle types
- Flexors (bend or flex a joint - excitatory) vs extensors (straighten or extend - inhibitory)
- Synergistic muscles (any two muscles whose contraction produces the same movement) vs antagonistic muscles (any two muscles that act in opposition to each other)
- Fast fibers (strong and quick movements but fatigue easily) vs slow fibers (more vascularized so have more staying power, steady and sustained movement)
- Muscles are a mix of slow and fast fibers
- Acetylcholine released by motor neurons at the neuromuscular junction causes contraction
- Motor pool: all motor neurons innervating the fibers of a single muscle
Reciprocal innervation
- Antagonistic innervated in a way that allows for smooth motor response
- Excitatory and inhibitory response
- Response quickest with excitation of all agonist neurons and simultaneous inhibition of all antagonist neurons
- Normal movement does not proceed this way - all muscles are always always slightly contracted, movement occurs by making slight adjustments to different muscles that work in opposition
Receptor organs of tendons and muscles
- Golgi tendon organs: embedded in tendons, detect muscle tension, basically a "fail-safe" for muscle and tendon
- Muscle spindles: receptors embedded in belly of muscle, detect changes in muscle length, changes relayed to brain to allow computation of body position, intrafusal muscle inside each spindle innervated by intrafusal neuron
Central sensorimotor programs
- Thought that all but highest levels of sensorimotor system have patterns of activity programmed into them, and complex movements are produced by activating these programs
- Cerebellum and basal ganglia coordinate various programs
Motor equivalence
A given movement (or goal) can be accomplished using different sets of muscles, also, the same set of muscles can be used to accomplish different movements
- Flexibility/adaptability of nervous system
- Central sensorimotor programs must be stored at a level higher than the muscle (different muscles can do the same task)
- Sensorimotor programs can be stored in secondary motor cortex
Development of central sensorimotor programs
- Hierarchically organized
- Capable of using sensory feedback without direct control at higher levels
- Programs for species-specific behaviors developed without practice
- Practice can generate and modify programs --> response chunking, shifting control to lower levels
Functional brain imaging of sensorimotor systems
- When learning a task... brain activity is DISTRIBUTED
- When a task is known... brain activity is LOCALIZED
6 common causes of brain damage
1. Brain tumors
2. Cerebrovascular disorders
3. Closed-head injuries
4. Infections of the brain
5. Neurotoxins
6. Genetic factors
Brain tumors
- A mass of cells that grows independently of the rest of the body (cancer)
- 20% of brain tumors are meningiomas (encased in meninges, benign, surgically removable)
- 10% metastatic - originate elsewhere, usually the lungs
Cerebrovascular disorders (examples)
- Examples: stroke and neurotoxic cascade
Stroke
- Sudden-onset cerebrovascular event that causes brain-damage (cerebral hemorrage - brain bleeding, cerebral ischemia - disruption of blood supply, 83% strokes are ischemic)
- Third leading cause of death in the US
Neurotoxic cascade
- Most damage due to excess neurotransmitter release - especially glutamate
- Blood-deprived neurons become overactive and release glutamate
- Glutamate overactivates receptors, esp. NMDA receptors leading to an influx of Na+ and Ca2+
- This triggers more release of glutamate and a sequence of reactions that kill the neuron
Closed-head injuries
- Brain collides with skull
- Most common cause of death of young people
- Different outcomes depending on severity
Concussions
Disturbance of consciousness following a blow to the head and no evidence of structural damage, multiple concussions can result in dementia
Blast injury
- Common in returning veterans
- Can result in widespread diffuse axonal injury
Encephalitis
Resulting inflammation of the brain by an invasion of microorganisms
Bacterial infections
- Often lead to abscesses, pockets of pus
- May inflame meninges, causing meningitis
- Treat with penicillin and other antibiotics
Viral infections
- Some preferentially attack neural tissues
- Some can lie dormant for years
Meningitis
Inflammation of arachnoid, the pia mater, and the intervening cerebrospinal fluid --> causes by bacteria, viruses, inflammatory diseases
Neurotoxins
- May enter through gastrointestinal tract or through skin
- Toxic psychosis
- Some neurotoxins are endogenous: autoimmune disorders
Most common neurotoxin?
