MT1 Flashcards

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1
Q

why do we have brains?
1. Daniel Wolpert
2. mentalism and cardiac hypothesis
3. brain hypothesis
4. dualism
5. phrenology

A
  1. brains responsible for movement and all behaviour is gov by movement since it is only way to influence with environment around us
  2. Aristotle proposed that every person has an independent non-material mind which governs behaviour through the heart which makes people unique
  3. As physician Galen noticed through open wounds that many vessels lead to the brain, thus brain must be where the mind is
  4. Rene Descarte proposed that immaterial mind located in the pineal gland and physical body are separte entities but each can interact with another
  5. brain is tissue governing the body with specific parts cobtrolling diff behaviours, the size of each part of the brain correlated with dev of behaviour which can be measured by palpating bumps of the skull; change behaviour by changing size of brain region
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2
Q

case study on language
1. case studies in neuropsychology
2. localization and lateralization of function
3. Broca’s area
4. Wernicke’s area
5. Wernicke’s model

A
  1. in-depth investigations of a phenomenon, often small sample size; reveal how the brain works through the dysfunction of a part and its affect on behaviour
  2. functions are located in one part of the brain and can be lateralized to one side of the brain
  3. part of left frontal lobe responsible for motor control of speech; dysfunction of Broca’s area is Broca’s aphasia where speech movements are lost but sound rep is not, therefore have trouble producing right sounds or finding right words but can understand speech
  4. Wernicke’s area is part of the left temporal lobe responsible for the organization of language; Wernicke’s aphasia where sound rep damaged, therefore can speak fluently but it will not make sense, typically have trouble understanding language
  5. auditory info travels from ears to temporal lobe, sounds are processed into auditory representations and stored in Wernicke’s area, sent to through arcuate fasciculus bending around lat fissure to Broca’s area, sound representations turn into speech movements and stored, area representations of speech movements in Broca’s area are sent to muscles involved in speech to produce appropriate sounds
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3
Q

disconnection
1. conduction aphasia
2. neuroplasticity
3. hierarchical org

A
  1. if arcuate fasciculus was dmged then speech sounds and movement retained but speech still impaired since signal cannot be conducted between regions
  2. Goltz challenged idea of localization by removing entire cortex of dog, no change in specific function, dog behaved like a normal dog, except with shorter sleep wake cycle and duller senses, though impaired abilities recovered suggesting brainstem can substitute for cortex indicating a lvl of neuroplasticity
  3. since removal of cortex did not eliminate function but only reduced all functions suggests information is processed in sequence and organized in a functional hierarchy, higher level areas control more complex aspects of behaviour via lower levels, dmg to higher levels produce dissolution (reverse evolution where behaviours are simpler like in animals that did not dev missing brain struc)
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4
Q
  1. Brain mapping
  2. Neuropsychology
  3. Neuron hypothesis
  4. Nervous system overview
A
  1. Korbinian Brodman used golgi staining techniques to observe nerve tissue using a microscope, discovered six layers of nerve cells with different characteristics (different functions), different parts of cells, and mapped the parts of the brain
  2. Study of the connection between human behaviour and brain, influenced by variety of disciplines
  3. Neuron is major unit of brain structure and function
  4. Split into CNS comp brain and spinal cord, PNS comp ANS and SNS (sensory and motor)
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5
Q

Wilder Penfield

A
  1. Work with epilepsy patient, reduce seizures caused by abnormal electrical activity by removing parts of the brain suspected to be the cause
  2. Stimulating different parts of the brain cause sensations in different parts of the body, somatosensory cortex (S1) localizes sensation of parts of the body to a representation in the brain, the more sensory neurons in a an area the larger the representation in the brain
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6
Q

Patient H.M.

