PSYCO 275 Ch 11

CHAPTER 11: Memory

- Model of Memory- More of a functional than an anatomical model

- Learning: how experience changes the brain- Memory: how these changes are stored and reactivated- Amnesia: any pathological loss of memory

Sensory Memory- Shortest, lasts from 250 ms to one second

o Visual sensory aka iconic memory – 260 mco Echoic aka auditory lasts about a second

- Important to allow you to hang on to info for a little bit longer to determine if it’s relevant or not, do you have to pay attention to it

- Gives you the ability to hang on to sensory info a little longer to help brain determine if info is relevant or important, should you direct attention to it

- Ex: sparkler – trace doesn’t actually exist, it just exists in your brain- Then, you can move it into your short term memory store

Short Term Memory- Can hold info up to 20 seconds now without rehearsal- But if you don’t continue to rehearse, if your attention is drawn away, then you lose it- Canadian studies, human research – in order to see duration of memory, you prohibit rehearsal of info

- Test this:o Flash letters on screen, get you to remember letters in the rowso To prevent rehearsal, they give you another task – another cognitive task that competes with ability to

rehearse like counting backwards from 3o Researchers stop you at different points: after 5 seconds you get some letters, after 10 you get fewer

and by 20 you get nothing, you can’t remember order of letters- Demonstrates that if you don’t allocate attention to it or rehearse the info, you forget it- Auditory rehearsal, phonological loop = using language components to rehearse info- Rehearsal, aka a phonological loop – language based

o Basic maintenance rehearsal: just rote repentanceo Elaborative rehearsal: taking info, but expanding on it, can pull already known things from long term

memory- Pull info from LTM to consolidate- Can pull old info into current STM-

- STM is more complex- Working memory- Not just about rote rehearsal- This part of memory has to do more than that- There can be a phonological loop – rehearsal helps transmission into LTM- But also: things that are in STM can not only be rehearsed with respect to a phonological loop but can also used

vision- Can put visual image to info and that further helps consolidate the info- Phonological as well as visual now- promotes stronger consolidation of memory- Word pairs:

o Juggler and dresso You can picture thato Justice and peace – harder to put image to words since more abstracto Words that were more concrete were the ones recalled the best

- Prefrontal cortex type of function- Huge area of association cortex- Prefrontal cortex: short term working memory - Working memory has a central cortex- PFC: higher order stuff like allocation of attention, - You need attention to transfer from ST to LT memory - Duration: STM lasts 20 s- Working memory is around 10s- STM also has a capacity- Only a certain amount of info a person can handle- 7 +/- 2 - So 5 to 9 pieces of information- But can chunk info together

Long Term Memory- Remember info as far as 3 years old- Infantile amnesia- Since areas for memory consolidation haven’t developed yet at that age- Can still have memories that exist for years- Not perfect, fallible- People can make mistakes with retrieval of information- Unlimited capacity

- Sensory info directs attention to STM- Rehearse it, work it, allocate more attention to get it into LTM-

- Ventral view of brain and coronal slice – shows missing areas which include the hippocampus

The Case of H.M.- Henry Gustav Molaison, 1926-2008- At age 5, fell off bike, had lots of grand mal seizures, couldn’t lead normal life- 27 years old, had surgery to remove epicenters in temporal lobe

o Regions in both hemispheres of medial temporal lobeo Medial bilateral temporal lobectomyo Included most of the hippocampus, amygdala, and adjacent cortex

- Post-surgery: HM woke up and lived the rest of life – seizure free, but had problem with memory- Mild retrograde & severe anterograde amnesia - But normal anterograde short term memory - Retrograde amnesia: backwards from time of surgery, lost sporadic memories back to age of 15

- More apparent was his anterograde: loss of memory for new memories- Couldn’t take info and transfer it into LTM store- Every day you have to have capacity to incorporate new info, etc- HM couldn’t do that anymore- Usually retrograde and anterograde separate, only see both in severe cases- Remember Jimmy G and Korsakoff’s – different kind of deficit

- HM became huge case study, brought about revelations of complexities of memory- Discovery that there was more than just short term and long term – there are other categories of memory

Formal Assessment of HM

Digit Span- Tests short term memory: tester gives you numbers and you immediately repeat them- Demonstrate 7 +/- 2 rule HM could do that fine even though his hippocampus was removed

o So when it comes to STM, maybe it’s not the hippocampus responsible for hanging onto memory in STMo Likely the prefrontal cortex which is still intact

