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Chika- SF2 > Brainstem Motor Pathways-Wilson > Flashcards

Brainstem Motor Pathways-Wilson Flashcards

1
Q

Describe the following for upper motor neuron disease:

  • tone
  • reflexes
  • Babinski
  • clonus
  • muscle bulk
  • fasciculations
A

spastic paralysis greater in flexors of arms and extensors of legs; when you move a joint you get resistance and that is dependent on the velocity of the movement (slow movement not a lot of resistance; fast movement produces lots of resistance)

accentuated stretch reflexes

present Babinski

clonus frequently present

slight atrophy of disuse only, late

no fasciculations

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2
Q

Describe the following for lower motor neuron disease:

  • tone
  • reflexes
  • Babinski
  • clonus
  • muscle bulk
  • fasciculations
A

flaccid tone

normal, decreased, absent reflexes

absent Babinski

absent clonus
marked atrophy of muscles

fasciculations present

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3
Q

What happens if there is lesion in the lateral corticospinal system at the pyramids?

A
  • produces paresis and a loss of voluntary movements, especially at the digits
  • positive Babinski sign
  • decreased cremaster reflex
  • produces hypotonia (loss of tonic stimulatory effect)
  • does NOT produce spasticity
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4
Q

What happens if there is lesion in the anterior corticospinal system at the pyramids?

A
  • manipulation of objects normal (10% do not cross and it’s only change of posture, lateral CST is for manipulation of digits)
  • frequent failing
  • lost of righting reflex
  • hypotonicity
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5
Q

Why does a lesion to the lateral corticospinal tract in the pyramids NOT produce spasticity?

A

you get other parallel pathways in addition to the corticospinal tract that go to the brainstem, its when you lose signals going to the brainstem, that results in spasticity; at this stage all the corticofugal fibers (going to the brainstem) have been given off so no effect on the corticoreticular or corticorubral pathways, so you won’t have spasticity

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6
Q

Are lesions of the corticospinal tract clean?

A

NO

you get other parallel pathways like corticoreticular and corticorubal neurons

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7
Q

What is the difference between rigidity and spasticity?

A

rigidity: increase in extensor and flexor muscle tone which can demonstrate clinically through resistance to passive stretch; independent of velocity; due to increase in tonic reflex of muscle spindle
spasticity: increase of muscle tone that is velocity dependent; the faster you stretch the muscle the more resistance there is; greatest in flexors of upper limb and extensors of lower limb; exaggerated deep tendon reflexes and clonus (because of increase gain and sensitivity in the phasic phase of the tendon reflex–>hyperreflexia )

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8
Q

What are the two types of rigidity? Characterize them both.

A

lead-pipe: resistance constant throughout the range of movement

cogwheel (Parkinson’s disease) or clasp-knife (pyramidal tract): increase in passive resistance that abruptly decreases, usually at the end of the an excursion; resistance-release jerking pattern

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9
Q

Where is spasticity greatest during upper motor neuron lesions?

A

greatest in the flexors of the arm and extensors in the legs

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10
Q

What are the major efferents from motor cortical areas?

A
  • basal ganglia
  • cerebellum via basilar pons
  • indirect motor pathways to the spinal cord
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11
Q

What are the indirect motor pathways to the spinal cord?

A
  • Red nucleus
  • Pontine reticular formation
  • medullary reticular formation
  • vestibular nuclei
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12
Q

Spasticity results from disinhibition of reticular and brainstem nuclei, and damage of what parts of cortex?

A

non-pyramidal parts of the cortex

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13
Q

Relate the activity of motor areas of the brainstem during excessive muscle tone.

A

the motor areas of the brainstem become overactive resulting in excessive muscle tone

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14
Q

Cortex control of motor activity through corticofugal connections is direct or indirect?

A

indirect

brainstem modulates the reflexive activity of the spinal cord

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15
Q

Depending on the stimulus under a certain context, you can have different motor responses.

A

reflexes can change, sometime they are operational and sometimes they are not

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16
Q

Rexed Lamina IX consist of what two distinct groups of motor neurons that innervate what muscles?

A

medial group- axial musculature

lateral group: appendicular musculature (cervical and lumbosacral enlargement)

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17
Q

Where is the lateral descending motor system that controls the lateral motoneurons of lamina IX located? Which muscles do these neurons innervate?

A
  • posterolateral funiculus

- innervate appendicular musculature

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18
Q

Where is the medial descending motor system that controls the lateral motoneurons of lamina IX located? Which muscles do these neurons innervate?

A

anteromedial funiculus (medial motor pathway extends slightly laterally and so anterolateral funiculus)

axial musculature and some muscles of the shoulder girdle

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19
Q

Describe the projection of lateral and medial motor system pathways.

A

Lateral Pathway:

  • contralateral
  • lateral ventral horn
  • limbs and distal musculature

Medial Motor System (anteromedial funiculus)

  • bilateral
  • medial ventral horn
  • axial and girdle musculature

Medial Motor System (anterolateral funiculus)

  • unilateral (ipsilateral)
  • intermediate ventral horn
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20
Q

What are the spinal segments and muscles of the medial descending pathway besides the motor neurons in Rexed lamina IX?