A
  1. When he was eight or nine got into a cyclist accident and began experiencing seizures which got progressively worse to point he would exp multiple a day, negatively impacting all aspects of his life
  2. Lobotomy removing large part of his hippocampus treated his seizures but lost the ability to convert short term memories to long term memories, could only remember 20 seconds but could acquire new motor skills therefore different parts of memory are encoded differently
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7
Q

Distributed sys
1. Binding problem
2. Streams of processing
3. Ventral v. Dorsal stream in vision

A
  1. How different aspects of experiences are processed by different parts of the brain and are put together seamlessly
  2. different parts of the brain put experiences together to produce a modaility (memory, vision, sound, etc); dorsal stream involves parietal lobe, ventral stream involes temporal lobe
  3. ventral stream responsible for object recognition during concious perception; dorsal responsible for localization during unconcious perception; both work together to bind info together to produce sensation and ability to interact with environment
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8
Q

brain damage: traumatic brain injuries
1. head injury
2. concussions

A
  1. TBI is dmg or injury to brain caused by external force or recurring pressure on skull occurring after birth, disrupts brain function, not hereditary, congenital, degen, or induced by birth trauma; can be open (skull penetration) or closed
  2. closed head injury that can’t be seen by neuro imaging tech which affects the way people think and remember and causes variety of symptoms; coup is site of blow, countercoup is the second area of damage produced by compression of the brain against the skull opposite to the coup; severe (counter)coup can be accompanied by bleeding or subdural hematoma; can occur without blow
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9
Q

dementia pugillistica
1. overview
2. p-tau proteins
3. risk of brian injuries
4. prolonged brain rest and recovery period
4. sport concussion stats

A
  1. boxer’s syndrome or chronic traumatic encephalopathy (CTE) is progressive degen brain disease caused by repeated head trauma which cause accumulation of p(phosphorylated)-tau proteins in neurons and glial cells,
  2. tau proteins are responsible for stabilizing microtubules in brain for transport of nutrients in nerve cells, phosphorylation of tau proteins destabilize microtubules leading to clumping which breaks down brain cells leading to declining cog ability, short term memory less, tremours, loss of coordination, difficult speech, and emotional disturbance
  3. athletes with E4 variant of apolipoprotein (APOE) gene have increased risk of dev brain injuries
  4. when told too ill, take on sick role psychologically and can worsen symptoms; after initial 1-2 days of rest, try to return to daily life until symptoms show, stop, rest, repeat; axonal health (myelination) makes it easier to recover from concussion, recovery also lengthed by mental health (post and pre concussion anxiety)
  5. concussions in sport are public health issue due to frequency and consequences; most prevalent in youths 10-20 since they are more likely to be active in sports and not follow safe practices, more in males and high in sports such as ice hockey, rugby, and ringette
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10
Q

neuron theory
1. overview
2. electrical activity in neurons and behaviour
3. TMS
4. learning

A
  1. neurons are autonomous ceells that interact but are not physically connected, neurons send electrical signals with a chem basis, neurons use chem signal to communicate
  2. Fritsch and Hitzig showed that electrically stimulating the parts of cortex via an electrode produces selective movement in certain parts of the body on the opposite side, suggests that cortex forms topographic neural-spatial reps of body
  3. non-invasively stimulate different parts of the brain by inducing electrical activation via magnetized coil on surface of skull to study how different parts of the brain produces different behaviour
  4. Sherrington theorized that neurons separated by junctions called synapses, Loewi discover that synapses release chemicals to influence adj cells; based on this Hebb proposed that when individual cells activated at same time, synapses are est or strengthen to form basis of memory, families of neurons form cell assemblies to rep units of behaviour underlying conciousness
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11
Q

contributions to neuropsych from allied fields
1. neurosurgery
2. psychometrics
3. brain imaging