- If you only tested digit span you wouldn’t know he had a memory issue- But recall that with neuropsychological testing, digit span is only one part of memory- Also did digit span +1:

o Ex: 58, then 583, then 583 10, base always same and keep on adding one - Normal individuals: 30 up to 50 digits in a row- Why can we exceed 7 rule?

o With rehearsal, since you are repeating the base: greater likelihood of transferring base into LTMo Retrieval: not just about things in STM – now using both STM and LTMo More you rehearse it, the longer the chunk that goes into LTM

- HM could only go up to 7, he couldn’t do 8 digits- Regardless of how much he rehearses it, doesn’t go into LTM, aka he only has STM- DS only verbal – so also tested other modalities

Block Tapping Memory Span Test + 1- Taps this block, you tap they tap this then that- Same idea as digit span: consolidating base, transferring it into LTM- Normal people can do a long series, but HM could do 5 (normal) but no more than 6- Disruption in memory not just based on phonological loop- Sensory motor output visual info, still couldn’t do task so is a global memory transfer problem- Demonstrated HM’s amnesia was global and not just limited to verbal information- Global amnesia: for information presented in all sensory modalities

-- - Hippocampus not as important for holding things in short term memory

- Variety of tests to see what he could or couldn’t do- He couldn’t form new LTM for explicit

o Explicit aka declaredo You have to consciously try to recall it

- As long as delay was shorter than 20s, his STM was intact- So could do regular digit span- More prefrontal cortex than hippocampus- Problem with digit span +1

- Couldn’t do either – so even using different modalities- Not specific to a specific system, was global

Mirror Drawing Test- First indication that HM’s anterograde amnesia didn’t involve all long term memories- Performance improved: but couln’t recall having ever done the test

Rotary Pursuit Test- Subject tries to keep tip of stylus in contact with target that rotates on revolving turntable- Improved performance retained over a 7 day period

Incomplete Pictures Test- Upon initial testing, HM’s results are the same as normal subjects

Incomplete Pictures Test

- Two pictures- At step 1, you are shown a few components and you have no idea what they’ll be, but by step 3, 4 pictures is

obvious- When first shown the cards, normal aka control and HM have same results- But after practice, after being shown Step 1 get it right more- HM gets better- But denies having ever seen the picture before- But when performing task, his behaviour is accessing the info- Just not at a conscious level- Didn’t expect him to improve this much-

Mirror Drawing Task- Drawing while looking in a mirror- Motor system eventually gets used to it – people over time get faster and more accurate- HM got better at the task, but can’t remember practicing it at all- He has retained information on how to do the task, but the practice associated with it, knowledge of the

episode, he has no memory of- From both of these tasks, researchers realized that Henry has problem retrieving info, consolidating info, about

info that you consciously attempt to retrieve aka explicit memoryo Semantic: facts, knowledgeo Episodic: egocentric, based on person, passage of time, chronological order, and event that has

happened to the individual - Implicit: memory not demonstrated through reporting it, but retention through action and behaviour

o How to drive a car, ride a bike – you don’t have to think about every stepo Procedural: skills and actions without consciously seeking out, how do I do this?

Ex: mirror drawing task

Pavlovian Conditioning- Learned and eye blink conditioned response ,retained it even two years later

Scientific Contributions of HM’s CaseThree major contributions

• Medial temporal lobes involved in memory• STM & LTM are distinctly separate• Memory may exist but not be recalled

– Explicit versus Implicit memory-

1) Medial temporal lobes play an especially important role in memory- Challenged previous view that memory functions were diffusely distributed throughout brain2) Supported theory that there are different modes of storage for long term and short term and remote memory- Discovery that bilateral medial temporal lobectomy abolished HM’s ability to form certain kind of memories

without disrupting his performance on texts of short term or remote memory- HM had problem in memory consolidation: translation of short term to long term memories3) Creation of two distinct categories of long term memories: implicit and explicit- Can have amnesic with no recollection of a previous experience while demonstrating memory for it by improved

performance- Implicit demonstrated, but without conscious awareness- Explicit conscious long term memories

Two structures that play a major role- Cerebellum and basal ganglia- Cerebellum also plays a role in classical conditioning

o Big role in implicit memory- Animal studies: cerebellum damage means they can’t learn from classical conditioning-

