History of Localizing the Mind PDF

Summary

These lecture notes detail the history of localizing the mind, starting with ancient Egypt and moving through to modern neuroanatomy. They describe key figures and theories about the brain and how different parts have different functions. The lecture includes discussions about the ventricular doctrine, phrenology, and more.

Full Transcript

Lecture 08/22/23 History of Localizing the Mind ● Ancient Egypt: mummified all parts of the body so that their leaders would go into the afterlife with all that they need BUT they would scoop out the brain and throw it in the trash ➔ Ventricular Doctrine (270 BC - 1500’s AD): - People started to be...

Lecture 08/22/23 History of Localizing the Mind ● Ancient Egypt: mummified all parts of the body so that their leaders would go into the afterlife with all that they need BUT they would scoop out the brain and throw it in the trash ➔ Ventricular Doctrine (270 BC - 1500’s AD): - People started to be like “wait a minute when someone’s head gets damaged they start to act different” (ex: more anger, loss of memory) -> so the head/brain must be necessary for more - They began looking at pockets in the brain that held fluid and believed that’s where thinking happened and that maybe all the rest of the brain was really just protecting that fluid ● By around the 1500s they began to assign processes to different ventricles that had fluid in them - First Ventricle: integration of sensory information - Second Ventricle: Cognitive processes - reasoning; judgment - Third Ventricle: Memory ➔ 1543 - Andreas Vesalius - Began to think that the fluid isn’t the cause for it (the thinking process) but that it was rather the brain itself, the matter (i.e.: the white matter) ➔ 1685 - Raymond de Viessens - Began to think that the white matter wasn’t necessarily it because when people’s brains get damaged, the white matter isn’t damaged (thinking it’s the grey matter) ➔ 1664 - Christopher Wren (drew for Thomas Willis) - Began to look more like a brain with different pieces, but they didn’t realize that there were different parts of the cortex. Rather they thought it was all one big thing that went together ➔ 1782 - Francesco Gennari - Began taking slices of the brain - This was important for differentiation. Different parts of the brain do different things, they’re not all the same ➔ Franz Josef Gall and Johann Spurzheim (late 1700s - early 1800s) - Localized psychological functions to different regions of the cerebral cortex - Famous for phrenology (idea that you can feel the head and from different bumps and indentations you could figure out what kind of person they are) Lecture 08/24/23 Cont. History of Localizing the Mind ➔ Franz Josef Gall ● Although he took a misstep with phrenology he was a brilliant anatomist - Showed that 2 halves of brain are connected with white matter tracks (commissures) - First comparative anatomist of brains (looked at cortex of more intelligent animals with bigger brains) Issues with phrenology 1) Assumed that the shape of skull reflects shape of brain 2) Choice of psychological qualities - Wasn’t well replicated -> 27 highly complex faculties 3) Didn’t take discrepant findings of non-replications seriously Localizationism vs. Globalism ➔ Pierre Flourens (1822) ● Basically said that the bumps in the head thing didn't make sense, but went further to say we should think about how different parts of the brain do different things (great anatomist) - Performed surgical brain removal on animals The Aggregate Field View came out of this ● The whole cortex participated in each behavior ● The idea that he came up with is that the more brain he took out the worse the animal was ● So essentially he believed that the amount of spared tissue was what was actually important ➔ Localization makes a comeback with Paul Broca in 1861! ● In 1861, Broca published a paper about a patient of his (Tan). Tan was only able to say tan although he seemed to have an idea of what other people were saying to him (when he got really mad he could swear) ● Brings the idea that damage to a specific brain area causes a specific deficit (in this case its the frontal lobe and speech) - Gall -> John Baptiste Bouillaud -> Ernest Aubertin ● Broca began looking for more patients with damage and doing experiments. 5 years later he wrote another paper that talked about all the patients he’d found ➔ John Hughlings Jackson (1870) ● He began looking at seizure patients: Progression of seizure followed an ordered path ➔ Santiago Ramon y Cajal (1900s) ● 1906 Nobel Prize in Psychology/Medicine (shared it with Camillo Golgi) ● “Neuronal doctrine” made by Cajal, he had the idea that each of the neurons were separate pieces vs. “Reticular theory” made by Golgi, he had the idea that it was one big map/all connected ● It ended up being that Santiago was correct Navigating the brain ➔ The nervous system ● Central Nervous System (CNS) ● Peripheral Nervous System (PNS) ➔ Layers of protection ● There are lots of things (grey matter) that protect the brain ➔ Ventricles ● Fluid-filled sacs (cerebrospinal fluid) ➔ The orientation ● Dorsal (superior); Caudal (posterior); rostral (anterior); ventral (inferior) -> Reference Figure 2.22 in the book ● Different slicing of the brain: coronal plane, horizontal plane, sagittal plane -> Reference Brain Atlas in canvas ● Know the four major lobes and sulci (so the four major divisions) -> Reference Figure 2.36 in the book ● Look at the Key Gyri (think about it