Lecture 5 - The Motor System Flashcards

1
Q

Where does the ‘journey’ of motor action begin?

A

The frontal cortex

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2
Q

Role of prefrontal cortex

A

Planning

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3
Q

Role of premotor cortex

A

Sequence organization

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4
Q

Role of primary motor cortex (M1)

A

Movement production (contains homunculus)

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5
Q

Motor cortex vs. SS cortex

A
  • The motor cortex lies in the frontal lobe just anterior to the central fissure
  • The sensory cortex lies posterior to the central fissure and extends into the parietal lobe
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6
Q

Rate encoding

A

Firing of motor neurons before a task is proportional to the muscle force required for that task

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7
Q

Mental rehearsal/visualization

A
  • Imaging movement produces a similar pattern of brain activity to planning movement (but less strong)
  • Often used in training athletes in technically demanding sports, may help improve performance
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8
Q

2 Views of modelling movement

A
  • Direct mapping of motor homunculus neurons to muscle fibres in the periphery
  • More likely that the regions of motor homunculus represents categories of movement (a movement repertoire)
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9
Q

Neural mechanism for sequencing motor actions?

A

Lesion to the premotor cortex in animals impairs the ability to coordinate motor sequences

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10
Q

What are mirror neurons?

A

In monkeys, neurons exist which respond to both seeing action and performing action

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11
Q

Where are mirror neurons found in the brain?

A

The premotor cortex and inferior parietal lobe

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12
Q

Which disorder was malfunction of mirror neurons thought to play a role in?

A

Autism - a disorder which involves difficulty in replicating/understanding actions (not strongly supported)

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13
Q

What neurons are responsible for the beginning voluntary motor action?

A

Upper motor neurons (Betz cells)

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14
Q

Axons pass through the thalamus via the ________

A

internal capsule

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15
Q

Motor neurons axons form motor _______, evident in the _________ and ________

A

tracts, cerebral peduncles (midbrain), pyramid (medulla)

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16
Q

Tracts synapse with ________ in the spinal cord, which in turn affect the muscle activity

A

lower motor neurons

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17
Q

If you lesion only a part of M1 associated w/ the hand + digits, what would happen? How could you reduce this?

A

The whole area would shrink, could be mitigated by rehabilitation

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18
Q

How can the FC be damaged?

A
  • traumatic head injury
  • tumor
  • neurological diseases
  • stroke (most common)
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19
Q

What happens in a stroke?

A
  • condition in which poor blood flow results in cell death and loss of brain function
  • arises due to issues in the cerebrovascular system that supplies the brain with blood
  • serious consequences for neurons, which depend upon blood for oxygen + glucose
  • two types: ischemic + hemorrhagic
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20
Q

Ischemic Vs. Hemorrhagic Stroke

A
  • Ischemic stroke: clot stops blood supply to an area of the brain
  • Hemorrhagic stroke: hemorrhage/blood leaks into brain tissue
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21
Q

What are the main arteries in the brain?

A

Anterior cerebral artery: supplies blood to dorsal medial + frontal parietal
Middle cerebral artery: supplies blood to frontal, parietal, and occipital
Posterior cerebral artery: supplies blood to occipital (least likely to be involved in motor complications)

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22
Q

What would happen if there was damage to motor neurons in the frontal cortex?

A

This would profoundly impair movement

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23
Q

What is CIMT?

A

Constraint-induced motor therapy (CIMT): developed by Dr. Edward Taub
- involves forced use of affected limb by suppressing the unaffected limb
- based on the principle that loss of sensory function (afferent input to the spinal cord/brain) does not always result in complete loss of motor function (efferent)

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24
Q

What kind of restraints to they use in CIMT (to restrict the functional limb)

A
  • braces
  • mitts
  • casting
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25
Q

CIMT and neuroplasticity

A
  • In individuals who regain motor function, there is increased grey matter
  • recovery is imperfect - but even a little bit is valuable
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26
Q

CIMT in practice

A
  • Involves shaping (the reinforcement of successive approximations of the movement)
  • Time-intensive (90% of waking hours) and labor-intensive (requires supervision)
  • Early goal is cortical stimulation rather than task completion (which is very difficult)
  • Focus on day-to-day tasks (writing, eating, doing the dishes, and so on)
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27
Q

How many motor nerves are there?

