Lecture 10 - Motor Control and Disorders of Action Flashcards
how do we control our movements:
Most actions required:
- multiple muscles
- precise timing
- multiple components of movement
Higher cognitive aspects of motor control incl:
- planning and timing
- sequencing
- imagery (mirror neurons)
- expertise
Key brain areas and their function in motor control
Primary Motor cortex = execution
Premotor cortex = preparation of actions
Prefrontal cortex = higher level of planning
Parietal cortex = sensory-motor links
Primary motor cortex (M1):
- mapped out somatotopically
- in the precentral gyrus
- Brodmann’s area 4
- responsible for the execution of movement
- contralateral control
Brain lesions:
Hemiplegia - Paralysis of one side
Hemiparesis - weakness of one side
(contralateral)
M1 coding of movements:
- 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.
population vector
the sum of the preferred tunings of neurons multiplied by their firing rates
M1 connections
- input from the supplementary motor area (SMA), premotor area and primary somatosensory area (for sensory information)
- output to spinal cord to control the muscles.
Frontal eye fields (FEFs)
- 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
two main types of eye movement
- saccades
2. smooth pursuit
saccades:
- these are the fastest eye movements that we commonly make - up to 1000deg/sec
- duration around 20 to 200ms
- perception is suppressed during movement
smooth pursuit
- smooth tracking movement
- approx up to 50deg/sec
- you need an object to track to do this
Premotor cortex:
- 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
what did Swinnen and Wenderoth 2004 find
- areas more active in more difficult bimanual tasks
- e.g. moving one hand in a circle forward and one backward
sequence learning (Tone et al 1988)
- 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
input to premotor cortex
- 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
Gerloff et al 1997
- 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
Frith et al 1991
- 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
PFC lesions - what do they cause (x4)
- 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
antisaccades:
- required to look in the opposite direction to targets
- must inhibit tendency to look at target
Norman and Shallice (1986)
- 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)
action errors applied to SAS
perservation : unable to change schemas when no longer appropriate
utilisation: schemas activated by the environment without SAS suppressing them.
parietal cortex lesions
parietal cortex damage = apraxia (inability to perform skilled purposeful movement
- this issue stems from premotor areas in the posterior parietal cortex.
Ideomotor apraxia
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
CEREBELLAR PATIENTS
- leads to action tremor
- also dysmetria (over and undershooting movements)
- deficits also in:
- coordinating across joints
- motor learning
- timing
role of cerebellar network in action
- 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
role of basal ganglia motor circuit
regulates excitability of frontal motor structures(SMA) and biases the likelihood of movement and the nature of the movement.
Parkinsons disease:
- how many it effects
- 3 main symtpoms
- 1 in 1000
- bradykinesia (slow movement)
- tremor
- muscle rigidity
cause of parkinsons:
death of dopaminergic cells in substantia nigra pars compacts in the BG (the pathways linking the substantial nigra and BG)
writing with Parkinsons
- micrographia (writing small in size)
- may reduce while writing (size) due to fatigue
Parkinson’s disease deficits
- 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.