A
  • will synapse on interneurons in Rexed lamina VIII activating long propriospinal neurons that will go to medial motor neurons pools
  • proximal and extensor muscles (most important)
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21
Q

What are the spinal segments and muscles of the lateral descending pathway besides the motor neurons in Rexed lamina IX?

A
  • will synapse on interneurons in Rexed lamina VII activating short propriospinal neurons (possible to move one limb without having to move the other limb unlike axial musculature in which both sides need to move) that will go to lateral motor neuron pools
  • distal and flexor muscles (most important)
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22
Q

What are the major lateral cortical descending pathways?

A

lateral corticospinal tract

rubospinal tract coming from the red nucleus

medullary (lateral) reticulospinal tract

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23
Q

What are the major anterior cortical descending pathways?

A

-anterior corticospinal tract

tectospinal tract: involves the superior colliculus; coordinates head and eye movements to look at objects in lateral gaze

pontine (medial) reticulospinal tract

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24
Q

What are the two descending vestibulospinal tracts?

A
  • medial vestibulospinal tract

- lateral vestibulospinal tract

25
Q

What are the indirect pathways the cortex can influence muscles of the limbs?

A

corticorubrospinal tract
(takes a stop at the red nucleus)

-will synapse into the red nucleus which will receive input from the interposed nuclei in the cerebellum and then will decussate to the other side and continue as the rubrospinal tract

26
Q

Describe the projection of rubrospinal tract.

A

-contralateral projection -going to muscles of the cervical enlargement (upper limb, ONLY)

27
Q

Where is the red nucleus located?

A

midbrain at the level of the superior colliculus

28
Q

What are the two parts of the red nucleus?

A

magnocellularis: large cells; caudal and oldest part
parvocellularis: small cells; rostral and newest part; gets lot of input from the dendate nucleus of the cerebellum

29
Q

The red nucleus receives input from where?

A
  • motor cortex (magnocellular)

- cerebellum specifically the interposed nuclei (magnocellular) and dendate nucleus (parvocellular)

30
Q

What is the alternative indirect method in which the cortex can affect muscles of the upper limb?

A

magnocellular part send axons that descend and cross to the contralateral side which will run parallel the (contralateral) lateral corticospinal tract

31
Q

Where does the rubrospinal tract decussate to overlap with lateral corticospinal tract in the lateral funiculus?

A

in the ventral tegmental decussation

32
Q

Rubrospinal tract innervates proximal musculature of the CONTRALATERAL upper limb but does not control what?

A

muscles going to individual fingers (does not have direct monosynaptic input to motoneurons affecting fingers)

33
Q

The majority of rubral neurons have what kind of response properties?

A
  • dynamic response properties that fire at the beginning of a movement to cause the initial generation of force
  • thus rubrospinal firing activity is related to the dynamics of force and limb velocity
34
Q

The majority of cortical neurons have what kind of response properties?

A

in contrast to rubral neurons, they show static activity to maintain the force of an ongoing contraction (are involved in force and velocity)

35
Q

What are the main targets of the rubrospinal tract in the spinal cord?

A

interneurons in Rexed Lamina VII (intrasegmental-propriospinal and intersegmental interneurons)

36
Q

What kind of effect does the rubrospinal tract have on flexor motoneurons?

A

facilitatory effect

37
Q

Where do the medial reticulospinal tracts come from?

A
  • Medial (pontine) Reticulospinal Tract from pons
  • Lateral (medullary) Reticulospinal Tract from medulla

they are largely antagonistic

38
Q

What does the pontine reticulospinal tract affect?

A
  • facilitate axial muscles
  • facilitate extensor muscles
  • modulate reflexes based on context
39
Q

What does the medullary reticulospinal tract affect?

A
  • inhibit axial extensors
  • facilitate flexors
  • modulate reflexes based on context
40
Q

T/F. Both reticulospinal tracts receives direct cortical input.

A

True

41
Q

Where are the vestibular nuclei located and which ones are the most important and why?

A

at the pontomedullary junction

medial and lateral vestibular nucleus which both give rise to the medial and lateral vestibulospinal tract respectively

42
Q

Describe the medial vestibulospinal tract.

A
  • originates from the medial vestibular nucleus
  • terminates medially in the ventral horn of cervical regions
  • does not extend below the cervical region (similar to rubrospinal, which is limited to the upper limb)
  • affects axial musculature of neck
  • adjustments to angular acceleration of head
  • is a BILATERAL projection (affects boths sides of the medial vestibular nucleus)
  • caudal continuation of MLF
  • medial goes mainly to semicircular canals

stimulation of the medial vestibular system means the head is turning in one direction than the other (maintains head position during movements)

43
Q

Describe the lateral vestibulospinal tract.

