Psyc2020 Quiz 3

Front 1

Define Emotion

Back 1

A feeling state characterised by physiological arousal, expressive behaviours, and a cognitive interpretation

Front 2

What are examples of the three types of emotional factors

Back 2

Physiological

- Heart rate

- Breathing rate

- Sweating

Expressive

- Facial expressions

- Body movements

- Voice

Cognitive

- Beliefs

- Appraisal

Front 3

What comprises the autonomic nervous system?

Back 3

Sympathetic (close to spine) : fight or flight (sns)

Parasympathetic (further away) : calming down (psns); rest or digest or feed and breed

Enteric : visceral (feel butterflies or sick to stomach) (ENS)

Front 4

What are some typical measures of responses of arousal?

Back 4

Galvanic skin response

Pulse

Blood pressure

Breathing

Fidgeting / startle

All of these are measured in a polygraph

Front 5

How does folk psychology say that emotions and physiological responses related?

Back 5

Perceived event --> emotional experience --> physiological behavioural changes

Front 6

What is the Cannon-Bard theory?

Back 6

-Perceived event --> physiological and behavioural changes and emotional experience

-Emotions are separate from ANS response and behaviour

Front 7

What is James-Lange theory?

Back 7

-Perceived event --> physiological and behavioural changes --> emotional experience

Front 8

What are problems with James-Lange theory?

Back 8

-Visceral responses not reliable measure

- Visceral response would take too long to cause emotion.

- Visceral responses can occur without emotions.

-- Maranon: Injection of adrenaline produced physiological responses but no clear emotional states.

-- Cannon: Disconnecting viscera from CNS by removing SNS in cats has no effect on emotional expressions.

- Emotions can occur without visceral response; e.g., in paralyzed people.

Front 9

What do Cannon and James disagree on?

Back 9

James: physiological arousal causes emotion

Lange: physiological arousal is the emotional

Front 10

Can behaviour affect emotional states?

Back 10

Facial feedback-hypothesis (eg. Darwin; Zajonc)

- Expressing a particular emotion puts us (to some extent) into that corresponding emotional state

- Strong version: first you laugh, then you infer thats funny or i'm happy

- Weak version: facial expression modulates emotion

Testing

- General method:

-- Asking ps to contract/relax facial muscles important for expressing emotions

-- Testing: intensity of emotion when corresponding muscle groups active

-- What muscle groups are active in happy/ angry expressions?

Front 11

Can behaviour affect emotional states? : Duchenne (1806-1875)

Back 11

-Stimulated facial muscles to create natural looking facial expressions

- To find out what muscle groups were involved in genuine expression

- Corrugator muscle involved in frown

-Orbicularis oculi and zygomaticus major in smile

Front 12

Evidence for the facial feedback hypothesis? : McCanne and Anderson 1987

Back 12

- instructed participants to supress or increase the zygomatic or corrugator muscle while imagining please or unpleasant scenes

- Checked with facial emg

- When reporting their emotions states suppression of zygomatic muscle led to less enjoyment

Front 13

Evidence for the facial feedback hypothesis? : Laird 1974

Back 13

-Stimulated facial muscles (touching them and asking participants to contract them) to create different emotional expressions (cover story, checked with EMG)

-Then had participants rate emotional state and funniness of cartoons

- Ps told to contract muscles producing happy expression reported being happier and that cartoons were funnier than people in sad condition

- Problem: participants probably realised which facial expression was gathered

Front 14

Evidence for the facial feedback hypothesis? : Strack, MArtin and Stepper 1988

Back 14

-asked participants to hold pen in mouth in 2 different ways (lip/teeth) or in their non-dominant hand while filling out questionnaire (cover story)

- Then ps had to rate funniness of cartoon

-People in teeth condition rated cartoons as significantly funnier than people in lips condition

Front 15

Evidence for the facial feedback hypothesis? : Botox Evidence

Back 15

- Hennelotter et al (2008),fMRI: botox ir msucles decrease actibity in brain reigon (amygdala and brain stem)

- Havas et al (2010): botox injection slow sentences but not happy sentences

Front 16

In Sum:

Back 16

- Theory that physiological / facial expressions cause feelings or are identical with them probably too extreme

- But: physiological states and expressions/ behaviour can modulate emotions

Front 17

What does Cannon-bard theory not cater for?

Back 17

- Thalamic/hypothalamic theory of emotion

-Cannon and Bard proposed a hypothalamic theory of emotion:

--(1) the hypothalamus evaluates the emotional relevance of environmental events;

--(2) the expression of emotional responses is mediated by the discharge of impulses from the hypothalamus to the brainstem;

--(3) projections from the hypothalamus to the cortex mediate the conscious experience (Bard, 1928; Cannon, 1929).

