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FALL 2021: CASI TERMINAMOS > PSY 401 Exam #1 > Flashcards

PSY 401 Exam #1 Flashcards

1
Q

basic neuronal anatomy

A

dendrites (come off the soma, receive signals) –> soma (contains nucleus) –> axon –> (covered by) mylein sheath –> (interrupted by) nodes of ranvier –> terminal buttons pic

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2
Q

of neurons in human brain; comparison

A

86 billion; not remarkable, similar to other primates of our size

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3
Q

physiological props of neurons: the action potential

A

resting state = -70mv
depolarization = getting closer to 0mv
threshold state = -50mv

Na+ channels open causing depolarization, mv goes up +++ –> AP / “spike”

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4
Q

physiological props of neurons: fuel/energy use

A

brain is 2% of body weight but uses up 20% of oxygenated blood from the <3

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5
Q

physiological props of neurons: active conduction

A

the purposeful regeneration of an AP @ each node of rancvier; propogation of an AP from the soma down the axon; if the summation of dendritic signals passes the threshold it’s ALL or NOTHING

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6
Q

myelin sheath and nodes of ranvier

A

where the axon is covered in myelin, Na+ or K+i ons CANNOT enter/exit and AP has potential to slow down; nodes of ranvier interrupt the MS exposing the axon and allowing Na+/K+ to exit, essentially “re-creating” the AP at every stop

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7
Q

basic neuronal anatomy: myelin sheath and nodes of ranvier

A

where the axon is covered in myelin, Na+ or K+i ons CANNOT enter/exit and AP has potential to slow down; nodes of ranvier interrupt the MS exposing the axon and allowing Na+/K+ to exit, essentially “re-creating” the AP at every stop

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8
Q

brain structure: thalamus

A

“switchboard” of the brain, conducts signals from (ex) sensory organs, cerebellum, amyg to up cortex; has bidirectional connections to every cortex area

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9
Q

physiological props of neurons: passive conduction

A

uninhibited flow of elec signals from dendrites to soma

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10
Q

brainstem

A

medulla + pons + midbrain

func: HOMEOSTASIS, HOUSES CRANIAL NERVES

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11
Q

thalamus

A

SWITHCBOARD, CORTICAL RELAY (BOTHWAYS)

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12
Q

hippocampus

A

spatial navigation and episodic memory [place cells] ; bigger in taxi drivers, pianists (includes memory of more abstract domains)

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13
Q

amygdala

A

personal relevance of stimuli; danger, emotions

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14
Q

basal ganglia

A

(front and temp lobe) bunch of nuclei that contribute to development of habits;

  • get lots of input from cortex, has 2 “no” or “go” pathways
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15
Q

cerebellum

A

regulates muscle tone, posture, smooth movement, timing, coordination

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16
Q

gray matter vs white matter

A

gray matter = cell bodies, located in within the cortex (in the cortex)

white matter = myleinated axons

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17
Q

cerebral cortex: 5th lobe!

A

insula: not visible externally, located beneath the sylvian fissure (which separates temp lobe from frontal and parietal)

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18
Q

gyri vs sulci

A

gyri: bulGes of cortical tissue
sulci: GROOVES within cortical tissue
https: //www.purposegames.com/game/brain-sucli-and-gyri-quiz

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19
Q

gyri & sulci: properties & benefits

A
  • BOTH subject to individual human differences
  • increased gyrification MAY have implications for increased cognitive abilities
  • allow for a large surface area of tissue to be squeezed into the small cranial space; reduces the distance signals have to travel; reduces amount of axon wiring needed
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20
Q

cytoarchitectonic organization of the cortex

A

HORIZONTAL: ctx arranged in 6 layers of cells, arranged based on similarities in form and connection (where/what they innervate)

VERTICAL: ctx permeated by columns; cells in which respond to similar fts of the external and internal environment

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21
Q

broadmann areas

A

(43) imperfect; better as a STRUCTURAL organization / sectioning of brain areas than a functional one; BASED on CYTOARCHITECTONIC org of cortex

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22
Q

corpus callosum

A

tract of white matter connecting L and R hemispheres

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23
Q

fasiculi

A

tract of white matter connecting different cortical areas within the same hemisphere

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24
Q

diffusion tractography

A

type of fmri that tracks water molecules along axon fibers in white matter, allowing the visualization of fiber connections p19

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25
Q

syndrome

A

a group of symptoms that statistically co-occur within patients ex.

