L5a The Acting Brain

Name 4 key motor functions

execution, preparation, planning and sensory-motor

What is the Degrees of Freedom Problem (includes the 3 things most actions require)

the challenge that most actions require multiple muscles, precise timings, and multiple components of movement – requires coordination

Name 4 ‘higher’ cognitive aspects of motor control

planning and timing, sequencing, imagery and expertise

What is the key brain area involved with execution (and which label)

primary motor cortex, 3

What is the key brain area involved with preparation of actions (and which label)

premotor cortex, 2

What is the key brain area involved with higher level of planning (and which label)

prefrontal cortex, 1

What is the key brain area involved with sensory-motor links (and which label)

parietal cortex, 4

How is the brain’s motor system organised across its four main cortical areas

hierarchically

Where is the primary motor cortex (M1) located

in the pre-central gyrus

How is the M1 organised and what does this mean

somatotopic organisation; different areas correspond to different body parts

Considering the somatotopic organisation of M1, activation in particular parts of M1 causes ?

movement of particular body parts on opposite side

What is the difference between hemiplegia and hemiparesis

paralysis of one side of the body vs weakness of one side of the body (both following a stroke)

What is vector coding in M1

individuals cells in M1 have a preferred direction of movement; population of cells code for this preferred direction of movement

There have been recent challenges to somatotopic mapping, what are the 2 parallel systems recently identified as operating in M1

body-part specific and somato-cognitive action network (SCAN)

What is the body-part specific system responsible for vs the SCAN

fine motor control of foot, hand, and mouth vs integrating goals and whole-body movement

How is the primary somatosensory cortex organised (same as M1)

somatotopic

What are 3 regions of inputs and 1 output of the M1

supplementary motor area, premotor area and primary somatosensory area, and spinal cord (output)

What are two key regions within the premotor cortex

lateral premotor cortex and supplementary motor area

What is the difference in the role of the lateral premotor cortex and the SMA

involved in externally generated actions (cued by the environment) vs internally generated actions

What type of movement are these two areas important in coordinating

bimanual movements

according to Swinnen and Wenderoth, which 3 areas are more active in more difficult bimanual tasks

cerebellum, SMA and pre-motor area

What changes in brain activity occur as a motor sequence becomes more automatic (refer to dorsolateral prefrontal, SMA, lateral premotor cortex and primary motor)

all activity decreases except for SMA which increases

What did the TMS study over SMA by Gerloff et al show – was activity blocked or increased, and how did this impact performance on sequences (simple or complex sequences), what does this suggest about the importance of SMA

repetitive TMS blocked SMA activity which only disrupted performance of the most complex sequence, suggesting SMA is important for complex sequential movements

3 roles of the prefrontal cortex in action control

choosing what action to perform, direction attention to action, and pursuing longer term goals and intentions

Impact of damage to M1 vs higher areas like prefrontal cortex

basic movement affected vs complex actions

4 disorders which can be caused by prefrontal lesions

perseveration, utilisation behaviour, disinhibition and frontal apraxia

What is perseveration

repeating the same action or response when it is no longer relevant

What is utilisation behaviour

acting on irrelevant or inappropriate objects present in the environment

What task is used to test disinhibition

antisaccade task

What does the antisaccade task involve

ppt must look in the opposite direction to the target – requires inhibiting tendency to look at target

What is frontal apraxia

inability to follow steps in routines tasks (e.g. making tea)

What model is seen to explain these motor disorders in the prefrontal cortex

Normal and Shallice model

In the Norman and Shallice model, what is contention scheduling and what does it do (based on two factors)

an automatic system that selects the appropriate action scheme based on sensory information and habit

Name the system that is required for novel/less automatic actions

supervisory attentional system (SAS)

According to this diagram, which system has more influence

SAS, can override or modify contention scheduling

The Norman and Shallice Model can explain motor disorders as a result of prefrontal damage, what component of the model is disrupted by prefrontal damage

SAS

how does the model explain perseveration

SAS fails to update contention scheduling when context changes

how does the model explain utilisation behaviour

SAS fails to suppress schemas activated by the environment via contention scheduling

How does the model explain everyday lapses

even in healthy people, routine action run automatically via contention scheduling which can lead to slip ups e.g. sugar in the fridge, when the SAS is occupied

Damage to which brain area leads to apraxia

parietal cortex

What is apraxia

inability to perform skilled purposeful movement

What is ideomotor apraxia

when the idea and execution of an action becomes disconnected but the person retains the knowledge of the action

fill in the gaps of what a patient with ideomotor apraxia can or can’t do

can recognise action, pantomiming action/copying, perform sequence

What are the two main subcortical motor areas and their primary function

basal ganglia (selection of appropriate movements) and cerebellum (coordination of movement)