A

9 (cranial nerves) all but I, II, and VIII have motor functions

28
Q

Laterality of cranial nerves

A

Lack of decussation means that cranial nerves mediate function on the ipsilateral side of the body (they do not crossover before entering the brainstem)
*Damage to most cranial nerves generally leads to impairment on the same side of the body

29
Q

Example of cranial nerve pathology

A

Bell’s Palsy

30
Q

The facial nerve (VII)

A
  • responsible for motor function within the face as well as sensory functions (e.g. taste; L04)
  • malfunctions in the facial nerve can cause motor impairments
31
Q

Bell’s Palsy

A
  • facial nerve travels through a ‘tight tunnel’ (bone)
  • Inflammation of the nerve can lead to it being compressed against the tunnel
  • compression impair motor function in the face
32
Q

Treating Bell’s Palsy

A
  • most patients recover on their own
  • in severe cases, corticosteroids (to reduce inflammation) might be recommended (value of antiviral drugs is unclear)
  • surgery (to improve passage of the nerve) is possible, but comes with high risks
33
Q

How many segments in the spinal cord?

A

31 segments + nerve pairs

34
Q

Cervical section of SC

A

C1-C8

35
Q

Thoracic section of SC

A

T1-T12

36
Q

Lumbar section of SC

A

L1-L5

37
Q

Sacral section of SC

A

S1-S5

38
Q

Coccygeal

A

1 segment

39
Q

Two types of motor impairment with SC injury

A

Tetraplegia (most severe), paraplegia (less severe)

40
Q

Sensory pathways are in the ________ region

A

dorsal (posterior)

41
Q

Motor pathways are in the ________ region

A

ventral (anterior)

42
Q

Dorsolateral column of the SC

A
  • lateral corticospinal pathway
  • rubrospinal pathway (contacts red nucleus)
43
Q

Ventromedial column of the SC

A
  • anterior corticospinal pathway
  • vestibulospinal (vestibular nuclei) - balance + head-turning
  • reticulospinal (reticular formation) - locomotion and posture
  • tectospinal pathway (superior colliculus) - orientation to stimuli, head/neck/eye movements
44
Q

Tracts are typically named for their starting location and terminal destination

A

corticospinal = cortex to spinal cord

45
Q

Two divisions of the corticospinal tract

A

Lateral corticospinal tract: carries commands for movement of limbs + digits (distal muscles)
Anterior corticospinal tract: carries commands for movement of the body’s midline (proximal muscles, e.g., trunk)

46
Q

Decussation of CS tracts

A
  • lateral corticospinal tracts decussates at the medulla, before the SC (~90% of fibres)
  • anterior corticospinal tract decussates at the level of the lower motor neurons in the SC (~10% of fibres)
47
Q

Rubrospinal tract

A
  • extrapyramidal (outside pyramidal) tract
  • involves red nucleus at the level of the midbrain
  • important for large muscle movement and coordinating fine movements
  • may be more functionally significant in other animals
48
Q

Anteromedial pathway system

A

Vestibulospinal pathway: (connected with vestibular nuclei for CN8) is important for balance and head-turning
Reticulospinal pathway: (connected with the reticular formation) important for locomotion and posture
Tectispinal pathway: (connected with superior colliculus) important for orientation to stimuli, head/neck/eye movements

49
Q

The problem with SC lesions

A

No sensory info coming in, no motor instructions going out

50
Q

What is potentially a neurorehabilitation method for paralysis of SC lesions?

