Final Exam Unit 4 Flashcards

1
Q

Association Cortex

A
  • “Associations” of processing as much info as possible before responding
  • Inputs come from

—Primary and secondary sensory and motor cortices

—Hippocampus

—Thalamus

—Brainstem

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2
Q

Parietal Association Cortex

A
  • Important for attending to stimuli in the external and internal environments
  • Electrophysiological studies identify attention-sensitive neurons here

—-Allow for recording of single neurons during various tasks

-Damage= contralateral neglect syndrome

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3
Q

Temporal Association Cortex

A
  • Important for recognition and identification of stimuli
  • Damage= agnosia

–Patient acknowledge presence of the stimulus but cannot identify it

-Ex: Prosopagnosia

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4
Q

Frontal Association Cortex

A
  • Important for selecting and planning appropriate behavioral responses
  • Integrates complex info from all other cortices
  • Responsible for appreciation of self in relation to the world and ability to select, plan, and execute appropriate behavior (“character”)
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5
Q

Cortical Structure

A
  • Neocortex
  • Six layers each with a distinct population of cells
  • Layer 1= superficial, 6=deepest
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6
Q

Neocortical circuitry

A
  • Each layer has a primary source of input and a primary output target
  • Input to the thalamus comes from layer 6; output from the thalamus goes to layer 4
  • Can have connection in the vertical and horizontal axis
  • Interneurons can link functionally similar groups of cells

—Layers communicate w/ each other

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7
Q

Where do association areas receive info from?

A
  • Association areas receive info that has already been processed by the primary and secondary cortices
  • Also receive info from other association cortices–> corticocortical connections

—-Form the majority of input; can be ipsilateral or contralateral *Everything is not connected to everything

*Each association has distinct but overlapping connections

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8
Q

Synesthesia

A

-When one sense is perceived by one or more additional senses

—Ex: seeing numbers, letters, or sounds as colors; sounds inducing sensations in body; words or numbers liked to specific tastes

-Researchers study these patients to better understand how we integrate different sense modalities

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9
Q

Electrophysiological studies

A
  • Record activity of neurons during tasks
  • To study, we use behavior paradigms that assess attention (parietal), ID (temporal), and planning (frontal)
  • Allow for recording of single neurons during various tasks
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10
Q

Contralateral Neglect Syndrome

A
  • Inability to attend to objects or even one’s own body opposite the lesion
  • Typically associated w/ lesion on RIGHT side

—Right hemi mediates attention to both the left and right halves of the body, while the left hemi focuses mostly on right side only

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11
Q

Prosopagnosia

A

-Inability to recognize and identify faces

—Rely on other inputs (voice, body type, perfume) to determine person

-Can be acquired or developed (most common)

—No defining abnormality or genetic marker is known

  • Brain imaging and electrophysiological studies show “patches” of neurons
  • Usually results from problems in the right side

*No problem remembering names

-Treatment= helping patients use other cues

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12
Q

Phineas Gage

A

-Damage to frontal lobe–> changes in personality -Worked at railroad, had a metal rod go through his skull

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13
Q

Stroop Test

A
  • Tests for frontal lobe damage by evaluating abilities related to planning and decision making
  • Only frontal lobe damage lesions led to significant impairment on the test
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14
Q

Psychosurgery

A
  • Popular between 1935-1940s
  • Used as treatment for mental conditions like schizophrenia
  • Treatment disappeared after development of psychotropic drugs in 1940s
  • Cut hole in the skull to damage area of skull

—Made patients more subdued

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15
Q

Cortical States

A

-Our brains function in a continuum between alert wakefulness to deep sleep

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16
Q

Circadian Rhythm Study

A

-Volunteers placed into room

–1st trial- had access to cues like a clock, window, meals at certain times–> cycle was 24 hrs

–2nd trial- cues removed (no idea what time it was)—> participants woke up later and later each day, but cycle was about 26 hrs (still similar)

–3rd trial- Cues reinstated–> when back to normal 24 hr cycle

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17
Q

Circadian Rhythms

A
  • 24 hr cycle
  • Thought to have evolved in order to maintain appropriate daily rhythms of homeostatic functions (regardless of amount of daylight)