Medial Temporal Lobe Amnesia- Patients with deficits similar to HM: preserved intellectual functioning ut damage to MTL- Repetition priming tests: assess implicit memory- For example, incomplete pictures test- Implicit simpler, but we also have explicit to give us flexibility: to apply knowledge in a different context

Priming• Repetition priming tests

– Used to assess implicit memory– Performance in identifying word fragments (stem completion) is improved when words have been

seen before– Ex., _ O B _ _ E R

- HM did just as well as normal- Couldn’t remember any of the words or seeing the list, but did task faster- So must have been some retention, just not available to him at an explicit consciously level- Demonstrated it over behaviour- Premise being subliminal advertising

- Memory isn’t necessarily in one area

- More like a network

- When you reactivate a memory, not just one area-

Semantic and Episodic Memories- Semantic: general facts or information- Episodeic: memories for particular events- People with medial temporal lobe amnesia have particular difficulty with episodddic memories

Case of KC- Damage to medial temporal lobes- Severe amnesia for personal experiences

- Cerebral ischemia: often suffer also from medial temporal amsneisa

Korsakoff’s Syndrome- Disorder of memeory – brain damage from alcochol, thiamine deficiency- Damage to medial dencephalon – thalamus and hypothalamus- Anterograde amnesia for explicit epooisodic memories- But as disorder progresses, you also see severe retrograde amnesia - Spefically, damage to the mediodorsal nuclei of the thalamus

Hippocampus and Consolidation- Hippocampus and related structures play role in consolidation- Memories temporaility stored in hippocampus until they can be transferred to a more stable cortical storage

system- Standard consolidation theory- Medial temporal love lesions: produce temporally graded retrograde amnesia- Another theory: multiple trace theory- Hippocampus store memories for as long as they exist- When a concsioucs experience occurs, it is rapidly and sparsely encoded in a ditriuted fashion throughout the

hippocampus and other involved structures- Retained memories are more resistant since each time a similar experience happens or the memory is recalled, a

new engram aka change in brain that stores a memory is established

Structures Involved in Memory Formation- Anterograde amnesia: usually a problem with explicit memory- Implicit long term and short term memory intact- Inferior temporal love – ventral stream, what, for vision -

Inferotemporal Cortex- Recall: in vision, this was our ventral stream “what” ability to aggregate information, put it together into

form, produce percept and identify objecto Role in visual perception of objects

- We can identify object because we have storage – keeps info close to hippocampus- Lateral region: deeper in medial region, round bottom portion of hippocampus called rhinal cortex- A part of it is called perirhinal which feeds into hippocampus and is specific for memory for objects

o Memory for objects – visual patternso Object agnosia – damage is usually medial, in this areao Usually people with it – their visual system completely fine and can put the percept together, they can

draw and copy perfectly – it is the link to their memory of what it is damagedAmygdala

- Key role in emotional learning: particularly fear, aggression - Ex: memories persistent over time usually have a strong emotional component, more permanently stored

o The more you activate limbic system (amygdala part of limbic system), you increase likelihood that info will be consolidated into LTM

- HM could condition fearo Recall: problem with explicit memoryo Emotional memories can be explicit (you can be aware of your emotions) but can also be implicito Ex: after surgery, found out friend died – extreme emotional event would forget and keep on asking

again, and have same emotional responseo Eventually stopped asking - couldn’t explain where his friend was but knew something was wrongo Emotional component to it and chose not to ask, demonstrated ability for emotional learning still intact

- Animal studies: if you remove amygdalao Animal that would typically create aggressive response to something is completely tameo Completely taken up generation of fearo Lesion disrupts fear learning

Prefrontal Cortex- Researchers: proposed there had to be some component that allocated attention, kept things in order- No surprise: working memory is in prefrontal cortex, the area where you have so many higher order executive

functions (like attention allocation, etc)- Prefrontal cortex intact in HM which is why he has an intact short term memory as long as there is no delay

can report things- PC Important for ability to understand recency – time associated with memory - Moment to moment awareness of what just happened- People with frontal lobe damage: problem with temporal stuff- Behavior is bizarre because they have trouble remember order and timing of things

o Temporal order of events and working memoryo Different parts of PC may mediate different types of working memory