Front 18

Describe the history of the limbic system

Back 18

-Papex, 1937 extended Cannon-Bard Theory

-MacLean 1949/52 added prefrontal cortex, hippocampus, amygdala and named it the limbic system'

- The circuit originally proposed by Papez consisted of the hippocampus, the ipsilateral mammillary body, the anterior nucleus of the thalamus,the cingulate cortex, the parahippocampal gyrus, and the entorhinal cortex, returning to the hippocampus. MacLean elaborated on Papez's earlier work, adding the prefrontal cortex, the septum, and the amygdala, and named this group of structures the limbic system.

- Papez 1937: Added anatomical circuits in the forebrain to Cannon-Bard theory, but ascending and descending projections from hypothalamus still most important. MacLean (1949, 1952; doctoral student), Note: Amygdala present but does not play a major role.

Front 19

What is the history of studying the relationship between the limbic system and fear?

Back 19

-Long history of research using rhesus monkeys: removal of hippocampus, amygdala, temporal cortex and other brain regions and observing their behaviour afterwards (eg Weiskrantz, 1956)

- Little insight from these studies: widely different tests used (studying appetite behaviour; behaviour when relaxed; response to arousing/calming stimuli). Results did not converge on specific brain regions

Front 20

Which parts of the limbic system are essential? :

Back 20

Hippocampus important for context/compound/trace learning:

- Context conditioning:

-- No distinct CS: environment serves as CS --Context A: CS+ (paired with US); context B: CS-

-- Example: Animal receives electro shocks upon tone in box A but not in box B. (Differential Conditioning)

Amygdala important for fear learning:

-Evidence:
-- Damage to lateral nucleus of amygdala interferes with fear conditioning (e.g., Amaral et al., 1992; LeDoux et al., 1990, Turner et al., 1980).

-- fMRI: Amygdala activity changes during conditioning, and these correlate with thalamus activity but not cortical activity (LaBar et al., 1998, Morris, 1998).

Front 21

Describe the components of classical conditioning

Back 21

-Classical Conditioning:

--Pairing of a neutral/non-feared stimulus (CS) with a negative or positive stimulus (US) that evokes certain response (UR).

- Terminology:

--US: Unconditioned Stimulus (= hardwired, instinctive)

-- UR: Unconditioned Response (= hardwired response).

--CS: Conditioned Stimulus (= to be learnt/associated with US).

--CR: Conditioned Response (= follows CS after learning).

Front 22

What progress was made with fear conditioning and the limbic system?

Back 22

John Watson & Rosalie Rayner (1920): Little Albert (9 months).

- Fear conditioning: Striking metal with hammer (loud noise) whenever

-Albert was close to furry animal (rat/rabbit). Albert acquired fear of furry things and this transferred to other furry things (incl beard)

Research Today:

- Differential Conditioning

- Measures: Startle response (eye blink); physiological components: Skin conductance, Heart rate / breathing.

- Results: Cortex important for differential conditioning (discrimination of information)

Front 23

Summary of limbic system and fear ect

Back 23

Amygdala important for fear acquisition (fear response?).

Cortex important for differential conditioning.

Hippocampus important for contextual learning.

Front 24

What does LeDoux's High road and low road tell us about the role of the amygdala?

Back 24

Thalamus --> Amygdala --> Response (Low Road)

Thalamus --> Cortex --> Amygdala--> Response (High Road)

Further refined Cannon/Bard - Papez/Maclean circuits - assign functions to specific parts of the limbic system

Front 25

What does Feinstein et al. tell us about fear and the amygdala in humans?

Back 25

Patients with focal bilateral amygdala lesions (Urbach-Wiethe disease):

a) No conditioning to aversive stimuli,

b) Failure to recognize fearful faces and

c) Absence of fear when exposed to fear-provoking stimuli (Adolphs, 1999; Adolphs & Tranel, 2000; Bechara, 1995; Davis et al., 2010; Feinstein et al., 2011).

- Tested here: 3 amygdala lesioned patients and 12 controls for fear after inhalation of CO2. --> In mice, chemosensors in

Amygdala mediate fear response (Ziemann et al., 2009).

Results:

- CO2 triggered fear / panic attack in all three patients.

- Physiological response (SCR) was the same or heightened.

- BUT: Anticipatory anxiety was missing.

- only 3 of the 12 matched, neurologically intact comparison participants panicked (Fig. 1a), a rate similar to that previously observed in adults without a personal or family history of panic disorder

Front 26

Take home message of amygdala

Back 26

-Amygdala important for conditioning to fear; anticipation / detection of threat.

- Amygdala not necessary for experiencing emotions (fear/panic).

-Brain structures that bypass amygdala can also evoke fear.

-Le Doux’ Theory does not cater for that.

What works in mice does not necessary work in humans.

Front 27

Can we erase effects of conditioning?

Back 27

Extinction: Presenting CS+ (trained stimulus) alone.

