Neuropsychology Deck Motor Systems On Flashcards

1
Q

Behavior: Definition

A

Purposeful, goal-directed body movements resulting from controlled skeletal muscle activity

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2
Q

Subcortical Motor Structures

A
  • Basal Ganglia: outputs back to cortex; modifies or changes grip force exerted by muscles under control of the cortex
  • Cerebellum: computational machine
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3
Q

Path of Movement stimuli to movement

A
  1. visual information locates target EXAM
  2. Frontal-lobe motor areas (pre-frontal cortex) plan the movement and issue the command
  3. Spinal cord carries the information to the limb
  4. Motor neurons carry the message to the muscles
  5. Basal ganglia judges grip force (if hand movement)
  6. Cerebellum corrects movement errors
  7. Spinal cord carries sensory info to brain
  8. Sensory cortx receives info: move accomplished
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4
Q

Cortical Path for Movement

A
  1. Posterior cortex provides sensory info to frontal cortex
  2. Prefrontal cortex plans movement in advance of the behavior
  3. Premotor cortex organizes movement sequences
  4. Motor cortex porduces specific movements (then modified by brainstem) EXAM (eg where do visually guided behaviors originate?)

Note: M1 in anterior parietal lobe next to posterior frontal lobe so close - no need for white matter tract

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5
Q

Hierarchy of Motor Control

A
  1. Posterior Cortex: provides information to Frontal Lobe (sensory/perceptual info to plan goals)
  2. Prefrontal Cortex: (most anterior part frontal cortex) - cognitive activity that may result in behavor or inhibition of behavior damage: disinhibition
  3. Motor Cortices: a) Primary b) Premotor c) Supplementary; all in frontal lobes and project directly to spinal cord via corticospinal tract
  4. Brain stem: integrates visual and vestibulary info with somatosensory input to modify movement: a) RAS b) Vestibular Nuclei - position c) Inferior olivary complex -coordination via projections to cerebellum
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6
Q

Basal Ganglia, Cerebellum & Movement

A
  • Basal Ganglia: large cluster of neurons and gets input from many cortical areas; projects to thalamus then to cortex re motor planning; modulates muscle force
  • Cerebellum: input from the spinal cord, projects to brainstem and thalamus, improves movement accuracy: compares descending motor command with info about resulting motor action
  • damage: wide stance walking - can’t maintain coordinated movements to preven falling
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7
Q

Central Pattern Generators

A
  • local circuits of interneurons in spinal cord and brainstem that drive rhythmic patterns of movement
  • organize muscle movements (e.g. alternating stepping movements) even in absence of input from the cerebral cortex
  • one central pattern generator sent to same muscles in both limbs can create mirror images
  • generates movement activity spontaneously via input from peripheral sensory neurons that adjust as needed
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8
Q

Motor Neurons

A
  • Upper motor neurons: layer V and VI of primary motor cortex; heavily myelinated - project to spinal segments &synapse with neurons in grey matter of sp. cord segment assoc. with that partic. muscle it is designed to control
  • Lower motor neurons: in grey matter of spinal cord; project out of sp. cord via ventral roots and synapse with target muscles (efferent)
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9
Q

Cortico-motoneuronal System

A
  • Hand control in primates: Direct, rapid and monosynaptic connections between the upper and lower motoneurons
  • Relatively Independent Finger Movements(RIFMs)
  • Some primates can only move fingers together like a claw (fewer cortico-motorneurons)
  • Extremely fast and no need for feedback (no interneurons)
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10
Q

Damage to Motorneurons

A
  • Upper motorneuron:
    • weak or absent voluntary movements
    • increased muscle tone (rigidity)
    • altered reflexes
  • Lower motorneuron:
    • reduced muscle tone
    • weak stretch reflex
    • atrophy of affected muscles
    • fibrillation
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11
Q

Sliding Filament Theory

A

Two myofibrils: actin and myosin

Contraction: rotate the cross-bridges of the myosin along the Actin strands causing them to slide along one another (like a rowing boat)

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12
Q

Muscle Wasting

A

if no synapsing of muscle and lower motoneuron at the neuromuscular junction - if not the muscle cannot retain its normal muscle tone (not always purposeful, can have resting rate of production of synapses)

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13
Q

Neuromuscular Junction

A
  • ‘synapse of pre-synaptic membrane of motoneuron and the postsynaptic membrane of muscle fiber
  • motoneuron releases acetylcholine, which binds to nicotinic ACh receptors which depolarizes the muscle fiber and causes a cascade that results in muscle contraction
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14
Q

Monosynaptic Reflex

A
  • direct connection between a sensory and a motor neuron - only one synapse
  • these are rare
  • example: knee jerk reflex
  • there is no interneuron in the circuit
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15
Q

Polysynaptic Reflex

A
  • more than one synapse because an interneuron lies between the incoming sensory neuron (in the integrating centre in grey matter) and the outgoing motor neuron in the circuit
  • more flexibility in the response
  • e.g.: need to flex bicep but to do so need to inhibity the stretch of the tricep which would fight against it so add an inhibitory interneuron to connect the bicep motor neuron to the tricep motor neuron and it will help to override the tricep stretch reflex
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16
Q

Reflex Arc

A
  • circuit for connecting inputs to outputs
  • sensory neuron makes an excitatory connection to a motor neuron so that when the sensory neuron stimulated it activates the motor neuron
  • if muscle being overstretched the sensory neuron will alert the motor neuron to contract the muscle
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17
Q

5 Components Reflex Arc

A
  1. Somatic Receptors (skin, muscles, tendons)
  2. Afferent nerve fibres - carry signals from somatic receptors to dorsal horn (sp. cord) or brainstem
  3. Integrating Center - synapse of the neurons
  4. Efferent nerve fibres - carry motor info from spinal cord via ventral route to signal muscles
  5. Effector muscle - innervated by efferent nerve fibre, carries out the response

