Midterm 2 Flashcards

1
Q

List the 4 misconceptions about brain injury recovery

A
  1. depends on the injured person’s efforts or attitudes
  2. full recovery is always possible
  3. all effects of dysfunction are externally visible
  4. people with dysfunction always have insight on their impairments
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2
Q

What is Anosognosia

A

an error of self-awareness, a failure to judge one’s own functioning.
Can be general or domain specific

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3
Q

List some types of dysfunction that can have Anosognosia

A

Schizophrenia/Bipolar
Contralateral neglect
Dementia (20-80% of AD)
TBI

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4
Q

list the three parts of the Crosson Hierarchical awareness model

A

Intellectual awareness
Emergent awareness
Anticipatory awareness
(bottom up)

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5
Q

Define Intellectual Awareness

A

The bottom of Crosson’s hierarchical awareness model
Person with anosognosia can report something about their deficit

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6
Q

Define Emergent awareness

A

Second tier of Crosson’s hierarchical awareness model
Person with anosognosia has ability to monitor how they are performing AND detect errors
‘i can see from your face i’m forgetting something’

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7
Q

Define Anticipatory awareness

A

Top of Crosson’s hierarchical awareness model
Person with anosognosia can predict how current deficits may impact future performance AND adjust behaviour and expectations accordingly
‘its not safe for me to do this yet’

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8
Q

List Consequences of anosognosia

A

Lower rate of engagement with rehab
Poorer compliance with taking medication
poorer use of compensatory strategies
creates need for more supervision and more structured living arrangements

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9
Q

diagnosis of anosognosia

A
  1. clinicians judgement through structured interview
  2. patient partner discrepancy: gap between their described ability and how others describe it
  3. self-appraisal performance discrepancy: patient first report their performance and then compare it to what it actually is
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10
Q

Neurological correlates of anosognosia

A

Frontal Lobe
Medial Temporal regions
Cingulate gyrus

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11
Q

Denial vs Anosognosia

A

Denial is avoiding/rejecting information that is stressful or painful. Patient would respond with anger, resistance and refusal to discuss.

Anosognosiac would respond with surprise or confabulation when confronted with evidence of deficit

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12
Q

How does age effect recovery

A

Margaret Kennard’s monkey studies
Children recovered much better than newborns or adults
- to do with neurogenesis and plasticity at childhood

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13
Q

Impact of lesion size on recovery

A

larger lesion= worse outcomes
bilateral lesions show less recovery than unilateral

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14
Q

Chronic vs Acute impact on recovery

A

Chronic tends to have less impairment
slower changes and compensatory processes can offset injury
Less opportunity for this when its sudden, acute TBI/damage

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15
Q

Environmental effects on recovery

A

rats and humans in an enriched environment (social/ stimulating/ supportive) like the rat condos show better recovery

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16
Q

List Secondary effects of injury

A

Edema, swelling in the brain, leads to pressure in brain and on skull

Blood flow changes following injury, these may be temporary

Diaschisis is sudden change of function in a part of the brain connected to a distant, damaged area

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17
Q

what is compensation/ compensatory strategies

A

the substitution of new behaviour, a new way to do an old thing
- using a walker for motor changes

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18
Q

What is plasticity

A

the rewiring of the brain’s connections to deal with results of an injury

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19
Q

what is the concept of localization of function

A

the idea that certain brain areas correspond to specific functions

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20
Q

Describe Franz Joseph Gall and his contributions

A

French Anatomist
Idea of phrenology (early kind of localization of function), bumps of the skull correspond to stable traits about a person since those brain areas are ‘overdeveloped’

Physiognomy: someone’s face predetermines their behaviour and character

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21
Q

Karl Lashley and his contributions

A

trained rats with a lesion on a maze task
finds that larger lesions lead to greater impairment

idea of equipotentiality: other regions of cortex take over functions following damage (idea of neuroplasticity)

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22
Q

Contributions of Paul Broca

A

Patient M.Lborgne can only say ‘tan’ but had intact language comprehension
(separation between ability to produce and understand speech)

found lesion in patients left front lobe

used lesion mapping studies to find Broca’s area, the speech producing area in left frontal lobe