—Homeostatic fxns regulated w/in 24 hr cycle

—-1. Body temp- drops during sleep

—2. Growth hormone- peaks while we sleep

—3. Cortisol= stress hormone–> peaks right before u wake up

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18
Q

Photosensitive Retinal Ganglion Cells

A
  • Located in the retina
  • Important for photo entrainment

—Regulate sleep and mood

  • Contain melanopsin (photopigment)
  • Are depolarized in the presence of light
  • Synapse at suprachiasmatic nucleus
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19
Q

Suprachiasmatic Nucleus

A
  • Retinal ganglion cells synapse here
  • “Master clock”–> removal leads to no more sleep-wake cycle

-Signal will eventually arrive at pineal gland- synthesizes melatonin

—Enters bloodstream to influence sleep-wake cycle in brain

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20
Q

Melatonin’s relationship with light

A

-Melatonin has an inverse relationship with light

—As light increases, melatonin release decreases

-Release peaks btwn 2-4 am

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21
Q

Sleep

A
  • Defined as a normal suspension of consciousness with the presence of specific brain waves
  • Brain waves measured using EEG
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22
Q

Electroencephalography (EEG)

A
  • Electrodes applied in specific positions to the scalp
  • Measures the activity of a group of neurons
  • Activity creates an electrical field where the most superficial areas are more negative
  • Four distinct rhythms were identified

—Alpha (awake)

—Beta (active/busy)

—Theta (sleep, deep meditation)

—Delta (deep sleep)

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23
Q

Why do we sleep?

A
  • Replenish brain glycogen levels
  • Allows body temperature to drop
  • Consolidation of memory
  • Clearing of wastes in the brain
  • Effectiveness of immune system

*We need less sleep with age

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24
Q

Sleep Stages

A

*I- marked by drowsiness, wave frequency decreases, amplitude increases

*II- frequency decreases more; sleep spindles = high frequency clusters

*III- Moderate deep sleep, further decrease in frequency and increase amplitude of waves

*IV- delta waves= lowest frequency and highest amplitude *REM- Rapid Eye Movement Sleep

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25
Q

REM

A
  • EEG pattern similar to awake state
  • Dreams occur here
  • Lasts about 10 minutes
  • Amount decreases as we age

—8 Hrs at birth; 2 at 20yo; 45 minutes at 70

*Paradoxical sleep- eye movement but muscles= paralyzed

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26
Q

Physiological Changes during sleep

A
  • Eye movement= only during REM
  • Neck movements only outside REM
  • Heart rate, penial erection, and respiration increase during REM
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27
Q

Neural Circuits for Sleep

A
  • Sleep= interaction between the brainstem, thalamus, and cortex
  • Stimulation of Reticular Activating System (junction of the pons and midbrain) leads to wakefulness
  • Stimulation of the thalamus= sleepiness
28
Q

Neurotransmitters for the Awake State

A
  • Cholinergic neurons from the reticular activating system
  • Noradrenergic neurons from the locus coeruleus
  • Serotonergic neurons from the raphe nuclei
  • Histamine-containing neurons from the tuberomammillary nucleus (TMN) of the hypothalamus

—Antihistamines cause drowsiness by inhibiting TMN neurons

29
Q

How is sleep produced?

A

-Neurons in the ventrolateral preoptic nucleus causes inhibitions of the “wakefulness neurons”

—Inhibits cholinergic nuclei, locus coeruleus, raphe nuclei, and tuberomammillary nucleus

30
Q

Limbic System Activation During REM

A
  • Limbic system is active while the frontal cortex is inactive
  • Explains why dreams tend to have a lot of emotions and are not always socially appropriate
31
Q

Insomnia

A

*Sleep disorder

  • Amount of sleep not long or deep enough
  • Can be caused by stress, jet lag, working night shifts
  • Can be associated with depression

—Balance between cholinergic, adrenergic, and serotonergic is disturbed

32
Q

Narcolepsy

A

*Sleep disorder -Individual enters REM sleep (directly) during the day

  • Often accompanied by cataplexy (loss of muscle control)
  • Treatment= stimulants (Ritalin, Modafinil or amphetamines)
33
Q