Need all 5 for a controlled reflex arc; fixed innervation ratios but can modify with experience and each muscle ratio varies depending on degree of control exerted over the muscle by the nervous system

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18
Q

Stretch Receptors

A

Two types:

  1. In series with the muscle - when the muscle contracts it puts force on the golgi tendon organ then it signals the level of force of the muscle
  2. In parallel with the muscle - it can’t tell the force, only the length of the muscle - muscle spindles

The control of muscle is necessary or else you would seize or convulse

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19
Q

Muscle Agonists/Antagonists

A
  • Opponent pairs
  • Agonists: muscles that work together
  • Input: heavily myelinated large caliber axons project to spinal cord and synapse with myelinated lower motorneurons, exit ventral root & go to muscle
  • Feedback: from muscle and tendon in via dorsal root from muscle spindles (length) and golgi tendon organs (force) - feeds into position of body part
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20
Q

Flacidity, Hypokinesias, Hyperkinesias

A
  1. Flacidity: floppy limb due to damage to lower motor neurons (disconnected from sp. cord)
  2. Hypokinesias: decreased ability to produce body movement - anormal basal ganglia activity (Parkinsonianism)
  3. Hyperkinesias: exaggerated unwanted motor movements (Tourette’s, Huntington’s Chorea) - also associated with basal gangia
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21
Q

Innervation Ratio

A
  • average # of muscle fibres that are innervated by a single motor neuron
  • low ratio: small muscles for fine motor skills (3:1 for extra ocular muscles). For every 3 muscle fibres there is 1 motor neuron axon that synapses to the 3
  • large ratio: for power muscles - e.g. calve has 2000:1 ( every 2000 muscle fibres there’s 1 motor neuron that synapses so not much control)
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22
Q

Corticospinal Tract

A
  • Corticospinal tract: primary motor pathway CNS
  • originates in precentral gyrus (M1) plus other cortical areas (corticospinal pathway)
  • Axons go from layer V M1 into the internal capsule then forms cerebral peduncles then the decussation of the pyramids (white matter structures of medulla)
  • Lateral Corticospinal Tract: M1 to decussate in pyramids then descend contralaterally for fine muscle control (limbs, digits)
  • Ventral Corticospinal Tract: M1, descend ipsilaterally to decussate on spinal segment (larger muscles of trunk)
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23
Q

Steps for Neural Control of a Muscle

A
  1. Lower motorneuron excites muscle
  2. The neuron dumps Ach into synaptic cleft of neuromuscular junction
  3. Ach binds to nicotinic receptors on the postsynaptic membrane of the muscle
  4. Muscle contracts
  5. Muscle spindle is strained and it sends afferent signal into the spinal cord via dorsal root
  6. This creates FEEDBACK
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24
Q

Motor Cortical Magnification Factor

A
  • volume of cortex devoted to a body part is NOT proportional to its size but to the complexity of its behavioural repertoire (what it can do)
  • Smaller the skeletal muscles, larger amount of cortex devoted to controlling it (facial muscles, oral cavity, hands)
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25
Q

Upper Motor Neurons

A
  • Originate in Layer V of primary motor cortex
  • 2 separate tracts:
    • Corticospinal Tract: Pyramidal Tracts; pass through pyramids in medulla, terminate in ventral horn and synapse with lower motor neurons - fine limb movement
    • Corticobulbar Tract: originates in M1; terminates in pons and medulla (voluntary control of facial and jaw muscles, swallowing, tongue movem) - output via cranial nerves to muscles of face - speech, eating, facial gestures
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26
Q

Penfield’s Montreal Procedure

A
  • stimulated areas in S1 and M1
  • Created the “homunculus” as a learning aid
  • Large areas of S1 devoted to tip tongue, tip index finger, tip thumb
  • Large areas of M1 devoted to control of thumb and forefinger, tongue, lips
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27
Q

Movement Sequences

A
  • dictionary of movement sequences - lexicon
  • 3 aspects of volitional behavior:
    • part of body to be moved - from proprioceptive feedback from receptors, joints, etc (low level)
    • spatial location to which movement directed (visual feedback - high level)
    • Function to be achieved (high level feedback - whether you have achieved your goal)
  • Feedback loops in all 3 and each different
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28
Q

Mirror Neurons

A
  • neurons that fire when we see others make a movement
  • Can be used to imitating and understanding others’ actions
  • they encode a complete action
  • are mirror cells in premotor area (which plans & organizes the behaviour before execution)
  • generally located in left hemisphere
  • important for gesturing and verbal language
  • import for recog of emotion (facial motor patterns)
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29
Q

Brainstem and Motor Control

A
  • Sends info re: posture, balance, control of autonomic nervous system
  • (reflexive and inate) eating, drinking, standing upright, walking, grooming
  • gateway into consciousness & planning and motor control
  • NON-VOLITIONAL - so not interrupted, reflexive (even if decorticated, animal still walk or groom)
  • eating: hypothalamus (re cessation) so if slow down, hypth will kick in & stop you
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30
Q

Basal Ganglia & Movement

A
  • Control of movement force
  • How?
    • receives signal from motor cortex, limbic cortex & nigrostriatal dopamine pathway (and sends them back via the Thalamus) - so, no direct connection between B.G. and spinal cord
    • sends signals to motor cortex and substantia nigra in brainstem
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31
Q

