Upper and Lower Motor Neurones and Pathway Flashcards

1
Q

Where are the cell bodies for upper and lower motor neurones found?

A

Both cell bodies within CNS

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2
Q

What are lower motor neurones? (3)

A

Final common path - when activated will call muscle contraction

Cell body projects from CNS to PNS

Controlled by upper motor neurones - these descend through brainstem/cord and synapse onto them

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3
Q

Where in particular are cell bodies for lower motor neurones found?

A

Ventral horn or cranial nerve nuclei (eg oculomotor nucleus, optic nucleus)

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4
Q

Which neurones are present in spinal reflexes?

A

Lower motor neurone

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5
Q

When are lower motor neurones activated during reflex?

A

Incoming impulses from sensory neurones communicate with muscle spindles

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6
Q

Are lower motor neurones inhibited?

A

Yes - inhibition dominates LMN from descending UPN synapsing onto inhibitory interneurons

They are also inhibited by sensory neurones synapsing onto inhibitory interneurons in spinal levels below during reflexes eg hamstrings in patella reflex

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7
Q

What are ‘primitive’ reflexes?

A

Present in babies (eg palmar grasp) but disappear as baby grows due to maturation of descending upper motor neurone pathways

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8
Q

LMN damage signs and why (5)

A

Weakness - due to denervation

Areflexia/hyporeflexia - due to denervation

Wasting - due to loss of trophic support to the muscle (growth factors) from the LMN across the neuromuscular junction

Hypotonia - loss of muscle activation

Fasciculation - up regulation of muscle nAchR’s to try and compensate for denervation, become extra sensitive to Ach

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9
Q

Where are origin of upper motor neurones found?

A

Pre-central gyrus (primary motor cortex) in frontal lobe

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10
Q

Where do upper motor neurones go and what do they do?

A

Synapse onto LMNs directly/indirectly in the ventral horn or cranial nerve motor nuclei (if supplying head and neck)

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11
Q

What type of neurones are present in basal ganglia and cerebellum?

A

NOT upper motor neurones - damage to them does not cause an UMN syndrome

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12
Q

Overall majority effect of UMNs on LMNs

A

Inhibition - most synapses are inhibitory for neurone, this explains the signs of UMN lesion

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13
Q

Where do the UMNs axons descend from and to - name the structures (9)

A

Corona radiata - lots of axons are sprayed out (fingers on a hand)
(between
Internal capsule - narrowed here (palm of hand)
Cerebral peduncle in midbrain
Pons
Medullary pyramids
Decussate of the pyramids (in caudal medulla - 85% cross over here)
Lateral corticospinal tract
Ventral horn
Synapse onto LMNs

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14
Q

What are the two options for UMN when synapsing?

A

Can synapse direct onto neurone
Or indirect via inhibitory interneurons onto LMNs

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15
Q

Where do the upper motor neurones decussate?

A

Decussation of pyramids - in pyramids of medulla

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16
Q

What do the decussated fibres of the UMNs form vs the others?

A

85% decussate forming lateral corticospinal tract
15% don’t decussate and form ventral corticospinal tract

17
Q

What is the lateral corticospinal tract involved in?

A

Fine motor control of the limbs - primarily the distal extremeties

18
Q

What is the route of the UMNs supplying the face via cranial nerve nuclei?

A

Leave pathway in the brainstem and form the corticobulbar (corticonuclear) tract, which innervate the lower motor neurones in the cranial nerve nuclei

19
Q

What is special about the CN VII the facial nerve nucleus?

A

Split into two halves - one supplies superior half of face and the other supplies inferior half of face

Superior half of nucleus supplying superior half of face receives contralateral supply from primary motor cortex BUT also ipsilateral supply (both hemispheres)

Inferior half of nucleus supplying inferior face only receives contralateral supply from PMC (just contralateral hemisphere)

20
Q

What does the special fact about facial nerve nucleus mean for pts presenting with facial nerve palsy?

A

UPN lesions involving the face = forehead sparing as there is supply from the opposite and ipsilateral hemisphere

Eg in stroke on R hemisphere, will get left facial nerve palsy with forehead sparing on left

But in true facial nerve palsy where facial nerve/nucleus is affected, the whole face will be paralysed (eg on L facial nerve lesion, L half of face will be paralysed as fibres have already decussated)

21
Q

What are the signs of upper motor neurone lesion? and why

A

Weakness - denervation

Hypertonia - loss of descending inhibition (net effect of UMNs on LMNs is inhibition)

Hyperreflexia - overactive reflex arc

Extensor plantar reflexes - loss of descending modulation (toe normally curls under and flexes when foot is stroked, opposite of this happens)

22
Q

What is spinal shock?

A

Phenomenon that occurs in the days following an UMN lesion

Initially flaccid paralysis with areflexia (like LMN lesions)

But then tone increases (hypertonia) and reflexes become exaggerated (hypereflexia)

Related to neuroplasticity of spinal cord

23
Q

What can be damaged in either LMN or UMN lesion?

A

Either cell body or axons of the neurones will cause the signs/lesion

24
Q

What signs do you get when you get UMN and LMN lesion?

A

You get LMN lesion signs as these are needed to transmit UMN signs
LMN signs dominate UMN signs basically