Ethanol
Toxic psychosis
Chronic insanity produced by a neurotoxin
"The Mad Hatter"
Hat makers often had toxic psychosis due to mercury exposure
Genetic factors of brain damage
- Most neuropsychological diseases caused by recessive genes
Angelman's syndrome
A neurogenetic disorder characterized by severe intellectual and developmental disability, sleep disturbance, seizures, jerky movements (especially hand-flapping), frequent laughter or smiling, and usually a happy demeanor.
Apoptosis
Programmed cell death, cause of all six types of brain damage
Common Neuropsychological Diseases
Epilepsy, Parkinson's, Huntington's, MS, Alzheimer's
Epilepsy
- Primary symptom is seizures (not all who have seizures are epileptic)
- Epileptics have seizures generated by own brain dysfunction
- Affects ~1% of population
- Difficult to diagnose due to complexity of epileptic seizures
WADA Testing
The test is conducted with the patient awake. Essentially, a barbiturate is introduced into one of the internal carotid arteries via a cannula or intra-arterial catheter from the femoral artery. The drug is injected into one hemisphere at a time. The effect is to shut down any language and/or memory function in that hemisphere in order to evaluate the other hemisphere. Then the patient is engaged in a series of language and memory related tests. The memory is evaluated by showing a series of items or pictures to the patient so that within a few minutes as soon as the effect of the medication is dissipated, the ability to recall can be tested.
Parkinson's Disease
- A movement disorder of middle and old age affecting about .5% of the population
- Tremor at rest is the most common symptom of the full-blown disorder
- Dementia is not typically seen, no single cause
- Associated with degeneration of the substantia nigra; these neurons release dopamine to the striatum of the basal ganglia
- Almost no dopamine in the substantia nigra of Parkinson’s patients
- Treated temporarily with L-dopa
- Linked to about 10 different gene mutations
- Deep brain stimulation of subthalamic nucleus reduces symptoms, but effectiveness slowly declines over months or years
Multiple Sclerosis (MS)
- Progressive disease that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis)
- Nature and severity of deficits vary with the nature, size, and position of sclerotic lesions
- Periods of remission are common
- Symptoms include visual disturbances, muscle weakness, numbness, tremor, and loss of motor coordination (ataxia)
- Epidemiological studies find that incidence of MS is increased in those who spend childhood in a cool climate
- MS is rare among Africans and Asians
- Only some genetic predisposition and only one chromosomal locus linked to MS with any certainty
Alzheimer's Disease
- Most common cause of dementia – likelihood of developing it increases with age
- Progressive, with early stages characterized by confusion and a selective decline in memory
- Definitive diagnosis only at autopsy – must observe neurofibrillary tangles and amyloid plaques
- Several genes associated with early-onset AD synthesize amyloid or tau, a protein found in the tangles
- Decline in acetylcholine levels is one of the earliest signs of AD
- Effective treatments not yet available, but immunotherapy is promising
Neuroplastic responses to nervous system damage
1. Degeneration
2. Regeneration
3. Reorganization
4. Recovery
Neural Degeneration
- Cutting axons is a common way to study responses to neuronal damage
- Anterograde vs Retrograde
Anterograde
- Degeneration of the distal segment between the cut and synaptic terminals
Retrograde
- Degeneration of the proximal segment - between the cut and cell body
Neural Regeneration
- Does not proceed successfully in mammals and other higher vertebrates - capacity for accurate axonal growth is lost in maturity
- Regeneration is virtually nonexistent in the CNS of adult mammals and unlikely, but possible in the PNS
Conditions for neural regeneration
- If the original Schwann cell myelin sheath is intact, regenerating axons may grow through them to their original targets
- If the nerve is severed and the ends are separated, they may grow into incorrect sheaths
- If ends are widely separated, no meaningful regeneration will occur
Neural Reorganization
Reorganization of primary sensory and motor systems has been observed in laboratory animals following
- Damage to peripheral nerves
- Damage to primary cortical areas
- Lesion one retina and remove the other –neurons that originally responded to lesioned area now responded to an adjacent area – remapping occurred within minutes
- Studies show large scale of reorganization possible
Neural reorganization in humans
- Brain-imaging studies indicate there is continuous competition for cortical space by functional circuits
(e.g. Auditory and somatosensory input may be processed in formerly visual areas in blinded individuals)
- People with traumatic brain injury show brain activation over a larger area than uninjured controls when performing about the same on memory task.