A

If we could measure signals we could perhaps transfer them directly to muscles or another apparatus (i.e. bypass the injury too SC)
*Many researchers are experimenting with implants to measure neural activity (e.g., Neuralink)

51
Q

Robot-guided movements

A
  • once you have the correct signal, you can direct it to a machine that can complete movements
  • the individual can learn to control their movements better through the machine (feedback is vital)
  • much research into this possibility
52
Q

What is the Basal Ganglia?

A

Network of structures involved in coordinating movement
- caudate and putamen (together referred to as the striatum)
- globus pallidus (internal and external)
- subthalamic nucleus
- substantia nigra

53
Q

The _________ through the BG is thought to play an important role in initiating movements

A

direct pathway

54
Q

The _________ is through the BG is thought to play a role in inhibiting unwanted movements

A

indirect pathway

55
Q

Which receptors inhibit/excite which pathways?

A

Inhibitory actions of the DA are mediated by D2 receptors (left, indirect) whereas excitatory actions are mediated by D1 receptors (right, direct)

56
Q

What is the defining feature of Parkinson’s Disease?

A

Loss of DA-projecting neurons (>60%)

57
Q

What is Parkinson’s Disease (PD)?

A
  • progressive disorder of the nervous system that affects movement
  • develops gradually, advancing over time
  • though primarily considered a motor disorder, involves non-motor symptoms
58
Q

PD motor symptoms

A
  • resting tremor
  • cogwheel rigidity: stiffness and jerky motions, decreased range of motion
  • bradykinesia/akinesia: slow to start/finish movements, less spontaneous movement, difficulty w/ repeated movements, decreased facial expressivity, short, shuffling steps
  • postural instability: loss of balance when standing or when pressure is applied
59
Q

PD non-motor symptoms

A
  • may occur before motor symptoms (predictor of later PD diagnosis)
  • many examples: loss of smell, constipation, sleep disorders (REM), mood disorders, orthostatic hypotension, cognitive deficits (dementia)
  • pathological gambling occurs more frequently (3.4-6.1%) than in the general population (0.25-2%)
  • other impulse control disorders are also more common, including binge eating, compulsive shopping, and ‘hypersexuality’
  • risk for impulse control disorders may be linked to medications for the disorder, though this is still controversial
60
Q

Etiology of PD

A
  • Environmental factors: pesticide exposure, agricultural occupation, prior head injury, rural living, beta-blocker use, well-water drinking
  • Genetic factors (family history): alpha-synuclein gene (x1.5 risk), ~18 genes linked to PD, heritability ~ 0.40 (out of 1.00)
61
Q

Increasing DA in PD

A
  • we cannot administer DA directly (won’t cross the blood-brain barrier) so we need another solution
  • L-DOPA, the immediate precursor for DA, can cross the blood barrier
  • If we administer L-DOPA (levodopa; in drug form), it will be converted to DA inside the brain, correcting the DA deficiency
62
Q

Increasing DA through other targets (target metabolism of DA instead)

A

Monoamine Oxidase B (MAOB) Inhibitors: delays breakdown of DA by MAO-B, used as monotherapy or in conjunction with L-DOPA, it can reduce the dosage of L-DOPA by 15%

Catechol O-Methyl Transferase (COMT) Inhibitors: delays breakdown of DA by COMT, mainly used in combination with L-DOPA, increases the half-life of L-DOPA, delays “wearing-off” effect of L-DOPA and other motor complications such as dyskinesia

63
Q

Concerns of increasing DA

A
  • L-DOPA non-selectively increases DA levels in the entire brain, not just in the substantia nigra (other systems are affected - e.g., cognitive)
  • Increased DA elicited by L-DOPA is not as precise as endogenous DA neurotransmission (sometimes effects are too strong or too weak)
  • L-DOPA has unpleasant side effects (nausea, dyskinesia, psychosis, and delusion)
64
Q

Deep Brain Stimulation (DBS) in PD

A
  • Electrodes can be planted in the subthalamic nucleus (more effective, preferred) or globlus pallidus internus to modulate the activity of these structures
65
Q

What is the role of the cerebellum in movement?

A
  • role in posture, balance, coordination, and adapting movements
  • contains a topographic representation of the body