in terms of superior, inferior, etc.) -> Reference Figure 2.34 in the book Cells Overview ➔ Neurons ● Lots of different types of neurons that take in information differently ➔ Glia/Gilal Cells/Neuroglia ● Glial Cells Reference my ans wers in the PollEverywhere for what they each do Review - IPAD notes Lecture 08/31/23 Dividing The Brain ➢ How is the brain divided? ● Gross Anatomy (the big structures) ● Fine Neuroanatomy: Cytoarchitectonics (the cells themselves and the architecture of the cells) ● Function ● Chemicals (neurotransmitters) ★ Helps us to understand what different parts of the brain might be doingf ➔ Fine Neuroanatomy: Cytoarchitectonics ● ● Neurons: different functions, have different number of dendrites (diff parts of the brain doing diff things) Cytoarchitectonics: - Can start staining the brain with diff chemicals and stains to highlight diff parts in the cortex “Brodmann’s areas” (Korbinian Brodmann) - 1909 - Was using nissel stain to divide the cortex (into about 50 different areas) - Did all of this before color publishing so he came up with a bunch of different patterns to represent diff areas in black and white - The numbers just represent the order in which he went in - He was able to show that this was pretty consistent across diff people ➔ Dividing by Function(s) ● ● ● ● Visual Processing: Occipital Lobe Auditory Processing: Temporal Lobe Somatosensory & Spatial Maps: Parietal Lobe Motor & Executive Functions: Frontal Lobe (decision making, judgement, reasoning, etc.) We also have systems in the brain ● Limbic system: important for emotion processing ● Basal Ganglia: different sections; important for motor control and motor coordination ➔ Dividing by Chemicals ● Neurotransmitters - Go all over the place and overlap (so not everything has its own neurotransmitters) - This is why doing things like drug therapy can be tricky because you could want to specifically affect one area and end up affecting another as well Information Processing ➢ Neuronal Signaling ● How do neurons work? - use electrical and chemical signals to send information between different areas of the brain, as well as between the brain, the spinal cord, and the entire body ● How does the “strength” of the input vary? - Action potential frequency - Depends on how many inputs you're getting (some have lots of dendrites) - Might be getting excitatory and inhibitory inputs and that determines if the cell is getting ready to fire or not - You could possibly getting lots of excitatory inputs and so it’s more excited ★ The neuron is doing a lot of processing since there’s a lot of info that goes into whether it’s going to fire or not ● How does the “strength” of the output vary? - ● “All-or-none phenomenon” -> action potential is either going to fire or it’s not “Refractory period” -> the period when the neuron has to recharge before it can fire again (limit) Gap junctions/electrical synapses (advantages/disadvantages?) (RARE) - 2 neurons that are next to each other and have direct connections into the cells -> they’re basically sharing that action potential (the chemicals going through) - Advantages: Very quick and coordinated between neurons - Disadvantages: don’t have any plasticity because it’s not taking inputs from a lot of diff places or basing on the chemical environment (not flexible) ⅓ - The Methods of Cognitive Neuroscience ● Neuroanatomy: The study of the nervous system’s structure -> identifying parts and connections - Gross neuroanatomy: focus on general structures and connections - Fine neuroanatomy: focus on components of individual neurons ★ Can visualize neural development - Prenatal neurons typically have lots and lots of connections and those prune away in adults ★ Visualize cell densities across different brain regions ➢ Histology: study of tissue through dissection ● Anterograde tracers: indicate where the injected region outputs to ● Retrograde tracers: indicate where the input to a particular neural region originated from Lecture 09/07/23 Neurology/Neuropsychology ➢ How does damage to the brain affect an individual? Think about Paul Broca’s patient in 1861 because that was the first real cause of neuropsychology (John Hughlings Jackson studied epilepsy) ➢ Etiologies of Neurological Disorders 1) Vascular Disorders (disorders of blood flow): ● Most common: Stroke -> a sudden disruption of blood flow to the brain 2) Tumors ● Gliomas: abnormal reproduction of glial cells ● Meningioma: originates in the meninges ● Metastatic: originate in other parts of the body 3) Degenerative and Infectious Disorders ● Alzheimer's 4) Epilepsy: excessive and abnormally patterned activity in the brain ● Seizure: transient loss of consciousness (dangerous) 5) Trauma ➢ Issues in Neuropsychology ● Case study vs. group study - Case Study: putting your all into one person and studying that person, looking into their history, etc. -> good for trying to map out a specific person - Group Study: if something is in the brain, is it specific to that person or is that the same case for everybody ➔ Con: if you’re putting in so much time searching for people around the world who have this issue then you’re not going to be able to put in enough time gathering specific data ● Single dissociation vs. double dissociation - Single dissociation: - Double dissociation: ➢ Postmortem Studies ● Through most of history, this was the only way to examine the human brain ● Still used today for detailed analyses of brain damage because some things don’t show well on an FMRI