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23
Q

Contributions of Wilder Penfield

A

During neurosurgery for epilepsy, he used electrodes to do stimulations across the surface of the cortex and asked patient what it felt like

Collected a huge database of what happens when stimulating certain brain areas

Produced a homunculi

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24
Q

Describe TMS

A

Transcranial Magnetic Stimulation, a coil held over the scalp that uses a magnetic field to temporarily disrupt the activity of brain area under it.
Can either suppress or stimulate activity
helps in localizing function

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25
Q

What are two modern methods of Localizing function

A

Transcranial magnetic stimulation and Single Neuron Recording

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26
Q

What is single Neuron Recording

A

Patients before surgery are implanted with electrodes to identify where the surgery should take place.
In this situation, research can be done opportunistically.
Researchers show images to find relationships between images and the neurons that fire.

Can get resolution of a single neuron.

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27
Q

List 3 methods of Structural brain imaging

A

X-Rays
Magnetic resonance imaging MRI
Diffusion tensor imaging DTI
CT scan (computed Tomography)

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28
Q

Describe X-rays

A

Electromagnetic radiation imaged into film
- rely on tissue density so more useful for things involving dense tissue

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29
Q

List the two other types of X-rays

A

Cerebral Angiography and Computed Tomography CT

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30
Q

Describe cerebral angiography

A

A contrast x-ray where they introduce a foreign contrast agent into the body through cerebral artery
used to locate large tumors, aneurisms etc.

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31
Q

Describe Computed Tomography CT

A

Rotates X-ray source and detector to reconstruct the image.
Uses many pictures from many angles and an algorithm to make a HD image
Used for skull fracture and intracranial hemorrhage

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32
Q

Describe how an MRI machine works (long answer)

A

Relies on hydrogen (water) and magnetism
step 1: external magnetic filed introduced to the body, all the hydrogen atoms line up

step 2: a second magnetic field is applied briefly that knocks down the lined up hydrogens

Step 3: (relaxation) once the second field is removed, measure the radio frequency RF signal produced when they realign with the larger field
Some places release more RF than others if theres more hydrogen there
This shows up as more brightness on the scan

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33
Q

List pros and cons of MRI

A

Pros: can get detailed small scale images,
high spatial resolution

Cons: slow and expensive, excludes patients with pacemakers in the body

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34
Q

Describe Diffusion Tensor Imaging DTI

A

A variant of MRI that relies on how water molecules move in the brain
detects white matter since water moves more in axons
allows us to build big white matter maps

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35
Q

List pros and cons of X-ray CT scans

A

Pros: quick and inexpensive
Cons: exposure to radiation

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36
Q

List 3 types of Functional Brain Imaging

A

Electroencephalography EEG
Positron Emission Tomography PET
Functional MRI fMRI

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37
Q

Describe the EEG

A

Wear a net of electrodes with gel underneath
Records changes in electrical activity of the cortex
Uses a net of electrodes over the scalp with gel for conductance
Outputs a wave form that is processed to form a reading

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38
Q

Pros and Cons of EEG

A

Pros: high temporal resolution, quick, inexpensive
Cons: hard to measure deeper brain structure activity
low spatial resolution

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39
Q

Describe the PET

A

Injecting a radioactively labelled substance and imaging it
Tracers for drugs or proteins show brain activity for the systems that interact with the specific drug/protein. Can show the metabolism of a drug

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40
Q

Pros and Cons of PET

A

Pros: useful for looking at specific systems or proteins and lifespan/ condition changes

Cons: expensive, poor spatial resolution

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41
Q

describe the fMRI

A

Relies on the BOLD response:
1. Neural activity triggers increase in blood flow to brain region

  1. increased ratio of high-to-low oxygen blood in the region

3.this changes magnetic properties of the brain and this becomes visible in the fMRI image

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42
Q

Describe the paired image subtraction

A

How the fMRI is used in research:
Control baseline for a task is designed that includes all the stimuli we want to rule out
then when we do the task, we can subtract the real image response with the baseline
to isolate brain regions to a stimulus

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43
Q

List the challenges of fMRI (6)

A
  1. epiphenomena: report of signal when there’s not, due to averaging across trials
  2. Poor temporal resolution, might miss brief but important events
  3. lack of causality
  4. leads us to focus on increases in activity, rules out baseline activity
  5. testing environment proves difficult for some
  6. Replicability and statistic flexibility (physician has to make pipeline choices)
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44
Q

What is the Default Mode Network

A

Regions of the brain that are active during rest, for inwardly focusing attention and mind wandering.