Cerebellum- Big role in procedural memory involved in memory of sensorimotor skills- Memory for action – not for consciously explaining how you do something, can just do something- Also for responsible for sensorimotor classical conditioning: for CS to produce a CR, reflexive response not

conscious- Not stored in cerebellum but routes through it- Just because you have a lesion and see a deficit doesn’t mean that area is where that function is processed,

more likely that you created a disconnection and damaged pathway that links areas together-

Mediodorsal Nucleus- One of the nuclei in thalamus (recall lateral geniculate, pulvinar, etc)- One in each lobe of the thalamus- Particular regions damaged in Korsakoff’s - extreme degeneration

- Mammillary bodies: part of limbic system- Also see damage here- Anterograde amnesisa, maybe a little retrograde

Basal Forebrain- Big role in acetylcholine production- Decrease in ACh concentration associated with Alzheimer’s- Ach: the neurotransmitter that increases activation through system – so if you can’t maintain activation of the

limbic system, you can’t consolidate memories

Hippocampus- Plays role in consolidation of long term explicit memory - especially spatial memory - You form a spatial map – over time you develop cognitive spatial map, demonstrated that in hippocampus

epically in posterior upper regions- Play a role in active when you put yourself in a particular place in the map- Neurons fire according to which position you are in- Neurons are specific to where you are in the map- Multiple maps that exist

- Entorhinal cortex:o Feeds into hippocampuso Plays role in spatial location and spatial memory

- Place cells o Present in certain regionso Respond when subject is in particular part of test environment

- Grid cells: like grid paper, you form a map and it forms a grid and neurons respond to your position in the grido Are in entorhinal cortex

- Experiments with rats: embed electrodes into single grid cells- Put them in new environment, and one neuron will only fire when rat is in one position - Taxi Driver Research:

o Do lots of spatial tasks so have larger area in hippocampus associated with spatial tasks

o Large posterior hippocampuso Also role in timing: so gives you ability to think about futureo Important for awareness of passage of time

• Place cells (in certain regions)– Respond when subject is in particular part of test environment– Hippocampectomy produces deficits on Morris maze & radial arm maze – Grid cells in entorhinal cortex

- Many hippocampal neurons are place cells- Neurons that respond only when a subject is in specific locations

- Grid cells: entorhinal neurons- Each have an etenxive array of evenly splaced place fields like grid paper- Respond relatively reflexively to location- Vs. place cells that respond to place and other features of test environment

- Hippocampus important for passage of time- Example in schizophrenics; garbled communication in hippocampus- Can’t have nice free flow of information- Problem with understanding time – what is past , what is present- Can contribute to symptoms that you see in schizophrenia- But not the only region involved - Episodic memory

Rhinal Cortex- Entorhinal: within rhinal fissure- Perirhinal : around rhinal fissure

o Object recognition

Synaptic mechanisms of Learning and Memory

Hebb- Proposed: creating physical changes at the neuronal level every time you form a memory- Something different at level of synapse

LTP: facilitation of synaptic transmissions following high grequency electrical stimulation applied to presynaptic neurons-

Long Term Potentiation aka LTP- “Neurons that fire together, wire together”

o Aka synapses are made stronger by repeated stimulation- Neurons that are active during learning, formation of a particular memory, their communication through the

system becomes more efficient over time, as well as more stable, fastero Physical changes that cause this

- Hebb also proposed that in order for this to happen: these changes happen only if presynaptic firing is followed by post synaptic firing you need co-occurrence

o Co-occurrence of firings in pre and postsynaptic neurons are necessary for learning and memory- LTP only happens if presynaptic firing is followed by postsynaptic firing

Three part process:- Induction: high frequeny stimulations induce LTP = learning- Maintenance: storing LTP = memory- Expression = recall

Induction of LDP or learning-

- Two types of receptors on postsynaptic neuron: NMDA and AMPA- NMDA receptors associated with calcium channels, let Ca2+ in when activated

o But they don’t open first time – only open when post synaptic neuron already somewhat depolarizedo So PSN already has some positive charge

- AMPA receptor associated with sodium channelo Open sodium channels right away

- First time release of glutamate, it will bind to both receptors but NMDA won’t open- PSN not depolarized yet- But AMPA opens sodium comes in positive charge in, PSN depolarizes- Next time glutamate binds to NMDA it opens- Threshold or gate- Changes don’t happen unless you demonstrate that there is a lot of communication and activation going on- Glutamate released- AMPA let sodium in over time- Builds up and now NMDA lets calcium move

