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Brain & Behaviour > Lecture 12 - Neural Basis of Motor Control > Flashcards

Lecture 12 - Neural Basis of Motor Control Flashcards

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1
Q

Movements

A

are brief unitary activities of muscle

  • Reflexes
  • Postural adjustments
  • Sensory orientation
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2
Q

Actions

A

are complex, goal-oriented sets of movements

  • Walking
  • Gestures
  • Acquired skills (speech, tool use, etc.)
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3
Q

Closed-loop movements:

A

Information flows from whatever is being controlled back to the device that controls it.

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4
Q

Open-loop movements:

A

Ballistic movements where once movement is initiated, there is no opportunity for feedback – accuracy is controlled through anticipation of error.

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5
Q

Overview of neural control of movement

A
  • primary motor cortex
  • nonprimary motor cortex
  • basal ganglia modulation
  • cerebral modulation
  • brain stem
  • spinal cord
  • muscles of body
  • muscles of head & neck
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6
Q

The neuromuscular junction

A

where the NS & the muscle connect

site where a motor neuron excites a skeletal muscle fiber is called NMJ
- chemical synapse consisting of the points of contact b/t the axon terminals of a MN & the motor end plate of a skeletal muscle fiber

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7
Q

The neuromuscular junction 7 Steps

A
  1. AP travels length of axon of a MN to an axon terminal
  2. VG Ca2+ channels open & Ca2+ ions diffuse into terminal
  3. Ca2+ entry causes synaptic vesicles to release ACh via exocytosis
  4. ACh diffuses across the synaptic cleft & binds to ACh receptors, which contain ligand-gated cation channels
  5. Ligand-gated cation channels open
  6. Na+ ions enter muscle fiber & K+ ions exit muscle fiber
    - greater influx of Na+ ions relative to outward influx of K+ ions causes MP to become less (-)
  7. Once MP reaches a threshold value, an AP propagates along sarcolemma
    - neural transmission to a muscle fiber cesses when ACh is removed from the synaptic cleft (occurs in 2 ways)
  8. ACh diffuses away from a synapse
  9. ACh is broken down by acetylcholinesterase to acetic acid & choline
    - choline is transported into axon terminal for resyn. of ACh
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8
Q

Effectors

A

e. g., the hands (distal) or neck (proximal).

- things muscle are moving

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9
Q

Eyes

A

effectors for vision.

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10
Q

Muscles arranged in agonist / antagonist pairs

A

e. g., biceps and triceps.

- pairs have to be treated differently (1 stimulated & 1 inhibited)

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11
Q

Primary site of interaction between muscles and the CNS is via…

A

alpha motor neurons.

  • determines the strength of muscle contraction.
  • basic building block for all movement
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12
Q

Alpha motor neurons

A

originate in the spinal cord, exit via the ventral root and terminate at extrafusal muscle fibres.

  • triceps are activated, biceps inhibited & vice versa
  • if not, muscles fight each other (more jerky, less smooth)
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13
Q

Acetylcholine

A

is the neurotransmitter released by action potentials in alpha motor neurons.

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14
Q

Intrafusal muscle fibres (muscle spindles)

A

– one sensory and one motor axon.

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15
Q

Excitation and Inhibition

A

descending fibers can be excitatory or inhibitory and form the basis of voluntary movements.

excitation to the agonist muscle (e.g., biceps) is accompanied by inhibition of the antagonist muscle (e.g., the triceps) – in this example the elbow is flexed! (muscles are contracted, limbs are flexed).

this prevents the reflex action of the antagonist muscle overcoming the voluntary action of the agonist muscle.
- otherwise, will be rigid

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16
Q

Efferent signals:

A

signals away from the CNS towards effectors (e.g. hand or eye).

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17
Q

Afferent signals:

A

signals from effectors towards the CNS (e.g. sensory feedback from skin).

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18
Q

Monosynaptic stretch reflex

A

1 synapse involved

  • responding to weight of objects. (weight is dropped into hand - but you bring it back up to balance it, reflex & 1 synaptic connection)
  • maintaining posture. (leaning forward & then bringing it back, upright posture restored)
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19
Q

Polysynaptic reflexes

A

couple synapses involved

secondary reflexes INHIBIT alpha motor neurons.

protective mechanism – inhibits further action when the amount of stretch may cause damage to tendons.
- using a weight that’s too heavy

interneurons synapse on alpha motor neurons of antagonist muscle.

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20
Q

Protective mechanism

A

inhibits further action when the amount of stretch may cause damage to tendons.