Observation: Fear-related behavior subsides.

Front 28

What happens during extinction?

Back 28

Extinction is not passive forgetting

- Spontaneous recovery: Emergence of conditioned fear some time after successful extinction.

- Renewal: Emergence of conditioned fear in different context after successful extinction.

-Reinstatement: Emergence of conditioned fear after encounter of US (shock) alone after successful extinction.

- Rapid reacquisition: Reacquisition after extinction faster than learning.

--Active suppression of fear response during extinction (learning)

--Extinction= learning something new about stimulus, not un-learning.

Front 29

What happens during extinction?: Neural Level

Back 29

Associative Learning at neural level:

- Changing connection strengths between neurons (synaptic weights).

- Changing wiring between neurons (Plasticity).

Hebbian learning rule:

- Plasticity: What fires together wires together. --Neurogenesis & changes in wiring of synaptic connections.

Front 30

Take home messages of 'unlearning'

Back 30

Extinction is not forgetting (spontaneous recovery, renewal, reinstatement, rapid reacquisition)

Extinction: active process involved changes in synaptic weights (similar to learning)

True unlearning of feat response does not happen during extinction

Front 31

Are we prepared to learn x but not y?

Back 31

-Some things in natural environment can be dangerous (large drops, rivers, snakes ect)

- Has evolution equipped us with threat detectors / preparedness so that we avoid dangerous objects more readily? Or is it innate?

- Could explain why phobias exist for some things (snakes ect) and not others (guns ect)

-Examples of approaches used in research

-Some innate factors that modulate learning speed and speed/effectiveness of extinction. To lesser extent: Also shapes perception, but learning history and actual emotions can dominate innate factors.

Front 32

What does Gubson and Walk tell us about innate fear?

Back 32

Toddlers do not crawl over ‘visual cliff’ (perceived drop of 1m) even when coaxed by mothers.

- Frequent conclusion: Fear of heights is innate.

- BUT: Infants avoid cliffs and steep slopes with locomotor experience, not automatically (e.g., Adolph, 1997, 2000).

- Initial purpose: show that depth perception is innate.

- Frequent conclusion: Fear of heights is innate. But that is problematic. Innate fear maybe not even innate? Infants may not be fearful. What we observe = Avoidance behavior.

-Reasoning often circular: They avoid because they are afraid; they are afraid because they avoid. Avoidance may not be based on fear: Heart rate not a reliable predictor for whether toddlers cross the cliff or not. No negative affect (crying, stiffening). Too close to the brink in avoidance: Infants would fall (and do; Adolph, 1997). Avoidance could be due to realistic estimate about affordances / abilities to cope with slope (Adolph, Kretsch & LoBue, 2014).

Front 33

Conclusion: Innate fears/ preparedness

Back 33

Have moderate modulatory function

Mostly tested with visual stimuli: perceptual factors

Experience and learning trump innate factors in shaping response

Front 34

Seligman & Maier (1967): Learned helplessness

Back 34

-3 groups of dogs: Group 1 and 2 dogs harnessed, subjected to electro shocks (yoked). Group 1 dogs could end shocks by pressing head against panel; Group 2 dogs could not (received stimulation from Group 1 dogs). Group 3 dogs: Harnessed but no shocks.

- Test in Shuttle box: Could escape shock by jumping over partition. BUT: Group 2 dogs never jumped (80%).

Front 35

What did Seligman & Maier (1967) infer from their intial findings on learned helplessness?

Back 35

-Retardation of Learning’ (better: Learning Transfer; Consequences of learning). -- Learned: Shock is inescapable. Don’t waste energy trying to avoid it.

- Linked to depression: Depression results from learning that outcomes are uncontrollable (Seligman & Maier, 1976).

-Learned Helplessness: Example how past learning / experience directly influences how a situation is perceived, and…

- How this perception leads to certain emotions / mood states.

Front 36

Experiment Hiroto (1974):Learned helplessness

Back 36

-People in 3 groups could stop loud noise vs. not vs. control (no noise).

- Testing in hand shuttle box: Noise could be stopped by moving lever from one side to another.

- Results: Subjects in no-noise and controllable noise learned to shuttle; but subjects in uncontrollable noise condition did not.

Front 37

What evidence is there for the fact that humans do not always learn to be helpless

Back 37

_ No helplessness when panic button available to escape noise, even when subjects do not press it (Hiroto & Seligman, 1975).

-No helplessness when students solve cognitive problems after inescapable noise (Klein & Seligman, 1976).

- When students were told that first task was good predictor of college performance & failed it, did worse on task 2. But when told that first task was learning experiment, failing task 1 led to no deficits on task 2 (Roth & Kubal, 1975).

-Failure on simple tasks produced cognitive decrements, lower expectancy of success and self-esteem, but failure on difficult tasks did not (Douglas & Anisman, 1975).

