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Human Neuropsychology Final Exam
You should be able to express, in point form, what the main points of each chapter are. That is, what are the questions being asked and what are the solutions? You should be able to define words in bold print. Chapter 17 – Cortical Networks & Disconnection Syndromes Case D.M: Psychiatrist with memory problems Cyst putting pressure on 3rd^ ventricle Inserted a cannulae to relieve the pressure Memory problems revolved BUT noticed that he couldn’t do puzzles o Disconnection problem – cannulae disconnected the 2-motor system of left and right side
1. What is a disconnection syndrome? Behavioral effect of cutting cerebral connections 2. Outline Downer’s experiment. Scenario A: Intact monkey, hemispheres are connected by commissures (optic chiasm & corpus callosum) Scenario B: Disconnection of commissures & left amygdala is removed right eye covered motor system doesn’t have visual input no motor response (tame monkey) Scenario C: Disconnection of commissure & right amygdala intact left eye covered monkey is able to perform species-typical behavior 3. What are the 3 types of cerebral connections? Association pathways: i. 2 main types: 1. Short, subcortical, U-Shaped fibers: can be between areas adjacent to one another (ie. ocular dominance columns)
a. Completely intact: reciprocal connections in all 3 areas b. White Matter dysfunction: Hypo decrease connections; Hyper increase connections c. Grey matter dysfunction: Hypo and Hyper (same meaning as above) d. Combined disconnection: Everything goes wrong
2. Long fiber bundles connecting distant cortical areas a. Can be inter/intra-hemispheres b. Several types & disconnection to any will cause a different effect Projection Pathways: i. Include ascending fibers from lower brain centers to the neocortex (ie. projections from thalamus and descending fibers from neocortex to the brainstem & spinal cord) Commissural Pathways: i. Connects the 2 hemispheres ii. Corpus callosum, anterior & posterior commissure, hippocampal commissure iii. If corpus callosum is cut, but anterior commissure is in tact, then the hemispheres can still communicate 4. What is Liepmann’s theory of apraxia? Neocortical disconnection changes in behavior Some apraxia types are the result of disconnection If patient is given verbal direction to use the left hand in a certain way, only the verbal LH would understand the command i. To move the left hand, a signal would have to travel from LH, through c. callosum, and to the RH that controls movement of the left hand ii. Disconnecting the c. callosum, disengages the RH in motor activity Lesion can also be in PPC 4, If the lesion were in posterior speech zone (22,39,40) then the result would be bilateral apraxia because verbal command cannot gain access to either left or right motor centers 5. What is agenesis of the corpus callosum? What are the symptoms? Born without a c. callosum Different symptoms of commissurotomy because when you’re born without a c. callosum, you also don’t have a cingulate gyrus
iii. If person is blindfolded and object is placed in left hand, and asked to point to object with left hand without blindfold, they can do it, point with right hand, they cannot do it, when asked to name it, they can’t
1. If object placed in right hand, person could name it Audition i. Has crossed & uncrossed aspects ii. This bilateral arrangement reduces the effect of disconnection iii. In dichotic-listening tasks, input from left ear is suppressed (person only reports words that go into the right ear) 7. Describe how agnosia and alexia could be disconnection syndromes. Geshwind says both can result from disconnection of posterior speech area from the visual association cortex Both symptoms can be caused by lesion that disconnects visual association region (left or right) from speech zone In class notes … Agnosia i. Visual agnosia disconnection between V1 from other regions in ventral stream Alexia i. Disconnection of 2 occipital regions into angular gyrus (Geshwind’s region) 8. What are cortical networks and hubs? How are they identified? 6 main types of networks: i. Attention ii. Default iii. Salience iv. Visual v. Sensorimotor vi. Auditory Networks can be seen by: i. DTI ii. Mathematically describe nodes and edges Provincial Hubs join together similar nodes within a module (analogous to residential roads) Connector Hubs join together modules (analogous to highways) Rich Club Hubs When each module is in a different cortical area. Rich Club Hub links modules together more extensive than regular hubs