Medial Prefrontal cortex, posterior cingulate cortex etc.

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45
Q

Define Visuospatial attention

A

Selectively processing one physical location in space to the exclusion of others

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46
Q

Behaviour of Contralateral neglect

A

Deficits in attending to and reporting on objects in space that are contralateral to the lesion.

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47
Q

causes of contralateral neglect

A

Caused by stroke, trauma, Alzheimer’s
right hemisphere damage
Cortical hypoperfusion in right hemisphere predicts neglect

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48
Q

List the treatments of contralateral neglect

A

Prismatic Adaptation
VR reaching practice
TMS

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49
Q

Apraxia Vs Ataxia

A

Both are disorders affecting movement performance:

Apraxia: planning difficulties
- damage to left PPC
- difficulty imitating meaningless gestures etc.

Ataxia: Coordination difficulties
Optic: disorder of visually guided reaching (Feature of Balint’s)
Dysmetria: impairment of movement accuracy

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50
Q

Anomia vs agnosia vs asterognosia

A

All recognition impairments

Astereognosia: inability to recognize/ discriminate by touch
because of lesions in primary somatosensory/ motor cortices

Agnosias: recognition impairment despite normal lower-level sensation
Visual agnosia: ventral stream lesions

Tactile Anomia: touch based recognition impairment. When objects in left hand of split brain patients can’t connect to speech-producing left hemisphere

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51
Q

Describe in detail the BOLD response

A

Electrical activity in brain

presynaptic neuron releases glutamate

some of this glutamate binds to nearby astrocyte

triggers astrocyte to release signaling molecules onto blood vessel

blood vessel dilates

more blood and oxygenated blood flow

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52
Q

Difference between retrograde and anterograde amnesia

A

Retrograde: old memories from before the injury are lost
Anterograde: inability to form new memories from the time of injury

53
Q

List some tests for contralateral neglect

A

Clock Drawing
Line cancellation
Drawing/ copying

54
Q

Describe the Posner Cueing task

A

reaction time test of visuospatial attention
congruent trials: target appears in the same box as the cue
Incongruent: target and cue are in different boxes

Comparing reaction time allows us to study visuospatial attention at a particular location

55
Q

What is the inhibition of return

A

In the cueing task, if the time between the cue and target exceeds 600ms, reaction time is impaired by the cue.
attention begins to fade by the time target arrives, you’re slower to return attention to the location.

56
Q

brain area dysfunction for contralateral neglect

A

All in right hemisphere
IPL and TPJ: inferior parietal lobe and temporo-parietal junction

the superior temporal gyrus

Ventral Frontal cortex

cortical hypoperfusion in right hemisphere predicts neglect

57
Q

Describe the individual differences in contralateral neglect

A

Ego-centric neglect: Neglect to one whole side of a larger picture

Object Centered neglect: neglect to one side of an individual object
(dysfunction of superior temporal gyrus)

58
Q

Describe the recovery forms of Contralateral Neglect

A

Allesthesia: person is able to respond to stimuli on neglected side BUT mislocate it
Simultaneous extinction: can respond to stimuli on neglected side UNLESS both side are stimulated simultaneously

59
Q

Describe Prismatic adaptation

A

Treatment for Contralateral neglect
Patient wears prism goggles (shifts everything to the right) so they have to actively reach to the left to reach an object.
This adjustment leads to some improvement in neglect once goggles are off

60
Q

How does TMS treatment for Contralateral neglect work

A

Low frequency rTMS placed over left posterior parietal cortex to INHIBIT IT
allows the right side to be more active. Doing this over time can reduce symptoms for a few weeks.