A
  • originates from lateral vestibular nucleus (Dieter’s)
  • largest
  • terminates in the intermediate ventral horn (Rexed lamina VII and VIII) group proximal limb muscles affecting balance
  • is IPSILATERAL and gives off numerous collaterals along the spinal cord
  • MOST IMPORTANT: activates preferentially antigravity muscles the EXTENSORS to help support posture
44
Q

If there is a vestibular lesion on the left, the patient will fall?

A

left

45
Q

If there is a vestibular lesion on the right, the patient will fall?

A

right

46
Q

Where does the lateral vestibulospinal tract get its input from?

A
  • primary afferents from vestibular ganglia, particularly the utricle
  • inhibitory input directly from Purkinje cells of the cerebellum
  • tonically inhibitory inputs from the motor cortex
47
Q

If there is a cortical lesion, how does that affect the activity of lateral vestibular nucleus?

A

it increases its activity as its tonic cortical suppression is removed due to the lesion

48
Q

Describe the stimulation of the lateral vestibular nucleus.

A
  1. Stimulation has excitatory influences on extensor tone and reflexes of upper and lower limbs (depending on site of stimulation).
  2. Stimulation produces EPSPs in extensor (antigravity) motoneurons and little effect in flexor motoneurons
  3. Stimulation enhances extensor activity during swing phase of gate
  4. Lesions reduce rigidity in decerebrate animals
49
Q

What is decerebrate rigidity?

A

-severing of SC or brainstem where you get rigidity, extension of vertebral column and lower limbs

Upper Limb:

  1. Extension
  2. Adducted
  3. Hyperpronated
  4. Flexed fingers

Lower Limb:

  1. Extension
  2. Plantar flexion of ankles

Spine: Opisthotonos
1. Spastic extension of the spine

50
Q

Describe the tectospinal tract.

A
  • originates from the deep layers of superior colliculus
  • decussates in the dorsal tegmentum
  • terminates medially in the ventral horn of cervical cord
  • coordinates neck and; eye movements
51
Q

How can we mimic decerebrate rigidity by lesion?

A

mid-collicular lesion

you lose descending input, flexor muscle tone

if vascular lesion, get lesion of purkinjie fibers, release of vestibular nuclei - hypertonia decreased by dorsal root lesion. ie, vestibular right to alpha motor neurons???

52
Q

The cortex and red nucleus have a facilitatory influence on flexor tone.

A large tumor or vascular lesion between the red nucleus and vestibular nuclei produces “decerebrate rigidity”, tonic contraction of the extensors. Why?

A

This is due to:
-loss of tonic inhibitory input from cortex and red nucleus
-overactivity of the vestibulospinal and pontine reticulospinal neurons
increased muscle tone in extensors.

53
Q

What is tone?

A

the balance between flexors and extensor???

54
Q

What exactly occurs with a lesion to the mid-collicular region?

A

lose the corticospinal and rubrospinal input thus reducing the effect of medullary reticulospinal tract and thus decreasing flexor muscle activity while at the same time the activity of the medial and lateral vestibulospinal and pontine reticulospinal tract is enhanced thus enhancing the activity of the extensors (upper limb, back, neck, lower limb)

55
Q

What are some experimental modifications of decerebrate rigidity?

A
  • noxious stimulation enhances rigidity (via spinothalamic drive to lateral reticulospinal tract)
  • the muscle spindle input has been reduced by cutting the dorsal roots
  • cutting CN VIII
  • stimulation of the anterior lobe of cerebellum decreases rigidity (Purkinje inhibition lateral vestibular nucleus); Purkinje cells provide tonic inhibition to vestibular cells
56
Q

Describe the postural rigidity in humans.

A
  • not as extreme as seen in animals (can’t make a complete cut like you can in animals)
  • seen best using a noxious peripheral stimulus to a bony pressure point (e.g. the sternum)
57
Q

What is decorticate rigidity?

A
  • pattern typical of chronic cerebral hemiplegia
    1. elbows, wrists and fingers flexed
    2. legs extended and rotated internally
  • lesion above red nucleus:
    1. cortex
    2. internal capsule
    3. (thalamus)
58
Q

Decorticate Rigidity: Upper Limb

A
  • Rubrospinal tract has a facilitatory effect on flexors of UL
  • Lesion of the corticospinal tract results in disinhibition of red nucleus.
  • Increased activity of rubrospinal tract enhances flexor tone that outweighs extensor tone in UE.
59
Q

Spinal Cord Damage

A

Acute: Spinal Shock (false lower motoneuron signs below the lesion)

1. areflexia
2. hypotonia

mechanism: loss of inputs from descending motor systems results in profound disfacilitation of spinal interneurons and lower motoneurons.

Chronic: Mass Reflex
1. hyperreflexia
2. light touch evokes bilateral 
		a. flexion of legs & trunk and 
		b. bowel evacuation
mechanisms:
1. development of denervation supersensitivity in spinal cord 
2. sprouting of the central terminals of primary afferent fibers

Chika- SF2 (63 decks)

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