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Brain and Behavior > Lectures 29-30: Motor Systems > Flashcards

Lectures 29-30: Motor Systems Flashcards

1
Q

Postural base

A

Positions that we take against force of gravity

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2
Q

The brainstem nuclei are critical for what aspect of motor control?

A

Postural base

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3
Q

What are the parts of the pyramidal motor system

A

Motor cortex, brainstem, spinal cord (and reciprocal connections)

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4
Q

Force-generating muscle fiber types, metabolism, function (2)

A

Fast-fatigable (glycolysis, power) and fatigue-resistant/slow (oxidative metabolism, posture-fine-scale movement)

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5
Q

Which muscle fiber type is able to generate a lot of force quickly?

A

Fast-fatigable

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6
Q

Intrafusal fibers are a part of the…function? Do they play a role in force generation?

A

Muscle spindle; adjust sensitivity of muscle spindle; NO

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7
Q

What motorneurons innervates extrafusal fibers?

A

Alpha-motorneurons

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8
Q

What motorneurons innervates intrafusal fibers?

A

Gamma-motorneurons

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9
Q

What is the significance of lower motorneuron pools?

A

All motorneurons in a pool/column innervate the same muscle

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10
Q

Final common pathway

A

Motorneurons, the route by which the CNS initiates and controls movement (includes alpha and gamma muscle fibers)

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11
Q

Motor unit

A

One alpha-motorneuron and all the extrafusal muscle fibers that its axon innervates

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12
Q

What is the relationship between alpha-MN size, motor unit size, and muscle fiber type?

A

Small alpha-MN innervates small motor units of “fatigue-resistent” muscle fibers; large alpha-MN innervates large motor units of “fast-fatigable” muscle fibers

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13
Q

Which fires first: small or large MNs? What is this called? Why?

A

Small MN fire first; size principle

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14
Q

Gamma motorneurons control what aspect of the motor capsule? What happens next?

A

Contractility of motor ends; feedback from non-contractile middle via sensory fibers

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15
Q

What sensory fibers carry back sensory feedback from the muscle capsule?

A

Group IA and Group II

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16
Q

Ways to stimulate muscle spindle (2)

A
  1. Stretch muscle overall; 2. Contract intrafusal fibers via gamma-MNs
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17
Q

When does a 1a fiber discharge (in what part of muscle)? When would 1a fiber be silent and how do we prevent this?

A

During stretch of muscle spindle; the fiber would be silent during muscle contraction but gamma-MN pulls polar ends of muscle spindle, maintaining load on spindle

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18
Q

The myotatic reflex requires how many neurons? What types? Describe this pathway.

A

Two; alpha-MNs and group Ia/II fibers; passive stretch –> Group Ia/II fibers carry information into dorsal horn –> synapse on alpha-MN –> excited agonist/synergist muscles (contraction)

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19
Q

How do antagonist muscles get involved in the myotatic reflex?

A

The same Group Ia/II sensory neuron synapse on an inhibitory interneuron, inhibiting motor activity of the antagonist muscle

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20
Q

What cell type shuts off the myotatic reflex?

A

Renshaw cells

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21
Q

Functions of deep tendon reflexes? (2)

A

Static posture and anticipatory activity (anticipation of future loads via gamma-MNs)

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22
Q

How is anticipatory activity possible?

A

Cortical input –> Gamma-MNs stretch polar ends –> Group Ia/II perception of “stretch” –> feedback to alpha-MNs –> contraction/relaxation of muscle pairs

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23
Q

Symptoms of LMN syndromes (3)

A

Flaccid paralysis (weakness, hypotonia, atrophy), hyporeflexia or areflexia (if LMNs have died), abnormal firing of LMNs (fasiculations)

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24
Q

Golgi Tendon Organs connect…and sense what using what types of fibers (2)?

A

Muscle to tendon; tension via contraction of collagen fibers on Group Ib axons

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25
Q

Golgi Tendon Organs are involved in what reflex? What does this prevent?

A

Inverse myotatic reflex; over-contraction

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26
Q

Describe somatotopy of ventral spinal cord motorneuron pools

A

(around a clock) flexor –> proximal –> extensor –> distal

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27
Q

Lateral spinal tracts and what they control largely (through access to what?)

A

Lateral coticospinal tract and rubropsinal tract; fine movements via access to distal flexors, extensors

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28
Q

Medial spinal tracts and what they control (through access to what?)