Front 38

Abramson, Seligman & Teasdale (1978): Learned Helplessness !

Back 38

In humans, attributions determine development of helplessness :

Attributions important for performance -helpless behaviour. But depression = mood disorder, not emotion disorder. Soare attributions also important for emotions?

Front 39

Schachter and Singer (1962): two-factor theory of emotion

Back 39

Emotion is arousal + cognition

- Emotion only occurs if:

-- Body is aroused

-- A reason for arousal located

-- The labelling of arousal determines emotion

--Arousal w/o cognition leads to no emotion

Test: make people attach a wrong cognitive label (misattributions)

- injected with Epinephrine aka Adrenaline (Cover Story) 4 Groups

Results

- Misinformed participants did not have an explanation for their arousal therefore formed emotion ‘happy’ when put in euphoria-inducing context.

-Informed participants attributed arousal to drug therefore least affected by context.

-Euphoria condition: Happiest were misinformed, followed by ignorant, placebo and informed.

- Anger condition: Angriest were ignorant, followed by placebo and informed.

Front 40

Dutton & Aron Misattribution experiment

Back 40

-Male participants met experimenter in two conditions: Had to cross narrow 230ft high bridge across river. Had to cross broad stable 10ft high bridge.

- Experimenter: attractive female who gave participants a survey to fill out & her mobile phone number in case they had questions

-Results

-- Participants who crossed the unsafe bridge more likely to call experimenter and ask for date (50%) than participants crossing safe bridge (12.5%).

- Interpretation: People crossing the scary bridge misattributed arousal (fear) to experimenter (attracted).

Front 41

Take home messages of attribution

Back 41

Attributions can have important effects on emotions

Determine what emotion is formed / experienced.

It is possible to have ‘misguided’ emotions (those arising from misattribution).

Similar theory: Cognitive Appraisal Theory. (--> Cognition causes arousal)

Front 42

Very rough history of theories of emotion:

Back 42

First approaches focused on ANS, visceral responses and behavior. Quest for brain structure where emotions are localised (first thalamus/hypothalamus, then amygdala). Conditioning procedures used to alter emotional response to a particular stimulus (and back – extinction) to identify important brain regions. Last enters cognition: Importance of cognitive appraisal in defining emotions (or defining arousal).

Front 43

SensorimotorSpinal Circuits

Back 43

-What is the ‘bit’ that interacts with the environment?

-Muscle = muscle fibres with membrane, attached to tendon

- Lowest level of the hierarchy = motor unit = motor neurone and the muscle fibre(s) it innervates

-The point of innervation = neuromuscular junction (first photos -Ach)

-- If this doesn’t work well there will be problems with interacting with your environment

Front 44

Descendingmotor pathways

Back 44

-From the primary motor cortex, signals descend to the muscles through 2 dorsolateral regions in the spinal cord and 2 in the ventromedial region in the spinal cord

- 2 main pathways from motor cortex that send signal all the way down to the muscle fibres ...

Front 45

Descending Motor Pathway: 2 Main pathways

Back 45

Dorsolateral tracts (end up in back/side of spinal cord)

-terminate in contralateral half of one spinal cord segment, and sometimes directly on a motor neurone

-limbs

-- Direct --Indirect

Ventromedial tracts (end up forward/central of spine)

- more diffuse, with axons innervating interneurones in several segments of spinal cord

- body

-- Direct --Indirect

Front 46

Describe the direct and indirect dorsolateral tracts

Back 46

Direct

- Start from motor cortex

- Then pass through medullary pyramid

-Make way straight down to dorsolateral portion of the spinal cord

- Cross over from where they began

- One side of brain controls other side of body

Indirect

- Rubro = red

- Pass through the red nucleus

- Cross over (a bit earlier in brain stem) More complicated

- Send off connections to facial muscles

Front 47

Lawrence & Kuypers (1968) transected dorsolateral corticospinal tracts in medullary pyramids of monkeys

Back 47

After surgery, monkeys could stand, walk and climb

But could not use limbs for other activities (e.g. Reaching for things; and could not move fingers independently )

Front 48

Describe the direct and indirect ventromedial corticospinal

Back 48

Direct

- Make way down same side of body from brain

- But at the level of the spinal cord, there are fibres that send information from left and right

- These ones end up in ventral medial portion and control trunk and limbs

Indirect

- Go through the brain stem and connect then with the reticular formation

- Make way down same side then end up at ventral medial portion of the spinal cord

-Control trunk and proximal limb muscles

Front 49

Lawrence & Kuypers (1968) transected ventromedial tracts

Back 49

-Monkeys had postural abnormalities

- Impaired walking and sitting

-controlof posture and whole-body movements, and they control the limbs movementsinvolved in these activities