or MRI scan ● Invention of CAT/CT scanning allowed living brain to be “seen” for the first time Structural Neuroimaging ➢ CAT scans and MRI scans (CAT scans are much thinner) 1) CAT scan: Computed Axial Tomography ● It’s computed which is why it took them a while to develop even with x-rays ● You must take pictures from all different sides and then compute what occurred 2) CT scan: computed tomography ● Easy to do because it’s not your full body so it helps with claustrophobia ● It puts x-rays in you so you must be careful with how many times you receive it 3) MRI (magnetic resonance imaging) ● Gives you better resolution than a CT, so you’re able to see more ● People still have CT scanners in hospitals and such because MRIs are essentially a huge magnet and if you have metal in your body, the MRI can essentially move it and that’s not good (it’s a specific kind of metal, so some metals are fine but they have to be able to say that for sure) ● MRIs are also super expensive, CT scans are cheaper ● Can show you different density of tissues/material (muscles, white matter tracks, spectroscopy, veins, arteries, structure, etc.) -> good for several things ● All these types of MRI scans have high spatial resolution but very low temporal resolution Cognitive Psychology ➢ Interested in how people think -> what’s going on in our brain ➢ The History: Philosophical Antecedents ● Rationalist - Logically go through it and make sure that your theories actually make sense - Acquire understanding through thinking and logical analysis - Plate (~400 BC) ● Empiricist - Acquire understanding via empirical evidence - Aristotle (~350BC) ➔ Rationalism vs. Empiricism ● Theories are insufficient without data, but data can only be fully explained with theories (full circle moment with theory and data) ➢ Before Cognitive Psychology ● Behaviorism (early 1900’s): - Scientific study of observable, quantifiable behavior - “Behavior is the ultimate topic of psychology” -> stimulus-response and reward/punishment contingencies - “Anti-mentalistic” - Idea that we just need to know how individuals behave - Thought = “subvocal talking” - Mental events are unobservable and unnecessary to a scientific explanation of psychology “The Behavior of Organisms” by B.F. Skinner; 1957 book “Verbal Behavior” by B.F. Skinner ➢ The Cognitive Revolution (1950’s) ● Article: “the misbehavior of organisms” -> said there’s something else going on that behaviorists just don’t seem to be accounting for ● Linguistics -> Noam Chomsky wrote a review of B.F. Skinner’s book “Verbal Behavior” where he basically stated that behaviorists can’t explain language and if they can’t do that then there are several cognitive processes that they’re unable to explain ● World War 2 happened around this time ● The invention of the computer also happened around this time (AI) -> you can’t just smack a computer or reward it to make it do something, you have to actually give it a step-by-step code; this brought up the question of whether the brain was essentially the same way ➢ Cognitive Psychology ● The things above led to cognitive psychology ● Biggest thing they look at is how fast you do it and how many mistakes you make because this can tell a lot about a person’s cognitive processing at the time ➔ Assumptions of Cognitive Psych 1) Mental processes exist! 2) Mental events take time (this ties into that observable part -> they can be measured) 3) People are active information processors 4) Information processing depends on internal representations which undergo transformations 5) Human cognitive processing abilities are limited Lecture 09/12/23 + Lecture 09/14/23 The Methods of Cognitive Neuroscience ➢ The Stroop Task ● It’s been almost 100 yrs and we still use it today ● The more cognitive tasks you’re doing the harder it is for your brain to do all (cognitive load) ● How much can you control your cognitive processes and how accurate it is? ● How automatic is your cognitive process of certain things? How well can you inhibit that automatic process? Control Condition: Nonwords (XXXXX) -> just looking at the ink color Experimental Condition 1: Color word matches ink color (BLUE) - Faster than control because of that benefit Experimental Condition 2: Color of word does not match ink color (GREEN) - Slower than control or more errors = “cost” ● What does this task do? - Demonstrates automaticity of cognitive processes - Demonstrates difficulty in stopping an automatic cognitive process Measures Executive control (and inhibition) ➢ Cognitive Psychology: Methods ● Overt behavior responses - Accuracy - Reaction time/response time ● Chronometric methodology: - Subjects’ response time can be used to measure the degree of processing required to perform a task or hypothesized mental computation ➔ Controlled Lab Experiments ● Reductionist Approach - Understand complex mental events by breaking them down into separate components ● Isolate process of interest, and control for other factors ● Remember independent and dependent variables! ➢ Sternberg’s Memory Search Task ● One of the first cognitive psych experiments ● Subject sees a bunch of letters on the screen and then there’s nothing on the screen (you keep the letters in your memory) THEN a letter pops up and the subject quickly presses yes or no to whether that letter was part of the original letters on the screen 1) Perceive Stimulus 2) Compare stimulus to what you have in your memory (search/comparison) 3) Decide (yes/no) 4) Respond if it was yes or no ● If