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21
Q

Cortical control of movement

A
  • some are involved in visual control & planning
  • others involved in movement

slide 13

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22
Q

Cortical control of movement

Motor plan:

A

an abstract representation of an intended action.

  • specify a goal for the action.
  • outline the effectors needed to achieve that goal.
  • create the plan.
  • execute the movement.
  • compare executed movement with plan on-line.

(ex: jump over another athlete and get ball in basket and make it down without hurting yourself)

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23
Q

Cortical control of movements

Efference copy:

A

refers to a copy of the motor plan to be executed. This copy can be used to compare the plan with the outcome.
- blueprint of how plan should go

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24
Q

Movement plans

Vocal motor plans:

A

We start talking later when we are about to read a long sentence. Than we do for a short one.

This suggests that the entire vocal motor plan is generated BEFORE we begin speaking.

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25
Q

Movement plans

Motor imagery:

A

the time it takes to imagine moving shows the same patterns as for real movements.

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26
Q

Real Movement vs Imagined Movement

A

Real movement:

  • small objects take more time to touch one to the other b/c they are smaller, therefore larger distance
  • larger objects - distance b/t is shorter, so that movement is quicker

Imagined movement:
- same slope (follow same motor plan as real movements)

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27
Q

Movement plans

Deafferented patients:

A

(no sensory feedback of moving limb) can perform simple motor tasks.

movements are not as precise and multi-joint movements are particularly difficult.

feedback plays a very important role in modifying motor plans on-line to improve accuracy.

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28
Q

_______ plays a very important role in modifying motor plans on-line to improve accuracy.

A

FEEDBACK

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29
Q

Movement plans – effector independence

A

the particular goal of a movement specifies its control and execution.

movement endpoint may be the most crucial element specifying the goal (but direction, speed and form are important too).

ex: can tell same person wrote a bunch of words b/c some of the end movements look the same (slide 17)

30
Q

Supplementary Motor Area (SMA)

A

in font of primary MC

plays a role in planning, preparation and initiation of movements.

topographic connection with motor cortex.

ipsi and contralateral motor cortex projections and connections to opposite SMA.

primarily involved in complex movements and sequences (also active for imagined movements).

31
Q

Anterior Cingulate

A

involved in novel motor plans.

single cell activity in monkeys shows increased firing prior to movement onset .

fMRI shows the AC is involved in monitoring performance, error feedback and evaluation of possible response conflict (e.g. Stroop effect).

RED vs. RED (one in red, one in green)

32
Q

Rough topography evident in the AC

A

caudal (manual movements, e.g., hand movements), rostral (eye movements), speech – somewhere between the caudal and rostral regions.

33
Q

Internally and externally driven motor plans

A

internally and externally driven motor plans may rely on different neural networks.

parietal, cerebellar and lateral premotor regions – spatially directed movements (novel situations). (ex’s: picking up water bottle)

SMA, basal ganglia, temporal lobe (hippocampus) – internally driven, familiar sequences of movements. (ex’s: tying a tie or shoe lace, or walking)

unlikely to be completely mutually exclusive.

34
Q

Motor strip

A

areas involved in fine motor control (hands, lips etc.) have more cortex devoted to them than other regions of the body

35
Q

Descending pathways - pyramidal and extrapyramidal tracts

A

all cortical motor tracts cross over at the medullary pyramids.

subcortical motor tracts can have ipsi and contralateral projections.

36
Q

Corticospinal pathway

A

connects motor cortex to spinal cord

LATERAL TRACT – controls distal muscles (arms, fingers, lower legs, feet).

lateral tract completely crosses over at the medulla (i.e., completely contralateral).

VENTRAL TRACT – important for posture and locomotion (projects both ipsilaterally and contralaterally).

37
Q

Corticobulbar pathway

A

connects motor cortex to SC

important for the control of the face and tongue.

crosses midline at the pons.

synapses on the pons at the:
V (trigeminal – chewing, pain & touch for face and mouth),
VII (facial – facial expressions),
IX (glossopharyngeal – tongue movement),
X (vagus – digestion, taste) and
XII (hypoglossal – tongue movements) cranial nerves.

38
Q

Corticobulbar pathway interesting

A

UPPER part of face represented both IPSI- and CONTRAlaterally (after unilateral cortical damage both eyebrows and eyelids can still be controlled).

LOWER part of face is exclusively CONTRAlateral (after unilateral cortical damage a FACIAL DROOP is seen).