- Only get calcium in when ell already depolarized- Calcium acts like messenger, change of events that create physical changes

• NMDA receptors do not respond maximally unless glutamate binds AND postsynaptic neuron is already partially depolarized

• Ca2+ channels do not open fully unless both conditions are met• Ca2+ influx may activate protein kinases that induces changes causing LTP

- NMDA receptors do not respond maximally unless glutamate binds AND postsynaptic neuron is already partially depolarized

- Ca2+ channels do not open fully unless both conditions are met- Ca2+ influx may activate protein kinases that induces changes causing LTP- Hebb: notion that in formation of memory pathways, you create physical changes at level of the synapse- Glutamate: different types of receptors

- Main receptor for glutamate, NMDA – calcium channel- But you have to have co-currence of firing- Only if post synaptic neuron is partially depolarized

- Other type of receptor: AMPA-- AMPA receptor: not specific- Doesn’t require depolarization, opens its sodium channels when glutamate binds

- NMDA won’t open yet because it needs depolarization, increase in positivity - If this is first time pathway is activated, NMDA won’t open yet- The more glutamate continues to release, the more those sodium SMPA channels open and as sodium increases

in concentration, positive inside, so cell depolarizes- Once you reach a certain threshold when glutamate binds again to NMDA calcium channels will open

Maintenance and Expression of LTP- There are pre and postsynaptic changes – protein synthesis (aka structural changes) underlie these long term

changes- LTP begins in postsynaptic neuron, which signals the presynaptic neuron with nitric oxide- Calcium activates protein kinases which are responsible for the changes in the postsynaptic neuron

o Sprouts more NMDA receptors – so when glutamate is released from presynaptic neuron it is more quickly bound, generating a faster response

o Also, receptors that already currently exist become more sensitive to glutamate – so maybe when glutamate binds to sodium channels, they bind for longer than normal which results in a greater influx of sodium so quicker depolarization

- Presynaptic enhances release of glutamate – higher concentration released and faster but how does it know?o An unconventional NT – nitric oxide gas – is produced in post SNo Recall: soluble gases only quickly produced, and you see retrograde transmission – travels from dendrite

back into presynaptic neuron where it creates physical changes- Believed that through repeated activation, these changes are stable over time and maintained- LTP doesn’t happen everywhere in the brain but happens in hippocampus and also beyond the limbic system in

pathways associated with memory- Astrocytes: supportive glial cells that are also involved in LTP

Chapter 16: Lateralization, Language and Split Brain

• Enhanced release

• Increase in sensitivity

• Increase in number

The Split Brain- You sever the corpus callosum, aka the major commissure between hemispheres - Not a lot of split brain patients exist - had severe epilepsy, unsuccessful with medication- Is a radical surgery - usually removing epicentre more popular- But patients do relatively well after surgery – if you limit it to one hemisphere, medication is more effective- Commissurotomy – aka cutting the commissure – limits convulsive activity

Sperry and Gazzaniga- Developed procedures to test split-brain patients, demonstrated that hemispheres have very different abilities- Split brain patients essentially have two separate hemispheres wanted to look at lateralization of function

o Does left do things different than the right? Are there higher order functions that one hemisphere does but not the other?

o Experiments: put info in left hemisphere, right hemisphere doesn’t have access to it – look at behaviour- If functions reside solely in one hemisphere and that hemisphere didn’t have the necessary info, person can’t

complete the task – because there is no communication between hemispheres - Experiment: in terms of getting information into a hemisphere, used divided visual field technique

o Remember contralateral relationship: patient fixates on central point, pathways are contralateral between visual field and hemisphere processing

o Then you flash information very quickly: long enough for them to see it, but take it away fast enough prevent eye movement so that they stay fixated and visual field stays divided

- Result: you can send different information to the two hemispheres and they can’t communicate-

- red = corpus callosum, which is severed- optic chiasm isn’t – completely intact

- Individual stares at fixation field- Flash: spoon to left visual field and apple on right visual field- SPOON:

o Left visual field, so ends up in right hemisphere visual cortex- APPLE:- Right visual field ends up in left hemisphere visual cortex- Sperry tries to get patient to demonstrate that they saw both words ask patient what they saw- For right handed individuals, 99% are left handed dominant for language, same for most left handers so with a

little bit a variability, almost everyone in a population has their left hemisphere dominant for language- Ex:- Right handed patient so you suspect language is in left hemisphere- Ask them what you just saw- If language is in left hemisphere, there are numerous pathways throughout left hemisphere visual info can

incorporate into language areas, and language can access visual information- Language centers in left hemisphere will access right hemisphere visual field – person reports seeing an apple- If asked if they saw anything else, they say no, since as far as language is concerned they report only info in left not

right hemisphere

- Then you wonder if info even get into the right hemisphere? What else can you do to get them to demonstrate it, how do you get them to access right hemisphere info?

