Motor Control 1

Question 1

What cortex makes up the majority of the cerebral cortex?

Answer 1

Association cortex

Question 2

Where is the main motor processing cortex?

Answer 2

The precentral gyrus (Brodman’s area 4), next to the primary somatosensory area S1, with which it has very strong connections

Question 3

What do motor cortical cells give rise to?

Answer 3

CS projections and alpha and gamma motorneurons. These cortical neurons have large pyramidal shaped bodies - hence pyramidal tracts

Question 4

What percentage of CS tract neurons make direct rapid contact? Where do the other axons end?

Answer 4

10%

Interneurons

Question 5

What percentage of CS tract neurons are myelinated?

Answer 5

50%

Question 6

Do CS tract neurons that originate from cortical cells in the motor cortex have connections to other parts of the brain? If so what are these referred to as?

Answer 6

Yes, they have collaterals which pass to many areas of the brain

Question 7

What is the purpose of the collaterals form the CS tract neurons?

Answer 7

They provide mechanisms and sensory system with updates of the commands being sent to the motorneurones

Question 8

Where does the major decussation of the CS tract fibres occur?

Answer 8

The brainstem, specifically in the medulla

Question 9

Do all of the fibres cross at the decussation?

Answer 9

No, 80% cross and are the major crossed lateral tract. 20% do not cross and are the minor uncrossed ventral tract

Question 10

Is there a pattern of the motor representation of the body within the cortex?

Answer 10

Yes, there is a clear, orderly mapping of the areas of the cortex and their corresponding areas of innervation, the motor homunculus

Question 11

Who first discovered the relationships that would be further developed into the map we now call the motor homunculus?

Answer 11

Penfield, a Canadian neurosurgeon operating on patients and stimulating different areas of the cortex whilst observing the responses of the body that manifested

Question 12

Why were Penfield’s patients surprised when the contractions occurred?

Answer 12

Because the motor cortex is not involved in the initiation of movements, and his direct stimulation of the cortex bypassed the initiation stage, therefore the patients expressed surprise because they had not “thought” about making the contraction happen

Question 13

What functions have some of the greatest allocations in the homunculus?

Answer 13

Dexterity, facial expression, speech

Question 14

What is the change in character in relation to general movements when there is damage to the MC or CS?

Answer 14

Clumsiness and primary distal involvement

Question 15

Is the MC involved in the initiation of movement?

Answer 15

No

Question 16

What is the readiness potential?

Answer 16

This refers to the increase in electrical activity in all of the cortical areas when the brain is thinking about carrying out a motor act

Question 17

What is the premotor cortex?

Answer 17

An area of the association cortex assigned a specific motor function. It is responsible for identifying goals and choosing a course of action

Question 18

What is the supplementary motor area?

Answer 18

An area of the association cortex assigned a specific motor role. It is responsible for programming voluntary movements.

Question 19

What factors are associated with mental rehearsal of a motor task?

Answer 19

Increased electrical activity, increased blood flow in the supplementary motor area

Question 20

What is the posterior parietal cortex responsible for?

Answer 20

The brain receives colossal amounts of sensory information, not all of which is useful. As a result much of it must be filtered out to leave sensory information that will lead to purposeful movement

Question 21

What is neglect syndrome?

Answer 21

A result of lesions on the posterior parietal cortex - an inability to respond to stimuli on the contralateral side of the body

Question 22

When does neglect syndrome occur?

Answer 22

Commonly after a stroke that has caused insult to the PPC

Question 23

What are the two main parts of the basal ganglia?

Answer 23

The striatum
Globus pallidus (pallidum)

Question 24

What information does the striatum receive?

Answer 24

A copy of the readiness potential. It is then processed by the striatum and pallidum

Question 25

What happens to the copy of the readiness potential once it has been processed by the striatum and pallidum?

Answer 25

It is relayed via the thalamus back to the motor cortex and premotor cortex (- identifying goals and choosing course of action)

Question 26

What connections do the basal ganglia make with the midbrain?

Answer 26

2, with the substantia nigra and the subthalamic nucleus

Question 27

What are the two different ways in which diseases of the basal ganglia manifest?