A

Tectospinal tract, vestibulospinal tracts (lateral and medial), reticulospinal tracts (lateral and medial); postural control via access to proximal flexors, extensors

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29
Q

Describe pathway of CST

A

Cortex –> cerebral peduncle –> pyramindal tract –> pyramidal decussation –> LCST (90%) and vCST (10%)

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30
Q

Where does the vCST travel?

A

Only to lower cervical

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31
Q

Lateral component UMNs mostly terminate on…

A

Interneurons

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32
Q

Describe pathway of RST

A

Cortex –> red nucleus –> decussation –> RST

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33
Q

RST facilitates what type of muscle? Inhibits what type of muscles?

A

Facilitates flexors, inhibits extensors

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34
Q

T/F: There is somatopy in the descending cortical motor projections?

A

True!

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35
Q

Tectospinal tract function. Where?

A

Facilitates head, neck rotation; high cervical only

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36
Q

Reticulospinal traction function.

A

Balanced control of axial/anti-gravity muscles

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37
Q

Describe pathway of RST

A

Cortex –> pontine/medial (excitatory, ipsilateral) and medullary/lateral (inhibitory, contralateral) reticular nuclei –> RST. FILL IN.

38
Q

Vestibulospinal tract function. What controls it?

A

Medial: neck; Lateral: excitatory influence on axial/anti-gravity muscles; cerebellum

39
Q

Describe pathway of LVST

A

Cerebellum (inhibitory) –> lateral vestibular nucleus –> LVST

40
Q

The anti-gravity muscles favor excitatory/inhibitory inputs?

A

Excitatory (two excitatory pathways: LVST and Pontine RST)

41
Q

If you make a midbrain cut what happens to anti-gravity extensor muscles?

A

Cut off motor cortex control and thus MRN inhibitory input –> hypertonus of anti-gravity muscles

42
Q

If you cut the DRG of an animal with a midbrain cut, what happens? Therefore?

A

The hypertonus will relax. Descending motor system actually acts on gamma-MN and NOT alpha-MN

43
Q

Spasticity and rigidity are both…

A

Forms of hypertonia (excessive muscle tone)

44
Q

What is spasticity. Upper or lower?

A

Hyperactive stretch reflexes, hypertonus more evident in axial/extensor muscle groups; damage to UMNs, internal capsule, cord

45
Q

What is rigidity? Disease of what structure?

A

Hypoactive stretch reflexes, hypertonus equal between extensors/flexors; basal ganglia disease (Parkinson’s)

46
Q

Cortical areas that control movement (4)

A
  1. Overall plan areas (pre-motor areas); 2. Primary motor cortex (M1); 3. Areas responsible for concept of extrapersonal space and motor goals (parietal); 4. Sensory-feedback areas
47
Q

Defining features of motor cortical areas (3)

A
  1. All “fire” before movement onset; 2. All have direction connections with spinal cord; 3 Unique histological features (output layers V and VI are dominant)
48
Q

What percentage of corticispinal neurons are small? What about large (and name)?

A

90% = small; 10% = Betz

49
Q

Describe the function of small corticospinal neurons

A

Slow, fine movements: firing proportional to force, selective to direction, sensitive to sensory feedback

50
Q

Describe the function of Betz cells

A

Ballistic, powerful movements: all-or-none firing, not directionally selective or sensitive to sensory feedback

51
Q

Pre-motor cortex is involved in what? What side?

A

Preparing upcoming motor acts based on sensory-related cues; contralateral

52
Q

Supplementary motor cortex is involved in what? What side?

A

Internally generated motor planning (rehearsal); bilateral

53
Q

UMN syndromes…EMG elicits?

A

Weakness, hypertonia, hyper-reflexia, spasticity, mild atrophy; EMG = decreased muscle recruitment

54
Q

LMN syndromes…EMG elicits?

A

Weakness, hypotonia, hypo-areflexia, significant atrophy; EMG = abnormal firing of LMNs, fasciculations

55
Q

Motor exam: observation (5)

A

Observe: gait, symmetry, bulk, atrophy, fasciculations

56
Q

MRC scale uses what numbers? Describe the key middle number

A

0 - 5; 3 = movement against gravity

57
Q

UMN deficit: weakness distributing (adductors vs abductors).

A

Adductors are stronger because abductors are affected MORE

58
Q

UMN deficit: In upper extremities, flexors or extensors affected?

