Psyc 301 LGs for Final Exam PDF

sensorimotor Describe the hierarchical structure of the sensorimotor system and name the major “levels” Describe: it controls the motor flow from highest to lower level. lower level process sensorimotor programs. - the sensorimotor system has real-time (online) feedback to adjust...

sensorimotor Describe the hierarchical structure of the sensorimotor system and name the major “levels” Describe: it controls the motor flow from highest to lower level. lower level process sensorimotor programs. - the sensorimotor system has real-time (online) feedback to adjust movement - Once the program is activated, the sensorimotor program can be processed without the control of higher levels. major divisions: abstract plan - association cortex (PPC & dorsolateral prefrontal association cortex DlPFC) - secondary motor cortex refining movement design - primary motor cortex specific motor sequence - brainstem motor nuclei - spinal motor circuits Basal ganglia & cerebellum are in parallel to those above to manage timing and sequence Discuss brain changes associated with movement practice - response chunking. movement sequences are grouped as units & phrases instead of separating parts. - e.g,. learning how to type, memory the words instead of single letters - shifting controls to lower level - frees up higher level of control Define motor equivalence Principle of motor equivalence: there is more than 1 way to carry out a movement. - reflexes are not enough, motor system need to be flexible - Those movement outputs are the same at higher control levels, but different at lower control levels. Identify 2 major areas of sensorimotor association cortex, and provide evidence of function and consequences of damage here Posterior parietal association cortex (PPC) Function: - receiving information & collecting info - integrates info about the current position of body parts with information about external objects you will act upon. - stimulation PPC can make patient feel like they are performing an action Damage to PPC - contralateral neglect - deficit of attention: right hemisphere damage →neglect of left side of the space - deficit of language: damage to the left hemisphere. - Apraxia - damage to left hem→ impaired voluntary movement performance - this is due to the problem with initiating movement, NOT due to weakness & coordination problem - symtoms are bilateral - errors: imitation of gesture performance of gesture of command use of tools and objects dorsolateral prefrontal association cortex DlPFC Function - evaluation & support cognition (problem solving, math, working memory, learning) & executive - evaluation of external stimuli and initiation of voluntary reaction - first neurons to fire when anticipating the motor action → decision to act begins here Damage - Impaired decision-making, problem-solving, and working memory. Name the defining behaviour of mirror neurons and identify where in the brain they are located Mirror neurons locations  - in ventral premotor cortex (second motor cortices) & hippocampus definition - Mirror neurons are activated during both execution and observation of specific motor acts. - related to empathy and theory of mind. (understanding what others are doing) Describe the organization of the secondary and primary motor cortices, evidence of function, and consequences of damage here Secondary motor cortices function - eight areas of secondary motor includes premotor & supplemental and cingulate - produce & guide complex movement Damage - Impairs coordination of complex movement sequences. Primary motor cortex (M1) function - Organization. somatotopically organized (Penfield: who discovered how different parts of the motor cortex correspond to specific body parts and movements.) Damage - deficit in moving one specific body part independently of others. - astereognosis (deficit in identifying object just by touching ) - reduce speed & accuracy & force of movement Link the roles of the cerebellum to consequences of damage here Cerebellum Cerebellum function - receiving info from - primary and secondary motor cortex - brainstem nuclei’s information about descending motor signal - motor response feedback via somatosensory and vestibular system - compare intended movement and actual movement - Ensures precise timing and sequence control. Cerebellum deficit - deficit to control direction & force & velocity & amplitude of movement (ataxia_Impaired movement precision /dysmetria辨距困难) - affecting balance & gait 步态 & eye movement - deficit to adapt patterns of motor output to changing conditions - difficulties in maintaining steady posture (proves by Rphomberg_standing with eye close → test for balance and steady posture)  - attention deficit & executive control & procedural memory & working memory & language and visual spatial processing - learning new motor sequence deficit Describe the two pathways of the basal ganglia and link these to Parkinson’s Disease and Huntington’s disease basal ganglia function - modulates motor outputs - critical for habit formation - support cognitive roles - promotes skill learning - many parts communicate to the brain & receiving and sending info to the brain pathway - STOP - inhibitory – rest state - basal ganglia inhibit motor and premotor areas - black - no movement - GO - excitatory - disinhibition - red - to activate motor cortex → inhibit the inhibition - yes movement Dopamine is involved in both pathways but more in GO. two pathways in balance involving cortex & basal ganglia & thalamus Deficit - Parkinson disease 僵硬 - Reduced "Go" and increased "Stop" due to substantia nigra neuron loss. - diminished movement & specifically less movement initiation - symptoms (initial): stiffness & resting tremor (during inactivity) - symptoms (later): muscular rigidity & slow