- Possible mechanism = reorganization
Phantom limbs
- Neuroplastic phenomena
- Amputee feels a touch on his face and also on his phantom limb (due to their proximity on somatosensory cortex)
Ramachandran's hypothesis
Phantom limb caused by reorganization of the somatosensory cortex following amputation
Recovery of neural function after brain damage
- Difficult to conduct controlled experiments on populations of brain-damaged patients
- Can’t distinguish between true recovery and compensatory changes

- Adult neurogenesis (generating new neurons) may play a role in recovery
Cognitive reserve
Education and intelligence – thought to play an important role in recovery of function – may permit cognitive tasks to be accomplished in new ways
NeuroTreatment of Nervous System Damage
- Reducing brain damage by blocking neurodegeneration
- Promoting recovery by promoting regeneration
- Promoting recovery by transplantation
- Promoting recovery by rehabilitative training
Reducing brain damage by blocking nerodegeneration
- Various neurochemicals (neuroprotective agents) block or limit degeneration: apoptosis inhibitor protein, nerve growth factor, estrogens
- Promote regeneration
Estrogens
- Profound effect on neuroplasticity.
- Evidence suggests a neuroprotective mechanism (especially in traumatic brain injury), due to selective inhibition of apotosis.
Nerve growth factor
Causes axon growth. Without it, apoptosis occurs. Has been linked to neuroprotection, and appears to promote myelin repair. Several clinical trials show promising results.
XAIP (Apoptosis inhibitor protein)
Stops apoptotic cell death caused by infection (and other mechanisms). However, it’s a balancing act: if XAIP isn’t well-regulated, can produce cancer, autoimmune disease, other neurodegerative disorders.
While regeneration does not normally occur in CNS, experimentally it can be induced, directing growth of axons by...
Schwann cells
Neurotransplantation
- Transplanting fetal tissue
- Fetal substantia nigra cells used to treat monkeys with induced Parkinson’s
- Treatment was successful, limited success with humans

- Transplanting stem cells
(e.g. Embryonic stems cells implanted into damaged rat spinal cord)
- Rats with spinal damage with improved mobility
Rehabilitative Training
- Monkeys recovered hand function from induced strokes following rehab training
- Constraint-induced therapy in stroke patients – tie down functioning limb while training the impaired one – creates a competitive situation to foster recovery
- Cognitive and physical activity associated with better recovery
- Facilitated walking as an approach to treating spinal injury
Learning
The acquisition of skill or knowledge (people who study learning deal with how experience changes the brain)
Memory
The expression of what you have acquired; the "record" of a learning process (people who study memory deal with how changes in the brain as a result of experience are stored and reactivated)
Standard consolidation theory
- Short-term memories are temporarily stored in the hippocampus
- In order for the memory to be retained and for the information to be retrieved and used later (long-term memory), it must be transferred to a more stable cortical system
- This process is called consolidation
Mechanisms of learning and memory
- The basis of long-term memory lies in the ability of neurons to make lasting changes in synaptic efficiency (the efficiency of synaptic transmission between neurons)
- Strengthening of synapses (enhanced synaptic efficiency) by repeated stimulation, a process called long-term potentiation (LTP), is one of the major and widely accepted cellular mechanisms underlying learning and memory
Hippocampal hebbian LTP
- Most LTP research has focused on NMDA-receptor-mediated LTP in the hippocampus, but LTP is also mediated elsewhere by different mechanisms
- Hippocampal LTP follow Hebb’s rule, which proposes that increase in synaptic efficiency arise from repeated and persistent stimulation from the presynaptic to the postsynaptic neuron
LTP (3-Part Process)
1. Induction (min)
- Can be experimentally induced by a single high-frequency electrical stimulation
It involves the protein kinase activity but no protein synthesis (protein synthesis independent)
2. Maintenance (min, hours)
3. Expression (hour)
- Triggered by a series of high frequency electrical stimulation
- Involves the synthesis of new proteins (receptors and other proteins that contribute to the growth of new synapses)
Induction of LTP
1. Glutamate (the main excitatory neurotransmitter in the brain) that are released from the pre-synaptic terminal binds to AMPA receptors and NMDA receptors.
2. AMPA receptors are activated, allowing Na+ to enter the cell. NMDA receptors are blocked by Mg2+.
3. The influx Na+ locally depolarizes the cell; this depolarization removes Mg+ blockade on NMDA receptors and allows for Ca2+ to enter through these receptors.