A

Extensors affected (arm flexed in)

59
Q

UMN deficit: In lower extremities, flexors or extensors

A

Flexors affected (can’t flex foot = foot drop) –> anti-gravity muscles

60
Q

Reflex scale, what is normal?

A

0 - +4, +2 = normal

61
Q

Babinski equivalent in upper body

A

Hoffman sign (finger flicking)

62
Q

Describe hemiplegic gait

A

Arm in flexion with extensor weakness, hand and finger tightly clenched, outward swinging of leg

63
Q

Spastic gait

A

Both legs are stiff, walking slow and difficult, hyperreflexia, clonus

64
Q

Frontal gait

A

Seen in normal pressure hydrocephalus; looks like feet are stuck to ground, small steps (magnetic gait)

65
Q

ALS involves both…must include some symptoms above

A

UMN and LMN; foramen magnum (because of cervical spondalosus on differential)

66
Q

Describe ALS. What will the history be like?

A

Progressive diffuse LMN w/ UMN dysfunction, pelvic floor muscles affected; history = fasciculations with weakness over weeks to months, clumsiness, difficulty swallowing

67
Q

UMN in ALS

A

Stiffness, spasticity, clumsiness, hyperactive reflexes, Babinski

68
Q

LMN in ALS

A

Weakness, wasting/fasciculations, hypo/areflexia

69
Q

What is spared in ALS?

A

EOMs, intact bowel/bladder, no cognitive or sensory changes

70
Q

What must be excluded in ALS?

A

Cervical sondylosis (so look at jaw jerk reflex), tumor, syrinx

71
Q

Primary lateral sclerosis (compare to ALS)

A

ALS minus LMN involvement (only UMN)

72
Q

Progressive spinal muscular atrophy (LMN/UMN and cause)

A

Only LMN involvement; congenital

73
Q

Treatment and prognosis of ALS

A

Treatment: Riluzole; Prognosis: months to 3-4 years after Dx

74
Q

How do you get UMN and LMN in cervical spondylosis?

A

UMN = spinal cord compression; LMN = nerve roots but NO INVOLVEMENT ABOVE FORAMEN MAGNUM

75
Q

Guillain-Barre (description and causes)

A

Acute autoimmune polyneropathy: rapidly progressing paralysis, ascending w/ dysautonomia; often follows infection (campylobacter jejuni)

76
Q

When you’re _____ with G-B, what is lost?

A

Weak; reflexes

77
Q

How do you Dx G-B? Treatment?

A

Increased CSF protein w/out increased cells (albuminocytological dissociation); plasmapheresis

78
Q

Miller Fisher sydrome

A

Like G-B, but w/ ophthalmoplegia and ataxia

79
Q

Steppage gait is characteristic of what disorder?

A

LMN neuropathy; patient picks up foot with conscious effort to avoid tripping over it by lifting up proximal leg

80
Q

What is the most common disorder of NMJ? Describe. Important clinical symptom.

A

Myasthenia gravis; antibodies targeted against AChR; reduction of numbers of AChR and damage to post-synaptic membrane; fatigable

81
Q

Differential diagnosis for Myasthenia gravis

A

Eaton Lambert, botulism, myopathy

82
Q

Myasthenia gravis treatment

A

AChE inhibitors, thymectomy, corticosteroids, IVIG/plasmaphoresis (can be quite effective)

83
Q

Myopathy (muscle problem) symptoms

A

Weakness is proximal (not distal), normal sensation, muscle pain/cramps, DTRs preserved relatively

84
Q

How to diagnose a myopathy

A

Look for elevated CK, EMG, muscle biopsy, genetic testing

85
Q

One important myopathy to know…

A

Statin-induced myopathy (tested w/ elevated CK)

86
Q

Classification of myopathies (general, 2)

A

Hereditary and acquired

87
Q

Myotonia is a disorder of the…symptom?

A

Muscle membrane; delayed relaxation after contraction

88
Q

Botulism and infant botulism cause and presentation

A

Toxin prevents ACh release, descending paralysis, respiratory failure; acute floppy baby (due to spore ingestion)

89
Q

You can get paralysis by these two animals. These both look like what?

A

Ticks, fish (from consumption); G-B syndrome

90
Q

What area of the spinal cord is affected in polio? UMN or LMN? What kind of paralysis?

A

Anterior horn cells; LMN lesion only; flaccid paralysis

91
Q

T/F: ALS sometimes has sensory involvement

A

False! ALS is motor neuron only

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