DAMAGE to the FACIAL NERVE (VII) leads to Bell’s Palsy.

39
Q

Rubro-spinal pathway

A

right red nucleus to SC

originates in the red nucleus of the midbrain.

receives input from motor cortex and cerebellum.

projects mainly to the cerebellum.

modulates motor control and co-ordination.

40
Q

Ventromedial Pathway

A

originates in BRAIN STEM NUCLEI (including the superior colliculus, pontine and medullary reticular formation).

important for co-ordination of eye, head and trunk movements (tecto-spinal).

involved in posture control.

Tecto-spinal - superior colliculus to SC

Vestibulo-spinal - vestibular nucleus to SC

Reticulo-spinal - reticular formation to SC

41
Q

Brain stem disorders

A

damage to the cranial nerves will lead to various neurological signs (e.g., facial nerve palsy or Bell’s palsy – from VII nerve damage).

LOCKED-IN SYNDROME refers to a complete paralysis due to bilateral lesions of motor pathways and lower cranial nerves in the pons and medulla – the oculomotor nerve (III) is spared allowing patients to communicate with eye movements and blinks – cognition is unimpaired and EEG is normal.

motor neuron disease or amyotrophic lateral sclerosis (ALS, also known as Lou Gherig’s disease) affects motor neurons in the cortex, brain stem and spinal cord.

aggressively progressive disorder that generally leads to death within 2 – 4 years after onset (which is typically in the 40’s).

42
Q

Locked-in syndrome

A

refers to a complete paralysis due to bilateral lesions of motor pathways and lower cranial nerves in the pons and medulla – the oculomotor nerve (III) is spared allowing patients to communicate with eye movements and blinks – cognition is unimpaired and EEG is normal.

43
Q

Motor neuron disease or amyotrophic lateral sclerosis (ALS, also known as Lou Gherig’s disease)

A

affects motor neurons in the cortex, brain stem and spinal cord.

aggressively progressive disorder that generally leads to death within 2 – 4 years after onset (which is typically in the 40’s).

44
Q

Cerebellum

A

10% of brain’s mass.

more than half the brain’s neurons!

cerebellum Latin for “little brain”.

45
Q

Cerebellum receives

A

receives sensory input from somatosensory, vestibular, visual and auditory sensory modalities.

also receives input from association cortices.

46
Q

Cerebellum

Organization

A

ipsilateral organization.

so movements of the RIGHT hand involve the LEFT MOTOR CORTEX and the RIGHT CEREBELLUM.

motor feedback loops are also important in the cerebellum – for motor learning, modulation of movements, matching the executed to the planned movement, etc.

47
Q

Cerebellum

Important & sections & includes

A

important for motor learning and modulation of motor control.

three sections – VERMIS, INTERMEDIATE and LATERAL ZONES.

deep cerebellar nuclei include; FASTIGIAL nucleus, INTERPOSITUS nucleus and the DENTATE nucleus.

48
Q

Cerebellum

Vermis (incl. fastigial nuclei)

A

vermis (incl. fastigial nuclei) receives SOMATOSENSORY and KINESTHETIC information.

projects to the ventromedial pathway and is important for POSTURE.

walking and balance are affected by damage to the vermis while fine motor control of distal muscles remains intact.

49
Q

Cerebellum

Intermediate zone (incl. interpositus nucleus)

A

intermediate zone (incl. interpositus nucleus) receives information from the RED NUCLEUS and the SPINAL CHORD.

forms a loop with the red nucleus.

damage leads to RIGIDITY and ACTION OR INTENTION TREMOR (distinct from resting tremor).

finger – nose test.

50
Q

Cerebellum

Lateral zone (incl. dentate nucleus)

A

lateral zone (incl. dentate nucleus) receives information from MOTOR and ASSOCIATION CORTICES via the PONS.

projects back to motor cortex via the red nucleus and the ventrolateral thalamus.

damage affects ballistic movements (leading to overshoot), co-ordination of multi-joint movements, learning new movements.

damage also leads to impairments in timing of motor and cognitive functions.

51
Q

Cerebellum – recalibration

A

damage to the lateral cerebellum impairs the ability to recalibrate movements in response to visual perturbations.

normals ADJUST movements to accommodate change induced by prisms.

normals then show an AFTER-EFFECT that indicates they made a compensation for the prisms – adjustments are very rapid.

cerebellar patients fail to adjust and therefore do not show an after effect.