- Can’t use language, so they can’t say or write but can potentially draw ito To tap right hemisphere information, they have to draw it with their left hando Recall: primary motor cortex in right hemisphere can access visual information in left visual field, can controls

left side of body doctor puts pen in left hand of patient and tells them to draw ito Patient says they don’t know what to draw, but encouraged to tryo They draw a spoon as soon as it’s drawn on paper, the left hemisphere can also access it – now they can say

it’s a spoon - Demonstrates that the two hemispheres aren’t communicating with another- Can also get them to reach under screen with left hand, and pick out object they saw

o Again, they report not seeing anything but will pull out the spoon with their left hand

o Left hand information is somatosensory info – recall that stereognosis is primarily in right hemisphereo Works because communication fully works within the right hemisphere, and RH knows you are looking for a

spoon the information just can’t cross over, there is no communication between the hemispheres

Experiment 1- You have a right handed patient, and present an apple to their right visual field can patient say what they saw?- YES: language is in left hemisphere, and visual information also goes to left hemisphere- Could also draw it with right hand- Or, as soon as they say apple out loud both hemispheres have access to it so could draw with left or right hand

Experiment 2: - RH patient, show hairbrush to left visual field – can they say what they saw?- NO: left visual field to right hemisphere, language in left side doesn’t have access to it- How do you get at info in the right hemisphere?

o Alternate method or respondingo Can get them to draw it with their left hand

- Right hemisphere has information, can express through behaviour sometimes you can have actions controlled by right hemisphere but left hemisphere language is the one that has to try to explain the behaviour

- Ex: fixating visual field, and you give instructions to do whatever is on the screeno Flash the word laugh on left visual field goes to right hemisphereo Patient laughs, but can’t explain why because instruction was in right side so left hemisphere has no idea o Left side will have to concoct a story confabulation not to deceive, but because left hemisphere where

language is located is trying to explain a behaviour when it doesn’t have information to give the true story- Ex: can also give two competing instructions

o Show “Pick up pencil” to right visual field, but “Stop” to left visual fieldo Right hand picks up pencil, but right hemisphere sees stop, left hands stops right hand

- Complex language is left hemisphere – syntax, putting words together – but doesn’t mean right hemisphere has no language capacity

- Originally believed that left was dominant hemisphere and right was just a backup, but now know right is just responsible for different things – for example, faces

- Recall: FFA fusiform face areao Homeotopic aka similar and present in both right and left hemisphereso Showing a face will activate both FFAs, but found that (through fMRI studies), the right hemisphere was very

specific to upright faceso looks specifically for upright faces so faster and more specific processing which fosters faster facial recognition

Chimeric figures task:- get patient to fixate on a point, and flash image- then you show them the full faces of the man or the woman and ask them which one they saw- if you ask them with speech they have to respond with language

o language is in left hemisphereo left hemisphere sees right visual fieldo so will point to the man

- or you can also ask them to used their right hand and point to who they sawo right hand controlled by left hemisphere which gets info from right visual fieldo so will point to the mano however, their reaction time is slower and they make more mistakes

- now ask them to used their left hand to point

o left hand controlled by right hemisphere so sees the woman in the left visual fieldo since right hemisphere FFA is specialized - processing is faster o with left hand, their response is faster and also more accurate, less likely to make mistakes during quick

identification Video Example

- Artist created images out of fruit or individual objects that looked like faces – does the patient see it as a whole/face or as the individual components?