you remove the number of items in a memory set then their response time will be faster (ex: showing 3 items in the memory set will lead to a shorter response time than 4 items) -> IF IT DOESN`T MATCH (i.e. the letter is NOT in the memory set) ● If it DOES match (i.e. letter IS in the memory set) -> you have an exhaustive search (you search an entire memory set even if you see that it’s there, you check all of them) - This search process is an automatic process which is why we do it. It goes so quickly that it’s easier for our brains to just search through them all (takes 38 milliseconds to look at each one) -> stopping that automatic process is going to take more time and effort than just letting it run through Manipulate the steps in different ways ● For example, if they wanted to manipulate the perception stage, they’ll “mask” the letter with a pattern or something -> the rest of the steps would stay the same BUT the perception stage would take longer Recording Neural Activity ➢ Human Electrophysiology 1) Electrocorticography (ECoG) ● Sub-dural, multielectrode recording ● Actually putting the electrodes on the brain ● Only done for cases of severe epilepsy to figure out whether the seizures are starting from ● On the surface of the brain, doesn’t go deep in so you’re not damaging the brain (still giving you more activity) ● What is it actually doing? It shows that when there’s a bunch of neurons together, those pyramidal cells are lined up in a certain way and when they’re getting excitatory their potential is changing -> that part of the brain is likely receiving info/active (gives you big electrical field that you can actually record) - Positive/negative are the same (ex: one isn’t inhibitory and the other is excitatory) it’s just how the neurons are positioned 2) Electroencephalogram (EEG) ● Put an electrode on someone’s head and record brain activity ● Hans Berger (1924) -> alpha frequency is the one at the bottom (the first one that got identified) ● Always at least 2 electrodes on the head because you have to have a comparison - Ongoing activity ● Important for showing the general states of a person (ex. Excited, asleep, etc.) but not good at showing specific instances 3) Event-Related Potential (ERP) ● The ways we can use EEG to look at specific events ● You’re looking at the potential that’s related to a specific event ● Tiny little part that’s JUST related to an event and kind of rides on top of the ongoing EEG ● Can show you all these different things that are happening in real-time (your brain is doing all of these things reallllyy quickly) ➢ Localizing EEG and ERPs ● Strength of EEG: the speed ● Limitation of EEG: localizing it (think about it in comparison to MRI which can pinpoint very specific things) However, we still have EEGs because MRIs are really slow (this can be a problem if you want to know the process) ➔ ➔ Forward solution ● If you get a good model from an MRI or something, you can use that model to determine what it looks like on the outside of the head Inverse Problem ● This is what we use in the real world ● You’re working backward 4) Magnetetoencephalogram (MEG) ● Looking at the magnetic field not electric field ● Continuous MEG and event-related fields (ERF) ● Anytime you have an electric potential you’re going to get a magnetic field (you can measure this magnetic field) ● It can localize stuff better than EEG (not always, but still) -> has the same timing as EEG - Still have that inverse problem since you’re still kind of guessing from stuff on the outside of the brain where these things are coming from ➢ Functional Neuroimaging (FMRI and PET) ● Both of them rely on blood supply/flow -> the idea is that blood flow goes where the brain is active -> will also pick up draining veins and such so that is a limitation (has a delayed response) ● First idea of this came up in the 1800s (Aneglo Mosso) -> had a teeter totter that people would lay on. He would have people either relax or think about something and he thought that blood flow would increase in the brain when they’re thinking about something and then the teeter-totter would drop lower in the head area (brain would get “heavier” because more blood). This obviously didn’t work very well 1) PET (positron emission typography) ● Not used as often as FMRIs ● The scans will look similar and then you can do some comparison ● In studies they’ll plot it on top of an MRI so you can see it better ● Can be used for different things in the body (not as often used for cognitive neuroscience) 2) Functional MRI ● The Structural MRI has more precision than the Functional MRI -> they’ll take the hot spots from the functional MRIs and typically place them on top of a structural MRI ● Looking at something specific regarding the blood flow (complex) -> decreased ratio of deoxygenated hemoglobin to oxygenated hemoglobin (BOLD effect) - BOLD = blood oxygenation level-dependent effect Tells you what parts of the brain are more active Activity = oxyhemoglobin becomes deoxyhemoglobin -> an increase in activity means an increase in deoxyhemoglobin Deoxyhemoglobin is magnetic so it’ll disturb your neurons (MRI signal decreases -> doesn’t go down by much and it’s really hard to see) After the neurons have been active there’s a huge increase in blood flow so there’s more oxyhemoglobin and it isn’t magnetic so the MRI signal increases ➔ First use of BOLD FMRI for functional mapping of the brain was done similarly to a PET scan (variable stimulus was given and they turned it