A
  1. long history of neurosurgery; Hippocrates gave directions for trephining (cutting hole in skull) to reduce pressure from swelling brain from TBI; modern era with intro of antisepsis, anesthesia allowing patients to remain conscious and contribute by providing info about effects of localized stim, and principle functional localization
  2. Binet and Simon produced a test to id children with learning disabilities with a mental lvl based on score of 80-90% typical children of a certain age; Terman revised the test so that the mental age rep by IQ was set at average to be 100; when Hebb gave IQ tests brain dmged people, those with frontal lobe lesions did not have decreased scores
  3. early neuropsych relations between brain and behaviour could only be made at autopsy such as Charcot discovering MS (degen disease characterized by hardening of nerves in the spinal cord leading to loss of sensory and motor func); brain imaging allows for quick localization of symptoms for diagnosis
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12
Q

brain imaging techniques
1. CT
2. PET
3. MRI
4. Diffusion tensor imaging

A
  1. produces 3D image by passes X rays through head, bone absorbs more x-rays than brain cells which absorb more than water, dead brain cells with more water, produces darker images than healthy cell, quick, cheap but low quality
  2. radiotracer injected and decays, releasing photons which are used to create reconstruction of brain activity based on use of radiotracer
  3. calculate location of moving molecules using electrical charge generated by their movement to produce high quality image
  4. MRI method using direction of water molecules to gen images of brain’s nerve pathways
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13
Q

brain damage: tumors
1. overview
2. assessment
3. types
4. symptoms

A
  1. majority arise in glial (gliomas) and meninges cells (meningiomas, often benign and easy to remove at surface of brain); caused by old cells that do not die normally, insides of cells leaking, or abnormal multiplying which increases mass in area
  2. req symptomatology from patient, neuroimaging, and neuropsychological testing to fully assess the extent and type of tumor
  3. malignant tumors lack defined cell membrane and are likely to recur following removal, can metastasize when cells are shed and travel to other sites, increasing probability that tumors will occur; benign tumors are contained within own membrane, not shedding cells or relasing chem therefore have a low chance of recurring after removal
  4. pressure in skull, specific disruptions related to location
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14
Q

degree and treatment of tumors
1. grades of tumors WHO
2. treatment

A
  1. benign, slow growing, respond well to surgery
  2. malignant, slow growing, increased chance of recurrence
  3. malignant, high change of recurrence, req aggressive treatment
  4. rapidly fatal
  5. best treatment depends on size, type, grade, location, metastasis, and patient capacity to tolerate treatment; radiation therapy uses internal or external high E rad to target and destroy cancer cells but may dmg healthy cells; chemotherapy meds target rapidly div cells such as cancer but also some healthy cells; targeted therapy uses drugs that selectively interfere with specific molecules contributing to growth and survival of cancer cells
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15
Q

multiple sclerosis
1. overview
2. risk factors
3. symptoms
4. prevalence

A
  1. chronic autoimmune disorder affecting CNS which damages oligodendrocytes (glial cells forming myelin in CNS) and attacks myelin, forming scar tissue which hardens the white matter leading to inflammation and disruption of signals
  2. increased risk with higher estrogen, twice more common in females, female immune sys more susceptible to MS dev, and low levels of vitamin D (more common in women), modest heritability and environmental factors
  3. often appears first between ages of 20-40 y/o, common symptoms are numbness and tingling, fatigue, pain, muscle spasms, and difficulty walking
  4. Canada has one of the highest rates, more prevalent in countries closer to the poles
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16
Q

viral brain infections
1. AIDS and HIV overview
2. Canada’s 90/90/90 targets
3. demographics of transmission of new HIV infections
4. HIV virus on cells

A
  1. AIDs dementia complex is dev from presence of HIV, virus attacks immune cells, HIV diagnosed by testing for below standard WBC count, if found early can take meds to decrease viral load to prevent AIDs progression; AIDS initial symptoms are like depression and advanced symptoms lead to motor and cog disturbances
  2. aim to have 90% people with HIV know their status, 90% of diagnosed receive antiretroviral treatment; and 90% of those receiving treatment achieving viral impression by 2020; certain prov have hit target but not ON
  3. about half through male/male sex, one third thorough heterosexual sex, 10% injection drugs
  4. HIV invades macrophages (WBC destroying microorganisms and dying cells), microglia (CNS macrophage), astrocytes (glial cells providing structural support to neurons), and vascular endothelial cells and commands them to release cytokines resulting in tissue damage and apoptosis; HIV can bind to receptors in brain to excessively increase Ca2+ leading to neuronal death
17
Q

