Lecture 10 - Motor Control and Disorders of Action Flashcards

1
Q

how do we control our movements:

A

Most actions required:

  1. multiple muscles
  2. precise timing
  3. multiple components of movement

Higher cognitive aspects of motor control incl:

  1. planning and timing
  2. sequencing
  3. imagery (mirror neurons)
  4. expertise
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2
Q

Key brain areas and their function in motor control

A

Primary Motor cortex = execution

Premotor cortex = preparation of actions

Prefrontal cortex = higher level of planning

Parietal cortex = sensory-motor links

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3
Q

Primary motor cortex (M1):

A
  • mapped out somatotopically
  • in the precentral gyrus
  • Brodmann’s area 4
  • responsible for the execution of movement
  • contralateral control
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4
Q

Brain lesions:

A

Hemiplegia - Paralysis of one side
Hemiparesis - weakness of one side

(contralateral)

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5
Q

M1 coding of movements:

A
  • cells in M1 have a preferred direction
  • population of cells code the direction of movement - this is VECTOR CODING
  • when movement is in preferential direction of cell this causes that group of cells to fire more than when other movement of direction occurs.
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6
Q

population vector

A

the sum of the preferred tunings of neurons multiplied by their firing rates

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7
Q

M1 connections

A
  • input from the supplementary motor area (SMA), premotor area and primary somatosensory area (for sensory information)
  • output to spinal cord to control the muscles.
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8
Q

Frontal eye fields (FEFs)

A
  • controls the voluntary movement of the eyes
  • Broadmanns area 8
  • eye movements are guided by external senses (vision and hearing) BUT bodily movements rely on proprioception (concerning position of limbs - this info from somatosensory cortex
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9
Q

two main types of eye movement

A
  1. saccades

2. smooth pursuit

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10
Q

saccades:

A
  • these are the fastest eye movements that we commonly make - up to 1000deg/sec
  • duration around 20 to 200ms
  • perception is suppressed during movement
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11
Q

smooth pursuit

A
  • smooth tracking movement
  • approx up to 50deg/sec
  • you need an object to track to do this
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12
Q

Premotor cortex:

A
  • the lateral premotor cortex - important for linking action with visual objects in the environment (EXTERNALLY generated actions) e.g. tapping to a beat
  • the medial premotor cortex is termed the SUPPLEMENTARY MOTOR AREA (SMA)
  • SMA is associated with well-learned actions - well-learnt sequences (INTERNALLY generated action) e.g. you decide to walk
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13
Q

what did Swinnen and Wenderoth 2004 find

A
  • areas more active in more difficult bimanual tasks

- e.g. moving one hand in a circle forward and one backward

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14
Q

sequence learning (Tone et al 1988)

A
  • looked at brain areas involved in the process of learning a sequence of 8 key presses
  • changes from effortful to automatic
    found the following changes:
    • decreased activity in dorsolateral prefrontal cortex
    • SMA activity increased
    • lateral premotor cortex activity decreased
    • primary motor cortex activity decreased
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14
Q

input to premotor cortex

A
  • lateral premotor cortex: receives visual signals via the parietal cortex (dorsal route)
  • medial premotor cortex (SMA) receives strong proprioceptive signals about current position of the limbs
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15
Q

Gerloff et al 1997

A
  • Ps had to do simple, scale, or complex sequence tasks
  • whilst applying TMS to free frontal regions
  • TMS disrupted complex task when on SMA
  • TMS over the primary motor cortex affected both ‘complex’ and ‘scale’
  • TMS over lateral prefrontal cortex had no affect s
  • SMA, therefore, has a critical role in organising forthcoming movements in complex motor patterns
16
Q

Frith et al 1991

A
  • Ps required to generate finger movements that were either predetermined (i.e. move the finger that is touched) OR freely chose which finger to move.
  • motor response in both tasks is the same
  • bUT dorsolateral prefrontal cortex (PFC) showed greater activation in free-choice task
  • SO PFC is involved when there is attention to action
  • for longer-term goals and intentions
  • not specific to action
17
Q

PFC lesions - what do they cause (x4)

A
  • perseveration - repeat same action when no longer relevant
    • utilisation behaviour - act on an irrelevant object in the environment (pick up someone’s glasses)
    • disinhibition - e.g. antisaccade task - releasing behaviours that shouldn’t be done
    • frontal apraxia - not able to follow steps in routine
18
Q

antisaccades:

A
  • required to look in the opposite direction to targets

- must inhibit tendency to look at target

19
Q

Norman and Shallice (1986)

A
  • proposed a model to explain goal-driven action
  • this is the SUPERVISORY ATTENTIONAL SYSTEM (SAS)
  • Content scheduling is the mechanism that selects a specific schema to be enacted
  • SAS only used for novel and less automatic actions
  • activation of schemas depends partly on the environment and partly on biasing influence of current and future goals (derived from SAS component)
20
Q

action errors applied to SAS

A

perservation : unable to change schemas when no longer appropriate
utilisation: schemas activated by the environment without SAS suppressing them.

21
Q

parietal cortex lesions

A

parietal cortex damage = apraxia (inability to perform skilled purposeful movement
- this issue stems from premotor areas in the posterior parietal cortex.

22
Q

Ideomotor apraxia

A

INABILITY TO PRODUCE APPROPRIATE GESTURES GIVEN AN OBJECT, WORD OR COMMAND

  • idea and execution disconnected
  • can recognise action performed by other
  • but fails in pantomiming action
  • can perform sequence but NOT components
  • e.g. pretending to brush teeth - patient can do this without miming the existence of the toothbrush
23
Q

CEREBELLAR PATIENTS

A
  • leads to action tremor
  • also dysmetria (over and undershooting movements)
  • deficits also in:
    • coordinating across joints
    • motor learning
    • timing
24
Q

role of cerebellar network in action

A
  • active during coordination tasks that require one movement to be synchronised with another
  • cerebellar loop coordinates the timing and trajectory of movement using sensory and motor information
25
Q

role of basal ganglia motor circuit

A

regulates excitability of frontal motor structures(SMA) and biases the likelihood of movement and the nature of the movement.

26
Q

Parkinsons disease:

  • how many it effects
  • 3 main symtpoms
A
  • 1 in 1000
  1. bradykinesia (slow movement)
  2. tremor
  3. muscle rigidity
27
Q

cause of parkinsons:

A

death of dopaminergic cells in substantia nigra pars compacts in the BG (the pathways linking the substantial nigra and BG)

28
Q

writing with Parkinsons

A
  • micrographia (writing small in size)

- may reduce while writing (size) due to fatigue

29
Q

Parkinson’s disease deficits

A
  • internal/external: more problems with internally generated movements - BG closely linked to SMA involved in internal motor activity
  • problems with complex movements and bimanual tasks
  • also cognitive effects - attention shifting etc.