movement & mask like face & pain & depression - HUntington’s disease 多动 - affect neurons across the brain specifically affect the striatum - reduce STOP → excessive movement - rare & highly genetically determined - no strong treatment List two treatments for Parkinson’s Disease - L-DOPA - this can combine in your body to produce dopamine - can’t add dopamine directly because dopamine is too big to pass BBB - Deep brain stimulation of substantia nigra additional things - sensory feedback - sensory system monitor the body’s response and feed that response back to the sensorimotor circuit. - sensory feedback provide information to help adjust and control movement - Exceptions of sensory feedback - ballistic movement (punch & swat) because they happen too fast and programmed. - reflexes (yank hand away) because reflexes is automatic and don’t rely on feedback, the response happen before brain process the situation BD 1. Outline the DSM-5 criteria for Clinical Depression, Hypomania, Mania, and Bipolar Disorders (BD) I and II. Clinical depression criteria - 5+ of the following symptoms are presented at the same time of 2-week period. (at least one of them is from 1 or 2) - 1. Depressed mood. - 2. Markedly diminished interest or pleasure in all, or almost all, activities. - 3. Significant weight loss or gain, or decrease or increase in appetite. - 4. Insomnia or hypersomnia. - 5. Observable psychomotor agitation or retardation. 运动神经刺激/迟缓 - 6. Fatigue or loss of energy. - 7. Feelings of worthlessness or excessive or inappropriate guilt. - 8 Diminished ability to think or concentrate, or indecisiveness. - 9. Recurrent thoughts of death; recurrent suicidal ideation without a specific plan; a specific suicide plan; or a suicide attempt. Hypomania - symptoms of the following but not leading to severe disruption of work/social rejection/hallucination /delusions - persistent mild elevation of mood - increased energy and activity - marked feelings of well-being and both physical and mental efficiency - increased sociability and talkativeness (or increased irritability in some) - increased sexual energy - decreased need for sleep - no hallucinations or delusions (i.e., no psychosis) Mania - Definition: Distinct period of abnormally and persistently elevated or expansive mood and abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week and present almost everyday. - Symptoms (3+ of the following are present to a significant degree) - Inflated self-esteem or grandiosity - Decreased need for sleep (e.g., feels rested after only 3 hours of sleep) - More talkative than usual or pressure to keep talking - Flight of ideas or subjective experience that thoughts are racing - Distractibility - Increase in goal-directed activity or psychomotor agitation - Excessive involvement in activities that have a high potential for painful consequences (e.g., unrestrained buying sprees, sexual indiscretions, foolish business investments). Bipolar II - at least one hypomanic episode symptoms - at least one major depressive episode (clinical depression symptoms) - NO manic episode. Bipolar I - same as Bipolar II - YES manic (one form of psychosis) Most BD does not exhibit rapid shifts in affect (e.g., sudden unpredictable anger). 2. Distinguish between Hypomania and Mania with the use of an example. Hypomania: - no psychosis symptoms (delusion) - no severe disruption of work and social life Mania - A more intense and severe mood elevation that causes significant impairment - psychosis (delusion) 3. Explain the concept of ‘Self-Illness Ambiguity’ with the use of an example. Definition: reflects difficulty in distinguishing their true self from the symptoms of the condition Example: "Am I just a sad person, or is this the illness talking?" 4. Outline the major risks associated with BD. - high stress - misuse of drugs & alcohol & suicide attempt Neuroplasticity Be able to define neuroplasticity. - definition: change in nervous system according to experience, change of the structure and function in the brain. The brain's capacity to reorganize itself by forming new neural connections throughout life.  - nervous tissue has an extraordinary degree of plasticity. —william james - hippocampus is important Be able to describe the historical trajectory of how we arrived at our modern understanding of neuroplasticity. - despair of neuroplasticity: once the development is ended, the growth and regeneration end, nothing will be regenerated. –Ramón y Cajal, - Hebbian theory. forming the basis of memory. "Neurons that fire together, wire together," – Donald Hebb. - This is the hope for neuroplasticity because this means that the brain is adaptable. Understand the three mechanisms of neuroplasticity discussed in this lecture. Functional plasticity - changes in neurotransmission (change how neurons communicate) Structural plasticity - changes in brain structure - dendritic spines (new grown connections or branches of the neuron) Neuogenesis - birth of new neurons (mostly during development) - Adult neurogenesis is controversial Understand what a critical period is and how it relates to neuroplasticity. - critical periods are time intervals where nerves have an incredible degree of plasticity, mostly not seen in adults. - critical period = high neuroplasticity. - higher in children, as people age plasticity goes down - PRO: great period for developing new skills (language) - CONS: High plasticity increases vulnerability to adverse(negative) experiences. Lots of research done on early life adversity (ELA) - e.g,. childhood trauma will shape them as well. Explain why the visual system can be used as a model of neuroplasticity. Visual system – cataracts 白内障 - Children born with cataracts obstruct vision in one eye. - amblyopia: the brain reorganizes to favour using the other eye during