- If you flash painting in right visual field left hemisphereo Patient reports not seeing a face, instead saw the elements rather than the whole

- Left visual field right hemisphereo Patient first sees that it is a face

- But this kind of processing isn’t just about faces and FFA right hemisphere is more for global processing while left is more for focal processing

o Elements vs. the whole: right is for the whole, while left is for the elementsSummary- RH: faces and more global processing- LH: more focal processing elements rather than the whole

Examples of Cerebral Lateralization of Function

• Left hemisphere– Language – Superior in controlling ipsilateral movement

• Right hemisphere– Spatial ability– Emotion– Musical ability

- Doesn’t mean right has no language ability- Recall: asymmetry in auditory cortex- Right hemisphere has larger Heschl’s gyrus aka auditory cortex- Better at extracting pitch and sound whether it be music or sound- Prosody: understanding sarcasm- Right hemisphere damage: usually normal language but lose ability to understand inflection and tone of voice

- Their own speech usually very monotonous -- Rh stronger musical ability - Left more ipsilateral tracts and controlling movement- Left hemisphere controlling left side - Right: superior for emotional processing- Perhaps related to FFA- And spatial abilities - RH: prosidy or tone of voice-

--

Speech Laterality and Handedness- We tend to see left hemisphere dominance for language, but can be variable- Handedness: left or right handed can play a role

o Dextral: right handedo 10% are left handed or sinestrals

- Left handedness: might be genetico Right handedness is dominant, and recessive gene is no specificityo Majority of individuals will have dominant right handed phenotypeo Then minor percentage of individuals who have no preference so randomly, so by random half become right

handed and half become lefto So percentage = 12% or so will be left handed o Can be influenced through environmental exposureo Over time, left handed people can become right handed by using it for a long time

- Right hemisphere = left hand- This development associated with handedness might be related to language functions- 95% of dextral are left hemisphere dominant for language – probably closer to 99%- Sinestrals: around 70% have left hemisphere dominance for language

o 15% have right hemisphere dominanceo 15% bilateral distribution of language – not saying both hemispheres do the same thing just both

involved in overall complexity- Doesn’t mean right hemisphere has no capacity for language

o Broca’s and Wernicke’s areas have homotopic pointso So regions in other hemisphere that match these points

- Right hemisphere can recognize words – as demonstrated in split brain patients

- Big role in tone of voice – Heschl’s gyrus bigger, so better for pitch of sound extraction- Also see a gender split- Males tend to be much more left hemisphere damage- Females: more of a split - more language in right hemisphere- When looking at patients who have had damage in left hemisphere like stroke- Men with left hemisphere legions compared to women – women don’t have as much aphasia from brain damage- Aphasia: problem with comprehension or production of language or both- Women: less aphasias from brain damage, suggesting that right hemisphere has some capacity for language and so

can compensate when there is damage in left hemisphere

Wernicke-Geschwind model of Language- Prior to this model: Broca and his “tan” aphasia

o Imaging, found out that his area had been damagedo That area just be involved in speech production = broca’s area

- Wernicke: his grad student, noticed that in addition to this, person had another strokeo Damaged more posterior regiono More posterior region was involved in speech comprehension = wernike’s area

- Geschwind and Wernicke came up with this model- Predominantly in temporal lobe - This area is involved in comprehnsions- Broca’s area involved in production- Different forms of language

o Speech: auditory – so have to involve auditory cortexo Reading: visual, so needs visual input from visual cortex that routes through angular gyruso To get language out, speech: primary motor cortex

- Primarily in left hemisphere- Area involved with language production Broca’s area- Wernicke’s area: comprehension

Listening to someone specking- Primary auditory cortex- So Wernicke’s area so close to it makes sense- Receives input from primary and surrounding secondary auditory cortex- Wernicke’s area creates comprehension- Feeds forward to Broca’s area - Major tract called arculaite fasciluclus- Relays information from Wernicke’s to Broca’s- Broca’s has incoming info: responsible for formulating response- Then output feeds into primary motor cortex – which is why Broca’s is so close to it

If reading outloud - Routes into angular gyrus first, then into wernicke’s area- Then to Broca’s -

Aphasias

- Can have damage to a region – and as a result, should see deficits in language- Called aphasias- When diagnosing, need to make sure problem isn’t motor related- And also that it’s not a psychiatric condition, or dementia, etc- Have to rule out other things to insure it is a purely language based problem- Imaging brain will help