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26
Q

neuropsychology

A

utilizing instances of patient brain damage to reveal insights about it’s function - structure relationships

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27
Q

aims of neuropsychology in language study (2)

A
  1. understanding the cognitive architecture of lang; determining which components can be independently disrupted (ex. nouns v verbs, comprehension v production)
  2. understanding the neural architecture of lang; which lesion sites are assoc w which lang deficits

(p2)

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28
Q

neuropsychology: types of brain damage (4)

A
  1. stroke
  2. traumatic brain injury (tbi) - closed v open
  3. neurodegen and infectious disease (i.e. primary progressive aphasia)
  4. tumors
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29
Q

neuropsychological methods: lesion overlap and subtraction analysis

A
  1. “overlap maps” created for 2 separate groups - ppl with lesion and ppl without it
  2. lesion overlap map for DEFICIT ppl - lesion overlap map for ppl WITHOUT deficit = image highlighting areas specifically assoc w deficit
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30
Q

neuropsychological methods: voxel based lesion-symptom mapping (VLSM)

A
  1. some task is administered to a group of ppl w different lesions
  2. each voxel is id’d as either damaged or not damaged and from here subjects separated into 2 groups (damaged v not damaged)
  3. performance on the task is compared between the 2 groups
  4. can conclude that “damage to this area is signif assoc w poor/normal performance on …”
31
Q

neuropsychological methods: voxel based morphometry (VBM)

A
  • same as VLSM*? but voxels assessed on a graded scale (from 0%-100% damaged) rather than a binary one
  • useful in measuring neurodegen disease!!
32
Q

neuropsychological methods: issues

A
  1. the spatial distribution of voxels/damage is not random, although it is computed as such (i.e. every voxel has the same prob of being damaged or not)
  2. the brain may reorganize in response to damage, altering normal structure-funciton relationships
  3. some impairments may be issues in CONNECTIONS (yt matter tracks) between brain regions, not in the brain regions/structures themselves
  4. hypo-perfusion/low blood flow may cause impairment, not necessarily structural damage
33
Q

functional neuroimaging: PET

A
  • positron emission tomography: tracks distribution of radioactive isotopes thru the brain, capturing
    “annihilation events”
  • more A events –> more blood flow –> more activity
  • POOR temporal resolution = best suited to blocked designs
34
Q

functional neuroimaging: fMRI

A
  • f magnetic resonance imaging: measures Blood Oxygen Level Dependent signals (BOLD)
    • BOLD signal is LOW when blood is DEOXYGENATED
    • BOLD signal is HIGH when blood is OXYGENATED
  • temp and spatial resolution are better than PET but vary
35
Q

fMRI: HRF

A
  • hemodynamic response function: plots the BOLD signal distribution over time
  • brain activity occurs —> available O2 in the area is used up [BOLD signal drops]–> new 02 blood arrives from arteries [BOLD sig goes up] –> 02 blood is used up & cycle restarts
36
Q

functional neuroimaging: study designs (2)

A
  1. blocked design: stimuli for 1 trial are presented consecutively / in a block to account for poor TEMPORAL resolution
    ex. AAAAAAA - rest - BBBBBBB
  2. event related design: stimuli from different types of trials are intermixed
    ex. A - B - C - rest - B - A - C
37
Q

functional neuroimaging: experimental paradigms (3)

A
  1. subtraction: brain activation maps for an experimental task are compared to that of a similar ctrl tasks to see overlap / areas of common activation
    • [exp condition - ctrl condition]
  2. correlation / parametric: brain function / activity of interest is assessed as a continuous measure rather than all or nothing [ex. levels of unintelligible speech]
    • pts do a tasks requiring a function of interest to diff degrees / levels of difficulty –> look for corresponding graded shifts in brain activation
  3. multivariate pattern analyses (MVPA): considers patterns of activity across a cluster of voxels rather than individually
    • helps answer the q: can 2 exp tasks be differentiated based on different patterns of activity in the same voxels?
38
Q

electrophysiology methods: issues

A
  1. intensity of stimulation needed to id particular language areas varies across and within patients
  2. stimulation doesn’t stay local –> may spread to other regions, causing less precise measurements
39
Q

paraphasis

A
  • changes to semantic or phonological content of a word
  • ex. calling a dog “cat” or a “dag”

p30-31

40
Q

electrophysiology methods: EEG

A
  • electroencephalogram; brain activity wave forms recorded from electrodes on the scalp
  • changes in amplitude and duration of waves reflect changes in mental state –> HOWEVER measurements are too vague to give concrete info about linguistic operations, etc.
  • p34
41
Q

electrophysiology methods: ERPs

A
  • event-related potentials; linking changes in EEG waveforms to specific responses to experimental stimuli; NON-INVASIVE
  • ex. N400
  • GRANT MORE PRECISION TO EEG MEASUREMENTS
42
Q

electrophysiology methods: INTRA-CRANIAL single cell recording

A
  • single electrodes connected to individual neurons, recorded activity can reveal what type of stimuli a cell codes for; records # of APs per second
  • ex. subject listens to speech, a single neuron responds to the sound of Cs and Rs
43
Q

electrophysiology methods: electrocorticography

A
  • type of INTRA-cranial cell recording
  • an electrode “Grid” is placed directly over the cortex; records “field potentials” - responses from a region of cortical cells
44
Q

anomia

A
  • difficulty word finding
45
Q

anarthria vs dysarthria

A
  • anarthria: inability to articulate words

- dysarthria: impairment to muscles needed for fine articulation, issues in speed, timing, accuracy of mvmnt