types of alcohol
1. ethyl
2. methanol
3. isopropyl
4. increasing alch conc

A
  1. All alcohols have a hydroxyl group, ethyl alcohol for consumption produced by natural fermentation when yeast cells interact with sugar, type of material with sugar produces different types of alcohol, able to ferment up to 15% alcohol, percentage ethanol ranges from low (3-4%), med (12-14%), to high (45-50%), small molecule able to easily travel through body and bind to receptors
  2. methyl alcohol simple structure but highly toxic; used in fuel and industrial solvents
  3. isopropyl alcohol used as rubbing alcohol or as disinfectant but danger to consumption
  4. Contaimination of ethyl alcohol leads to formation of other volatile organic compounds in addition to ethanol producing higher alch content; distillation increase alch conc by decreasing water, add alch to increase content, or freeze alcohol to remove water but also results in higher conc of impurities
18
Q

update of Canada’s Low risk Alcohol Drinking Guidelines
1. CAMH guidelines
2. consequences of drinking
3. reasons for new guidelines

A
  1. set different guidelines for males and females; one standard drink will be different amounts for each type of alcohol
  2. <=2 drinks/per able to avoid neg consequences, 3-6 is increasing risk of cancer, >7 increase risk of CVD or stroke, and any additional drink health problems and diseases increases exponentially
  3. cancer is leading cause of death in Canada and alcohol is carcinogen causing at least 7 types of cancer; drinking less alcohol is among top 10 healthy habits to prevent cancer
19
Q

Relationship of alch consumption to all cause CVD and cancer related mortality in US adults (2017)
1. objective
2. methods
3. results and conclusion
4. 90+ study

A
  1. examine association between alch consumption and all cause mortality, cancer, and CVD in US adults
  2. large scale scale study on adults linking 13 waves of national health surveys to national death records
  3. light and moderate (5-7 drinks/week) alch might be protective against all-cause mortality and CVD, heavy drinking assoc with increased risk of all cause and cancer mortality
  4. people who drank moderate amounts of alcohol or coffee lived longer than those who abstained
20
Q

no amount of alcohol is good for health (2018)
1. objective
2. methods
3. results and conclusion
4. prospective study
5. retrospective study

A
  1. estimate alch use and alch attributed deaths worldwide for people between 15-95 y/o
  2. large scale study using individual and pop lvl alch consumption with prospective and retrospective studies on risk of alch to estimate prevalence of current drinking, distribution of alcohol consumption and alch attributed deaths
  3. alch use is leading risk factor for disease worldwide, 10% of global deaths in teens and younger adults showing the safest level of drinking is none, in conflict to most health guidelines, therefore view of health benefits of alcohol needs revising
  4. longitudinal study to observe outcome fo interest
  5. data collected after outcome of interest has occured
21
Q

health behaviours and effects of alch
1. stats Canada
2. short-term effects of alch
3. metabolism of alch
4. signs of intoxication

A
  1. heavy drinking is consuming 5 or more drinks on one occasion, 12 or more time over past year; males and ages 18-24 more susceptible; drinking increase during COVID across all ages
  2. normally excitatory and inhibitory signals have a homeostasis in the brain; alch increases inhibitory signals by increasing GABA and decreasing excitatory neurotransmitters such as glutamate or DA
  3. one drink/hr can be effectively metabolized as 10% alch absorbed in stomach, presence of food slows absorption since it delays movement into small intestine allowing ADH to metabolise alcohol in stomach before reach small intestine, 90% by small intestine into bloodstream, liver will metabolized 95% (at 15 mg/dL/h or 1 drink/h) and 5% excreted by lungs; anything over 1 drink/hr leads to accumulation which presents as intoxication
  4. usually at 2 drinks, relaxation, reduced social inhibition and judgment, coordination, memory deficits, reduced coordination and delayed reaction time but varies depending on time period of consumption, presence of food, other drugs, physiology, location of consumption, and how often you drink
22
Q

sex differences and metabolism of alcohol
1. tolerance mechanism
2. sex differences in tolerance
3. alch and other drugs metabolism
4. sex differences in effects of alch
5. sex difference in alcholism

A
  1. alchohol broken into acetaldehyde by ADH and into actetic acid by ALDH, ALDH and ADH can also convert methanol to formaldehyde and formic acid respectively, inactive ALDH not able to break down acetlyaldehyde, accumulation generate sick feelings therefore more likely to abstain and low chance of dev AUD, heterozygous version have mod alcohol tolerance partially protected from alcohol dependence
  2. males have higher activity levels of ADH1B, have higher rate of metabolism and lower BAC comp females, thus have higher tolerance; males also have 60% more active gastric ADH
  3. liver enzymes cytochrome P450 family convert alcohol to AL, also metabolise many other drugs, when consuming more than one drug compete for same enzymes leading to high and potentially dangerous level of other drugs
  4. females more susceptible to negative effects, estrogen’s role in inflammation speed up liver damage, have greater sensitivity to heart problems caused by alcohol, greater reductions in grey and white matter, greater thiamine deficiency leads to greater lead accumulation
  5. males have lower number of DA cells, less satsifaction from same amount of alch, tend to drink more, have greater susceptibility to alcoholism
23
Q

Receptors
1. Up regulation
2. Down regulation
3. Agonism vs. Antagonism
4. Neuroadaptation

A
  1. Increase # of receptors, increased sensitivity to ligand, by depolarizing cell (decrease electric potential), increase chance of triggering AP
  2. Decrease # receptors, decreased sensitivity to ligand by hyperpolarizing cell (increase electric potential across membrane), decreased chance of triggering AP
  3. Agonist ligands bind to receptor activating response, antagonist (inhibitor) binds to receptor and blocks other motels from activates the receptor
  4. Changes occurring in NS in response to prolonged exposure to stimulus
24
Q

Neurotransmitters & effects of alcohol
1. Glutamate
2. GABA
3. Dopamine
4. Opioids

A
  1. Excitatory, alcohol acts as antagonist to glutamate decrease activity, chronic use leads to neuroadaptive upregulatory response of GABA receptors, increasing glutamate activity producing hyperexcitability assoc with withdrawal and memory loss
  2. Inhibitory neurotransmitter, initial increase in GABA hyperpolarizes cells, chronic use leads to near neuroadaptive decrease in GABA resulting in tolerance and signs of withdrawal like hyperexictability, seizures, and tremors
  3. Initial increase dopamine signaling to mesolimbic tract (reg reward, motivation, and emotional processing), chronic decrease DA reinforce drinking to feel reward, feel negative affect with withdrawal, show firing rate, release, and metabolism
  4. Acute increase in endogenous opioids for feel good and pain relief, chronic neuroadaptive response decreases endorphin levels leading to dysphoria, increase use to decrease dysphoria reinforces alcoholic behaviour
25
Q

Vomiting and alch administration
1. Alch induced vomiting
2. Voluntary alch consumption by rats (Peris et al., 2006)
3. Alch induced brain dmg from chronic consumption

A
  1. High alch conc is detected by chemoreceptors in the area postrema, induce vomitting to reduce alch in sys and burden on liver
  2. using jello shots, able to get rats to voluntarily consume alcohol, resulting in increase in firing of DA neurons in reward pathway from the nucleus accumbens near hypothalamus to ventral tegmental area in midbrain to prefrontal cortex
  3. MRI shows that alcoholic brain has larger ventricles due to shrinkage of brain tissues; DTI shows white matter dmg (myelin loss) and enlargement of microtubules leading to degradation of membranes in alcoholics
26
Q

neurological assessment
1. olfactory nerve
2. optic nerve
3. fundus
4. photoreceptor

A
  1. nerve I, responsible for sense of smell, test using something familiar with strong scent (coffee, orange peel)
  2. nerve II, responsible for vision, test visual acuity using Snellen charts, colour vision tested with Ishihara plates, visual fields (peripheral vis) tested by having patient look straight ahead while moving fingers in each quadrant, visual inattention can be tested by moving both fingers at same time, visual field decrease with age; test pupil reflex by blocking light from one eye and shining light into other, if functioning well then both pupils with constrict
  3. the interior surface of the eye including retina, optic disc, macula, and fovea, and posterior pole (space between optic disk and macula), optic disk is blind spot where optic nerve attaches to retina
  4. convert photons into AP interpreted as vis info, macula is highly specialized with many photoreceptor for fine detail, fovea is high conc of photoreceptor for highest visual acuity
27
Q

neurological assessement
1. oculomotor nerve, trochelar nerve, and abducens nerve
2. trigeminal nerve
3. facial nerve
4. vestibulocochlear nerve

A
  1. II, IV, and VI involved in movements of the eye, test by having patient look straight ahead and follow your fingers with eyes only as you move fingers in all directions
  2. V involved in sensory supply to face and movement of muscles of mastication, three branches ophthalmic, maxillary, and mandibular, test sensory by using light touch such as feather to touch each part of three parts of face, test motor supply by asking patient to clench teeth, observe and feel the contraction of masseter and temporalis muscles
  3. VII, responsible for movement of facial muscles, patient makes faces to test motor supply, crease forehead, close eyes against resistance, puff out cheeks, bare teeth
  4. VIII responsible for hearing, Rinne test place tuning fork on mastoid process and compare to tuning fork next to ear, next to ear should be louder
28
Q

changing face of neurological assessment
1. neurological assessment
2. functional brain imaging
3. cognitive neurosci
4. managed care

A
  1. Post WWII, push for dev of psychological assessments for leading to divergence of psychological assessment from trad med since imaging cannot tell all
  2. historically neurological conditions inferred from behavioural symptoms, advances able to id change in cerebral functioning in variety of disorders but sometimes cannot predict extent of behavioural disturbance in people with certain types of brain injury such as concussions
  3. in 1990s dev specialized tests with cutoff scores to id certain conditions; many demographic factors influence cerebral org and many test req problem solving (intelligence) making it difficult to work with cutoff scores due to high variability; right frontal lobe unresponsive to neuropsych assessment but with cog testing, show it is responsible for functions such as social cog
  4. nueropsych tests are time consuming and expensive comp medical imaging, suggest psychologist must dev and promote assessments that focus on most appropriate diagnostic matters, id cost saving conditions, time efficient, and integrate planning, progress, and outcome of treatment
29
Q

rationale of neuropsych assessment
1. standardized test batteries
2. individualized test batteries
3. composite test batteries
4. factors affecting test choice
5. goals

A
  1. fixed criteria for organicity (natural impulses towards growth) atypical behaviour assumed to have a bio basis
  2. req particular theoretical knowledge, qualitative assessment tailored to the patient
  3. administered in formally and have comparison norms but also use qualitative performance and pattern of results
  4. consider more sensitive tests for smaller dysfunctional brain regions; demographic differences interact with brain pathology and intelligence change performance making interpretation of results difficult thus neuropsych assessments must be flexible
  5. id level of cerebral functioning and localize dysfunction, facilitate care and rehab, documents recovery of function after TBI, and promote realistic outcomes
30
Q

neuropsychological test and brain -activity
1. intelligence testing
2. Weshcler IV results
3. caveat of est intelligence
4. problem of effort

A
  1. most neuropsych assessments use measure of general intelligence often with Weshcler IV scale to determine baseline of cog func, tests general ability, verbal comprehension, perceptual reasoning, working memory, and processing speed
  2. ADHD has sig decrease in WM and PR while TBI patients show decrease in PS; left hemisphere lesions produce low verbal IQ, right hemisphere produce low performance, diffuse produce low performance (except in occipital lesion)
  3. post injury testing useless without pre injury est of intelligence; can be est based on edu, occupation, and socioecon bg
  4. malingering is intentionally exaggerating phys or psych symptoms, usually motivated by other incentives to receive diagnosis; control by adminstering effort tests such as forced choice digit memory where even amensiac patient can score perfect; 20% people with TBI or exposure to toxic substances likely to malinger