on and off in variable time) ➔ Over time they realized you don’t need to have a bunch of trials and look at this plateau because this is a quick process -> instead you just need one stimulus and look at the pattern for that (single-trial/event-related design) ★ Block-design FMRI design vs. Event-related FMRI design ● Block-design is a little more powerful because it’s easier to see when it’s down or up, event-related is noisier ● Event-related is more flexible because you can randomize your conditions and such ➢ Advantages of fMRI over PET ● Higher spatial and temporal resolution ● No radiation ➢ Advantages of PET over fMRI ● More comfortable environment (can help with claustrophobia) ● No danger from foreign materials (metal) in the body ● Allows other things to be tracked in the brain (besides just blood flow) -> *brain metabolism (glucose), neurotransmitter receptor density, brain amyloid imaging (possible marker for Alzheimers) Optical Imaging ➢ Functional Near-Infrared Spectroscopy ● Using near Infrared light to look at the brain ● Shining light into the brain and looking at the reflectance -> as the oxygen levels change, the reflectance changes as well ● Not as precise as the other methods we talked about ● Can be useful because it’s totally mobile, you can just strap it on an individual’s head and they can walk around -> easier for kids and better for measuring activities that require you to move ● It works because the skin, tissue, and bone are mostly transparent to NIR light ● More activity in neurons -> more glucose consumed (oxygen used to metabolize the glucose) ● Oxygenated hemoglobin & deoxygenated hemoglobin have different absorption spectra ● fNIRS measures changes in relative hemoglobin concentration Neurostimulation ● Stimulating the brain and looking at what that does ➢ Damaging the brain for science Non-Human animal studies ● Selective lesioning (damaging part of the brain) -> taking out a part of the brain that you believe does something and if you remove it the animal should no longer be able to do that thing ● Chemical deactivation (“temporary lesioning”) - Give them a chemical that causes it to be temporarily deactivated ● Selective freezing ● Genetic knockout procedures - create animals that lack certain kinds of cells or receptors Human studies with induced lesions??? (TMS, tDCS, tACS -> non-invasive) ● TMS (transcranial magnetic stimulation) - Stimulate one part of the brain and look at what happens if you stimulate that area (causes neurons to be active) - Used to use an oval-shaped coil but there’s not many parts of the brain that are shaped like this so now they use a figure-8 coil because it gives you a more precise area ➔ TMS: 2 techniques (just when you come into the lab, not ongoing) ● Create temporary “patients” (also known an rTMS repetitive TMS) - You keep pulsing an area for like 10 minutes or so and for 10 minutes after the brain is still recovering and there isn’t activity (that area of the brain isn’t being used temporarily) - Avoids problematic tissues in patient studies: plasticity, reorganization, compensatory processing, and not having a “pre-lesion” assessment ● Test timing of cognitive processes (also known as “single pulse” TMS) - You’re seeing when in time an area of the brain was important/involved in process (precise chronometric studies) - TMS studies have shown an area of the brain may be critical at multiple times ★ Limitations of TMS ● Each pulse results in a loud click/snap ● Tactile sensation at site of stimulation ● May stimulate facial nerves ● Need to consider: - Control sites of TMS (“sham-TMS” -> you hear click but nothing happening) - Control conditions - Timing ● Expensive equipment (and if you’re using MRIs in conjunction then you have to pay for that as well) Electrical Stimulation ● Invasive stimulation methods - Pre-surgery mapping ➢ Transcranial direct current stimulation (tDCS) ● Not a strong electrical current, actually pretty weak ● Transcranial ● Enhancing or depressing the baseline a little ● 2 electrodes, a battery, and a device to control the strength of the current - Anodal electrode (increases excitability) - Cathodal electrode (decreases excitability) ★ Advantages vs TMS ● Less invasive ● Permits decreasing or increasing excitability ● Much cheaper ★ Disadvantages vs. TMS ● Low spatial precision ● Limited understanding of mechanisms ● Relatively weak ➢ Transcranial Alternating Current Stimulation (tACS) ● Same set-up Lecture 09/19/23 Perception ➢ ESP: Extra-sensory perception ● Is there a way we can sense things beyond our 5 typical senses ● Dr. Paul Joire (1892) -> influenced by Franz Mesmer’s work on hypnotism ● Joseph and Louisa Rhine (1933) at Duke University began looking into these - Used “Zenner Cards” -> idea was that there was a pack of them and there were like 5 different shapes on them. Could the experimenter flip over the card and the participant be able to guess the shape of the card without seeing it? Not just by chance, beyond that -> they found the answer to be yes, it wasn’t up to chance - When other experimenters did this they could not replicate and found confounding variables (ex: could see the reflection in the glasses of the experimenter) ● There's no evidence that we can get stuff beyond sensation and perception ➢ A few case studies about perception ● Case 1: Franz list (musician) -> explains to the orchestra the sound he wants them to make through color (ex: that’s too violet, more rose please, etc.) ● Case 2: Michael -> feels