46
Q

electrophysiology methods: features of ERPs

A
  1. latency: time after stim presentation when waveforms reach peak
  2. amplitude: strength of an effect (in mvs)
  3. polarity: positive or neg spike (arbitrary, except for when compared to a control condition)
  4. tomography: the scalp distribution of wave responses; where responses are observed/where electrodes are placed
47
Q

electrophysiology methods: TMS

A
  • transcranial magnetic stimulation; can be used to facilitate AND disrupt elec activity of cortical neurons
  • good spatial precision
48
Q

aphasia

A

impairment to language function resulting from a brain injury ACQUIRED after normal linguistic competence is developed

49
Q

aphasia categorization: issues (5)

A
  1. often based around problems in production or comprehension, this DOESNT align with the levels of linguistic theory [phono, morpho, syn] AND eurocentric bias [repetition task, favors euro langs that have more standard syntactic constraints]
  2. impairments are always on a continuum, NOT all or nothing
  3. Not every symptom of a syndrome must be present in order to give a diagnosis
  4. Brain damage often extends past one specific area; lesion-deficit connections are not always v clear
  5. Syndromes are not always stable over time, shift acutely
50
Q

Broca’s aphasia: production

A
  1. nonfluent speech
  2. apraxia of speech
  3. dysarthria
  4. agrammatism [noun heavy]
  5. repetition is ok, lots of omissions [usually of clases cerrados]
51
Q

apraxia of speech

A
  • disrupted articulatory planning
  • patient can say “pa” “ta” and “ka” but can’t put them together to say the more complex “pataka”
    p7
52
Q

agrammatism

A
  • deficit assoc w disruption of syntactic rules
    ex. dropping FUNCTION words [“-ed’s”, prepositions, conjunctions] keeping content words
  • affects clases cerrados más que abiertas
  • BA!
53
Q

Broca’s aphasia: comprehension

A
  1. difficulty understanding complex phrases/sentences [compared to simple, single word]
54
Q

Broca’s aphasia: lesion site

A
  • Left Posterior Inferior Frontal Gyrus (IFG)
    Left Superior Temporal Gyrus

+ underlying fiber tracts [arcuate fasiculus, frontal aslant trac]

55
Q

Wernicke’s aphasia: production

A
  1. hyperfluent speech, very little meaning conveyed [syntactic structure maintained]
  2. phonological paraphasia
  3. neologisms
56
Q

phonological paraphasia

A

[WA!]

  • disruption of phonological properties of words in speech ex. “paker” instead of “paper”
57
Q

neologisms

A

[WA!]

  • result of extreme phonological paraphasia - nonsense words
58
Q

Wernicke’s aphasia: comprehension

A
  1. very poor, sometimes nonexistent
  2. repetition: poor, neologisms and phonol. errors

p12

59
Q

Wernicke’s aphasia: lesion site

A
  • Posterior Superior and Middle Temporal Gyri + underlying white matter
60
Q

Conduction aphasia: lesion site

A
  • damage to the connections between the left superior temporal gyrus [WA] and the left inferior frontal gyrus [BA]
  • not limited to here!
61
Q

Conduction aphasia: production

A
  1. fluent [less than WA, moreso than BA]
  2. LOTS of paraphasia [phonol.]
  3. AWARE of their errors! try to correct them!
62
Q

Conduction aphasia: comprehension

A
  1. well-preserved

2. repetition: NOTABLY IMPAIRED; will try to correct and sometimes paraphrase

63
Q

global aphasia

A
  1. disruption of virtually ALL linguistic function
64
Q

anomic aphasia

A
  1. PRODUCTION is most affected, hesitation and pausing when word finding
  2. REPETITION IS INTACT!
65
Q

transcortical aphasias: motor

A
  1. Trouble INITIATING and PLANNING speech, mostly nonfluent
  2. Comprehension: relatively preserved, prone to ECHOLALIA
  3. REPETITION IS INTACT!
66
Q

echolalia

A
  • OCCURS IN TRANSCORT MOTOR APHASIA

- deficit in which patients repeat parts of what is said to them

67
Q

transcortical aphasias: sensory

A
  1. production: phonemic paraphasia, often misdiagnosed as psychotic/schizo
  2. comprehension is impaired
  3. REPETITION IS INTACT!
68
Q

transcortical aphasias: mixed

A
  • a mix of TCMA and TCSA; REPETITION IS INTACT!
69
Q

primary progressive aphasia (PPA)

A
  • aphasia that occurs as a byproduct of neurodegenerative disease
70
Q

PPA: nonfluent variant

A
  1. labored speech, agrammatism, phonological error
  2. gradually worsening comprehension of single words and simple sentences
  3. repitition impaired; Posterior IFG and spreads
71
Q

PPA: semantic variant

A
  1. fluid production, semantic errors
  2. comprehension impaired
  3. repetition INTACT; anterior temporal lobe damage [both hemis]
72
Q

PPA: logopenic variant

A
  1. fluent production, ANOMIA, phono errors
  2. comprehension of complx sentences is impaired
  3. repetition of complx sentences is impaired; damage in left temporoparietal junction [posterior]

**COMMON TO ALZHEIMERS*

73
Q

what are grandmother cells? what cog neuro method has been used to id them?

A
  • hypothetical neurons that respond to 1 particular image; single cell recordings

FALL 2021: CASI TERMINAMOS (7 decks)

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