critical period in childhood, enhancement of the non-deprived eye. - Even if the cataract is removed, vision will still be poor for that affected eye, because the brain has changed. - This is not seen in adults, because the neuroplastic critical period closes. Be able to link neuroplasticity and age to Charles Bonnet Syndrome. Charles Bonnet Syndrome (CBS) - visual cortex neuron fires themselves without environmentally relevant sensory input → hallucinations - loss sight in an eye in adult → no neuroplasticity reorganization → visual cortex neurons begin to fire on their own Know the relationship between neuroplasticity, PTSD, and depression. - PTSD & depression → Consistently lower hippocampal volumes are observed  - neuroplasticity adapt to PTSD and depression Be able to define iPlasticity and describe an experiment that demonstrated this phenomenon. Definition - iPlasticity = induced juvenile-like plasticity in adulthood (用药物诱导出和青 少年时期一样的plasticity period) - Psychedelics迷幻药 and representatives from each type of antidepressant 抗抑药can induce this juvenile-like period of plasticity - Experiment: MICE EYESIGHT Monocular deprivation of an eye sight with antidepressants will induce a shift in eyesight dominance just like young mice (induced juvenile-like plasticity) Know how drugs of abuse can exert detrimental neuroplastic changes. How do drugs induce plasticity? - Psychedelics(psilocybin (magic mushrooms), ketamine) & antidepressant change the receptor called TrkB to be more receptive to protein which promote neuroplasticity called brain-derived neurotrophic factor (BDNF) - BDNF is only released by active neurons → iPlasticity is activity dependent plasticity. iPlasiticity & activity-dependent plasticity - because neurons need to active to release BDNF, so neurons are more sensitive to environmental experience - Activated ensembles will be strengthened, while unused ones may be pruned or weakened → why combining antidepressant treatment with therapy is Gestaltian. - Gestaltian: effects of both together can be more powerful than either alone. Addiction exploits neuroplasticity - All drugs of abuse act on the mesolimbic dopamine pathway. - the mesolimbic dopamine pathway is the reward and motivation pathway. - Addictive substances cause neuroplastic changes in this pathway due to their potent effects → mesolimbic pathway begins to over value the drug & increasing the motivating to get the drug & overuse behaviour (compulsive强迫的 /uncontrollable) Be able to suggest several ways to increase neuroplasticity. - exercise - Exist in an enriched environment - Engage in cognitive exercise or meditation - Learn to navigate a complex environment - Take antidepressants Psychiatric Dysfunction Identify motivating factors for classifying psychiatric illnesses - guide treatment choices - allow clinicians to communicate - serve parties who required diagnosis (e.g., insurance, legal system) - permit research - to causes - to treatment responsiveness - to prognosis Name the three components a condition must have to be included in the DSM DSM= Diagnostic and Statistical Manual of Mental Disorders - atheoretical (focus observable symptoms rather than explaining their causes) - operationalist (provides clear, measurable criteria for diagnosis, e.g,. what symptoms are needed to identify BD) - categorical (instead of spectrum) Components to be included in DSM-5 - characterized by clinical significant disturbance in an individual’s cognition & emotion regulation & behaviors - (those behaviors) reflect mental functioning dysfunction in psychological & biological & developmental processes - e.g,. Imbalances in brain chemicals like dopamine (biological) - e.g,. deficit in managing emotions - significant distress or disability in social, occupational, or other important activities. Components NOT to be included in DSM-5 (explicit exclusion) - expectable or culturally approved response to a common stressor or loss - e.g,. loss of a loved one - socially deviant actions (political, religious, or sexual) - conflicts that are primarily between the individual and society (unless the conflict is caused by dysfunction in psychological & biological & developmental processes Recognize criticisms of the DSM criteria - level of details (unevenness of symptoms for each MD) - “there are almost 24,000 possible symptom combinations for panic disorder in DSM-5, compared with just one possible combination for social phobia” - Overlap - 2 people could be diagnosed with the same mental disorder, but not having overlap in symptoms. 相同病症，症状不重合 - different disorders can have overlapping symptoms. (PTSD & MDD)不同病症，症 状高度重合 - authority - who defines those impairment - comparator - who the symptoms compare to? (more talkative than usual→ compare to self) - excessive guilt (compare to normative) - feelings of worthlessness (no compare)  Define normative assumptions, deinstitutionalization and recognize these in historical examples and trends Normatic assumption Descriptive evaluation of right or wrong What is or would be - ought & should - the class would be 10 people example 1: manic & hypomanic - “Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).” example 2: ADHD - fails to give close attention & make careless mistakes - “Often leaves seat in situations when remaining seated is expected.” These examples shows that normative assumption affect what is considered as illness History of normative assumptions - 19th c. masturbation is illness - drapetomania = is treated as an illness causing black slaves to attempt escape - homosexuality in DSM-1,2 but removed from DSM-3 Deinstitutionalization - replace long-stay psychiatric facilities with community mental health services (started in 1960s) - Possible with antipsychotic drugs such as chlorpromazine - balloon theory = without proper