Note: BOTH glutamate binding and partial depolarization of neuron must be met in order for NMDA receptors to respond maximally
4. Ca2+ activates a number of protein kinases that may induce changes causing LTP
Maintenance and expression of LTP
- Both pre- and post-synaptic changes causing LTP are involved
1. Insertion of additional AMPA receptors at synapses (post)
2. Phosphorylation of AMPA receptors, which results in increase in receptor activity and ion channel conductance (post)
3. Increased neurotransmitter release probability (pre)
4. Synthesis of new receptors and proteins involved in structural changes
- Structural changes underlying LTP include actin cytoskeletal reorganization, growth of new dendritic spines, enlargement of preexisting spines, splitting of single postsynaptic spines into two functional synapses
Strengthening of synapses by LTP
Initial state --> initiated stimulation --> Potentiated
Evidence of LTP from animal models
- Learning can produce LTP-like changes
- Drugs that impact learning often have parallel effects on LTP
- LTP can be elicited by high frequency electrical stimulation of presynaptic neuron
- NMDA receptors blockers, Ca2+ chelators, and protein synthesis inhibitors can block LTP
Morris Water Maze
- Used for mice to test hippocampus dependent/independent leaning and memory
- Hidden platform in water maze, test for spatial learning and memory
- Learning and memory is quantified by how long it takes to find the platform
Additional memory tests
- Radial arm maze
- Radial arm water maze
- Barnes maze
- T-maze
- Y-maze
Fear conditioning experiments
- Pairings of noise and shock on mice
- When noise was played, mice froze, % freezing was recorded
- Hippocampal-dependent and amygdala-dependent
Electrophysiology recordings
LTP can be experimentally induced by high frequency electrical stimulation
Cognitive map theory
Cognitive maps are mental representation of a spatial location (tells us where we are relative to the environment); the hippocampus is thought to be involved in the construction and storing of cognitive maps
Place cells
Respond to specific place in environment, thought to provide cognitive representation of the spatial environment in the brain, only begin to fire once an animal has familiarized with the spatial environment
Grid cells
Entorhinal cortex, input to hippocampus, cells with an extensive array of evenly spaced place fields (makes up a pattern reminiscent of a grid of equilateral triangles)
Patient HM
- At the age of 27, H.M. underwent bilateral temporal lobectomy to control for his epilepsy
- Both his left and right hippocampus was removed in this procedure
- The surgery controlled his epilepsy, but left him with severe anterograde amnesia
Retrograde amnesia
Loss of memory that was previously formed due to an injury
Anterograde amnesia
Loss of ability to create new memories due to an injury
Formal assessment of HM's amnesia
- Digit span + 1 test – H.M. was not able to repeat a sequence of more than 7 digits even after 25 trials (most people correctly repeat ~15 digits after 25 trials)
- Mirror drawing test: H.M. improved on this task, despite not being able to recall having performed this task before
What did we learn form HM?
- The medial temporal lobes are involved in memory
- Short-term and long-term memories are distinctly separate
- H.M.’s problem seems to be the inability to convert memories from short-term to long-term (“memory consolidation”)
- There are 2 kinds of long-term memories: explicit (declarative) and implicit (non-declarative)
Short-term memory
- Held in an active, readily available state for a short duration
- Limited capacity
- Time sensitive
Long-term memory
- Stored for a longer period of time; involves memory search
- Unlimited capacity (in theory)
Explicit (declarative) memory
- Conscious memories
- Episodic: memories of specific events/episodes (ex: what you did yesterday, your high school graduation, etc).
- Semantic: memories of facts, concepts, names
Implicit (non-declarative) memory
- Unconscious memories
- Procedural: memories of the performance of an action, skills (ex: how to tie shoes, how to ride a bike)
Where are memories stored?
- Diffusely throughout the brain
Memories stored in prefrontal cortex
Temporal order of events and working memory; tasks involving a series of responses
Memories stored in hippocampus
Spatial location and navigation
Memories stored in amygdala
Memories associated with emotional events
Memories stored in cerebellum
Sensorimotor skills
Memories stored in striatum
Habit formation
Memories stored in inferotemporal cortex
Visual inputs
What consolidates memory?