61
Q

What is Balint’s Syndrome

A

A severe disruption of attention due to damage to large region of the brain.
Patients are functionally blind except for one object in visual field at a time
(Bilateral damage to parieto-occipital lobes)

62
Q

Behaviour/components of Balint’s syndrome

A

Simultanagnosia
Oculomotor Apraxia
Optic Ataxia

63
Q

What is simultanagnosia

A

Component of Balint’s syndrome
Inability to perceive simultaneous objects of events in visual field
- smaller visual window of attention

64
Q

What is oculomotor Apraxia

A

Component of Balint’s
‘sticky fixation’, problem of planning and initiating eye movements
difficulty tracking something
an attentional impairment: inability to attend to object to move the eyes there.

damage to saccade-planning areas in parietal cortex

65
Q

What is optic ataxia

A

Component of Balint’s
Disorder of visually-guided reaching
damage in superior parietal lobe

66
Q

Treatment of Balint’s

A

Neurological change is difficult due to distribution of brain damage but coping strategies include:
dialing a phone, practice using a fork

67
Q

What is PPS peri personal space

A

The space around our bodies that is prioritized by the attention system

68
Q

List 2 conditions related to visuospatial attention near the body

A
  1. claustrophobia: larger PPS
  2. autism: smaller PPS
    peri personal space
69
Q

Causes of Amnesia

A

Surgical intervention, seizures, stroke, TBI

70
Q

What were patient HM’s removed brain structures

A

Bilateral removal of hippocampus, amygdala and the entorhinal cortex.
(medial temporal lobe structures)
to treat epilepsy

71
Q

Patient HM’s effect of surgery

A

Profound anterograde amnesia and some retrograde amnesia

72
Q

Patient HM’s performance on memory tasks and why its significant

A

Digit Span task
Gets a normal score on digit span task BUT much lower score on the ‘digit span + 1’ task

Normal people benefit from practice on the +1 task, HM CANT. he has normal short term working memory BUT CANT hold things in long term memory.

Showed us that memory has different pieces that can be separated (evidence for at least 2 types)

73
Q

List the 3 forms of memory and the functions coming off and to them (like draw it yk in ur brain)

A

sensory input–>
SENSORY MEMORY(unattended info lost)
–> attention–>
SHORT TERM MEMORY (maintenance rehearsal/unrehearsed info lost)
–> encoding –> <–retrieval<–
LONG TERM MEMORY

74
Q

Which part of the memory system does HM struggle with

A

encoding short term to long term memory

75
Q

What are the divisions of long term memory

A

Explicit and Implicit
Explicit: Semantic memory + Episodic Memory

Implicit: Procedural memory+ priming+ classical conditioning

76
Q

What is explicit long term memory

A

Effortful recall, involves the hippocampus, frontal and temporal lobes

77
Q

Semantic vs Episodic memory + relevant patient

A

Semantic = general fact (capital cities etc.)
Episodic = Personally experienced events

Patient KC continued to learn new semantic information but was unable to form new memories for personal events

78
Q

What is priming

A

A type of implicit memory demonstrated by how amnesiacs perform better on word recall if primed with word stems. Suggests that exposure to the words is remembered at some level

79
Q

What is classical conditioning in memory

A

a type of implicit memory
amnesiac patients can still hold associations from events that happened in the past that they no longer remember.
(Physician handshake with a pin leading patient to not want to shake his hand later)

80
Q

How does Long term memory become permanent?

A

The process of consolidation:
Hippocampal indexing theory–> many brain areas active when you experience an event, hippocampus serves as the index card to ‘point’ to all the aspects of the memory
When this set of activities is fired again over time (retrieving the memory), the neurons become ‘wired together’
then the memory can be activated without the hippocampus
BOOM long term stable memory!