9. What is commissurotomy? Disconnection of commissure tissue (callosal agenesis) i. LH talks, reads, writes, serial movements, interpreter ii. RH Understands some verbal instruction, little reading, can match pictures to words, better than left at copying designs, facial expression & recognition, sense of self, recognition of family & other social relationships 10. What are the 2 key principles in the development of networks? Modularity minimize cost of long wiring (long connections use lots of energy) Functional Integration Need some long connections (ie. frontal parietal) Development involves organizing patterns inter-regional interactions Experience influences development 11. How are hubs and connectivity related to brain dysfunction such as dementia or psychiatric disorders? (in a general way) Abnormal connectivity Neurodegeneration can start in one module and then through rich club hubs, ‘invade’ other modules 12. How can contralateral neglect be caused by a disconnection? Where? Damage to right parietotemoral junction is most commonly associated with neglect MRI shows white matter damage also show strong association to neglect 13. What disorders can be related to hyper/hypoconnectivity? Hyperconnectivity: i. Synesthesia increase connection between the sensory systems (taste shapes, hear color etc.) ii. Hallucinations increase ventral stream connections iii. Phobias increase connection between visual stimuli & amygdala (very specific) Hypoconnectivity: i. Schizophrenia Decrease in frontal-hub activity ii. Autism Increase in some networks but a decrease in others iii. Traumatic Brain Injury (TBI) disruption of networks **Chapter 18 – Learning & Memory
- Who is Clive Wearing?** Extreme amnesia He has the most severe amnesia ever studied – no change in memory for over 30 years Caused my encephalitis, only has 2 memories – playing music, and his wife Only has moment-to-moment consciousness, no memory for musical training
ii. Animals and people iii. Fruits and vegetables
4. What are 5 theories of memory? Be able to explain consolidation, reconsolidation, and multiple trace theories. When does consolidation occur? Consolidation: i. Memories are built in the hippocampus but then moved ii. Explains why new memories are lost with hippocampal injury. Because the memories cannot get made, and the new ones have moved whereas, cortical injury effects the old memories iii. Image shows how consolidation works Reconsolidation: i. Each time a new memory is recalled, it gets reconsolidated because it becomes easily altered and stored as a new memory ii. Similar to the game of telephone, each reconsolidation, changes the memory slightly Multiple Trace Theory: i. There’s multiple types of amnesia (see above), therefore, there should be many types of memory… ii. 3 types: 1. Autobiographical 2. Factual Semantic 3. General Semantic (language) iii. Main points: 1. Memories are stored in parallel in different regions 2. Memories change over time – older memories can become facts (general semantic) and therefore move 3. Different kinds of memories are susceptible to different brain injury Trace Transformation Theory: i. Perceptual features of events richly represented in posterior hippocampus ii. Overtime, details are shifted to anterior hippocampus (preserves only gist of memory) iii. Memory is then moved to PFC that keeps similar memories grouped together further changing memories Scene Selection Theory: i. Hippocampus creates memory by assembling neocortical elements into spatially coherent scenes that form the basis of recalling memory events
ii. Basically, representations are in the cortex & hippocampus is the one that assembles the memory
5. What did Maguire’s study demonstrate for the vmPFC-HPC pathway? What does this imply for memory storage? fMRI studies in subjects are asked to recall old memories (memories from 10 years ago vs. memories from 2 weeks ago) Hippocampus activity was different for each memory But PFC activity was similar for new memories 2 years later, when asked to recall the once “new” memories, which are now 2 years old, PFC activity is different. Memory storage in PFC is more diffuse while in HPC it is more localized (??) 6. Distinguish between explicit, implicit, and emotional memory. What are the key structures in each of these memory types? Explicit: Conscious (top-down) i. Episodic Personal & Autobiographical ii. Semantic Facts & Knowledge iii. Key structures: Hippocampus Implicit: Nonconscious (bottom-up) i. Skills ii. Habits iii. Priming iv. Conditioning v. Key Structures: Basal Ganglia Emotional: Conscious & Nonconscious i. Attraction ii. Avoidance iii. Fear/Phobias iv. Key Structures: Amygdala 7. Outline HM’s memory story. How is it different from KC’s symptoms? H.M i. One of the most famous memory studies ii. Had really bad epilepsy iii. Bilateral medial-temporal lobe resection to try to stop the seizures iv. Got really bad amnesia v. Surgery caused scarring in both hemispheres vi. Oxidation of one of the surgical clips marked the para-hippocampal gyrus vii. Good IQ, no deficit in perceptual tasks, retrograde memory was ok
iii. Case K.F left posterior-temporal (TPJ) lesion
1. Virtually no verbal short term memory for digits, letter, words, and sentences 2. Intact verbal long term memory, paired associates 3. Shows that info does NOT go STM LTM (LTM is a set of networks, and STM is neuronal activity) iv. Object recognition (factual or semantic): Ventral Stream depends on the rhinal cortices v. Right temporal lobe removal impaired facial recognition, spatial position, and maze-learning vi. Left temporal lobe lesions functional impairments in recalling word lists, consonant trigrams, and nonspatial associations Prefrontal Cortex: i. Gets input from parietal cortex & inferior temporal cortex ii. Recall Trace Transformation Theory memory is moved to PFC where it groups together similar memories iii. According to HERA: 1. Left PFC is more involved in encoding rather than retrieval of both semantic and episodic memories 2. Right PFC is more involved in episodic retrieval iv. Feeds into amygdala (recall neural circuit of emotional memory) Posterior Parietal Cortex: i. Bilaterally engaged in retrieval 10. What is diencephalic amnesia? Who is Case NA? What are the causes and symptoms of Korsakoff’s disease? Diencephalic Amnesia: Form of amnesia resulting from loss of neurons in the diencephalon (midline thalamuc and mammillary bodies of the hypothalamus) Case NA: i. Fencing foil up is nose ii. Damage to medial thalamus Korsakoff’s Disease i. B1 (Thiamine deficiency from alcohol)