What is cerebellar ataxia

movement disorder caused by cerebellar damage

3 consequences of cerebellar ataxia

action tremor, dysmetria, and deficits in motor functions

What is dysmetria

over and undershooting of movements

4 deficits caused by cerebellar ataxia

balance and posture, coordinating across joints, motor learning and timing

What connects the basal ganglia and the cerebellum

thalamus

Which number represents essential tremor vs cerebellar tremor vs tremor in patients with Parkinson’s disease

4 v 2 vs 3

3 main motor symptoms of Parkison’s disease

slow movement (bradykinesia), tremor and rigidity)

What is the neurological cause of Parkison’s disease

dopaminergic cells, nigra pars

fill in the gaps of deficits associated with Parkison’s disease

internally, bimanual, sequences, attention shifting, everyday cognitive failures

The basal ganglia is seen as ‘Gain Control’, what is the difference between its direct pathway and indirect pathway

allows desired movements to occur vs prevents undesired movements occurring

What is this?

basal ganglia circuitry

What is the input and the output (and where they receive/project)

putamen (receive inputs from cortical areas) and GPm (projects back to cortex)

Which pathway in the BG is this

direct pathway (excitatory)

What happens at 1. (think what signals, from where?)

excitatory signal from cortex

What happens at 2. (think what signals, from and to where)

increased inhibitory signal from Putamen to GPm

What happens at 3. (think what signals, from and to where)

reduced inhibitory signal from GPm to thalamus

What happens at 4. (think what signals, from and to where)

increased excitatory signal from thalamus to motor cortex

explain the steps in the indirect pathway (inhibitory)

What is the impact on movement of the direct pathway vs indirect pathway

movement facilitated vs suppressed

What is the selection mechanism of the BS using either direct or indirect pathway

desired movement is ‘disinhibited’ (released) via direct pathway, while competing movements are simultaneously inhibited via indirect pathway

Can you remember which 3 neurotransmitters are key in the BG circuits

glutamate (excitatory), GABA (inhibitory) and dopamine

Lack of dopamine in Parkinson’s has opposing effects on 2 pathways, how does lack of dopamine affect the direct pathway

becomes underactive

How does lack of dopamine affect the indirect pathway

becomes overactive

How does lack of dopamine in each pathway then affect GPm activity

both lead to increased GPm activity

How does this then impact activity of the thalamus and motor cortex

increased inhibition of the thalamus, reducing excitation of the cortex

What are 3 treatments for Parkison’s disease

L-dopa, newer dopaminergic drugs and surgery

What is the function of L-dopa and what is its drawback

restores dopamine levels but induces uncontrolled movements (dyskinesias)

One example of a surgery for Parkinson’s disease

deep brain stimulation

What is the method of deep brain stimulation

a stimulator delivers electrical stimulation to targeted areas

What are the 3 target areas of deep brain stimulation

thalamus, subthalamic nucleus (STN), and globus pallidus (GPm)

Study this diagram for a moment, does deep brain stimulation increase or reduce the effect of the direct or indirect pathway

reduce effect of indirect pathway

Where did reduced activity in the circuit begin and what activity followed in GPm, thalamus and motor cortex?

STN -> reduced excitation of GPm -> reduced inhibition of thalamus -> greater excitation of the motor cortex -> more normal movement restored

What is the main symptom of Huntington’s disease (contrast with Parkinson’s)

chorea – uncontrolled movements

Considering Huntington involves uncontrolled movements (so competing movements aren’t supressed), which pathway might be responsible and is it underactive or overactive

underactivity of indirect pathway

Label the disrupted circuit (for 1, this is the initial cause of the condition)

neurodegeneration, inhibition, increased, reduced

Similarly to Huntington disease, Tourette syndrome also involves unwanted/intrusive movements (differently to Parkinson’s), what type of condition is it

developmental

What is the neurological basis for Tourette Syndrome in the BG – an increase of what neurotransmitter in which brain area causing what impact on which pathway ?

increased dopamine from the SNc -> overactivity of the direct pathway -> disinhibition of an unwanted movement

What is ‘aberrant selection’ in Tourette syndrome

an aberrant focus of activity in striatum -> activates direct pathway -> disinhibits undesired movement (tic)

State whether each pathway is underactive, overactive, or unaffected, and the effect on movement

underactive, overactive, too little movement. Unaffected, underactive, too much movement. Overactive, unaffected, unwanted movement