Front 50

Cerebellum

Back 50

a) Input from primary and secondary motor cortex

b) Feedback from motor responses from somatosensory and vestibular systems

- Gait (walking), speech and balance, and learning new motor sequences

-- Cerebellar ataxia

--- Common effect of damage to the cerebellum

--- imprecision of movement and reaching out and touching fine points in space

-fine-tuning and learning functions

- navigation within the environment

Front 51

Basal ganglia

Back 51

-Complex, heterogenous interconnected nuclei

-They modulate movement

-cognitive functions – habitual responses, implicit learning

Front 52

Primary motor cortices (right and left)

Back 52

- Info passed across through the corpus callosum

- also in the cortex is the supplementary motor area

-- gate keeper to movement

-- activation means the whole system is held in readiness

Front 53

Thalamus

Back 53

Two pathways

- Direct

-- Just one connection from basal ganglia to thalamus

- Indirect

-- Various pit stops along nuclei

- Very well balanced pathways

- Imbalance = parkinsons

Front 54

Parkinsons

Back 54

- Input to basal ganglia and specifically into the putamen come from the substantia nigra compacta (SNc)

- Have projections from the SNc, which are in the tegmentum, and there are projections to the putamen from the SNc

-There are two types of connections and what they do depends on what receptor type they are involved with

- The neurotransmitter = dopamine and dopamine is an inhibitory NT so it dampens the system

Front 55

Thereare two types of receptors in the putamen

Back 55

D1

- Excitatory connection from the SNc to the putamen

D2

- Inhibitory connection

- Good example of how the system whether it’s cognitive functions or whatever it may be, the system does not just depend on active, but there has to be a balance.

-Need to activate and stop making movements

-Each of the nuclei will then receive inhib or excitatory conditions from one nucleus to the other

-- In tuned balance between the direct and indirect pathways but within one pathway there isn’t

Front 56

Direct and Indirect pathways : Parkinsons

Back 56

- Depend on Dopaminergic connections from substantia nigra

-Connections can be excitatory OR inhibitory: the output of one nucleus either excites (enhances) or inhibits (suppresses) the output of the next nucleus

- FINE BALANCE between activation of these nuclei in the intact system

- IMBALANCE in Parkinson’s disease leads to extra or reduced movements

Front 57

What role does the tegmentum play in parkinsons

Back 57

- 80% drop off of substansia nagra= motor problems

- Therefore, pathways from substansia nagra to putamen no longer working

- Balance between direct and indirect pathways knocked out

- Balance within direct pathway is also knocked out

Front 58

Positive parkinson symptoms

Back 58

- Patients may present primarily with

-- Tremor. Usually starts in distal musculature . Resting tremor

-- OR rigidity and akinesia

-- With/ without cognitive dysfunction, dementia, depression

- Tremor- resting (disappears when limb is in use or in sleep- contrast with cerebellar intention tremor)

- Rigidity- resistance to passive movements, leading to postural problems, loss of righting reflexes.

- Rigidity + tremor may feel like “cogwheel rigidity” on passive movement by examiner -Forward leaning; backward leaning

- Postural hypotension = many falls

--Blood pressure drops when you stand

Front 59

Parkinson's negative symptoms

Back 59

- Reduction in spontaneous movement (hypokinesia)

- Slow initiation of movement (akinesia);

-Progressive slowing or freezing during a movement and

- Reduced range and scale of movement

--Micrographia

--- Writing becomes smaller and smaller

-- Slow gait, often with freezing and small steps

-- Rapid festinating gait

-- Poor arm swing

-- Postural instability = many falls

- Dull, weak voice without inflections (hypophonia) and slow speech

- Mask-like, unemotional expression

Front 60

What role does L-Dopa play in parkinsons?

Back 60

- can reduce symptoms

-side effects:

--hypotension

--confusion

--eventually drug fails

Front 61

Huntington's disease

Back 61

- Huntington described the three peculiarities of the disorder:

-- Hereditary nature

--Autosomal dominant with complete lifetime penetrance, chromosome 4

-- Manifestation in adulthood Tendency to ‘insanity and suicide’

- Destruction of GABAergic (and some cholinergic neurones in striatum (caudate and putamen, and to some extent the globus pallidus)

- Progressive striatal atrophy: Medial caudate first (small spiny neurones), then putamen, then tail of caudate

- Defective metabolism precedes loss of tissue

Front 62

First signs of Huntington's disease

Back 62

Depression, anxiety, irritability, impulsivity, aggression

Front 63

Following signs of Huntingtons

Back 63

-Restlessness, clumsiness, poor coordination, forgetfulness and personality changes