support, without long-stay psychiatric facilities → MD patients became more at risk and unhoused. Comment on the relationship between mental illness and violence - without the addition of drugs → no relation of mental illness and violence. - normal people violent level = MD patients - “a great deal of what is responsible for violence among people with mental illness may be the same factors that are responsible for violence among people without mental illness.” Schizophrenia 1. Recognize the main criteria that go into a diagnosis of schizophrenia Criteria A: - 2+ symptoms of the following present a significant portion of time during 1 month period (less if treated properly) 1 must from 1/2/3 1. Delusions 2. Hallucinations 3. Disorganized speech (e.g., frequent derailment or incoherence) 4. Grossly disorganized or catatonic behaviour 5. Negative symptoms (i.e., diminished emotional expression or avolition意志力) Criteria B: - After the onset of the disturbance begins, levels of function in areas (work & interpersonal relations & selfcare) is below the previous achieved level. - if the onset of schizophrenia onset happen in childhood or adolescence → failure to achieve expected level of function (interpersonal, academic, or occupational functioning) Criteria C: - The continuous disturbance lasts at least 6 months, including at least 1 month of active symptoms(of criteria A) and other times with milder or negative symptoms like odd beliefs or unusual perceptions Criterion D: - Schizoaffective disorders (e.g,. bipolar I, depression with mania) have been ruled out Criterion E: - The disturbance is not attributable to the physiological effects of a substance such as drugs and medications. Note: schizophrenia is the split of mind including personality & emotions perception & memory. 2. Distinguish between positive, negative, and cognitive symptoms of schizophrenia Postive symptoms positive = symptoms that normal people don’t have - hallucinations - perceptions without sensory cause - Often auditory voices, noises, music - e.g,. hearing non-existent voices - command hallucination → high risk of suicide & self harm - delusion - beliefs that are not realistic or culturally proper. false belief that isn't based in reality. - can be varied - E.g., the world is full of hidden signs for me; I am being closely watched; more bizarre Negative symptoms impairment of normal function - Blunted emotional responses (“affective flattening”情感扁平化) - impoverished content of thoughts and speeches (disturbed attention) - Grammar is reasonably intact but content wanders or is incoherent –“loosening of - reduced social motivation associations” Cognitive abnormalities (or “disorganization symptoms) - Impaired working memory and executive function - Impaired source monitoring - Impaired source monitoring tendency to misattribute own actions and thoughts to external  causes, errors confusing imagination and real memory. 3. Name some risk factors for schizophrenia - genetics - urban environment - 1st or 2nd trimester maternal infection or malnutrition 孕期感染/营养不良 - Perinatal complications围产并发症 - Cannabis or stimulant use兴奋剂和大麻 - Paternal age >35 years 4. Identify common brain changes Structural change - Widespread decreased grey matter, particularly in frontal and temporal cortices. → enlarged ventricles - obvious thinning of dorsolateral prefrontal cortex (this part is critical for working memory) - volume loss is not due to cell death, it’s the reduction of cell process & shrinkage of cell connection (axons & dendrites) - prefrontal cortex: loss of dendritic spine density (cell connection) Fewer GABAergic interneurons (support cell activity) - hippocampus - Atypical layering structure - Atypical neuron shape Functional - abnormal (most hypoactive) frontal and temporal lobes including hippocampus. 5. Compare the efficacy of the various nonpharmacological and pharmacological treatments for schizophrenia Non-pharmacological treatments非药物治疗 - Cognitive Behavioural Therapy (CBT) + medication → management of positive and negative symptoms. Pharmacological treatment - antipsychotic drugs = most common treatment for positive symptoms - typical (older) E.g., chlorpromazine (Thorazine), haloperidol (Haldol) → side effect: movement disorder (parkinson) - atypical (newer) E.g., olanzapine (Zyprexa), aripiprazole (Abilify) → side effect: metabolic side effects (weight gain, diabetes…) - not so good for treating negative symptoms 6. Compare and contrast the dopamine and glutamate theories of schizophrenia Dopamine theory of schizophrenia - it indicates maybe schizophrenia is caused by too much activity at dopamine receptors, suggest dopamine plays a key role - This theory was based on several findings:  - Parkinson’s disease have marked dopamine depletions缺乏多巴胺; and antipsychotic drugs produce symptoms that are similar to Parkinson’s disease.补充 多巴胺 - Drugs known to increase dopamine levels (e.g., amphetamine, cocaine) produce symptoms of schizophrenia. - Antipsychotic drugs’s efficacy: it works better when they block dopamine D2 receptors. - Problems of dopamine theory: - The newer “atypical” antipsychotic drugs produce a wide variety of changes in brain, but is NOT better than older antipsychotic drugs. - It takes 2/3 weeks for antipsychotic drugs to work, yet their effects on dopamine receptor activity are immediate. - Most patients show no significant improvement to the first antipsychotic they are given. Glutamate hypofunction theory of schizophrenia - PCP and ketamine are drugs that can cause symptoms like psychosis (loss of touch with reality) and negative symptoms (e.g., lack of motivation). They work by blocking NMDA receptors. - NMDA = a specific type of receptor of glutamate - Glutamate = excitatory - GABA = inhibitory - interneurons receive glutamate → enough excitation → release