Motor Control 1 Flashcards

1
Q

What do most actions require?

A
  • Multiple muscles
  • Precise timing (e.g. between the 2 hands)
  • multiple components of movement
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2
Q

What do higher cognitive aspects of motor control include?

A
  • Planning and timing
  • Sequencing
  • Imagery (cg mirror neurons - simulate or imagine movements in real time without making the movement)
  • Expertise (e.g. sport, musical instrument)
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3
Q

What brain area is associated with execution of actions?

A

The primary motor cortex

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4
Q

What brain area is associated with preparation of actions?

A

The premotor cortex

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5
Q

What brain area is associated with higher level of planning?

A

The prefrontal cortex

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6
Q

What brain area is associated with sensory motor links?

A

The parietal cortex

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7
Q

Where is the primary motor cortex (M1) located?

A

The pre-central gyrus

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8
Q

What type of organisation does the M1 have?

A

Somatotopic organisation

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9
Q

Does the M1 produce body movement contralleterally or ipsalaterally?

A

contralaterall

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10
Q

Who was the somatotopic organisation of the M1 originally discovered by?

A

Wilde and Penfield by direct probing of the brain during surgery

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11
Q

Does stroke affecting one side of the brain affect movement on the same or opposite side of the body?

A

Opposite side

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12
Q

What is hemiplegia?

A

paralysis of one side

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13
Q

What is hemiparesis?

A

weakness of one side

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14
Q

What is the coding of movements in the M1?

A
  • cells in M1 have a preferred direction of movement
  • populations of cells code the direction of movement- vector coding
  • motor cortex sends impulses down motor cortex to evoke movement in muscles
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15
Q

Where does the M1 get it’s input from?

A

supplementary motor area, premotor area and primary somatosensory area

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16
Q

Where does the M1 give it’s output to?

A

Spinal cord which controls muscles

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17
Q

Are eye movements controlled by the same cortical area as the body?

A

No

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18
Q

What are the two main types of eye movement?

A
  1. Saccades

2. Smooth pursuit

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19
Q

What are saccdes?

A

The fastest movement we make. Perception is suppressed during the movement

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20
Q

how quick are saccades?

A

up to 1000 deg/ sec

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21
Q

what is the duration of saccades?

22
Q

What are smooth pursuit eye movements and when are they observed?

A
  • smooth tracking movement

- observed when tracking a stimulus

23
Q

How quick are smooth pursuit movements?

A

Up to around 50 degree/ sec

24
Q

What is the lateral premotor cortex involved in?

A

Externally generated actions e.g. tapping your finger in time to a metronome, crossing the road in response to a green man

25
Where is the supplementary motor area?
Medial premotor cortex (closer to the middle)
26
What is the supplementary motor area involved in?
Internally generated actions e.g. well learnt sequences, crossing the road without a green man
27
What are the areas more active in difficult bimanual tasks?
Cerebellum, SMA, pre-motor area
28
What happens with sequence learning?
- movements become faster and more accurate | - movements change from effortful to automatic
29
What do changes in movements from effortful to automatic include?
- decreased dorsolateral prefrontal activation - increased supplementary motor area activation - decreased lateral premotor cortex activation - decreased primary motor activation - subcortical (cerebellum and basal ganglia) activity
30
What happens when virtual lesioning TMS was applied over the SMA (supplementary motor area)?
It only interfered with performing the most complex sequence
31
What is the prefrontal cortex involved in?
- choosing what action to perform - when someone is paying attention to their action (when it is difficult or they are learning) - longer term goals and intentions (what to do and what not to do) - Not specific to action
32
What can prefrontal lesions produce?
- Perseveration - Utilisation behaviour - Disinhibition - Frontal apraxia
33
What is perseveration?
Repeat the same action when it is no longer relevant
34
What is utilisation behaviour?
Act on irrelevant (or inappropriate) object in environment (e.g. picking up someone else's glasses)
35
What is disinhibition)
Repeating movements that shouldn't be done (e.g. antisaccade task - do the opposite of what you are meant to look at because can't inhibit pre-potent tendency to look at the target
36
What is frontal apraxia?
Not being able to follow steps in routine tasks (e.g. making tea)
37
What is the Normal and Shallice model?
- contention scheduling - selects appropriate schema (e.g. tea making schema) - Supervisory attentional system (SAS) is require for novel/ less automatic actions
38
How does the normal and shallice model explain perseveration and utilisation behaviour?
- Perseveration: unable to change schemas when no longer appropriate (lack of flexibility) - Utilisation behaviour: schemas activated by environment without SAS suppression
39
Damage to what leads to apraxia?
Damage to the parietal cortex
40
What is apraxia?
Inability to perform skilled purposeful movement
41
What is the posterior parietal important in?
Locating where things are (where things are mapped out in the world) and also important for forming and understanding movements
42
What is ideomotor apraxia?
- idea and execution disconnected - retain knowledge of action - can recognise action performed by another - fail in pantomiming action - can perform sequence but not components of action
43
What can cerebellar damage lead to?
- action tremor (tremor of the body during action) | - dysmetria - over and undershooting of movements
44
What deficits does dysmetria cause?
deficits in: - coordinating across joints - motor learning - timing
45
What are symptoms of Parkinson's disease?
- Bradykinesia: slow movement - Tremor (when resting_ - Rigidity
46
Akinesia is a symptom of Parkinson's disease. What is this?
Trouble with movement
47
Freezing is a symptom of Parkinson's disease. What is this?
Where a person finds themselves frozen and rooted to the spot
48
What sort of gait do people with Parkinson's have?
Shuffling distinctive gait
49
What causes Parkinson's?
Death of dopaminergic cells in the substantia nigra pars compacta in the basal ganglia
50
How can Parkinson's be treated?
By giving people dopamine replacement medication
51
How many of the dopamine cells in the substantia nigra have already died away by the time someone exhibits Parkinson's?
80%
52
Why do parkinson's patients have problems with internally generated movements?
Because the Basal Ganglia is closely connected to the SMA which is involved in the control of movements