- Altered speech and writing, saccadic changes

-Bradyphrenia and bradykinesia

-- Slowness in initiating thinking and movement

- Poor motor dexterity, unsteadiness, reduced speed

- Athetosis, chorea

-- They often appear to be fragments of normal behaviours

-- They involve multiple joints and thus resemble voluntary action

-- They are briefly suppressible, and decrease during sleep

-- They increase with stress and with voluntary movements like walking

-- Quasi-undulating character is idiosyncratic to individuals

Front 64

Neuropathology of Huntingtons: Tourette's

Back 64

-Intermittent tics :Motor &/or Verbal

- Echolalia

- Coprolalia

- Involuntary

- Partly suppressible

- Anxiety increases

- Sleep deprivation increases

- Premonitory sensory phenomena

- Genes, environment

- Imbalance of GABAergic activity in basal ganglia (Leckman, 2002)

- Management when severe: neuroleptics such as haloperidol and risperidone

- Before tic onset significant activations were found in mesial and lateral pre-motor areas, while at tic onset sensorimotor including SPL (superior parietal lobe) activations were observed.

- So cortical areas involved, as well as basal ganglia

- BALANCE between excitation and inhibition . Not just basal ganglia, Also cortical involvement

Front 65

Primary Motor Cortex (where and what)

Back 65

-In precentral gyrus of frontal lobe

- Major hub of convergence of cortical motor signals

- AND one of major outgoing point of signals

Front 66

Primary Motor Cortex: Damage

Back 66

- hemiplegia

- Weakness (loss of power) in the body part represented by that site

Front 67

Secondary motor cortex

Back 67

Front 68

Sensorimotor Association cortex -Input

Back 68

Front 69

SensorimotorAssociation cortex -Output

Back 69

Front 70

Dorsolateral prefrontal

Back 70

Front 71

Ataxia

Back 71

- Inability to use visual information to guide movement of hands

-- Deficit more severe in periphery of visual field

---Worse when reaching for something you can't see it

-- Visual fixation preserved

- Incorrect / awkward movements

- Errors in accuracy (over/undershoots)

Front 72

Apraxia

Back 72

- Inability to act, i.e., to move the moveable parts of the body in a purposeful manner (Liepmann, 1977)

- A disorder of skilled movement resulting from neurologic dysfunction (Rothi, Ochipa and Heilman, 1991). (Presupposes ability to move is intact, and is not due to sensory loss, weakness or ataxia, or other movement disorder)

Front 73

Wolpert, Goodbody and Husain 1998

Back 73

-PJ: 50yo F

- Head injury when 43yo, 30min loss of consciousness

-Jerking of the right arm at 48years, focal seizures, presented for assessment

- MR: cyst encroaching on the cortex and subcortical white matter of left superior parietal lobe

- No visual neglect or extinction, no other visual deficits

- Complaint: perceives her right arm and leg to drift and fade unless she is able to see them

-Superior parietal lobe is critical for sensorimotor integration by maintaining an internal representation of the body’s state

Front 74

Intrinsic spatial coding:

Back 74

-knowing what our own body parts are doing

-Intrinsic coding is essential when

-- a body part is going to be obscured from vision at some stage in the movement planning and execution

Front 75

Alien/Anarchic hand syndrome

Back 75

- Hand does its own thing as if its not of the same being as the 'owner'

- No suppression because goal is not generated appropriately

- Don't perceive it as their own hand

Front 76

Mirror neurons: William James: (1890)

Back 76

-awakens to some degree the actual movement which it is object”

- Observing, imagining or in any way representing action excites the programmes involved in that action

- The ideomotor principle

Front 77

Mirror neurons: Gallesse, Rizzolatti et al 1990s

Back 77

-mirror neurones in monkeys respond

1. to sight of goal-directed actions only as long

2.as the goal is achieved, even if it is out of sight

3. to sound of an action (multimodal)

4. when action is performed by an agent (hand-object interactions, not to tools) - ?????

Front 78

Mirror neurons: in monkeys

Back 78

- Premotor and parietal cortices activated by perception of action and execution; activation is greater when movements are to be replicated later

- mirror neurone system facilitates action understanding, allowing planning of our actions and understanding of others’ actions (Rizzolatti et al; Jeannerod et al)

...

Front 79

Mirror neurons in humans

Back 79

- similar system in humans as in monkeys

-Action GOALS, rather than action per se

-Non-human models CAN elicit action observation effects

- Context matters

- Experience matters Individual differences matter

...

Front 80

Mallan et al. rationale

Back 80

Previous research shows that fear conditioned to outgroup face is resistant to extinction, which might be the same type of prepared learning that occurs for fear-relevant animals.

Front 81

Mallan et al. hypotheses

Back 81

Mallan et al. reasoned that if it is in fact prepared learning:

1. It will occur for a different racial outgroup (Chinese faces as outgroup for Caucasian Australians).

2. It will occur for blink-startle responses, a more reliable and specific measure of fear than electrodermal responses used previously.

3. It will be irrational, i.e., if you tell people the CS+ face will no longer precede a shock, extinction will not happen faster.