inhibitory GABA signal to other neurons. If glutamate signalling becomes abnormal, this can lead to - glutamate signal is off→ no release of GABA→ Less GABAergic transmission (i.e., decreased inhibition of downstream cells) leading to - A widespread pattern of too much activity (unbalanced excitation vs inhibition) Executive (dys)functions Describe the tripartite model of executive function, name the three components, and identify a test for each Working memory - holding and mental working with information in mind - test: digit or pointing span → how many can you remember Inhibitory control - Resisting temptations, not acting impulsively or prematurely, resisting automatic behaviour (stroop test) - to test - Stroop. You see the word "RED" written in blue ink, and you're asked to say the ink color (blue), not the word (red). - flanker (see the graph) resisting the temptation of getting distracted. Cognitive flexibility - Fluidly changing perspectives & methods to solve problems - adjusting to new demand - switching between priority of tasks - tests - wisconsin card sort (adapt to changing rule, e.g,. sort card by color and then the rule changed to sort by shape) - trail making with alternation (1-A-2-B-3-C) switch between different tasks Differentiate the orbitofrontal and dorsolateral subdivisions of the prefrontal cortex (location, behaviour) Location: Orbitofrontal circuit dysfunction - impulsive & socially inappropriate - poor safety judgment & poor punishment and reward anticipation - diminished guilt & regret → NOT learning from mistakes Dorsolateral circuit dysfunction - Distractible & disorganized - Perseverative 坚持不懈(wisconsin card sort changing the rule, but still stick to the old rule OR doing too much than the required) - Difficulty multitasking & time management & prioritization Identify consequences major frontal lobe damage - Abulia –lack of drive - Return of primitive reflexes (frontal release sign) - If you touch an adult's palm, they might automatically grab your hand like a baby would. - utilization actions: using someone else’s object while you shouldn’t. Provide a profile of ADHD: major symptoms, neurobiology, and treatment symptoms of ADHD (Attention deficit hyperactivity disorder) - extreme inattention, hyperactivity, impulsivity - 5-7% of children; ~2-3% of adults - Diagnosis intersects with societal norms - more likely to be diagnosed among classroom younger students - rapid rise in adult diagnosis - Presentations vary with gender –underdiagnosis of hyperactivity in girls (means girls are more likely to have inattention symptoms) Neurobiology of ADHD - Reduced activity and volume of PFC - Slower maturation of PFC in ADHD people than normal people - Slower thinning process of brain cortex in ADHD (this is related to hyperactivity & impulsivity) - the brain outer layer needs to  get thinner as we age to help the brain become more efficient. A dual-pathway model of ADHD - Executive circuit - inattention = dysfunction - involved regions: dlPFC and caudate - reward circuit - lack of motivation = dysfunction - involved regions: OFC, ACC and nucleus accumbens Treatment ADHD - ADHD = LOW dopamine system & hypoactive dopamine - Major treatment: medications that act upon dopamine and norepinephrine systems in PFC and subcortical regions. Other info on executive functions - executive function mainly involve the prefrontal cortex - higher orders of executive function based on the working memory & inhibitory control & cognitive flexibility Planning Organizing Multi-tasking Self-awareness Regulating emotions Inhibiting inappropriate behaviour Motivation Concentrating - ADHD is Initially characterized as a problem of “moral control” (1902) Neuroplasticity & Cognitive Rehabilitation 1. Define neuroplasticity, neuropathic pain Neuroplasiticity - The brain’s capacity to change following - “experience-dependent change” - plasticity can be seen at many levels: Modified gene expression & protein Changes in dendritic spine density and morphology; axonal sprouting Neurogenesis Up or down regulation of synaptic pruning Strengthening or weakening synapses (LTPvs LTD) Reorganization within brain areas Increased or decreased connectivity between distant brain areas Neuropathic pain - caused by a lesion or disease of somatosensory nervous system - Many causes including: spinal cord injury, diabetic neuropathy, MS, cancer, trigeminal neuralgia… - give a feeling of burning & tingling & painful cold & electric shock - affect 7-10% adult 2. Identify two principles of neuroplasticity and name evidence for each Plasticity depends on age - Evidence: rats live in complex or simple house → decreased Infant spine density in cortex & increased Adult spine density in cortex → the nature of plasticity really depend on age Plasticity depends on brain area - Evidence: Rats given amphetamine → decreased Spine density in Orbitofrontal cortex & increased spine density in mPFC. 3. Discuss 3 examples of the plasticity of cortical maps and an example of plastic changes to the cortex in the absence of visual input Cortical maps - A convenient way to measure plasticity. - Plasticity of cortical maps is the brain’s ability to reorganize itself, letting different areas take on new tasks after changes like injury or practice. Examples of plasticity of cortical maps plasticity is helpful plasticity is NOT helpful - cortical map + use frequency(of the - cortical map + overuse → disorder sensory representation) → involved involving involuntary muscle brain region of somatosensory movement and postures of the cortex will be enlarge overused body part - e.g., Reading Braille - E.g., playing piano often, increases sensory some fingers always move representation of the together → Somatosensory reading finger maps expand and overlap, causing movement problems - Cortical maps after injury → phantom limb患肢 phenomenon related to cortical map reorganization. - The brain still interprets signals from the missing limb as pain or other sensations, even though  the limb is gone cortical plasticity change & absence of the visual input - In children who are born blind, primary visual cortex assumes non-visual functions → the cortex takes on new functions such as processing audio signal and touching. - Different across individuals but stable over time 4. Define central sensitization and name three manifestations of this Central sensitization: manifestations - plastic change of CNS in processing pain to be more sensitive. - allodynia: feel pain to non-painful stimuli - primary hyperalgesia: already painful sensation became more painful - Secondary hyperalgesia: Increased pain in areas around the injury. Mechanism - New, spontaneous & Overactive activity in spinal cord (if myelin is damaged) - Increased excitability and receptive field size of CNS neurons → perceive non-painful stimuli (e.g., touch) as pain, when touch and pain signal are unbalanced. - damage inhibitory circuit in brainstem & spinal cord → normal pain inhibition process lost. 忍痛功能消失 5. Describe cognitive rehabilitation therapy – what is it, what are some potential areas of application, and how does it relate to the idea of plasticity? Cognitive rehabilitation therapy: - Definition: treatments aimed to improve cognitive functioning through the combined action of compensation, plasticity, and recovery - Training the affected behaviours (targeting recovery + plasticity) - e.g., mnemonic strategies to remember words, looking to neglected side - Offering external supports (targeting compensation) - e.g., use a notebook, neck muscle vibration - Potential area of application: - Particularly studied for TBI and stroke - visual scanning for neglect after right-hemisphere stroke; - compensatory strategies for mild memory deficits; - social-communication deficits after TBI; Aging & Neurodegeneration Comment on Canadian demographic trends related to aging growing trend of senior population. Implication of career for medical system & tech development Consider: Are younger adults good at forecasting the experiences of older adults? Provide evidence. No, because young people underestimated senior people’s emotional stability and emotional complexity, while overestimate their loneliness Name and describe four physical changes affecting the aging brain Normal brain aging changes - Volume loss - Overall volume shrinks by 5% per decade after 40, accelerating after 70 - the shrinkage varies across structures! frontal cortex > basal ganglia > temporal lobe > other - Neurotransmitter depletion - dopamine & serotonin decline - Cerebral blood flow decrease - Accumulation of white matter damage (linked to hypertension=high blood pressure) Distinguish between normal and abnormal cognitive and physical changes of aging Normal changing: - small degree of Alzheimer’s pathology (amyloid plaques and neurofibrillary tangles) - small degree of neuronal loss Describe common socioemotional changes of aging Common socioemotional change of aging - small & intentionally chosen social network with emotionally close partners - Higher emotional stability & emotional complexity (positive and negative emotions together in life) - compensation: older brains = larger activity regions than younger for the same  task. 老人会用到更多的neuron当process一个任务的时候 Distinguish between normal aging, MCI, and AD in terms of memory performance and activities of daily living MCI = mild cognitive impairment - Mild changes in attention and memory serious enough to be noticed by others - cognitive impairment is worse than the normal aging - intact daily living activities - prodrome of AD, but not always - Important to rule out other possibilities(e.g., vascular cognitive impairment, depression) - 5-15% are converted into dementia - up to 20% are MCI people over 65. Clinical testing: patient history & mental status exam(MoCA) & brain imaging Clinical discussion: Clinical discussion should include possible etiologies, lifestyle factors, future planning. Dementia - multiple cognitive and daily life activities impairments - people’s cognitive function progressive decline - dementia is a syndrome can be caused by many disease → Alzheimer’s disease (most common) - onset = middle to late adulthood AD = Alzheimer’s disease - Most common cause of dementia - Earlier symptoms: - confusion - irritability - anxiety - deterioration of speech (difficulty in forming speech) - Later symtoms - Later symptoms: difficulties with even simple responses or behaviours (swallowing & speech) Identify symptoms of AD and predictors of progression to this illness from MCI Predictors of progression from MCI to AD. - Older age - APOE ε4 status (people who with this gene is at higher risk of AD) - homozygous (2 copies) risk > heterozygous (carrier with one copy of APOE ε4) > non carrier - Medial temporal lobe atrophy on MRI - Positive amyloid on PET scan - Molecular markers in CSF (low Aβ, elevated total tau and phosphorylated tau) Explain the clinical significance of Apo-E status Apo-E status - Everyone carries two Apo-E (apolipoprotein E) genes. - plays a role in cholesterol transport - regulate normal metabolism of amyloid beta - amyloid beta: A protein that build up at extracellular space and form sticky plaques Name and describe the 3 defining characteristics of AD Defining characteristics of AD Neurofibrillary tangles - A tauopathy: tau protein are misfold & hyperphosphorylated过度磷酸化build up - act as prions. - one misfold causes the other to misfold as well. - Intracellular - cell structure is compromised = weaken cell Amyloid plaques - (“beta amyloid”) proteins Volume loss - Progressive loss of cell & synapse - first in medial