[31] Upper and Lower Motoneurones Flashcards

1
Q

What are the upper and lower motoneurones responsible for?

A

Controlling movement

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2
Q

Where does the upper motorneurone have its cell body?

A

In the primary motor cortex

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3
Q

Where is the primary motor cortex found?

A

In the pre-central gyrus of the brain

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4
Q

What is the result of the UMN being located entirely in the CNS?

A

Any upper motoneurone signs indicate a CNS lesion

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5
Q

What does the UMN synapse with?

A

The LMN

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6
Q

What happens to the LMN once it has synapsed with the UMN?

A

It enters the PNS

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7
Q

Where are lesions affecting LMN found?

A

Either in the CNS or the PNS

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8
Q

Where to the LMN come from?

A
  • A large proportion come from the ventral horns of the spinal cord
  • Some come from motonuclei in the brainstem
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9
Q

Which brainstem motonuclei have LMN coming from them?

A
  • The oculomotor nuclei
  • The trochlear nuclei
  • The trigeminal nuclei
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10
Q

Where do the LMN coming from the oculomotor neurones supply?

A

The extraocular muscles

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11
Q

Where do the LMN coming from the trochlear nuclei supply?

A

The superior oblique

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12
Q

Where do the LMN coming from the trigeminal nuclei supply?

A

The muscles of mastication

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13
Q

Describe the relationship between the cranial nerve nuclei and the vertebral columns

A

The cranial nerve nuclei are upwards extensions of the vertebral columns

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14
Q

Where to the LMN have a pivitol role?

A

In the spinal tendon reflexes

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15
Q

How do the spinal tendon reflexes work?

A

When the tendon gets hit, the muscle spindle gets stretched. This information is sent to the dorsal root. In the cord, it then travels down to the ventral root. Here, the sensory fibre synapses with a LMN supplying the muscle, causing contraction of the muscle

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16
Q

What must happen to the antagonist in order for tendon reflexes to work?

A

They antagonists must be inhibited by reciprocal inhibition

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17
Q

How does reciprocal inhibition work?

A

A colateral branch of the sensory neurone coming from the muscle spindle travels down the cord to a lower spinal cord segment. Here, it synapses with an inhibiitory interneurone, which synapses with LMNs, inhibiting their supply to the antagonistic muscle, causing relaxation

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18
Q

What are the signs of LMN damage?

A
  • Weakness
  • Wasting
  • Areflexia or hyporeflexia
  • Hypotonia
  • Fasciculations
  • Fibrillation
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19
Q

When does muscle wasting caused by LMN damage occur?

A

A few weeks after the damage

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20
Q

Why does muscle wasting occur a few weeks after LMN damage?

A

Because LMN provide growth factors that are required for muscle bulk

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21
Q

What are fasciculations?

A

Un-coordinated muscle contraction caused by ectopic ACh receptor expression

22
Q

Are UMN found in the basal ganglia and the cerebellum?

23
Q

What is the main effect of the UMN on the LMN?

A

Inhibitory, via inhibitory interneurones, but they also have a small excitatory projection

24
Q

Where do the UMNs have their cell bodies?

A

Within the motor cortex

25
Where do the UMN go from the motor cortex?
They run through the corona radiatat
26
What is the corona radiata?
A structure with 1000's of UMN axons radiating through the hemispheres
27
Where do UMN run after passing through the corona radiata?
The internal capsule
28
What is the internal capsule?
A white matter structure where all corona radiata axons converge
29
Where does the internal capsule sit?
Between the lentiform nucleus and the thalamus
30
Why is the internal capsule clinically significant?
Because it is frequent affected by stroke, with lacunar infarcts commonly occuring in the internal capsule
31
Describe the topographical organisation of the internal capsule?
In transverse section, the V shaped internal capsule is organised into 3 parts- the anterior limb, the posterior limb, and the genue (point where the capsule bends). The fibres supplying the face are found in the genue, and the parts supplying the upper limbs -\> trunk -\> lower limb are found on the posterior limb (as you get more posterior)
32
Where does the internal capsule join with the midbrain?
At the cerebral peduncles
33
Where do the UMN go from the cerebral peduncles?
The medually pyramids
34
What happens to the UMN in the medullary pyramids?
They move from the ventrally situated medullary pyramids to a lateral position on the opposite side of the brain stem, at a site called the decussation of the pyramids
35
Why is the decussation of the pyramids significant?
Because it explains why the right side of the brain controls the left side of the body, and vice versa
36
What % of corticospinal fibres go into the lateral corticospinal tract?
80%
37
What are the fibres that don't decussate at the medually pyramids called?
The ventral corticospinal tract
38
Where do the fibres in the ventral corticospinal tract cross the midline?
At the level they want to innervate
39
What are the lateral corticospinal tracts important for?
Controlling the distal parts of the limbs
40
What are the ventral corticospinal tracts important for?
Controlling the trunk musculature
41
What phenomenon results from the UMN supply to the face?
Forehead sparing
42
What pathway does forehead sparing occur via?
The corticobulbal pathway
43
What route do UMN take in the corticobulbal pathway?
They pass from their origin in the motor cortex, through the corona radialis and internal capsule, to the facial nerve nuclei.
44
What are the facial nerve nuclei divided into?
Superior and inferior portions
45
What innervation does the superior portion of the facial nerve nuclei recieve?
Bilateral UMN innervation
46
What innervation does the inferior portion of the UMN recieve?
Contralateral UMN innervation
47
What is the superior portion of the facial nerve nuclei dedicated to?
The upper 1/2 of the face
48
What is the inferior portion of the facial nerve nuclei deicated to?
The inferior 1/2 of the face
49
What is the result of the UMN innervation to the facial nerve nuclei in an infarction of the genue of the internal capsule?
The upper 1/2 of the face (the forehead) is spared, as it is recieving bilateral innervation, so you therefore only get contralateral partial facial paralysis
50
What does complete paralyis of half of the face suggest?
Ipsilateral damage to the facial nerve