Basal Ganglia Pathways

A
  1. Direct Pathway (positive feedback loop): Cortex to Putamen to Globus Pallidus internal to Thalamus and back to excite cortical activity (result: amplificaiton)
  2. Indirect Pathway (negative feedback loop): Cortex to Putamen to Globus Pallidus external to Subthalamic Nucleus to Globus Pallidus internal to Thalamus and back to inhibit cortical activity (NOTE: there are at least 2 additional synapses in the indirect pathway so latency into cortex is slower)
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32
Q

Disorders of the Basal Ganglia

A
  1. Parkinson’s: loss of dopamine cells in the substantia nigra; muscular rigidity / shuffle walk / hypokinetic symptoms / lack facial expression (corticobulbar tract issue)
  2. Huntington’s Choria: hyperkinetic; destroys cells in caudate putamen; gentic, exaggerated movements (try to control anti-gravity musculature)
  3. Tourette’s Syndrome: damage to caudate putamen; unwanted tics and, at times, vocalizations (expression & speech are corticobulbar)
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33
Q

Cerebellar Damage

A
  • loss of timing and perception
  • problems with movement accuracy
  • calibrates the actions the body wants to perform
  • show no evidence of learning if lesioned (i.e. can’t acquire the ability to correct motor movement to perform a visually guided behavior)
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34
Q

7 Deficits w/ Cerebellar Lesions

A
  1. Ataxia: wide gait walk (from alcoholism)
  2. Dysmetria: loss of calibration for objects within reach
  3. Dysdiadochokinesia: loss of control to do alternating movement of limbs (like flipping hands over together)
  4. Asynergia: absence of coordin. muscles/body parts
  5. Hypotonia: reduction in muscle tone
  6. Nystagmus: disordered eye movement - oscillations, wiggling - try to fixate but can’t, no fovia feedback
  7. Action Tremor: rhythmic oscilatory movement (e.g. resting hand tremor or head tremor, not volitional)
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35
Q

Consciousness Definition

A

Awareness of external objects and thoughts or sensations arising from within one’s self

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36
Q

Orienting Reflex

A
  • reflexive responses that lead to the evaluation of the novelty of an external stimulus (unpredictable)
  • the OR habituates with stimulus repetition (matched against a pre-exising neural code)
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37
Q

Mental Chronometry

A
  • measures reaction time - either simple reaction time or choice reaction time (greater latency)
  • Processing cost: more complex, more time it takes to react, more “cost”
  • Difference between the two latencies of simple and choice reaction times is indicative of how much time the brain takes to make the decision
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38
Q

Functional Imaging

A
  • Flow of H2O (blood mostly water) and measure the brain metabolism of participant while they are performing a task versus at rest
  • will have increased blood flow in areas where there is more metabolic demands (activity)
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39
Q

Oddball Paradigm

A
  • Atttention on 2 stimulus - one infrequent with high info content, one frequent with low info content
  • The oddball stimulus will evoke a different response than the frequent stimulus
  • Selective attention task
  • used to assess affect of drugs on attentional capacity of a person to volitionally switch their attention
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40
Q

Theory of Attention and Glucose / ATP

A

Attention may be a mechanism for allocating metabolic resources (oxygen, glucose) to specific neural areas to conserve energy (need more glucose to make more ATP etc.)

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41
Q

Endogenous / Exogenous Attentional Triggers

A
  • Endogenous triggers: hunger emotion fatigue, fear
  • Exogenous triggers: familiar face, loud sound, moving object in visual field
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42
Q

Rubin’s Vase

A
  • can’t see the vase and the face at the same time - one or the other
  • hard to control which one you look at
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43
Q

Hemineglect

A
  • Failure to attend to one half (usually left) of the visual field, divided vertically; it’s a disorder
  • typically damage to right parietal lobe
  • a deficit in attention to and awareness of one side of the field of vision i
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44
Q

Biased-Competition Model of Attention

A
  • neural processes compete with each other for metabolic resources (vision, hearing, taste, smell…)
  • consciousness has limited capacity so not all enters so instead resources are allocated
  • so..previous experiences or attitudes or instructions (i.e. biases) can affect which you “attend to” (stop sign warning example)
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45
Q

Definition of Learning

A
  • relatively permanent changes in behavior produced by experience
  • Learning creates declarative and non-declarative memories
  • most important evolution for learning: speech - transfer of info from one NS to another (or written) hs changed the nature of experience
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46
Q

Perceptual Learning

A
  • Identify objects and situations
  • naming things
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47
Q

Stimulus-Response Learning

A
  • making a response when a particular stimulus is present
    • classical conditioning
    • operant conditioning - instrumental learning
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48
Q

Motor Learning

A
  • forming new circuits in the motor system
  • basis for all behaavior
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49
Q

Relational Learning

A
  • identifying connections between and among stimuli
  • integration of knowledge
  • can include thoughts as well - i.e. connections between “learned things”
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50
Q

Stimulus Response Learning

A
  • always have an antecedant stimulus and response
  • always causal relationship
  • perception detects the stimulus and the motor system makes elicits a behavior and the respose is the consequence of that behavior
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51
Q

Classical Conditioning

A
  • Pair two different stimuli with a reflexive response (i.e. UCS that produces UCR)
  • Add a NS (neutral stimulus)
  • then…pair the NS and the UCS many times
  • when the NS alone generates the “now” CR (previously UCR) you have :conditioning
  • ie: start with a behav. already present and pair it with something that does not normally elicit that response to create a conditioned response
  • Pavlov
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52
Q

Operant/Instrumental Conditioning

A
  • Pair a behavior with a consequent stimulus
  • If stimulus reinforcing: behavior more likely to occur in the future (positive reinforcement)
  • If stimulus punishing: behavior less likely to occur in the future (negative reinforcement)
  • reverse of Classical Conditioning

