Lectures 29-30: Motor Systems Flashcards Preview

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Flashcards in Lectures 29-30: Motor Systems Deck (91):
1

Postural base

Positions that we take against force of gravity

2

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

Postural base

3

What are the parts of the pyramidal motor system

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

4

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

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

5

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

Fast-fatigable

6

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

Muscle spindle; adjust sensitivity of muscle spindle; NO

7

What motorneurons innervates extrafusal fibers?

Alpha-motorneurons

8

What motorneurons innervates intrafusal fibers?

Gamma-motorneurons

9

What is the significance of lower motorneuron pools?

All motorneurons in a pool/column innervate the same muscle

10

Final common pathway

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

11

Motor unit

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

12

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

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

13

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

Small MN fire first; size principle

14

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

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

15

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

Group IA and Group II

16

Ways to stimulate muscle spindle (2)

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

17

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

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

18

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

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)

19

How do antagonist muscles get involved in the myotatic reflex?

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

20

What cell type shuts off the myotatic reflex?

Renshaw cells

21

Functions of deep tendon reflexes? (2)

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

22

How is anticipatory activity possible?

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

23

Symptoms of LMN syndromes (3)

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

24

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

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

25

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

Inverse myotatic reflex; over-contraction

26

Describe somatotopy of ventral spinal cord motorneuron pools

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

27

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

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

28

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

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

29

Describe pathway of CST

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

30

Where does the vCST travel?

Only to lower cervical

31

Lateral component UMNs mostly terminate on...

Interneurons

32

Describe pathway of RST

Cortex --> red nucleus --> decussation --> RST

33

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

Facilitates flexors, inhibits extensors

34

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

True!

35

Tectospinal tract function. Where?

Facilitates head, neck rotation; high cervical only

36

Reticulospinal traction function.

Balanced control of axial/anti-gravity muscles

37

Describe pathway of RST

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

38

Vestibulospinal tract function. What controls it?

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

39

Describe pathway of LVST

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

40

The anti-gravity muscles favor excitatory/inhibitory inputs?

Excitatory (two excitatory pathways: LVST and Pontine RST)

41

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

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

42

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

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

43

Spasticity and rigidity are both...

Forms of hypertonia (excessive muscle tone)

44

What is spasticity. Upper or lower?

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

45

What is rigidity? Disease of what structure?

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

46

Cortical areas that control movement (4)

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

Defining features of motor cortical areas (3)

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

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

90% = small; 10% = Betz

49

Describe the function of small corticospinal neurons

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

50

Describe the function of Betz cells

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

51

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

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

52

Supplementary motor cortex is involved in what? What side?

Internally generated motor planning (rehearsal); bilateral

53

UMN syndromes...EMG elicits?

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

54

LMN syndromes...EMG elicits?

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

55

Motor exam: observation (5)

Observe: gait, symmetry, bulk, atrophy, fasciculations

56

MRC scale uses what numbers? Describe the key middle number

0 - 5; 3 = movement against gravity

57

UMN deficit: weakness distributing (adductors vs abductors).

Adductors are stronger because abductors are affected MORE

58

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

Extensors affected (arm flexed in)

59

UMN deficit: In lower extremities, flexors or extensors

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

60

Reflex scale, what is normal?

0 - +4, +2 = normal

61

Babinski equivalent in upper body

Hoffman sign (finger flicking)

62

Describe hemiplegic gait

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

63

Spastic gait

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

64

Frontal gait

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

65

ALS involves both...must include some symptoms above

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

66

Describe ALS. What will the history be like?

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

67

UMN in ALS

Stiffness, spasticity, clumsiness, hyperactive reflexes, Babinski

68

LMN in ALS

Weakness, wasting/fasciculations, hypo/areflexia

69

What is spared in ALS?

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

70

What must be excluded in ALS?

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

71

Primary lateral sclerosis (compare to ALS)

ALS minus LMN involvement (only UMN)

72

Progressive spinal muscular atrophy (LMN/UMN and cause)

Only LMN involvement; congenital

73

Treatment and prognosis of ALS

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

74

How do you get UMN and LMN in cervical spondylosis?

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

75

Guillain-Barre (description and causes)

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

76

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

Weak; reflexes

77

How do you Dx G-B? Treatment?

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

78

Miller Fisher sydrome

Like G-B, but w/ ophthalmoplegia and ataxia

79

Steppage gait is characteristic of what disorder?

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

80

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

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

81

Differential diagnosis for Myasthenia gravis

Eaton Lambert, botulism, myopathy

82

Myasthenia gravis treatment

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

83

Myopathy (muscle problem) symptoms

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

84

How to diagnose a myopathy

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

85

One important myopathy to know...

Statin-induced myopathy (tested w/ elevated CK)

86

Classification of myopathies (general, 2)

Hereditary and acquired

87

Myotonia is a disorder of the...symptom?

Muscle membrane; delayed relaxation after contraction

88

Botulism and infant botulism cause and presentation

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

89

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

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

90

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

Anterior horn cells; LMN lesion only; flaccid paralysis

91

T/F: ALS sometimes has sensory involvement

False! ALS is motor neuron only

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