81
Q

How does anterograde amnesia link to Hippocampal Indexing theory

A

When someone has injury, memories gone through the process that no longer need the hippocampus are stable
BUT new memories can’t use the hippocampus indexing to go through the process to LTM
so HM can’t form new memories

82
Q

Explain Procedural memory

A

Form of implicit memory
HM is able to learn skilled motor movements and benefit from practice despite having no memory of performing the task before

83
Q

Cause of Korsakoff’s syndrome

A

Result of brain damage due to thiamine (vitamin B1 deficiency)
Often due to heavy alcohol consumption

84
Q

Effects of Korsakoff Syndrome

A

Severe anterograde amnesia and mild retrograde amnesia (only explicit memory)
Confusion, abnormal eye movements, hypothermia

85
Q

Damaged structures in Korsakoff syndrome

A

Thalamus hypothalamus, diffuse damage to cortex, hippocampus

86
Q

Treatment for Korsakoff’s

A

Thiamine supplements+ nutrition
25% show full recovery with right treatment

87
Q

What is the corpus callosum

A

The largest white matter tract that connects the left and right hemisphere of the brain

88
Q

Describe the surgical procedure for split patient

A

Commissurotomy is done (a callosotomy) for patients with severe epilepsy to stop epileptic discharge spreading from one hemisphere to another (the cause of a seizure)

89
Q

Describe the experimental procedure used to provide visual information to only one hemisphere at a time (split brain)

A

ppt stares at a fixation point
right hemisphere sees left visual field
left hemisphere sees right visual field
information is ‘dropped’ into a hemisphere based on which visual field its in

90
Q

What can split brain patients tell us about sense of self

A

the left hemisphere requires a lot less visual information to state that its a photo of themself

91
Q

What split brain research tells us about each hemisphere

A

In search tasks: left hemisphere is more strategic
- left hemisphere is the interpreter for the actions of the right hemisphere

92
Q

Compare patients with callosal agenesis to adult split brain patients

A

Normal Language and IQ
minimal disconnection syndrome
BECAUSE plasticity in childhood allows alternative cross hemispheric pathways to be reinforced

93
Q

Define Sensation

A

the detection of internal or external stimulation, raw information from the environment traveling afferently through the senses

94
Q

Define perception

A

the awareness and interpretation of sensory information by the brain
Perceptual deficits can occur without sensory impairment

95
Q

What is the primary visual cortex

A

the first place the cortex knows about visual information. V1 resembles information spatially, like how it was in the world
no complex visual features coded here

96
Q

Consequences of Damage to the V1

A

patients report being cortically blind
BUT they can guess visual information better than chance
decent spatial navigating and coordination

97
Q

What is the secondary visual cortices

A

Made up of almost 24 different regions
process input from V1 to extract higher level features
shape/ colour/ pattern

98
Q

Damage to secondary visual cortices

A

Akinetopsia- selective loss of visual motion perception

99
Q

What is the visual association cortices

A

Made up of the dorsal and ventral steam
receive input from both visual cortices and from one or more sensory systems
multi-modal experience

100
Q

List the two different between the dorsal and ventral streams theories

A

“what vs where” theory
Ventral= the ‘what’
Dorsal= the ‘where’

‘action vs perception’ streams theory
Ventral = perception
Dorsal= action

101
Q

Tell me about patient DF

A

Extensive bilateral ventral stream lesions
Can’t match card orientation BUT can put the card through the slot

Can’t discriminate verbally about properties of different blocks BUT can reach for the larger one if asked

Ventral perception stream disrupted, dorsal (action) stream intact

102
Q

Effects of Ventral stream damage

A

forms of Agnosia
loss of ability to recognize objects or shapes visually

103
Q

Apperceptive agnosia

A

failure in object recognition linked to issues in early perceptual processing
if theres a processing step to recognition, they are unable. Lose higher level features of an object

104
Q

Associative agnosia

A

Normal visual perception but unable to use information to recognize things
can copy an image perfectly BUT can’t tell you what its an image of

105
Q

What is prosopagnosia

A

Failure of race recognition with intact object recognition
can be developmental or acquired by stroke/injury

106
Q

Part of brain responsible for face perception

A

Ventral stream areas
occipital face area
fusiform face area FFA
Anterior temporal cortex

107
Q

Prosopometamorphopsia

A

some areas of face perception are overactive
see distorted faces

108
Q

Name all the major levels of the sensorimotor system

A

Association Cortex
Secondary motor cortex
Primary motor cortex
Brainstem Motor Nuclei
Spinal Motor circuits