Skinner Box

manipulate the eviron. to increase probab. of the behavior - when rats got food, reinforced; increases prob. they will press lever again

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53
Q

Fixed / Variable Intervals

A

Fixed Interval: get reinforced every “x” minutes (or every e.g. 2 weeks with pay check)- get a dip in “curve” in between then up again in anticipation - no incentive to work faster or produce more

Variable Interval: behavior reinforced on an inconsistent schedule (interval: time between reinforcements) so have to perform the behavior consistently “just in case”

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54
Q

Variable/Fixed Ratio Schedules

A

Variable Ratio Schedule: response is reinforced after an unpredictable (or average) number of responses: creates a steady, high rate of responding (slot machines); reinforcement dependent on your behavior

Fixed Ratio Schedule: response in reinforced after a specified # of responses - produces a high, steady rate of responding (brief pause after reinforcement) cuz want the reinf. as soon as possible (car salesman example)

Ratio: the amount of responses

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55
Q

Long Term Potentiation

A
  • changes synaptic efficiency and that increases the probability that when “x” is present the circuit will fire
  • Hippocampus and parahippocampal area important for long-term potentiation
  • used to explain long term memory
  • connections between neurons strengthen
  • first 24 hours the LTP can be interfered with (e.g. shock) - rat on pedestal
  • “long-lasting enhancement in signal transmission between 2 neurons after repeated stimulation”
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56
Q

Perforated Synapses

A
  • After LTP can be generated (production of 2 receptor areas for synapse) to increase the probability of binding
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57
Q

Mirror Neurons

A
  • neurons that fire when the individual is watching an action being performed
  • could be the neurological basis of observational learning
  • e.g.: baby mimicking a facial expression
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58
Q

Memory Stages

A
  1. Sensory memory - brief (.25 of a second) representation of a stimulus
  2. Short Term Memory - working memory
    1. limited capacity - 7 items
    2. Duration is about 30 seconds
  3. Long Term Memory - large capacity and long duration - NO limit at all

Note: a) In order to demonstrate learning, you have to show you remember something and b) in order to demonstrate memory, have to demonstrate the person didn’t know it before

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59
Q

Classifications of Memory

A
  1. Declarative memory - explicit and readily available to conscious recollection
  2. Episodic – memories of events
  3. Semantic - memories of facts
  4. Nondeclarative memory - implicit, unconscious knowledge
  5. Perceptual – previously experienced stimuli
  6. Motor (procedural) – learned behavioral sequences
  7. Stimulus-response – learned responses to specific stimuli
60
Q

LT Memory and Reconsolidation

A
  • Reconsolidation: consolidate a previously stored memory that you recall
  • Can change something on the recall
  • Why eye-witness testimony unreliable
  • LTM is coded into cetegories and stored
  • REM sleep may play into categorizing new items within LTM
61
Q

Recogntion/Recall/Relearning

A
  • Recognition: cue is matched against a LTM (face?)
  • Recall: general cue is used to search memory (exam)
  • Relearning: learn material a 2nd time - less time to relearn 2nd time shows memory
62
Q

Acetylcholine and Memory

A
  • acetylcholine is the primary neurotransmitter which nerves use to signal muscles to initiate or cease movement; activates pain responses, regulates sleep
  • involved in encoding of new episodic memory
  • lost early in Alzheimer’s - memory loss
  • cholinergic pathway involved in memory/learning
63
Q

Limbic System and Memory

A

EXAM - know 7

  1. Thalamus
  2. Hypothalamus
  3. Epithalamus
  4. Frontal Cortex
  5. Olfactory Cortex
  6. Reticular Formation
  7. Amygdala

Events that occurred that produce emotion are recalled more accurately & more efficiently than others

64
Q

6 Functions of Limbic System

A
  1. Preservation of the Individual
    1. fight or flight
    2. Eating / Drinking
  2. Preservation of species
    1. Sexual behavior
    2. Social Behavior
  3. Emotional behavior
  4. Memory
  5. Emotional valence of sensory stimuli
  6. Motivation
65
Q

Episodic Memory Processing

A
  1. Sensory information
  2. Short term memory
  3. Rehearsal - produces consolidation
  4. Long term memory

Note: Don’t rehearse episodic memory but DO rehearse procedural memory (i.e. every time you use cutlery you are re-learning / rehearsing)

66
Q

Varieties LTM

A
  • Explicit / Declarative: (conscious recall)
    • Semantic Memroy (general knowledge - e.g. what had for breakfast, facts, events)
    • Episodic Memory (personal experiences)
  • Implicit / Nondeclarative: (no conscious recall)
    • procedural memory (learned actions/skills)
    • not subject to forgetting
    • e.g. piano playing, riding bike, using utensils
    • stimulus-response / motor memories
67
Q

Hippocampal Place Cells

A
  • pyramidal cells within hippocampus sensitive to spatial location where episodic learning occurred
  • i.e.: you code for “place” - dog pees on pole leaving olifactory clue to enhance episodic memory in other dogs
  • Each place cell responds maximally to one location, known as its spatial receptive field
68
Q

Serial Position Effect

A
  • Tendency of a person to recall the first and last items in a series best, and the middle items worst
69
Q

Theories of Forgetting

A
  • Proactive interference: old info interferes with recall of new info
  • Retroactive interference: new info interferes wtih recall of old info
  • Decay: memory trace fades wtih time
  • Motivated forgetting: loss of painful memories
  • Retrieval Failure: info still in LTM but can’t be recalled because recall cue is absent
70
Q

Reasons for Inaccuracy of Memory

A
  • Source amnesia: attribution of a memory to the wrong source
  • Sleeper effect: piece of info from an unreliable source is initially discounted then later recalled (but the source is forgotten)
  • Misinformation effect: incorporate outisde info into our own memories
71
Q