Sleep!
Short-term memories are stored in ____ changes in the activity between neurons
Unstable
Long-term memories are stored in ____ structural changes that involves the protein synthesis
More stable
Post-traumatic amnesia
People who experiences a severe blow or non-penetrating injury to the head that results in loss of consciousness (concussions) typically do not remember the events that led up to the blow or what occurred in the period thereafter, although all other memories seems intact.
- This period of amnesia suggests a temporary failure of memory consolidation due to a temporary disturbance to the brain; memories around the event are permanently lost
Reconsolidation
- Each time a memory is retrieved from long-term storage, it is temporarily held in labile (unstable) short-term memory
- Retrieved memories held in short-term are once again susceptible to posttraumatic amnesia until it is reconsolidated
- Clinical implications in treatment for PTSD (post-traumatic stress disorder)


*Keep in mind: a key molecular event for consolidation and reconsolidation (formation of long-term memory) is protein synthesis
Stages of Memory
Encoding: acquisition and consolidation
Storage: creation of a permanent record of the encoded information
Retrieval: recall the stored information in response to some cue for use in a process or activity
Pathological loss of memory disorders
-Alzheimer’s disease
Progressively severe anterograde and retrograde amnesia, some loss of short-term and implicit memories
Neurodegeneration and extensive damage to many brain areas involved in learning and memory (hippocamps, prefrontal cortex)

-Korsakoff’s syndrome
Associated with extensive alcohol consumption
Extreme confusions, personality changes, and progressively severe anterograde and retrograde amnesia
Damage to thalamus, hypothalmus, neocortex, hippocampus, and cerebellum
Decision making
Evaluate given information, arrive at a judgment, and, based on this, make an optimal choice among alternatives
Conventional economic theory assumptions
1. Compute value of options
2. Choose optimal option based on rational processing
3. Errors are influenced by “market forces”
Behavioral economic assumptions
1. Rational thinking and market forces don’t account for all decision-making behaviors
2. Irrational behavior exists
- It is systematic, rule-based
- Therefore predictable
Dual-Process View of Decision Making
Humans operate in two different reasoning modes:

- Analytic Mode
deliberate
conscious
slow
verbally mediated

- Heuristic Mode
automatic
non-conscious
fast
nonverbal
Heuristics: Cognitive Shortcuts
We are hard-wired to move from effortful to effortless
- A way of achieving cognitive efficiency
- Supported by the neural system
- May come at a cost
Context and relativity
1. We don’t make decisions in isolation
2. Number of choices makes a difference
3. Type of choices makes a difference.
Anchoring and Imprinting
1. We have an initial impression, which is affected by a number of factors
2. Initial opinion is adjusted to arrive at final judgment
- Initial impression provides anchor for future assessments
- Bias towards initial opinion leads to inadequate adjustments
- Effects can be long lasting

Example: Real Estate
- Selling: Initial price biases future offers upwards from appropriate value
- Buying: if initial house viewed is expensive, price range of buyer is adjusted upwards.
Herding
- If we see someone else has made a decision, we “decide” it is the best decision
- Initial decision anchors future decision
Self-herding
- If we have made a decision (even on impulse) we are more likely to repeat that decision (even if it is not the best one)
- In essence, we demonstrate herding behavior with ourselves (if we made the decision before, it must have been the right decision)
Loss Aversion
- People react more strongly to losing than to winning
- Some estimates based on research are that the effect is 2-fold
- Leads to risk aversion—people are more likely to choose small, sure gains over large gains coupled with possibility of loss
- May explain the “endowment effect”: the finding that people value items they own more highly than the same items that they don’t own
- Also the concept behind the marketing ploy of “free trials”
The unreasonable benefit of nothing
- Most people gravitate towards the idea of getting something for no cost, even if the ultimate gain is less
- Pattern is similar across all ages (young children and adults)
- Violates most economic theory
- Pervasive in marking
NeuroEconomics
The multi-disciplinary study of decision making, especially how decisions shape the brain and how the brain constrains decision making
Game Theory (Interactive Decision Theory)
The study of strategic decision making in an interactive context
Aim is to create mathematical models that predict cooperation and conflict
Has been used in economics, political science, and psychology, biology.
Initial research on zero-sum games
When one person's net gain exactly equals net loss of the other player.