Answer 27

Difficulties in starting voluntary movements
OR
Difficulty stopping unwanted movements

Question 28

What are the symptoms of Parkinson’s disease?

Answer 28

Akinesia, extreme difficulty starting voluntary movements - ‘frozen’
Loss of associated movements e.g. swinging arms when walking, shuffling gait with stooped posture
Loss of facial expression - ‘dead-pan face’

All of these contribute to loss of movement = hypokinetic

Question 29

What features, counterintuitively, feature in addition to the akinesia in patients with Parkinson’s?

Answer 29

Hyperkinetic features - resting tremor of limbs shake at rest, tremor disappears when movement is in progress
- rigidity, increased muscle tone affects both flexors and extensors - spastic rigidity

Question 30

What are some hyperkinetic disorders?

Answer 30

Huntington’s Chorea - jerky spasmodic movements at rest and incorporated into normal voluntary movements
Athetosis - slow writhing movements which affect the extremities. When trunk and limb muscles are affected results in torsion spasm and adoption of grotesque positions
Ballism - violent flailing movements of the limbs

In all os these hyperkinetic disorders, it is as if unwanted movements have been released

Question 31

What are the basic features of the BG which allow understanding?

Answer 31

The cells of the pallidum have a high level of spontaneous activity. Therefore, control of movement relates to voluntary regulation of this spontaneous activity

The striatum exerts a profound inhibitory effect on the pallidum via the neurotransmitter GABA

Organising cortical input arrives via the striatum

At rest, when no voluntary movements are in progress, excitation of this pathway inhibits pallidal activity and the body is still

When a voluntary movement is to be initiated, pattered inhibition in the form of the readiness potential allows organised excitation to be transferred to the MC

Question 32

What is the aetiology of Huntington’s chorea?

Answer 32

Stratal degeneration so that the organising cortical input is lost. AS a result the spontaneous activity of the pallidum passes unchecked to the MC without regard to voluntary desire i.e. a form of motor gibberish

Question 33

What is the aetiology of Parkinson’s disease?

Answer 33

The inhibitory pathway from the striatum to the pallidum is kept in check by an inhibitory pathway from the substantia nigra, which thus ensures that the pallidum does not get too much inhibitor from the striatum. The nigostriatal pathway uses DOPAMINE

In parkinson’s the pathway degenerates, making it very difficult to initiate a voluntary movement, forcing the patient to concentrate very hard to bombard the striatum with inhibition

As many as 90% of postmortem fibres can degenerate, it is thought that clinical symptoms only appear once 80% of SN neurons have degenerated

Tremor and rigidity are poorly understood, but may be due to disruption of pathways from the BG to the brainstem

Question 34

What is another component which must be taken into account interns of the BG in order to understand treatment? What it its effect?

Answer 34

Cholinergic striatal interneurons, which exciting the stratal palladial projection. These decrease motor activity

Question 35

What is the governing principle of treatment strategies for diseases of the BG?

Answer 35

Only treatment and management is possible, not a cure, the degeneration is ongoing

Question 36

What is the objective of treatment in Parkinson’s disease?

Answer 36

To compensate for the loss of dopaminergic neurones SN pathway

Question 37

What is the key pharmacological treatment for Parkinson’s?

Answer 37

L-DOPA, the precursor to DA. It is able to cross the BBB. Much of it is taken up by the body so only around 0.01% reaches the SN. Efficacy can be combined by adding selective extra cerebral decarboxylase inhibitor such as carbidopa to reduce peripheral breakdown

Question 38

What is the objective of treatment in Huntington’s chorea?

Answer 38

Increasing efficacy of the remaining striatal interneurons with ACh mimetics and DA blockers. It is not very successful and may produce Parkinsonism
Huntington’s is autosomal dominant, responds poorly to treatment and is associated with dementia

Question 39

Outline the balance of neurotransmitters in relation to the SN/BG and relevant diseases

Answer 39

Normally, dopamine from the SN and ACH from striatum are in balance

In Parkinson’s, DA is low because of SN degeneration so excess ACh effects - treat with L-DOPA or ACh antagonists

In Huntington’s, striatal degeneration means not enough ACh and so excess effects of DA - treat with ACh mimetics or DA antagonists