Anterograde / Retograde Amnesia

A
  • Anterograde Amnesia: difficulty forming new memories for events that happen after brain trauma; loss of relational learning ability; no new declarative memories
  • Retrograde Amnesia: inability to recall events that happened prior to the trauma, previously formed declarative memories
72
Q

Korsakoff’s Syndrome

A
  • severe anterograde amnesia associated with chronic alcoholism caused by a vitamin B1 deficiency (needed for laying down new memories)
  • Also confabulate - unknowingly make up false episodic memories - they think it’s true
73
Q

Henry Gustav Molaison’s Case

A
  • surgical treatment for epilepsy: bilateral removal of parahippocampal gyrus and amygdala, 2/3 hippocampus medial temporal lobe
  • perpetually lived in the “now”
  • dense anterograde amnesia
  • no longer convert short term to LTM (episodic)
  • began to lose recognition of his own face (changed as he got older so did not recognize himself)

BUT: Procedural memory was fine

74
Q

Memory impairment re future

A
  • The “future” requires memory
  • ability to predict what you are going to do will be impaired because it requires recall - search memory about what you “were going to do” at that time
  • also can’t prepare to reach goals if you can’t remember what they are - would not know to study for an exam if you did not remember you had one
75
Q

Anatomy of Speech Production

A
  • Hypophonality: Whispering
  • Air goes from longs to larynx then vibrates at different frequencies, producing voice pitch
76
Q

Formants

A
  • A formant is a concentration of acoustic energy around a particular frequency in the speech wave
  • position and height depends on the position of the tongue in the oral cavity (which is controlled by the cranial nerves
  • Formant transitions carry speech information
77
Q

Producing Speech Sounds

A
  • Limit to ability you can produce speech sounds over long distances eg. use vowels to howl
  • ability to speak depends on your ability to rehearse the words over and over again and learn how to articulate them (re motor process)
  • Neural output from language centers in brain then through speech centre in frontal lobes then to motor nerves of speech apparatus
78
Q

Innervation of Face / Oral Cavity

A
  • LOW innervation ratio re these parts - (i.e. for fine motor coordination) e.g. 3:1 for the eye
79
Q

Cranial Nerve V: Trigeminal Nerve

A
  • Facial muscles
  • Mandible: conrol of jaw, tensor veli palatini for back of throat and tensor tympani of middle ear
  • Sensory info from head, jaw, face and sinuses AND tactile sensations from ANTERIOR 2/3 of tongue
80
Q

Cranial Nerve #VII Facial Nerve

A
  • At junction of pons and medulla
  • innervates ALL muscles of facial expression
  • muscles in upper part of face are controlled by bilateral innervation from upper motor neuron tracts (hard to raise just one eyebrow)
  • muscles in lower part of face are controlled ONLY by contralateral innervation
  • Sensory component mediates taste NOT tactile
81
Q

Neural Basis of Smiling

A
  • UPPER motoneuron: from corticobulbar tract - voluntary movements of cheeks and lips CN VII (a lesion won’t affect involuntary expression as controlled by exrapyramidal tract)
  • LOWER motoneurons: a lesion will paralyze entire side of face so neither volun. or involun. input from upper motoneurons will generate facial expression
82
Q

Cranial Nerve VIII - Acoustic Nerve

A
  • Originates in the medulla
  • involved in the feedback process with the reception and production of speech, creating speech sounds (without the feedback: can’t tell what you are doing)
  • Hearing is critical as feedback for speech learning and speech production
83
Q

Cranial Nerve IX - Glossopharyngeal Nerve

A
  • Sensory aspect carries info from posterior 1/3 of tongue, velum, pharynx and tonsils (ie. gag reflex)
  • activates the stylophangeus muscle - swallowing reflex
84
Q

Cranial Nerve X: Vagus Nerve

A
  • Originates in medulla
  • One of the motor nuclei of CNS controls the phyaryngeal constrictor muscles and the larynx
  • Damage: hypophonality (breathiness)
  • Also innervates the palate
85
Q

Cranial Nerve XI: Spinal Accessory

A
  • originates in medulla
  • innervates the muscles that raise the velum - back of the throat (which controls the coupling of oral and nasal cavities) - so they are interconnected for lots of sounds like “m”
  • Controls muscles of neck
86
Q

Cranial Nerve XII: Hypoglossal

A
  • originates in medulla
  • controls tongue movement
  • lesions of lower M.N. of this nerve result in non-symmetric eversion of the tongue (sticks out to the side)
87
Q

Psycholinguistics / Neurolinguistics

A
  • relationship between language (grammer not actual speech) and the brain
88
Q

Receptive / Expressive Language

A
  • Receptive Language: mediated by left temporo-parietal region (left hemisphere)
    • in 95% of right handers and 75% left
    • Wernicke’s area - no clear boundary, different in everyone
    • lesion studies not best because anatomical differences in this area in everyone
  • Expressive Language: mediated by region in left inferior frontal gyrus
    • Broca’s area is confined to the pars opercularis
    • Arcuate Fasciculus joins Broca and Wernicke
89
Q

Arcuate Fasciculus

A

3 Pathways: (if damaged get speech symptoms)

  1. Deep AF pathway: connects Wernicke and Broca
  2. Shallow pathway 1: connects frontal / inferior parietal cortex
  3. Shallow pathway 2: connects Wernicke with inferior parietal cortex
  • auditory processing affecting language, music perception / motor programming of speech sounds
  • language processing in the left hemisphere
90
Q