Front 82

Mallan et al. participants, stimuli and assigned?

Back 82

Participants: 64 Caucasian-Australian UQ Students (33 male; mean age19.81)

Stimuli: Male Caucasian and Chinese faces in frontal pose with neutral expressions·

How were subjects assigned?: Randomly allocated to conditions of the IVs

Front 83

Mallan et al. IVs

Back 83

What were the independent variables (namesand conditions)?: ·

- Race of conditioned stimuli (Caucasian vs Chinese)

- Instruction:(no instruction vs instructed extinction)

Front 84

Mallan et al. Dvs and measures

Back 84

Blink startle :the magnitude of the blink when startled by loud white noise.

electro dermal response: the conductivity of the skin (determined by amount of sweating).

Front 85

Mallan et al. procedure for aquisition

Back 85

Four photos of faces of the assigned race presented one-at-a-time 8 times each - two are CS+ faces and two are CS- faces.

Participants received electrotactile stimulus (‘unpleasant but not painful’ zap) every time the CS+ faces appeared.

Participants never receive the electroctactile stimulus after the CS- faces.

Electrodermal responses and blink-startle responses collected to check fear acquisition.

Front 86

Mallan et al. procedure for extinction

Back 86

CS+ and CS- faces shown 12 times each without any shock, so the CS+ face no longer predicts a shock.

No Instruction condition – experimenter enters the room and inspects ‘zapper’ electrodes and says nothing about whether there will be more shocks.

Instructed Extinction condition – experimenter enters room, tells participant there will be no more zaps, and physically disconnects the electrodes while the participant watches. -- Blink-startleand electrodermal responses taken throughout the extinction phase.

Front 87

Mallan et al. results

Back 87

Fear learning, as indexed by larger electrodermal responses to, and larger fear-potentiated startle during the CS+ relative to the CS- was evident in all groups during acquisition.

Resistance to extinction of differential electrodermal responses and differential blink startle modulationwas evident in the Chinese no-instruction group, but not the Caucasianno-instruction group.

Front 88

Does Mallan et al. provide evidence for prepared learning to out-group

Back 88

No evidence of fear learning of other-race faces is irrational so it does not support the idea that it is the same as prepared learning for fear –relevant animal stimuli

Front 89

Arnold Pick

Back 89

- In 1892, he described a man who had presented in life with progressive loss of speech and dementia.

- When the patient died his brain was found to be atrophied.

- This shrinkage had been caused by brain cells dying in localized areas.

Front 90

Frontotemporal dementia (FTD/Pick's): Abnormal Spontaneous Behaviours

Back 90

- Inappropriate jocularity

- Echolalia (repeating the examiner's words), echopraxia (repeating the examiner's gestures)

-Disinhibited approach or utilization behaviours (more later)

-Unkempt, depressed in early stages

- Primitive reflexes such as grasp, suck, and snout, toes

Front 91

Frontotemporal dementia (FTD/Pick's): Clinical Course

Back 91

- Psychiatric abnormalities related to the classic frontal lobe syndromes:

-- aggressive and social inappropriateness (may steal or demonstrate obsessive or repetitive stereotyped behaviours), apathy and disinhibition

-- lack of concern, apathy, or decreased spontaneity.

Front 92

Frontotemporal dementia (FTD/Pick's): speech and language

Back 92

- Abnormalities often begin early and progress fast .

- Memory impairment relatively less severe than speech/language and behavioural changes

-Verbal output that is often nonfluent, with poor naming of objects

Front 93

Frontotemporal dementia (FTD/Pick's): movement disorders

Back 93

- Akinesia, plastic rigidity, or paratonia on motor examination

- Perseveration

Front 94

Frontal lobotomies

Back 94

- Anecdotal reports – patients were ‘stimulus-bound’:

- reacted to whatever was in front of them and did not respond to imaginary situations, rules, or plans for the future.

- Some gained significant weight, and / or became sexually promiscuous

- Could not form / sustain goals

- Distracted by circumstances

Front 95

W.R (Knight and Grabowecky, 1995)

Back 95

- Man who lost his ego

- W.R. had suffered a seizure in his last year of college

- No identifiable cause (on PET of CT) at the time

- CT re-done: extremely large astrocytoma traversing along the callosal fibres, invading extensively the lateral prefrontal cortex in the left hemisphere, and considerably in the right

-Poor prognosis: death within ~1 year but still didn't care

Front 96

what are the frontal lobes for?

Back 96

-“stimulus-bound”: utilisation behaviours

-Personality

- Supervisory functions: working memory, inhibition, control, decision-making

- Acquired sociopathy – not caring about issues that would normally evoke an emotional response

Front 97

Lateral prefrontal cortex

Back 97

-On the face of it, (unilateral) damage to this area presents “mild” deficits: Intelligence and language intact.