things in his arm based on the texture of food ● Case 3: Vladimir -> different letters are different colors (and different color shades) (ex: the yellows include E and Is) Synesthesia: When the senses mix ● ‘Together’ ‘sensations’ (1892) ● A lot of time people don’t realize that other people don’t have this (this is their normal) ● How do we test this? - Ask people to do a visual search - Stroop-type task (ask them to name the ink color of a letter or number) -> have a harder time when it doesn’t fit the colors they see them as (experience more interference) ➔ Different types ● Grapheme -> color synesthesia ● Number -> Spatial ● Visual motion -> sound ● Sound -> color (shape/form) ● Lexical -> gustatory synesthesia ● Alphanumeric personification ● Somatosensory -> emotion ➢ Visual Perception ● Visual = “exteroceptive perception” ● Perception at a distance (similar across mammals) ➔ Neuroanatomical Approach 1) Retina -> light comes in through the cornea, through the lens, and hits the back of the retina (that’s where the rods and cones are) -> first part of the human body that takes in the visual a. Photoreceptors (over 250 million) - Rods: low levels of light - Cones: color vision b. Bipolar cells c. Ganglion cells (2 million) -> optic nerve - Optic nerves divide in the brain: - 90%: retinogeniculate pathway to geniculo-cortical pathway (where most of our conscious perception occurs) - 10%: other subcortical structures 2) Lateral Geniculate Nucleaus ● 6 layered organization ● Organizational principles: - Layers 1, 4, & 6 from contralateral nasal hemiretina - 2, 3, & 5 from ipsilateral temporal hemiretina - Top 4 layers = Parvocellular or P-system - Bottom 2 layers = Magnocellular or M-system 3) Primary Visual Cortex ● Broadmman’s Area 17; V1; Striate -> all refers to the same thing (the back of the brain) ● 3 pathways: - M pathway - P-blob pathway - P-interblob pathway 4) Prestriate cortex (Extrastriate cortex) ● 3 subregions: - M pathway -> thick strip region - P-blob pathway -> thin strip region - P-interblob pathway -> interstripe pathway ➔ Know: Information from retina converges to go through optic nerve and then diverges into 3 separate streams from LGN through V1 to extrastriate regions. ➔ Know: multiple visual areas -> processing diff aspects of visual world (in monkeys) BUT is there evidence that human vision is similar? We can turn to cognitive psych and see that it is **MAKE SURE TO KNOW WHAT V1, V5, V4, ETC> DO** Cognitive Psychology 1) Visual Search - Feature search -> just searching for one feature (quicker) - Conjunction search -> have to search through 2 different aspects (shape & orientation) (takes more time) ● Allows us to examine what makes an elementary visual feature ● Fits well with cell recordings ● Unique color, shape, or motion pops out (pop out equally well) ● Feature Integration Theory (Treisman, 1980) 2) Illusions ➔ Know: From behavioral responses ➢ Human Neuroimaging ● PET studies of color and motion in the human brain - Experiment 1: Color - Condition 1: Stationary display of multi-colored patches - Condition 2: Stationary display of gray patches - Experiment 2: Motion - Condition 1: moving display of black-and-white patches - Condition 2: stationary display of black-and-white patches Lecture 09/26/23 Synthesia ➢ What is linked? Could be several things (mixing can be at diff stages of our processing): ● Form and Color (7 vs. VII -> diff color) ● Concept and Color (7 vs. VII -> same color) ➢ Real “perception” of color? ● If someone sees a 7 in green ink they’re able to tell you that it’s green BUT they’ll feel like something is wrong with it ➢ Fovea ● We can see color good in this area because this is where the cones are ● People with certain forms of Synthesia they can identity the color of something (ex. A red 7) but when the number is moved toward their periphery they’ll began to see it as the color they associate with it ➢ White matter tracts and synthesia ● Some regions show higher white matter connectivity in synesthetes compared to control ➢ How does this occur? ● Crossed-wiring? - New connections -> extra connections that other folks don’t have - Incomplete neural pruning ● Disinhibition of neural connections? - Sometimes people can temporarily lose or gain synthesia so there’s the idea that it’s not permanent neural connections BUT rather that it’s something that we suppress but all have - “Acquired synthesia” (in non-synesthetes) -> people have something in the brain that causes them to acquire it (ex. Concussion, drugs, etc.) - Anectodal reports of synthetes losing synthesia when taking medications ★ Suggests that maybe everyone has these connections but in some folks it’s evident and shown but in others it may be that they’re repressing this ➢ Synthesia in everyone? ● Associating color with personality (ex. Cool blue) ● “She dresses very sharply” ● “Someone is acting salty” ● Matching colors to subjects (ex. English is red) ➔ Newly discovered: Motion-sound synesthesia Neural Plasticity ➢ MEG study: ● Musicians that used string instruments vs. Non-musicians ● Found that the musicians had a higher reaction/activation when their finger was touched than the healthy controls ● Went deeper and looked at how long they’d been playing these instruments -> Longer they’ve been playing the stronger the activation/respons ● So -> using it more makes it stronger and stronger ➢ Visual deprivation ➔ FMRI study: Tactile stimulation during 5 days of being completely blindfolded ➔ For the first few days, when the finger is touched the visual cortex isn’t activated. But on day 5 when the finger was touched the visual cortex was activated again. On Day 6 when they removed the blind fold it didn’t activate again. ➔ Suggests that the connection to the visual cortex is usually just sitting there but doesn’t have a need to be activated ➢ Engineering new inputs (adaptation to new inputs) ➔ Retinal Inputs ● Put device behind the eye and it picks up the signals and stimulates the different nerves in the eye and sends it off to the optic nerve (basically making new retina for someone) ➔ Prosthetic Limbs ➔ Cochlear Implant ● There’s a microphone that sends a signal to the attachment in the back of the head and it sends the signal down the cochlea. This is for people whose hairs don’t work and this gives them a little sound ● Cochlea is distributed by frequency coding and they can’t set that up exactly but to the best of their ability (can only get like 12 different frequencies) Object Recognition Neuropsychology of vision ➢ Scotoma: “field cut” - spatial region of the visual field in which the patient is incapable of detecting anything visually ➔ Case study ● Patient D.B. ● Right striate cortex was surgically removed ● Reported being blind in left visual field ● The person studying D.B. noticed that if he was walking and something was in his left visual field he would walk around it/avoid it but claimed he couldn’t see it. D.B. could move his eyes to visual stimuli in his blind spot “Blindspot” (weiskrantz, 1986) ● Residual function could reflect: 1) Spared V1 tissue (little pockets still there) 2) Extrageniculate vision (other pathway - the 10%) -> e.g. superior colliculus (very important for eye movements and doesn’t need V1) ➔ Extrageniculate Vision (Rafal et al., 1990) ● Move their eyes to a target in their good field ● Found that their eyes would move slower to the target when there was a distractor in the bad field or blind field ● Saccade latencies: significant effect ● BUT: when they asked them to press a button to represent this (manual) they found no effect -> were never conscious of it ➔ Hamster lesion studies (schneider, 1969) ● Had patterns and one of them was associate with a treat ● If you take out their visual cortex (V1) they can no longer do that task (discrimination task) of finding the one of the treat ● BUT they can still do the localization task ● If you take our their colliculus it’s flipped -> can’t do localization task, can do discrimination task 3) Residual cortical functions that bypass V1 ● Overall (blindsight summary): - V1 is important for complete visual awareness (and ability to consciously discriminate objects) - Superior colliculus important for orienting to objects even without conscious perception - Other visual areas may support perception features not bound to objects (distrubted system) ➢ Computational issues with object recognition ● Viewer-Centered: Every position, every illumination scenaria has its own template in memory - Only later is the semantic knowledge merged from across diff viewpoints - Require huge number of template matching units ● Object-centered: Sensory input defines basic properties that are fit together in a certain way and it doesn’t matter how you view it because the pieces are still in that orientation ● Is object recognition “viewer-centered” or “object-centered”? - Problem: Variability in sensory info (e.g., viewing positions; illuminations; color constancy (ex. shadow); occlusions) -> Would need a different template to represent all possibilities ➔ fMRI evidence: object vs. viewer centered ● Repition Suppression Effect: Once you see something the next time you see it you don’t have the same level of activation to it (your brain just saw it, it’s not going to use so many more resources again) ● ● ● Left fusiform area: Even in a different view you still don’t take as many resources, same activation level (object centered) Right fusiform area: In a different view, your activation level spikes back up as if you hadn’t seen it before (viewer center) Suggests that our brain is doing both ➢ Do “grandmother cells” exist? ● Cells in inferior temporal cortex (monkeys) ● Problems with this hypothesis: - would require so many cells -> implausible - Assumes that final percept is driven by a single cell - Can’t account for categorization ➔ Alternative: Ensemble Coding (more efficient and explains a lot of the mistakes we make) - Recognition is due to collective activation over many complex feature detectors (explains why we confuse similar items) - Accounts for novel object recognition - More robust systems - “Selectivity” in single-cell recording is only relatively selective ➢ Bottom-Up and Top-Down with object recognition ➔ Bottom-Up ● Shape Perception: Lateral Occipital Cortex (LOC) ➔ Top-down ● Frontal lobe involvement in object recognition (MEG study) Lecture 09/28/23 Agnosia ➢ Failure of object recognition (patients with brain damage) ★ Definition: Difficulty in recognizing objects that cannot be attributed to 1) an impairment in sensory processing OR 2) a general loss of knowledge ● Visual Agnosia is the most common type ➢ Varieties of Agnosia 1) Visual Agnosia 2) Auditory Agnosia: Inability to recognize sounds that is not due to simple auditory perception problems - Amusia: inability to recognize music notes/melody (you can recognize the diff sounds but it doesn’t come together as a melody) - Phonagnosia: inability to recognize familiar voices 3) 4) 5) 6) Somatosensory Agnosia: Inability