temporal lobe: entorhinal cortex, amygdala, hippocampus (all involved in memory) Name theories and treatments of AD AD Theories - Amyloid cascade hypothesis - Neurofibrillary (tau) hypothesis Treatments for AD - Cholinergic agonists (i.e., cholinesterase inhibitors), prevent breakdown of ACh (a chemical for memory) - prevent decline in learning and memory - NMDA receptor antagonist抑制剂 (reduces actions of glutamate) - prevent damage to neurons - Manage risk factors: depression, smoking, social isolation Identify biomarkers for AD and consider the implications of these results for patients Biomarkers - CSF biomarkers can help detect AD (just like amyloid and tau) but not 100% true. - can inform diagnosis & treatment & referral decision Implication of returning the Biomarker result to patient - Returning biomarker results should be done carefully, as it can provide relief for patients who realize their struggles are not just in their head. It helps them understand their condition and make sense of issues they've been facing, guiding treatment and support. Patient oriented research & social determinants of health 1. Explain the importance of understanding social determinants of health for brain dysfunction and recovery. Provide examples of the impact of SDoH on risk, treatment access, & treatment outcomes Importance: SDoH increase risk for neurological disorders - e.g,. lower educational level risk > high education treatment access & outcomes of SDoH: - Example: higher risk of Stroke in Black Americans - discrimination & stress & hypertension & diabetes - not likely to receive public health education about the acute sign of stroke - high neighbourhood segregation (people are classified into sections) → people receive different health service → wait long to receive treatment - More likely to receive a toxicology screen → 医院可能会因为对某些群体的 偏见（比如认为他们更可能使用毒品）所以进行验毒测试 - Example: higher risk of TBI in Indigenous Canadians - Road conditions (unpaved, poorly maintained) - intergenerational trauma → intimate partner violence - lack of access to culturally appropriate health care. - Learning to “live well” vs. fixing problems - Attention to spiritual health as part of overall wellness - Incorporation of traditional healers in the health care system - distrust of help from settlers due to early colonization. 2. Walk through a scenario in which cultural factors interact with dementia care Cultural factors can influence neurorehabilitation - when patients view their condition & the helpful treatment ≠ treatment offered. Example: Indigenous views of dementia - they think it’s a normal part of life - caregiving is interdependence(家人互相依靠） & reciprocity （互相提供）based on their shared cultural values - focus on acceptance and adaptation - Traditional remedies & ceremonies to maintain health 传统疗法和仪式来保持健康 - causes: normal aging & adoption to western diet & less active lifestyle & 环境污染 3. Contrast traditional and patient-oriented approaches to research traditional research patient oriented approach to research - extractive model - Research team determines research topic & method & location & condition & time & content - Participants are seen as data sources to be “mined” - One time monetary compensation - NOT return knowledge to  communities - result only published in closed access journals → limit accessibility 4. Identify perceived barriers to the inclusion of persons with lived experience in research Challenges for patient engagement research - resources intensive (expensive & require time) - What if patients shift research agenda away from original purpose? - tokensim 参与者不说实话，为了作秀 - lack of supportive infrastructure & research culture缺少相关经验的基础设施 5. Provide arguments for the inclusion of persons with lived experience in research Ethical - patient engagement should be with subject that related to their own condition For researchers increase - should increase Enrolment and retention of patients response参与和保留参与者回 应让他们感觉被重视 - Alignment of research objectives with patient priorities - should get to know the research area, rapport with the patient lived community.做 好背景功课 Improves - data collection tool - dissemination (=spread out) of study findings and mobilization of findings For patients, develops - Own voice and agenda, experience as a collaborator - Feeling of empowerment, value, confidence, life skills Improves - trust - patient involvement in decision making & organization of care - help identify what is the focus of the context = priority setting 6. Recognize possible models of patient engagement Artificial intelligence 1. Recognize the five characteristics of Big Data as they apply to brain health data Five Characteristics of Big Data in Brain Health - Volume: Large amounts of data (e.g., MRI scans, health records). - Variety: Different types of data (structured like imaging, unstructured like text). - Velocity: How fast the data is collected. - Veracity: Data accuracy and quality. - Value: Insights and benefits derived (e.g., predicting Alzheimer’s).