- Behaviour is “reflexive”, elicited by environmental circumstances, and purposeless : Stimulus-driven

- AND cannot keep interpreting the environment based on previous knowledge

Front 98

Working Memory : Baddeley and Hitch 1974

Back 98

-Unitary STM concept not enough to explain how information is maintained and worked on over short periods

- Limited capacity over the short term

-Performing mental operations (NOT rehearsal) on contents of store

- Contents may be new sensory info AND / OR retrieved info

Front 99

Lateral prefrontal cortex and working memory

Back 99

- McCarthy et al. 1994

- spatial vs working memory task

- fMRI

- Spatial wm task: respond when a stimulus appears at a location that has been used previously

- Control colour task: respond when a red object appears

Front 100

Wisconsin Card Sorting Test

Back 100

-still a working memory component: combine info from present and recent past, manipulate it and come up with a new response

-Impaired performance: inability to ‘find’ category and / or to shift to the new category

-Perseveration with same category even after changed conditions

- The WCST Information must be INTEGRATED with information that was relevant in previous trials (what the category was, what the E said)

-S must retain knowledge about the relevance of features, and manipulate this information on-line

Front 101

WCST and switching performance Konishi et al 1998

Back 101

- Computerised WCST Function of prefrontal cortex:

-- Inhibit dimension that is not relevant

--Dynamically sift and filter through possible alternatives

Front 102

Temporal Organisation of Memory

Back 102

- people with frontal lobe dysfunction struggle to order

- Test: give cards and ask order

Jasper:

- Ps with frontal lobe lesions

- Arranging cooking a meal

- Couldn't

| Chronogenesis |

Front 103

Frontal lobe and goal orientated behaviour: Shallice and Burgess

Back 103

-gave list errands and failed task

- problem with sub- routines of goals

Front 104

Frontal lobe and goal orientated behaviour: Duncan

Back 104

- goal neglect

- identify/select goal and develop appropriate subgoals

Front 105

Anterior cingualate cortex

Back 105

- Was thought to be part of the limbic system (modulation of autonomic responses)

- Now shown to have attentional / monitoring functions

- Input from limbic structures, including amygdala, the thalamus and the striatum, as well as the brainstem

- Output to prefrontal cortical areas

Front 106

Corbetta and colleagues

Back 106

- Ss asked to selectively attend to a single visual feature (colour, shape, motion) = PASSIVE

- Or monitor changes in all three features at the same time = DIVIDED ATTENTION

BUT

-ACC as a way-station / hub / amplifier of emotional signals

- Emotional signals can be interoceptive (eg heart rate, breathing) or exteroceptive (meaning in environment eg horrible scenes)

--Interoception – internal / own body signals

--Exteroception – external / ‘world’ signals

- ACC - experiential processing and response to emotion cues – conscious experience of emotion

Front 107

Lane et al. : The Levels of Emotional Awareness Scale (LEAS)

Back 107

- 12 female Ss, highly selected for emotionality seven emotions (interest, amusement, happy, sad, fear, disgust, anger) emotion-generating film and recall tasks, subjects were asked to feel the relevant target emotion.

-For the control film and recall tasks, subjects were asked to feel emotionally “neutral.” Relate to CBF: hypothesized that greater emotional awareness would be associated with increased activity in those structures previously implicated in emotional experience:

--thalamus, hypothalamus, ventral striatum, amygdala, ACC, anterior insula, orbito-frontal cortex, and/or mesial prefrontal cortex.

Front 108

The Orbitofrontal Cortex

Back 108

- Ventromedial prefrontal cortex

- Lateral-orbital prefrontal cortex

- Social and emotional judgement

- Social and emotional decision-making

Front 109

Decision making : “Elliot”

Back 109

- Tumour invading OFC bilaterally

- Lack of concern for social rules, decreased social awareness and empathy

Front 110

Decision making: Bechara

Back 110

- Anticipation of rewards and punishments Skin conductance, card playing

- Not responding as much as controls

Front 111

J.S a case of acquired sociopathy

Back 111

- JS, 56yo male, engineer

- Premorbid: quiet and rather withdrawn, no psychiatric history

- right frontal trauma, incl orbitofrontal

- High levels of aggression and callous disregard of others

- Lack of remorse

- In contrast to CLA and inmates, JS showed (acquired sociopathy)

Front 112

Mirror hand illusion: Mallan et al.

Back 112

- reach to target

-mirror or no mirror
-reach errors varied systematically according to the position of the hand image relative to the real hand

-greater the difference between fake image and real hand greater the reach errors

Front 113

Rubber hand illusion: Botnik and Cohen

Back 113

-Synchronous(multisensory integration) and asynchronous stroking of hands

-reach was closer to fake hand aftersynchronous

-proprioceptive drift

Types of illusory effects:

-Subjective: ownership, referal of touch

-phsyiological: temp and immune change