Broca’s Aphasia- Production of language: person has problem with producing language- Not because it’s a motor problem, not htat motor cortex can’t send signals- Broca isn’t giving motor cortex appropriate signals for output- Usually patient has telegraphic speech- Interconnecting words missing, struggling with key words as well- “walk dog” when trying to say that they are going to walk the dog- Some might be better with writing than speaking, but some both have deficiits- Formulation of response , onse step before motor cortex that is the problem- Also called expressive aphasia- But still have full comprehension if wernicke’s area still inctact0 just problem with getting communication back

out- Also understand that their language production is lacking – so very frustrating for them-

Wernicke’s Aphasia- Intact broca’s area

- No problem talking, can produce language- Bbut have prolems compredhending language- Can’t even comprehend own language

• “You know that smoodle pinkered and that I want to get him round and take care of him like you want before"

- Word salad- But might be perfectly correct geramatically just makes no sense- Receptive aphasia: receiving communcitaiton -

- Extremely rare to have one purely broca’s or wernicke’s- Usually see a mix-

Damage to Arcuate fasciculus- Passage from roca’s to W- Conduction aphasia- Disconnection: - Inability to repeat words just heard- Comprehension & speech normal- Intact wernicke’s and broca’s- Can understand conversation and formulate response- Suggesting AF isn’t the only way these two areas communicate- Just a major connection- Language can incorpaotate higher order areas- Might not evenknow they have aphasia- But problem with rote repintion- Repeat after me- Cat chased the dog- Can’t repeat word for word- So AF required for complete transfer, carbon copy- While higher order is more for abstract thought, etc-

Left angular gyrus• Alexia (inability to read)• Agraphia (inability to write)

- Can have these conditions without each other- Can’t read: visual processing issue- Usually invles more posterior- Partly parietal, partly temporal- Agraphia: can’t write or type

B and W’s areas- Usually damage in one won’t affect the other-

Wernicke-Geschwind Model: Problems

• Lack of evidence that damage to various parts of cortex has expected effects– Surgery that destroys only Broca’s area has no lasting effects on speech– Removal of much of Wernicke’s area has no lasting effects on speech

- Can hae a person with damage to Broca’s area but with no associated problems- When it comes to loking at people with surgery- Can take images- General images- But with surger you have excact images, whathas been removed-

Lack of permanent disruption of language related abilities after surgical excision f the classic W-G language areas

- Yellow = damage removed- Dotted – areas inoled in language- Would expect certain deficits, ut don’t demonstrate typical aphasia

- So very verialbe from person to person-

Current Status of W-G Model

• Empirical evidence supports:– Important roles played by Broca’s & Wernicke’s – Many aphasics have damage in these areas– Anterior damage associated with expressive deficits & posterior with receptive

• No support for more specific predictions:– Damage limited to identified areas has little lasting effect on language– Brain damage in other areas can produce aphasia– Pure aphasias (expressive OR receptive) rare

- Many people who are aphasic wually have damage in these areas- One of the two or maybe oth- In general- More anterior frontal lobe damage, broca’s area is more associated with expressive aphasia- More posterior damage, tend to have receptive aphasia, comprehensions problems- General rule fits model- Ut many exceptions to the rule- So doesn’t fit every single person- Handedness and gender play a role- And damage in other areas can cause language problems

- Pure aphasias – only b or W very rare-

Functional Brain Imaging and Localization of Language

• Bevalier’s fMRI study of reading– Sought to establish cortical involvement in reading

• Reading sentences versus control periods (strings of consonants)– Areas of activity were tiny & spread out– Active areas varied between subjects & trials– Activity was widespread– Yet, if you average across subjects…

- Had people read- Looked at activation of brain- Wanted to find which cortical areas were activated- Person was just reading strings of consonants – reading b, g, z, k etc reading letters outlide- Baseline coniditon- Then had to read sentences- Subtract to find differences- Which area was particular to reading words, higher order production - Areas were different from person to person, great variability- But with averaging- This is what you get:

FIGURE 16.16 The areas in which reading-associated increases in activity were observed in the fMRI study of Bavelier and colleagues (1997). These maps were derived by averaging the scores of all participants, each of whom displayed patchy increases of activity in 5–10% of the indicated areas on any particular trial.

- Looks like WG model- WG might fit as an overall general rule- So kind of the average you see, but doesn’t mean you can take the average and apply ti on an individual basis- Everyone bariable and different- General left heimpshere for language, but how’s its spread out in the hemipshere doesn’t always perfectly fit

the model

- Some people: can’t have spontateous production- But can repeat-