ii. Anterograde & Retrograde Amnesia iii. Confabulation (compulsive lies about anything and everything) iv. Meagre content (out of it) v. Lack of insight vi. Apathy vii. Normal IQ
11. What is the role of the perirhinal and entorhinal cortex in memory? Basal forebrain? Perirhinal Cortex important in episodic memory coding in the hippocampus and plays a part in retrieval. Codes object features and assocaitons Entorhinal cortex memory retrieval with hippocampus Basal Forebrain Cholinergic neurons. When neurons die here, you get Alzheimer’s 12. What are 4 likely causes of Alzheimer disease? Loss of cells in basal forebrain Development of neritic, amyloid plaques (caused by misfolding of proteins) Cumulative effect of a bunch of small brain bleeds (related to high blood pressure) Diabetes of the brain related to insulin drop & Type II diabetes 13. What type of changes in the brain might account for memory? Neuronal connections i. Contant length ii. # of vesicles iii. Post-synaptic receptor iv. Spine apparatus Complexity of the cell is positively correlated with complexity of the task (cells in language area are more complex than finger area) LTP is associated with learning When we produce cortisol, increase levels cause cell death in the hippocampus (decrease memories) Response to stress activates HPA axis which leads to CRH and AVP production in paraventricular nucleus of the hypothalamus i. Hormones are released into bloodstream causing a release of ACTH from anterior pituitary ii. ACTH stimulates the creation and release cortisol from adrenal cortex into blood iii. HPA axis modulation is done by negative feedback loops 14. What is the story of S? What price did S pay for such a good memory? Highly superior autobiographical memory Could look at long series of numbers are remember them for days, months, even years Found out to be a mnemonist (thought of each number as an image) Cost:
Predicts that i. Left PFC is more involved in encoding than retrieval in both semantic & episodic memories ii. Right PFC is more involved in episodic retrieval iii. PPC is bilaterally engaged in retrieval (reason being, it could be some kind of general processing related to intelligence or default network) Caption for image: i. During acquisition, activation appears in left vlPFC ii. During recall of same material, activiation in right premotor cortex, PFC, and parietotemporal cortex bilaterally
20. What neurological diseases affect long term memory? (see Section 18.6) Transient global amnesia i. Causes: 1. Concussion, migraine, hypoglycemia, epilepsy, interrupted blood flow in brain from stroke ii. Loss of old memories and inability to form new ones iii. Condition is acute with sudden onset and usually short course iv. Can be one-time event Herpes simplex encephalitis infections i. Associated with temporal lobe damage Extensive anterograde amnesia while showing normal intelligence, language, and implicit memory ii. Associated with additional damage to lateral temporal cortexand insula Retrograde amnesia Alzheimer’s disease i. Both progressive loss of cells and development of cortical abnormalities ii. First diagnosed with presence of anterograde first and retrograde later iii. First brain area to show affect is medial temporal cortex iv. Medial temporal is associated with anterograde v. Damage to other temporal areas and frontal cortical areas is associated with retrograde Korsakoff’s syndrome i. Combo of alcoholism and malnutrition ii. 6 major symptoms 1. Anterograde amnesia 2. Retrograde amnesia 3. Confabulation (lies on lies) 4. Meager content
5. Lack of insight 6. Apathy iii. Symptoms can appear suddenly iv. Cause: thiamine (vitamin B1) deficiency, so can be managed by supplements, but cannot be reversed 21. What is anomia? Difficulty in finding words, especially when naming objects 22. Distinguish between conscious and unconscious memory. Concious: something you are aware that you are recalling (explicit & emotional memory) ie. writing exams, speaking 2nd^ language Unconscious: something you are not aware that you’re recalling it (implicit and emotional) ie. speaking first language 23. What is highly superior autobiographical memory? Kinda bullshit (??) Can seem that the person has superior autobiographical memory Ex.) John Dean’s memory i. Nixon’s lawyer ii. Seemed to have insane autobiographical memory could speak about any life event in great detail iii. Not the case, they compared the testimony with video recording, and nothing lined up iv. Conclusion: memory is not a ‘tape recording’ of what happened, but rather an overall encoding of experience **Chapter 19 – Language
- What is language?** Historically, Wernicke-Geschwind model saw language as: i. Compression taken from sounds in Wernicke’s area ii. Then it is passed to the arcuate fasciculus pathway iii. Then over to Broca’s to be made into speech Now, it is seen as the use of sound combinations for communication Includes idea that with the use of sounds, communication can be transcended to other sensory modalities 2. What are the core language skills? Categorizing assigning tags i. Makes the brain easier to perceive all info coming in ii. Ventral visual stream is important in object categorization iii. Dorsal stream may be important in making relatively automatic distinctions between objects Labeling categories more than just tags i. Also includes events & relations (ie. Snoopy is more than just a dog)