Aphasias

A
  1. Conduction Aphasia: patient can’t repeat unfamiliar words (damage to arcuate fasciculus)
  2. Expressive Aphasia: inability to generate normal speech (damage to frontal cortex Broca’s)
  3. Fluent Aphasia: problems understanding spoken and written language - Wernicke’s - garble
  4. Global Aphasia: difficulty communicating orally AND with comprehension
  5. Deep dysphasia: word repetition deficits
  6. Transcortical sensory aphasia: impaired comprehension, naming, reading and writing
  7. Transcortical motor aphasia: transient mutism
91
Q

Reading Disorders

A
  • Dyslexia: Acquired and Developmental
    • Acquired: reading impairment in person who previously had normal reading ability
    • Developmental: never acquire normal level of reading during childhood

Both associated with structural and functional brain abnormalities

92
Q

4 Acquired Dyslexias

A
  1. Visual word form dyslexia: impaired sight reading
  2. Phonological dyslexia: trouble reading pseudowords and non-words
  3. Surface dyslexia: - what read and say not same, extract stuff from text that isn’t there
  4. Deep dyslexia: semantic substitutions, can’t read non-words or abstract words
93
Q

Linguistic Info Processing Routes

A
  1. Grapho-phonological (indirect) route: slow down the word and sound it out - get meaning from the sound (Teporal Lobe)
  2. Lexico-semantic (direct) route: store the visual appearance of the word with meaning (may bypass Broca’s) - Occipital Temporal Junction
94
Q

Agraphia

A
  • inability to write
  1. Phonological: can’t spell non-words and real words spelled visually
  2. Orthographic: can’t spell irregular words; regular and non-words spelled phonetically
  3. Deep agraphia: can’t spell phonetically; make semantic substitutions
95
Q

Prosody/Narrative/Inference

A
  • Prosody: intonation pattern or sound of an utterance; rhythm of speech
  • Narrative: abiliy to construct/understand story line
  • Inference: ability to “fill in the blanks”
96
Q

Hebb’s Rule

A
  • Neurons that fire together wire together
  • Creates stronger connections, synaptic efficiency
  • increases the probability that when one neuron fires the others in the circuit will as well
  • related to learning
97
Q

Homo Sapiens/Homo Economicus

A
  • Homo Sapiens: relative preferences: change moment to moment
  • Homo economicus: absolute preferences: never changing regardless of the comparison - having the infinite ability to make rational decisions and rationally calculate the costs/benefits of a decision
98
Q

Prospect Theory

A
  • way people choose between probabilistic alternatives that involve risk, where the probabilities of outcomes are known
  • how people choose between prospects and how they estimate the perceived likelihood of each of these options. (often biased)
  • overweight small probabilities to guard against losses
  • they will take the “sure” gain but gamble instead over a sure loss to try & lose “0”
  • Amygdala and Insula (how to minimize loss)
  • Dorsolateral prefrontal cortex (how to maximize gains)
99
Q

Framing Effect/ Endowment Effect

A
  • Framing Effect: people can be manipulated into picking a particular option, depending on how you frame the question
    • framed as loss: choose the other
    • framed as gain: choose that one
  • So..frame the risky one in a loss context and the certain one in a gains context
  • Endowment Effect: people demand a higher price than they paid to sell an object they own as it has become endowed wtih greater value
100
Q

Delay Discounting

A
  • Rewards that occur in the future have some risk of not being collected so they are discounted
  • “Delay Discounting” reduces the value of the reward that is paid further in time (seen as a bigger risk)
101
Q

Attribution Effect

A

We explain our own behavior by the situation but other’s behavior is explained by their character

102
Q

Intuitive and Rational Decision Systems

A
  • Intuitive Decision System (System 1)
    • non-conscious, intuitive level
    • independent of measured intelligence and attentional capacity
    • can’t say why you made that decision
  • Rational Decision System (System 2)
    • conscious explicit level
    • can say why you made the decision
    • sequential processing which takes longer cuz slower
    • depends on intelligence and attention
103
Q

Rule re Lateral Frontal Lobe and Decisions

A

Info in from outside (i.e. evaluation of incoming information) is processed in the lateral region of the frontal lobe

(H. Economics) - Rational System 2 Process

Info from inside the brain (cognition) is processed in the medial part of the frontal lobe

(H. Sapiens) - rapid System 1 process

104
Q

Lateral Prefrontal Cortex and Decisions

A
  • needed to suppress irrational decisions
  • evaluates outside info (e.g. advice) - so it may inhibit an irrational decision you may have come to without the advice
  • If this area suppressed or interfered with: more impulsive decision making
105
Q

Brain and Risk Seeking Behavior

A
  • Risk Taking Behavior: Ventral Striatum and Ventromedial Prefrontal Cortex - associated with the Endowment Effect
  • Risk Adverse Behavior: Anerior Insula
  • If damage to insula…more likely to gamble
106
Q

Amygdala and Framing Effect

A
  • Amygdala more active during risky options when the question was framed as a “gain” and less active when it was framed as a “loss”

So: if you are not susceptible to the framing effect the frontal lobe will overcome the emotion associated with risk perception and instead take a more objective look

107
Q

Neural Basis: Subjective Value Decision Process

A
  • Medial areas are more active when choosing rewards that are smaller and occur sooner
  • Lateral areas are more involved when choosing rewards that are larger and later
  • Medial prefrontal cortex - internal judgements
  • Those ppl that are more patient: their subjective value does not deteriorate as fast
  • Impulsive people it decays quickly
108
Q

Evaluation - Orbitofrontal Cortex

A
  • receives input from sensory areas
  • amygdala (modulates to determine good/bad) gets the sensory input and projects to the orbitofrontal cortex which then projects throughout the brain and then assigns a subjective value
109
Q