Restless leg syndrome

A

*Sleep disorder

  • Feelings of crawling, pricking, or tingling in one or both legs and feet
  • Occurs when sitting or laying down for long periods of time
  • Results in fragmented sleep
  • Seen mostly in elderly or people w/ chronic diseases
34
Q

Language and Speech Location

A
  • Lang= located primarily in the association cortices of the left temporal, parietal, and frontal lobes
  • Left hemi-concerned with lexical, grammatical, and syntactic aspects
  • Right hemi- emotional content
35
Q

Areas of Comprehension and Production of Language

A
  • Primary motor cortex
  • Broca’s area–> lang production left hemi
  • Primary somatosensory cortex
  • Wernicke’s area–> language comprehension (left hemi) -Primary auditory cortex
  • Primary visual cortex
36
Q

Broca’s Aphasia

A
  • Inability to produce language (also known as motor or expressive aphasia)
  • Halting speech
  • Tendency to repeat phrases or words (preservation)
  • Disordered syntax, grammar, structure of individual words

*Comprehension intact

37
Q

Wernicke’s aphasia

A
  • Inability to understand spoken language (also known as sensory or receptive aphasia)
  • Fluent speech
  • Little spontaneous repetition
  • Syntax and grammar= adequate
  • Contrived or inappropriate words
  • Comprehension not intact
38
Q

Split-Brain Patients and Language Lateralization

A

*Could not see object in either trial

-When holding on object in their right hand (left hemi)

—-Patients were able to name the object

-When holding an object in left hand (right hemi)

—-Patients could not name object but could provide descriptions

39
Q

Normal Individual vs Split brain–> Presentation of object

A
  • In a normal person- if object is presented in L visual field, it goes to R hemi then to left broca and wernicke’s areas–> can ID object and state what it is
  • In split brain:

–Object presented in L visual field, goes to R hemi and cannot cross to left (cannot ID or state what it is)

–Object presented in R visual field–> goes to left hemi and patient can name object

*Although we assign the role of lang to left hemi, overall communication is achieved via interaction of the two hemispheres

40
Q

Left Hemisphere Functions

A
  • Analysis of R visual field
  • Stereognosis R hand
  • Lexical and syntactic language
  • Writing
  • Speech
41
Q

Right Hemisphere Functions

A
  • Analysis of left visual field
  • Stereognosis L hand
  • Emotional coloring of language
  • Spatial abilities
  • Rudimentary speech
42
Q

Planum Temporale

A
  • Located in the temporal lobe
  • Significantly larger in the left hemisphere

—Seen in 67% of patients studied, while 97% of the population show preeminence of language in the left hemisphere (doesn’t match)

43
Q

Wada Test

A
  • Helps map language functions in the brain
  • Anesthetic is injected in the left carotid artery–> ends up in left hemisphere

—Allows you to observe lang functions of right hemi

—Patient develops aphasia

-Major language function in the right hemisphere for 3% of people (left-handed people)

44
Q

Imaging and Language

A
  • PET, fMRI, TMS
  • In patients with intact corpus callosum, answers are delayed when using the left hand in reporting identities of objects
  • PET and fMRI show that large areas in BOTH hemispheres are activated during diff language tasks

—Helped corroborate the idea that language is not left hemisphere specific and the involvement of more than just Broca’s and Wernicke’s areas

45
Q

Electrical stimulation and language mapping

A
  • Done in dominant hemisphere
  • Specific brain regions are different for diff individuals
  • Bilinguals seem to store “translations” in different areas -Areas in the temporal cortex (around Wernicke’s area) are not word-specific
46
Q

Damage to the Right Hemisphere and Language

A
  • Damage usually leads to problems with the emotional and tonal components of language (intonation, rhythm)
  • Aprosodia- Inability to express, repeat, or comprehend the variations in pitch, loudness, rate, or rhythm
47
Q

Temporal Lobe and Language

A
  • Seems to be organized based on categories (people, tools, animals, etc)
  • Damage that is limited to a specific small area can result in language deficit to a specific category of objects
48
Q

Sign Language and Lesioning

A
  • People that communicate with ASL use similar brain areas as people that communicate by speaking and hearing
  • Lesion in L hemi- results in deficit in sign generation and comprehension
  • Lesion in R hemi- Results in decrease in emotional processing and emotional tone of sign language
49
Q