3. Other homonid studies have shown that a. Neanderthal linguistic capacity b. Language began with the common ancestor between H. sapiens and Neanderthal’s was ~ 500 000 years ago (still rapid) 4. Ability to read & write a. These abilities have fine movement & transition in common b. Therefore, could have appeared close in time 5. Size of social group a. The more complex a social structure is, the more limited it is in size b. Language allows the group to get bigger as it allows or coordinated hunting, foraging & defense c. Social size is positively correlated with brain size d. Social media? i. OFC volume predicts social network size in humans ii. Bigger Facebook group => bigger OFC volume vi. Changes in language-related brain regions 1. Broca & Wernicke areas found in primates but changed in humans, especially with addition of pathway (dorsal & ventral) 4. What is the McGurk effect? We understand language much better is we can see the face 5. What do you conclude from studies of language-like processes in apes? They are unable to develop human like language (their larynx is too high) They can learn associations 6. What is the evidence for the localization of language? Seen in stroke patients When have stroke in middle of cerebellar artery aphaisa Damage to W&B area Key points: i. Most of the brain takes part in language one way or another ii. Most patients in language studies are stroke patients with MCA iii. Symptoms evolve after stroke and become less severe iv. Syndromes described as fluent or non-fluent consist of numerous varied symptoms, each of which likely has different neural basis 7. What role does the right hemisphere play in language? What is the one important language ability that the right hemisphere cannot do (in right- handed people)? Language comprehension Prosody
Injury causes variety of effects (odd word selection, difficulty in comprehension, reduced word fluency) Cannot do Production
8. What are the effects of 1) brain stimulation on language; 2) lesions on language? Electrical stimulation: i. Many effects speech arrest, inability to vocalize, hesitation, slurred, repetition, misnaming ii. Depends on exact location of stimulation iii. How Penfield did the thing Transcranial magnetic stimulation (TMS): i. Slows processing in Broca’s ii. Posterior Broca’s is involved in production of words iii. Anterior part of Broca’s is involved in the meaning of words Lesion i. A lot don’t cause apahsia ii. No pure sensory or motor aphasia iii. Can’t lose all of Wernicke’s area iv. Bad brain is better than no brain 9. What do PET and fMRI studies tell us about language that is different from the Wernicke-Geschwind model?
i. Various types (see image)
13. Distinguish between the dual language pathways. Dorsal Pathway i. Goes from posterior regions up to area 6 & go to 44 ii. Phonemes into movements iii. Mapping sound & sight onto articulation iv. Damage cannot articulate words but can understand Ventral Pathway i. Convert sounds into meaning (semantic) ii. Area 22 45 iii. Area 38 47 iv. Damage can read or hear but doesn’t understand Both paths involved in syntax 14. Know the two general types of aphasias. Aphasia language disorder apparent in speech (agraphia) or in reading (alexia) 15. Automatic language (eg., swearing) is believed to be located where? Does not involved the cortex Comes from the caudate of basal ganglia 16. How do we assess aphasia? Test batteries (take a long time & need special training i. Auditory & visual comprehension ii. Oral & written expression include tests of repititon, reading, naming, and fluency iii. Conversational speech
Brief aphasia screening although faster & easier to administer, they cannot replace the detailed battery tests (good for discovering the presence of language deficits i. Conversational analysis
17. Summarize the evidence for localization of language. Basic lines of inquiry i. Anatomical studies ii. Studies of brain lesions in humans iii. Studies of brain stimulation in awake patients iv. Brain imaging studies Brain imaging studies, aphasia analysis, and neural modeling show they a large network in the temporal, parietal, and frontal lobes (both hemispheres) contribute to language Found that Broca’s area is a lot more complex than originally thought, i. Area 44 & 45 have 2 parts ii. Area 6 is related to facial movements (facial expressions) Also found that posterior zone is much more complex 18. What is the story of the role of the FOX P2 gene? What regions of the brain are different? Original Idea: Fox P2 emerged in H. sapiens and drove speech evolution People (Family KE) without FoxP2 gene don’t have language But animals without the Fox P2 gene still have language BUT Fox P2 was found in Neanderthals & thus older than we thought AND Fox P2 appears to control synaptic plasticity in basal ganglia AND Fox P2 appears to play a role in vocal learning in birds & bats The gene is more than basal ganglia, it’s related to a bunch of changes in the cortex Brain regions that are different:
