Final Flashcards

1
Q

Prosody

A
  • tone, rhythm, etc.
  • anything in language that doesn’t have to do with the language itself but the way it’s spoken
  • associated with right hemisphere
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2
Q

Posterior language area

A

At junction of temporal, occipital and parietal lobe

  • thought to be central unit that puts together concepts and their language representation
  • word comprehension
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3
Q

Wernicke’s area

A
  • in left temporal lobe
  • spoken word recognition
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4
Q

Broca’s area

A
  • in left inferior frontal lobe
  • associated with motor tasks of language production
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5
Q

Transcortical sensory aphasia

A
  • failure to comprehend meaning of words
  • word perception and fluency might be okay but with limited comprehension of what is heard or said
  • repeat after ppl
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6
Q

conduction aphasia

A
  • inability to repeat words
  • rest of speech and comprehension generally fine
  • damage to arcuate fasciculusa
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7
Q

Arcuate fasciculus

A
  • interconnect Wernicke’s and Broca’s areas
  • damaged and ppl can look up word in association cortex but can’t say it back (conduction aphasia)
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8
Q

Pure word deafness

A
  • impaired auditory word recognition
  • damage to Wernicke’s area
  • can hear, interpret non-speech sound, read and write
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9
Q

Wernicke’s aphasia

A
  • aka fluid or receptive aphasia
  • combination of pure word deafness and transcortical sensory aphasia
  • poor language comprehension, fluid speech with prosody but meaningless
  • damage to wernicke’s and posterior language area
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10
Q

Pure alexia

A
  • inability to read or recognize written words but can write
  • damage to visual word-form area
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11
Q

Visual word-form area

A
  • in left hemi of fusiform gyrus (opposite to FFA)
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12
Q

Surface dyslexia

A
  • inability to recognize whole words but can read phonetically
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13
Q

phonological dyslexia

A
  • inability to read unfamiliar or non-words, loss of phonetic reading
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14
Q

Broca’s aphasia

A
  • inability to produce speech
  • articulation problems
  • agrammatism: difficulty using grammar
  • anomia: difficulty finding appropriate word
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15
Q

Volitional face paresis

A
  • can express emotions but can’t control muscles to fake them
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16
Q

Emotional face paresis

A
  • can fake emotions but can’t express them naturally
  • often seen in ppl w PD
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17
Q

streams of thought vs streams of feeling

A

cerebral cortex vs limbic system

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18
Q

In what theory of emotion are physiological rxns caused by emotions?

A
  • common-sense view
  • dif to study bc damaging brain areas of animals might stop physiological responses but can’t tell whether emotion still present
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19
Q

What theory of emotion involves feedback from PNS responses that gets to the brain to elicit emotions

A

James-Lange theory

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20
Q

What might a person with an amygdalectomy experience?

A

Patient S.P.:
- inability to feel fear or identify in other ppl’s faces
- can fake it

Patient S.M.:
- unusual eye movement: didn’t naturally look at other ppl’s eyes
- got better at recognizing emotions after taught to look at eyes

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21
Q

What might you expect of a patient’s brain with a damaged V1 to look like if shown fearful face?

A
  • amygdala will show activity
  • person might not be conscious of stimuli but will still mimic fearful face
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22
Q

Suffocation gets fear response even when amygdala is damaged. Why is that?

A
  • regulated by medulla oblongata
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23
Q

Role of vmPFC in emotions

A
  • seems to regulate (down-regulate, inhibitory influence) emotions
  • myelination in this area finishes at around 20
  • damage to this area causes childish behavior
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24
Q

Atherosclerosis

A
  • buildup of fat and cholesterol obstructing artery
  • one of the reasons for strokes
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25
Q

Ischemic stroke

A
  • thrombus: blood clot formed within blood vessel
  • embolus: part of tissue dislodged from site of original and occludes artery
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26
Q

Hemorrhagic stroke

A
  • rupture of cerebral blood vessel letting blood out
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27
Q

Malignant vs non-malignant tumor

A
  • malignant has no distinct border so it may invade neighboring tissues and metastasize
  • non-malignant encapsulated in clear distinct border so cannot metastasize but may still grow and compress surrounding organs
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28
Q

Causes of seizures

A
  • an imbalance of excitatory/inhibitory neurons
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29
Q

Partial seizures

A
  • localized to one brain area
  • simple doesn’t produce loss of consciousness, complex does
30
Q

Generalized seizures

A
  • involve most of brain
31
Q

Only infections agent that is just a protein ?

A

Prion protein

32
Q

Huntington’s disease

A
  • very clear genetic basis
  • causes misfolding of huntington’s protein
  • protein highly expressed in basal ganglia
  • short life-span, memory loss, uncoordinated movement
33
Q

Ubiquitin

A
  • protein that breaks down misfolded protein into their amino acids
34
Q

Parkin

A
  • protein that “marks” misfolded protein to be ubiquitinated
  • mutations in parkin gene is one cause of PD
35
Q

A patient has a neuron degeneration in substantia nigra and reduced dopamine signaling in basal ganglia. What disease do they have?

A

Parkinson’s disease

36
Q

Treatments for PD

A
  • no cure
  • L-DOPA alleviates motor symptoms because elevates dopamine signaling
  • DBS in overactive parts of basal ganglia
37
Q

Tau protein

A
  • microtubule protein that becomes disfunctional in AD, disrupting intracellular transport
38
Q

Beta-amyloid

A
  • protein that misfolds in AD due to dysfunctional secretase, accumulating around hippo and neocortex
39
Q

Secretase

A
  • class of enzymes that cut beta-amyloid precursor protein to be assembled
  • cuts it in wrong spot in AD
40
Q

Negative symptoms of schizophrenia

A
  • social interaction
  • doesn’t speak much
  • reduced emotional expression
  • reduced motivion

Negative symptoms typically emerge first

41
Q

Cognitive symptoms of schizophrenia

A
  • poor abstract thinking
  • disorganized and irrational thinking
  • deficits in learning and memory
42
Q

Positive symptoms of schizo

A
  • delusions and hallucinations
43
Q

Habituation of the gill withdrawal reflex was related to what change ?

A
  • change in # of vesicles on presynaptic side
  • vesicles not being released by sensory neuron towards motor neuron
44
Q

Endocannabinoids vs nitric oxide

A
  • both retrograde signaling mol
  • endo for LTD and nitric oxide for LTP
45
Q

NMDA receptor

A
  • coincidence detector (b/w glutamate binding and depolarization)
  • if glutamate binds and neuron at rest, will open but Mg2+ will clog pore quickly because wants to enter
  • If depolarized a little (over -40mV), Mg2+ doesn’t want to enter anymore and will let Ca and Na in
46
Q

AMPA receptor

A
  • lets in Na ions and causes EPSPs
  • mediates “normal” excitatory glutamate signaling
47
Q

CaMKII

A
  • enzyme controlling amount of AMPA receptors on postsynaptic membrane
  • activated by calcium influx through NMDA receptors
48
Q

Relational learning (stimulus-stimulus)

A
  • explicit memory
  • learning relationships among individual stimuli
  • basis of episodic and semantic memory
49
Q

Stimulus-response learning

A
  • pavlovian, classical conditioning
  • instrumental, operant conditioning, aka reinforcement learning
50
Q

Glioma

A
  • example of malignant tumor originating from glia stem cells
51
Q

grand mal seizure

A
  • generalized seizure
  • preceded by aura
  • tonic phase (muscle contraction) then clonic phase (rhythmic jerking movements)
52
Q

Petit mal seizure

A
  • aka absence seizure
  • generalized and complex (loss of consciousness)
  • type of seizure most children get
53
Q

Seizure treatment

A
  • benzodiazepines
  • increasing inhibitory synapse effectiveness
54
Q

Multiple sclerosis

A
  • autoimmune disorder that de-myelinate
  • prevent APs from propagating
  • damage occurs in white matter
55
Q

Lithium

A
  • very effective way to treat mania
56
Q

Perinatal Hypoxia

A
  • brief loss of oxygen during birth
  • can lead to neural death linked to schizo
57
Q

Phonagnosia

A

difficulty recognizing familiar voices

58
Q

PKU (Phenylketonuria)

A

Metabolic disorder causing brain damage

59
Q

Aripiprazole

A
  • partial dopamine D2 receptor agonist
  • using in schizo as anti-psychotic
  • partial so upregulates activity where too low and downregulates activity when too high
60
Q

Monoamine theory of depression

A
  • depression is driven by low levels of monamines
  • SSRIs take very long to alleviate depressive symptoms which doesn’t support this theory
61
Q

What would happen if you genetically modify a neuron so that it expresses a lot less K+ leak channels?

A
  • its resting potential would be a lot less negative
  • because less K+ would be able to leave cell
62
Q

What happens if you genetically modify a neuron’s K+ leak channels to be a permeable to Na+ instead?

A
  • resting potential will become positive (around +60mV)
  • because Na will enter the cell until electrostatic force = and opposite to force of diffusion
63
Q

Perceptual and motor learning

A
  • implicit types of memories
64
Q

Dopamine hypothesis of schizophrenia

A
  • suggests imbalance in dopamine levels b/w nucleus accumbens of stiatum (too much dop) and PFC (too little dop) causes schizophrenia
  • high dop levels in nucleus accumbens seem to underlie positive symptoms of schizo and antipsychotics (D2 receptor blockers) work well to alleviate those symptoms but not negative symptoms
  • low dop levels in PFC seem to underlie negative symptoms which are similar to those of damaged PFC
  • hence the use of aripirazole to treat both negative and positive
65
Q

Electroconvulsive therapy (ECT)

A
  • very effective in treating MDD and BD
  • very common
  • works very quickly
  • electrically induced seizure that puts brain in “healthy” state, can slow go back to unhealthy depressive state
66
Q

Abnormally quick brain growth at young age is synonymous with

A

ASD

67
Q

Role of sleep in MDD

A

Ppl with MDD:

  • have bad sleep
  • start with REM sleep and spend much less time in slow-wave deep sleep
  • sleep deprivation helps depressive symptoms but return after a normal night’s sleep
68
Q

HPA axis

A
  • hypothalamic-pituitary-adrenal gland axis
  • refers to hormone signaling cascade that increases glucocorticoid signaling in blood (primarily cortisol) in response to stress
69
Q

stress stimulates

A
  • the HPA axis
  • the sympathetic branch of ANS
70
Q

What do glucocorticoids do?

A
  • regulate a lot of essential tasks such as heart rate, metabolic and immune function, skeletal growth, reproduction, etc
  • prioritize fight or flight by increasing blood-glucose levels as well as blood flow
  • deprioritize other functions such as growth and sex hormone signaling, immune functions, etc.
71
Q

cingulotomy

A
  • cutting of fiber bundle b/w PFC and anterior cingulate
  • helps treat severe cases of OCD