Values/Goals/Plans/Actions

A
  • Values to Goals, Goals to Plans, Plans to Behavior/Action
  • Once have the evaluation: feeds into supplementary motor area that programs responses to create a goal (what to do) then into plans (how to reach the goal) then manip. of muscles to achieve the goals that will = behavior

S ⇒⇒(Cog Decision⇒⇒Response) (last 2/3 all frontal lobe)

110
Q

Steps to Decision-Making

A
  1. Values into Goals: orbitofrontal cortex (subjective value) - also modulates emotions (amygdala) re decisions
  2. Goals into Plans: Prefrontal areas and Dorsal anterior cingulate cortex (goal tracking: frontopolar cortex)
  3. Plans into Behavior/Action: Presupplementary and supplementary motor areas - internally guided movements (also plan-selecting: dorsomedial prefrontal cortex)
111
Q

Fear Conditioning

A
  • some species (humans too) exhibit fear conditioning that can enhance consolidation of episodic memory
  • once a fear memory has been established it is relatively permanent
112
Q

Bottom Up/Top Down Emotion

A
  • Bottom Up: immediate in-grained response to a stimulus (car pulls out in front of you); physiological reaction in the body causes the emotion (James-Lange Theory); more visceral, fight or flight type
  • Top Down: conscious responses to the way we think about a situation; 3 steps: Stimulus / Self-talk about what’s happening / Feel something based on stimulus (Cannon-Bard Theory)
113
Q

Cannon-Bard Theory

A
  • Top-down theory
  • information about the emotion spreads from brain to body
  • sensory info to cortex and hypothalamus / perception of emotion / hypothalamic pathway coordinates body’s part of the emotional response
114
Q

Modern “Two Factor” Theories

A
  • Emotions can be both bottom up and top down
  • Schacter and Singer experiment with the injected saline and epinephrine
  • Emotions are based on both physiological arousal and cognitive label (cognitive - arousal theory)
  • If someone is aroused they attribute it to their perception of the most plausible cause
115
Q

Valence/Arousal Network

A
  • Valence Network: pleasantness and unpleasantness of emotion
  • Arousal Network: the intensity of the emotion

Arousal will affect performance: the greater the arousal, the greater chance the episodic memory will be stored

116
Q

Amygdala input to Brain Regions

A
  1. Lateral hypothalamus - increased HR, BP
  2. Dorsal Motor Nucleus of Vagus - ulcers, urination
  3. Parabrachial nucleus - increased respiration
  4. Ventral tegmental area - behavioral arousal (dopam)
  5. Locus Coeruleus - increased vigilance (adrenalin)
  6. Dorsal lateral tegmental nucleus - cortical activation Acetylcholine (Ach)
117
Q

Yerkes & Dodson Law

A
  • there is an optimal level of arousal to help attention and focus and if depart from that performance will change
  • performance will drop if you are either under or over that optimal level
  • Use ratio scale to measure
  • linked to task complexity:
    • complex tasks are performed better at low levels of arousal
    • simple tasks are performed better at higher level of arousal
  • Rehearsal of a task will bring it from complex to simpler and can then be performed even if higher arousal (like pilot example)
118
Q

Hippocampus and Emotion / Memory

A
  • Anterior hippocampus: encoding and retrieving emotional content in episodic memories
  • Posterior hippocampus: mediating spatial navigation abilities

Location and emotion of memories are 2 aspects that are recalled from episodic memory

If you reconstruct the smell, location and emotion of an episodic memory it can facilitate recall

119
Q

Learned Emotion: CER

A
  • CER: Conditioned Emotional Response
  • emotional relationships among learned objects
  • an emotional response can be learned through operant or classical conditioning methods
120
Q

6 Basic Emotional Reactions

A
  1. Happpiness
  2. Anger
  3. Fear
  4. Sadness
  5. Surprise
  6. Disgust
121
Q

2 Neural Pathways Facial Expressions

A
  1. Voluntary Facial Movements: primary motor cortex (corticobulbar projections)
  2. Involuntary Facial Movements: extrapyramidal motor system with input from the limbic system (emotional state)
122
Q

Ventral Striatum

A
  • Centre for pleasure and reward
123
Q

Insula and Emotion

A
  • The insula regulates the sensory, subjective experience of emotions (produces whole body sensations associated with emotional states)

feel good component of the drinking is in the insula

124
Q

Motivational Drive

A
  • Neural state evoled to increase the chance of species survival - can be external or internal
125
Q

Generic Control System

A
  • comparison of what intend to do or want and what you actually did (control)
  • Set point:reference - i.e. “just enough water” to quench thirst - drink ⇒ produces actuating signal and feedback (dilution of protein in the blood),feeds back to the “error detector” to compare what needed re H2O and what you drank. Difference between them is a #. If the # is Zero - took exactly what needed (no longer thirsty) Note: most homeostatic processes never go to zero
126
Q

Internal / External Drives

A
  • Internal: Hypothalamus - e.g. energy and water balance, thermoregulation, stress response, circadian rhythm, defensive behaviors, sex
  • External: Amygdala: response to: outside threats, reproductive opportunities, social situations, parental attachmen, afiliation
127
Q

Inernal Homeostasis

A
  • maintain levles of nutrients, water, temperature, electrolyte balance, etc.
  • How: autonomic, neuroendocrine or behavioral responses (eat, drink, area restricted searches for food or water)
128
Q

Energy Balance

A
  • homeostatic drive
  • ghrelin - to signal hunger
  • leptin - to signal you to stop eating (satiation)
  • both feedback so could continue to eat if the leptin has not kicked in yet (eat slowly so it catches up)
129
Q

3 Types of Hypothalamic Responses

A
  • Endocrine
  • Autonomic
  • Behavioral

None are directly related to homeostasis process control but can result in behavioral changes