to recognize things based on touch Gustatory Agnosia (rare): Inability to recognize things based on taste Olfactory (rare): Inability to recognize things based on smell *Anosognosia: loss of awareness of one’s physical (or mental) impairments ➢ Subtypes of Visual Agnosia 1) Apperceptive Agnosia: - Most low level problems - Problems with perceptual processing and categorization - Very impaired in tests of degraded stimuli, unusual views test, and shadows test - Patient’s ability to achieve object constancy is disrupted - Very impaired at identifying overlapping objects - Associated with right hemisphere lesions (posterior part of brain) 2) Associative Agnosia: - Loss of visual semantic (what it is) knowledge regarding the structure of objects - Relatively good at parsing overlapping stimuli. But, they can’t name the objects they just parsed - Verbal knowledge is unimpaired, but can’t recognize the meaning of visually-presented objects - Perform well on “unusual views” tests but may fail to associate it with the same object in canonical view in “matching-byfunction” tests - Often associated with left hemisphere lesions ★ These have led to warrington’s model of agnosias ● Info first goes to right hemisphere (more simple perception) and once you have those pieces it goes to the left hemisphere where there semantic categorization happens 3) Integrative Agnosia - Difficulty integrating parts into a whole - OK at unusual views and OK at shape matching (similar to associative agnosia on these 2 tests) - But fail completely with overlapping figures - Copies drawings as pieces, not as a whole (different than associative agnosiasts) ➢ Category Specificity ● Animate vs Inanimate objects ● Most agnostic patients: Worse identification of animate objects Case study - Patient J.B.R: - 90% correct on identifying inanimate - 6% correct on identifying animate ● Warringeton and McCarthy (1994): Patient made more errors with inanimate objects (possible doubl dissociation) - BUT no double dissociation was actually found because the set of stimuli they used were more difficult ● Riddoch et al. (2008) - 2 patients: - Ventral extrastriate lesion: More impaired on animate - Dorsal extrastriate lesion: More impaired on inanimate Theories: 1) Living things are more difficult to discriminate because they share more silent and distinctive features than do non-living things ● Gaffan & Heywood (1993) experiment: - Healthy subjects - Pictures appeared for only 20 milliseconds and had to guess what was there - Errors > 35% - Important: all subjects made more errors on living things 2) Nonliving things evoke additional representations ● Visual and sensorimotor codes ● Fits with fMRI (graspable) ● Fits with the patient not being able to recognize combination lock and thinking it’s a phone but his fingers knowing what to do with combination lock 3) Separate brain areas for living vs. non-living objects - Even in blind subjects that are getting info auditorily (lateral vs. medial occipital regions) ★ All 3 of these theories have been supported through diff studies so they’re not necessarily competing Prosopagnosia ➢ Deficit in the ability to recognize faces ➢ Brings up the question of whether there’s a specific part of our brain that recognizes faces? Or is face recognition just harder? ● Prsopagnosiic sheep farmer -> could recognize all the sheeps differently but can’t do the same with faces ● Eyeglasses experiment -> a integrative agnostic patient showed the opposite effect (could recognize the faces but couldn’t recognize objects) ● Inverted face effects -> healthy controls do better with upright faces BUT prosopagnosic patients are better with inverted faces Face Processing in Healthy Brains ● ERP studies - ● ● “N170” component (happens with faces) -> suggests there’s a process in the brain specific to faces fMRI studies - FFA: fusiform face area Monkey electrophysiology (single-unit) Fuisform face area? Alternative view ● “Perceptual Experitse Network” - Have shown that this part of the brain can get active when bird or car experts see these things. Made “greebles” and stated that it can also activate FFA ● Modularity vs. General Processing ● However, “expertise” activity: 1) Is less than face activity in FFA 2) Extends beyond the FFA (largest in lateral occipital complex) ➢ What and Where ● Human Neuropsychology 1) Agnosia - Deficit in object recognition - Occipital-temporal lesions (“what” pathway) 2) Optic Ataxia - Can easily recognize objects, but cannot use visual information to guide their actions - Usually parietal lobe lesions (“where” pathway) Where Pathway: ● Goodale and Milner (1992): Agnosia Patient -> lost the “what” pathway, but “where” pathway was intact - Perception condition: couldn’t figure out the orientation to hold the paper in - Action condition: got it right every time, shows the where is telling them what to do as well (not just static info about something is but how does one respond to that stimulus) ➢ Perception vs. Action ● Estimating steepness of a hill (witt & proffitt, 2007) - Rotate disk (or state verbally) -> usually people overestimated - Manually tilt board -> accurate - If increase “difficulty” (fatigue, carry backpack, etc.) -> overestimate it even more (tilt board: unaffected) - Downhill perception -> stand on box vs. skateboard (people who didn’t know how to ride a skateboard perceived it as steeper, but when you asked time to tilt the board they were more accurate)

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