Risky Decision Making in the Brain
(Gonzalez, Dana, Koshino, and Just (2005))
- fMRI while considering the “Asian Disease problem”
*Results
- Frontal and parietal activity, indicating involvement of immediate memory and mental imagery
- Gains frame: Brain less active when faced with certain alternative, relative to risky alternative
- Loss frame: Brain less active when faced with risky alternative relative to certain alternative
Cost Benefit Choices and the Brain
- Research has linked the lateral habenula to depression and avoidance behavior, but a recent study suggests it is involved in making cost-benefit decisions. .
- Study: rats had to choose between a small frequent reward (1 food pellet) and a less reliable, but potentially larger reward (4 pellets)
- Rats chose the larger reward only when there was very little waiting
- Pattern typical of humans: larger rewards when “costs” are low and smaller rewards when the “risks” are higher.
- Experimental Manipulation: When the lateral habenula was ablated in the rats, they chose either option at random.
Implications of Cost Benefit Choices and the Brain
- Deep brain stimulation, which is thought to inactivate the lateral habenula, has been reported to improve depressive symptoms in humans
- Findings suggest these improvements may not be because patients feel happier, but because they no longer care as much about what is making them feel depressed
Timing of Decisions
- Different areas of the brain activate during decision making, depending on timing and nature of decision
- Research has demonstrated that the orbitofrontal cortex is responsible for value-based decisions, but only those made in the moment (impulsively)
- If the decision has already been made before, the OFC isn’t activated
Brain lateralization of language
Highly left lateralized
Broca's area
Speech production
Wernicke's area
Speech comprehension
Wernicke's aphasia
- Damage to left superior temporal gyrus
- Impaired comprehension
- Fluent speech, but meaningless
Pure word deafness
- Perceptual deficit specific to speech
- Normal speech production
- Literally cannot understand a single word
- Auditory comprehension at chance level, writing and music comprehension normal
Broca's aphasia
- Intact comprehension, impaired speech production
- Effortful, non-fluent speech
- Damage to left inferior frontal gyrus, some suggest must be insular damage as well
Conduction aphasia
- Good comprehension, good production
- Problems with repetition
- Caused by damage to the arcuate fasciculus
Traditional View: The Evidence
- There is a lack of evidence that damage to various parts of the cortex has the expected effects.
- Surgery that destroys only Broca’s area has no lasting effects on speech.
Effects of Cortical Damage on Language Abilities
No aphasic patients have damage restricted to Broca’s or Wernicke’s areas.
Aphasics almost always have damage to subcortical white matter.
Large anterior lesions are most likely to produce production deficits.
Large posterior lesions are most likely to produce comprehension deficits.
Tests of Cerebral Lateralization
- To determine which hemisphere is dominant
- Sodium amytal test: anesthetize one hemisphere and check for language function
- Dichotic listening: report more digits heard by the dominant half
- Functional brain imaging: fMRI or PET used to see which half is active when performing a language test
Lateralization of Attention
- Attention is not as lateralized as language
- Both hemispheres involved in attending to contralateral visual field, but RH also involved in attending to ipsilateral visual field
Hemispatial Neglect
- Difficulty attending to left visual field
- Not a deficit in low level visual processes
Corpus callosum
- Largest cerebral commissure
- Transfers learned information from one hemisphere to the other
- When cut, each hemisphere functions independently
Commissurotomy in Human Epileptics
- Commissurotomy: many of those who undergo the procedure never have another major convulsion.
- Sperry and Gazzaniga: developed procedures to test split-brain patients
Differences between the Left and Right Hemispheres
- For many functions there are no substantial differences, between hemispheres.
- Key point: Lateralization of function is statistical rather than absolute.
Analytic-synthetic theory
- All theories propose that it’s better to have brain areas that have similar functions in the same hemisphere
- Vague and essentially untestable
- “The darling of pop psychology”
Flexors vs extensors
- Flexors (bend or flex a joint - excitatory) vs extensors (straighten or extend - inhibitory)
Synergistic vs Antagonistic muscles
Synergistic muscles (any two muscles whose contraction produces the same movement) vs antagonistic muscles (any two muscles that act in opposition to each other)
Fast muscle fibers vs slow muscle fibers
Fast fibers (strong and quick movements but fatigue easily) vs slow fibers (more vascularized so have more staying power, steady and sustained movement)