Babbling

A
  • Babies babble to help them learn how to produce the appropriate sounds used in spoken communication
  • Babies who only use ASL babble with their hands *Babbling= immature versions of adult language
50
Q

Critical Period

A
  • When language acquisitions at its peak
  • Period starts to decline after 7yo
  • Applies for primary and secondary language
51
Q

Memory

A
  • Recovered experiences that can be brought into consciousness, or changes in behavior
  • Declarative (dates and facts) vs Nondeclarative (procedural; learn or store but cannot verbalize)
52
Q

Temporal Categories of Memory

A

-Immediate memory-fractions of second to seconds

—Ex: scanning a room- things we see but don’t pay attention to

  • Short-term= reciting a phone number, working memory, attention
  • Longterm

*All memories can enter a more long-term memory state or are forgotten

–Remembering requires conscious or unconscious rehearsal/ practice–> leads to change in neuronal circuit

53
Q

Phylogenetic Memory

A
  • Memories arising from the experiences of a species over the eons
  • Expressed as instinctive behavior
  • Ex: birds and primates expressing fear of shapes that resemble predators
54
Q

Priming

A
  • Change in the processing of a stimulus due to an encounter with the same or related stimulus
  • Concious or unconscious awareness
  • Ex: priming people with a list of words and then asking them much later to complete a test where they have to write words down with certain first 3 letters

—Participants fill out words they have seen more often and at a faster rate

—Litte to no concious memory of seeing the words from list A

55
Q

Importance of Association and Memory

A
  • We are not good at remembering random pieces of info
  • Giving meaning/ making associatiins helps in remembering

—Ex: learning all of the digits of pi by singing

56
Q

The Importance of Motivation and Memory

A
  • Participants were shown picture of food and non-food items and later asked to ID pictures they had seen before
  • Those who were hungry remember the food items better

*We more easily remember things we are interested in

57
Q

Classical and Operant Conditioning

A

-Classical-Pairing an innate reflex with an unrelated stimulis

–Ex: ringing a bell led to salivation in dogs

-Operant conditioning- learning via reward or punishment

58
Q

Savant Syndrome

A

-People with limited mental abilities who are extraordinarily competent in a particular domain

–However, cannot take care of themselves

–Excellent at calculation, historical dates, language, drawing, etc.

-Acquired Savant= Orlando Serrell

—Hit with a baseball, able to peform complex mental calculations, can recall the weather for every day since his accident

59
Q

Forgetting

A
  • We tend to forget things that have no importance to us
  • We gradually forget any unused or unreheared info

—-Allows us to focus on what is important (bigger picture)

60
Q

Types of Amnesia

A
  • Anterograde Amnesia– Inability to create new memories following the insult
  • Retrograde Amnesia– Inability to retrieve info established prior to the insult
61
Q

Hippocampus

A
  • Located in the medial temporal lobe
  • Part of the limbic system
  • Communicates with the mamillary body and dorsal thalamus
  • Posterior hippoccampus= important for spatial memory

—Cab drivers tend to have more developed posterior hippocampus than controls cuz have memorized routes

62
Q

Rat Experiment

A

-Rats with and without hippocampal damage were placed in pool with murky water and could not see a hidden platform

—Rats w/ hippocampal damage could not use visual landmarks for orientation and learn where the platform was after multiple trials

—Rats w/o damage learned where platform was after a few trials by using visual landmarks

63
Q

Clinical Case H.M.

A

-Had bilateral medial temporal lobe resection to treat severe seizures

—Amygdala, uncus, hippocampal gyrus, and anterior two thirds of the hippocampus were removed

  • IQ was normal
  • Retained ability to recall old memories and acquire nondeclarative memories
  • Could not form new memories
64
Q

The Cortex and Memory

A

-Retrograde amnesia= more likely with head trauma and neurodegenerative diseases involving the cortex

—-Alzheimer’s disease–Plaque and tangles develop on cortex

*Old memories stored throughout the cortex

65
Q

Memory and Aging

A

-As we age, we lose brain volume due to shrinkage

—Number of synapses decrease, but number of neurons seems to remain the same

—-Therefore, we lose the connectins btwn neurons

-Leads to difficulty remembering names and details

—Doctors must distinguish btwn normal aging and disease states