130
Q

Short & Long Term Allostasis

A
  • Short term allostasis: prepares body for challenges like feeding, fleeing, fighting, sex
  • Long term allostasis: harmful (suppression of immune system) - chronic stress responses - it is trying to “right” the balance of some external event (which can go on a long time…ie. chronic stress)
131
Q

Dopamine Pathways (3)

A
  1. Nigrostriatal pathway: substantia nigra (in brainstem) to striatum (in limbic system) - motor control
  2. Mesocortical pathway - ventral tegmental (in diencephalon) to prefrontal cortex (planning) - for cognition
  3. Mesolimbic pathway: transports dopamine from the VTA to the nucleus accumbens, amygdala, and hippocampus. Associated with addiction and depression. Reward pathway.
132
Q

Primary and Secondary Rewards

A
  • Primary rewards will directly affect homeostasis - food, water, (are primary reinforcers)
  • Secondary rewards: can take long time (Van Gogh)
133
Q

Prediction Error

A
  • difference beween what you want (the “reference”) and what actually occurs
  • The control system ceases if the prediction error drops to zero (no need to cycle) - happens the more the response is “expected”.
  • Based on prior experience and patterns of response, the brain expects (or predicts) what will happen with a certain stimulus or situation.
134
Q

“Needing” and Set Point

A
  • “Needing” happens as a result of a change in the “set point” (i.e. drugs - once effect reduces, the set point changes - happens with repeated use)
  • The “set point” is the desired or target value at which you will function optimally or what body thinks is optimal
    *
135
Q

4 Opioid Receptors

A
  • Mu - analgesia and euphoria / amplifier
  • Kappa - produce unpleasant reactions (but still reinforcing)
  • Delta - same as mu but also antidepressant
  • Nociceptin - regulates instinctive / emotional behav.

If you stimulate the Mu and and Delta it makes aversive stimuli seem more pleasant

136
Q

Addictive Substances and Reward Value

A
  • higher than normal reward value
  • Also: if bombarding the receptors brain will produce fewer receptors - leads to tolerance (if fewer receptors, less stimulation, less pleasure) - usually endogenous receptors that diminish
  • once have tolerance: reward values go down
  • Incentive Sensitization: rewarded even by cues
137
Q

Pathalogical Conditioning

A
  • bypassing normal system
  • addictive drugs produce a strong positive prediction error signal
  • Explanation prediction error signal:
    • The dopamine reward response: codes discrepancy between reward and its prediction (‘prediction error’) - unpredicted reward elicits a positive prediction error, a fully predicted reward elicits no response, and the omission of a predicted reward induces a depression (negative pred. error)
138
Q

Nucleus Accumbens and Addiction

A
  • Addictive substances cause nucleus accumbens to release dopamine
  • Positive reinforcement: stimulate circuit from nucleus accumbens to ventral tegmental area (PLUS: do NOT need a “positive experience” to experience positive reinforcement)
139
Q

Reward and Dopamine Pathway

A
  • Ventral tegmental area and substantia nigra ⇒nucleus accumbens and ventromedial prefrontal cortex (internal states) reward and pleasure.
140
Q

Face Perception

A
  • fusiform face area in inferotrmporal cortex (ventral visual pathway)
  • Temporal Pole / Inferior Temporal Pole
  • Amygdala / Insula - recognizing social/emotional cues on the faces
  • Insula: produces emot. relevant context for sensory experience
  • Damage: prosopagnosia
  • re emotion: by looking at others’ facial features we can perceive emotional states in them
141
Q

Superior Temporal Sulcus

A
  • Social-emotional cues - Superior Temporal Sulcus
  • Top gyrus of the temporal lobe - processes the cues like gaze, movement of hands, facial expression)
  • Disorders: autism, schizophrenia
  • (lack some necessary neuroinfrastructure to be able to tell what is happening by looking at others’ faces
142
Q

Theory of Mind

A
  • The ability to perceive others and understand the mental states of others and to recognize that they are different from our own
  • First Order: ability to preduct the thoughts of another person (I wonder what she would like…)
  • Second Order: understand what a 3rd person would think about the 2nd person’s thoughts
  • Sally Anne task - 1st Order and Informational Theory of Mind (specific to humans)
  • Before 5 can’t do T.O.M. abilities as not myelinated in frontal lobes
143
Q

Mirror Neurons T.O.M.

A
  • In monkeys saw them active in F5 which is near the Supreior temporal sulcus
  • F5 is near Broca which connectcs to Wernicke via and Arcuate Fasciculus so that tract may be involved
144
Q

T.O.M. General Intelligence

A
  • no correlation
  • no overlap with brain regions
  • so if no T.O.M. ability can still be of general intelligence
145
Q

Disorders T.O.M.

A
  • Autism: abnormalities in brain regions associated with the T.O.M.
  • (STS has less grey matter and abnormal patterns of activation during social cognition tasks)
  • Schizophrenia: reduced grey matter in medial and lateral prefrontal cortex, temporal poles, anterior insul (spindle neurons there), premotor cortex
  • spindle neurons: self-awareness - prerequisite for social cognition (ability to differentiate “self” from others)
146
Q

Pupil Size and Emotional State

A
  • the pupil size of the observer mimics the pupil size of those they are observing
  • pupil size is effeced by emotional states
  • (change in pupil size: amygdala, anterior cingulate, superior temporal sulcus, insula) - all associated with emotional responses
147
Q

Reward Prediction Error

A
  • The difference between the actual outcome of a situation or action and the expected outcome is the reward prediction error
  • A positive RPE indicates the outcome was better than expected while a negative RPE indicates it was worse than expected; the RPE is zero when events transpire according to expectations.