52
Q

Cerebellum – visuomotor transformation

A

Heathly control - adapt to it
- prism initially will affect our beh., but show gradual transformation to get closer in accuracy, when we take goggles off we’ll show after effect but then we’ll gradually improve & go back to baseline levels

Cerebellar patient - show same direct effect of prism, but not gonna show visuomotor transformation so will remain distant from target all the time, when they take goggles off they’re not gonna show an after effect so they immediately pop back up to baseline levels

53
Q

Cerebellar Disorders

A

ataxia – a (without) taxia (to order, or arrange).

ataxia is a disorder of the co-ordination of movements including directional errors, decomposition of movements into sub-components.

gait ataxia – lurching, unsteady or wide based gait – typical of midline cerebellar lesions or chronic alcoholism.

54
Q

Ataxia

A

a (without) taxia (to order, or arrange).

ataxia is a disorder of the co-ordination of movements including directional errors, decomposition of movements into sub-components.

55
Q

gait ataxia

A

lurching, unsteady or wide based gait – typical of midline cerebellar lesions or chronic alcoholism.

56
Q

Basal Ganglia

A

input mainly to the STRIATUM – caudate and putamen.

output is almost exclusively via the internal globus pallidus and part of the substantia nigra.

output is mainly ascending (via the thalamus).

57
Q

Basal Ganglia area

A

Internal Capsule

Globus Pallidus

Putamen

Head of Caudate

Corpus Callosum (genu)

Lateral Ventrical

58
Q

Circuitry of the basal ganglia

A

excitatory and inhibitory connections within the basal ganglia allow for fluid control of movement.

preparation for voluntary movements, auto-pilot for well-learned movements, timing and switching, planning, learning and execution.

DIRECT route connects striatum with GPi (inhibitory connection).

INDIRECT route connects striatum to GPe, STN and the GPi (eventual excitatory pathway).

59
Q

Circuitry of the basal ganglia

DIRECT route…

A

connects striatum with GPi (inhibitory connection).

60
Q

Circuitry of the basal ganglia

INDIRECT route…

A

connects striatum to GPe, STN and the GPi (eventual excitatory pathway).

61
Q

Circuitry of the basal ganglia

direct route leads to…

A

LESS INHIBITION OF THE THALAMUS (i.e., striatum inhibits GPi which in turn inhibits its normal (inhibitory) action on the thalamus), thus leading to greater excitation from the thalamus to the cortex.

62
Q

Circuitry of the basal ganglia

direct route allows

A

sustained action or initiation of action.

63
Q

Circuitry of the basal ganglia

indirect route

A

EXCITES the GPi thereby INCREASING ITS INHIBITION OF THE THALAMUS.

suppresses unwanted movements.

64
Q

Damage to indirect route of circuitry of the basal ganglia =

A

too many unwanted movements

65
Q

Damage to direct route of circuitry of the basal ganglia =

A

difficulty initiating voluntary control

66
Q

Giving the signal to go!

A

The basal ganglia can be thought of as a trigger center for movements – through the balance between the inhibitory and excitatory connections one movement plan is executed over a myriad of other possible actions.

like a dam - all possible coming from cerebral cortex & most active response gets picked & carried out

67
Q 
The strength of contraction of a muscle is determined by activity of
A) intrafusal muscle fibers.
B) golgi tendon organs.
C) afferent fibers.
D) gamma motor neurons.
E) alpha motor neurons.
A

E) alpha motor neurons.

68
Q 
A \_\_\_\_\_\_\_\_ is formed by the synapse of an efferent nerve terminal onto a muscle fiber.
A) myofibril tangle
B) motor unit
C) neuromuscular junction
D) intrafusal contact
E) muscle spindle
A

C) neuromuscular junction

69
Q

One function of the monosynaptic stretch reflex is to
A) coordinate the movements of the flexors on each limb.
B) smooth out muscle contractions.
C) provide feedback to the brain about motor activity.
D) alter the speed with which an arm moves while throwing a ball.
E) help maintain posture.

A

E) help maintain posture.

70
Q 
Which of the following pathways controls movements of the fingers?
A) lateral corticospinal tract
B) rubrospinal tract
C) tecto-spinal tract
D) nigrostriatal bundle
E) corticobulbar pathway
A

A) lateral corticospinal tract

71
Q 
Which of the following pathways controls movements of the tongue, face and some eye
muscles?
A) lateral corticospinal tract
B) ventral corticospinal tract
C) spinothalamic tract
D) rubrospinal tract
E) corticobulbar pathway
A

E) corticobulbar pathway

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