109
Q

Describe the Hierarchical organization of the motor system

A

When we want to make a movement, Neurons synapsing send the plan down and out to the body
Decisions get more specific as we go down
The basal ganglia and cerebellum work in parallel with the sequence,
manage the timing and monitor how well its going

110
Q

Principal of motor equivalence

A

there are many different ways to achieve a task. similar outcomes can be accomplished with many combinations of muscle activities

111
Q

The parts of the association cortex

A

Posterior parietal association cortex
Dorsolateral prefrontal cortex dLPFC

112
Q

What does the posterior parietal association cortex do

A

Receives input from visual, auditory and somatosensory systems
integrates information about the position of body parts and objects around us
puts the world into coordinate systems

Also the ability to move hands, interact with objects and move eyes

113
Q

Effect of Damage to the PPC posterior parietal (association) cortex

A

Contralateral neglect (if on the right)

Apraxia (Impaired voluntary movement performance) if damage is on the left

114
Q

What is apraxia

A

impaired voluntary movement performance
errors are pronounced for:
- un meaningful movements (imitation)
Performance of gestures on command (thumbs up)
Use of tools in unusual contexts
associated with damage to the left PPC

115
Q

Function of the dLPFC

A

The evaluation of external stimuli and initiating voluntary reactions (outputs go to lower levels of motor hierarchy)

The first neurons that fire when anticipating a motor action (the decision to act begins in dLPFC)

also involved in other cognitions

116
Q

What changes with movement practice?

A

First learn new movement: activity in PPC and dLPFC
higher up levels of the hierarchy are used when you learn and practice it first

when you learn it, control shifts down the levels of the motor system
higher up functioning is freed up to focus on other things

Response chunking = treating the learned sequence like a unit instead of discrete units put together

117
Q

Function of secondary motor cortices

A

receive projections from association cortex and send them to primary motor cortex
involved in producing and guiding complex movements in space

118
Q

Where are mirror neurons located and why are they special

A

Located in the ventral premotor cortex
they are the small subject of neurons that fire when you see someone else perform an action
could be related to theory of mind

119
Q

How is the primary motor cortex organized

A

Somatotopically
Neurons corresponding to hand are near the ones for arm etc.

120
Q

Consequences of lesions to the Primary Motor Cortex
(3)

A

Maybe unable to move one body part in isolation
Astereognosia (inability to recognize things by touch)
Movements slower/less accurate

121
Q

Function of the Cerebellum in the sensorimotor system (3)

A

receives information about the same thing from many brain areas simultaneously
compares actual movement to intended movements
understands what adjustments need to be made
important for timing, sequencing in an ONLINE WAY

122
Q

Consequences of Cerebellar Damage and how its demonstrated

A

Dysmetria (inability to precisely control movement)
Loss of ability to adapt their motor output
POSITIVE ROMBERGS TEST= cerebellar damage

PRISM GOGGLES TEST: throwing darts
healthy ppl learn to compensate for the goggles and then take time to adjust back once they’re off
Cerebellar Damaged ppl are unable to adapt to the goggle, theres nothing to unlearn when they take them off

123
Q

Function of the Basal Ganglia in the sensorimotor system

A

Keeps its two pathways in balance: the stop and go pathways

124
Q

how do the two basal ganglia pathways work

A

At rest, the BG inhibits motor/premotor areas
It has a pattern of tonic inhibition: no movement
[stop pathway]

go pathway:
Use dopamine from the substantia nigra to ‘turn off’ the tonic inhibition (disinhibition)
allows the motor and premotor areas to initiate movement

125
Q

Name two disorders characterized by dysfunction to basal ganglia

A

Parkinson’s disease
Huntington’s disease

126
Q

What happens in Parkinson’s disease

A

Most dopaminergic neurons of substantia nigra die
- less go pathway activity so overactive inhibtiion
becomes hard to initiate a movement and hard to stop

Leads to stiffness, resting tremor, muscular rigidity and slow movement

127
Q

Treatment for Parkinsons

A

L-DOPA, a dopamine PRECURSOR
Deep brain stimulation of substania nigra

128
Q

Describe Huntingtons disease

A

disorder affecting striatum in the BG
LESS STOP PATHWAY
excessive movement, brief, sudden, purposeless
genetically determined