​ 2. Distinguish between artificial intelligence, supervised machine learning, unsupervised machine learning, and artificial general intelligence AI: - a way to handle big brain data - it’s an artificial system that appear to think like human Machine learning: - subset of AI - Systems that can learn from experience & data to form pattern without direct human programming， they learn the pattern to apply to new data (classify, predict, decide) - CAPTCHA - machine learning can produce “black box” which means the output result has no explanation from the steps Supervised learning - Models are trained on known, labelled data  - E.G,. electronic medical records from patients who do vs do not develop psychosis → this has label - Requires huge volume of data and human labour Unsupervised learning - Models learn from unlabeled data - E.G,. all twitter posts containing the word “dementia” → because this is raw input without categorization. - Requires huge processing power Artificial General Intelligence (AGI): A hypothetical AI capable of solving any task on its own (not currently possible) 3. Demonstrate applications of AI to brain health with examples (risk prediction, clinical decision-making, neurotech, brain modelling, diagnosis & prognostication) AI’s application Risk prediction example - Goal: predict Alzheimer’s Disease diagnosis using brain scans - method: train ML model using labelled MRI data (heathy vs. Alzheimer’s Disease) to train ML model → to predict AD using neural activity. Identify most predictive brain regions Clinical decision-making - Goal:surgically remove epileptogenic brain region to treat seizures using intracranial EEG (electrodes implanted on surface of brain) - Method: Using unlabelled features of the raw EEG output to identify seizure origin → so that it can be removed. Neurotech build - goal: control prosthetic limbs with neural activities 脑活动控制假肢 - Method: train ML (machine learning) model to learn mapping between brain activity and limb movement Brain modelling - Goal: understand how rat brains represent space = representation of how the brain works - Method: train ML model to navigate space by simulate real neural activity of rats 通 过模拟老鼠的脑部活动来用machine learning模型完成导向 - result: successfully representation of real rats grid cell in entorhinal cortex. Diagnosis & prognostication - goal: diagnose the acute disease quickly such as stroke - model type: supervised ML model trained on head CTs & radiology annotations - result: accelerated time for diagnosing 4. Analyze ethical issues at the intersection of AI and brain health using terms like culpability, moral accountability, bias, and privacy Ethical issue of AI & neuroscience Accountability - Culpability: Responsibility based on intention, knowledge, or control - AI introduces potential harms no one person could predict or prevent - e.g,. if neurosurgery robot makes an error, who is culpable? - Moral Accountability: Duty to explain one’s reasons and actions to others - AI processes may be unexplainable to their users - e.g., doctors may not be able to explain ai’s decision because we don’t fully understand Bias & Discrimination - there are groups that are under-represented by AI models → they receive less care - e.g,. small races & ages & neuro conditions.. (mostly white people is represented) Privacy - AI outputs can be sensitive, such as future disease risk, personal preferences, emotional states → those information should be private & limit accessibility - problem: no privacy & no consent form & AI can detect previous anonymous patient by linking data. BCI Define BCI Brain computer interfere - artificial interface of the brain that bypasses(=without using) natural mechanism for speaking & typing & gesturing, inputs (vision & hearing & touch) and provide feedback - It's a device that lets the brain interact with the world without using mentioned normal ways - convert brain signal to control external object such as prosthetic limb & computer Identify types of sensors used in BCI (non invasive, semi invasive, and invasive) and recognize examples non invasive sensor - Signal is weaker, dispersed by bone, skin, hair - examples EEG semi invasive - example - recordingElectrocorticography (ECoG) electrodes place outside the dura mater (epidural) or under the dura mater (subdural) - Only performed as part of medically necessary procedures invasive - Requires craniotomy - Signal is much stronger - Accuracy can be much higher - scar tissue build up around invasive sensors → causing signals weaken or fail over time example - Cortical implants: only well-established invasive recording sensor - Neuropixels: in development 神经像素 - Multi electrode array with hundreds of sensors along a single thin probe探 测针 - Can record from hundreds of neurons simultaneously可以同时记录数百个 神经元 - Stentrodes: Wire & electrode implant threaded into brain’s blood vessels (in development) - Neural Lace (developing) - many flexible probes - inserted via surgical robot who perform the surgery Describe applications of BCI systems - Control a myoelectric prosthesis - Control an assistive device, wheelchair - Control a speech synthesizer通过分析动作目的来用ai完成想说的话 - This is an example of an ECoG system that synthesizes speech based on movement intentions - Biodirectional BCI - Myoelectric prosthesis: Electrodes implanted in motor & somatosensory cortices用motor cortex的信号操作假肢，为了让假肢更真 实，还用somatosensory cortic传递感觉such as touching - Deep brain stimulation =DBS → treat Parkinson Two intracranial electrodes implanted into basal ganglia, thalamus, or brain stem, with an implantable pulse generator (IPG) → send pulses to brain to  help movement and reduce symptoms other applications: OCD, Tourette syndrome, major depression disorders, addiction, anorexia… Discuss ethical issues relevant to BCI and link these issues to examples or research evidence Ethical issue of BCI Corporate accountability & end of use - What happens to a device after a research study? - Who is responsible to pay for removal or maintenance? User safety - Complications from implantation , potential scarring植入并发症&留疤 - Unknown interactions with plasticity of developing brain - Unknown effect of removal User burden: difficulty or stress a person experiences when using a technology, especially if it’s complex or uncomfortable. Autonomy: BCI might reveal the person’s true thought without the patient wanting it. & cause involuntary limb move. Cyborgization & personhood: - patient do NOT feel melt with tech & hybrid because they don’t want to lose sense of identity. - they prefer “controlling a tool” Judging agency:Who is responsible for BCI wrong outputs (users OR tools)