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C&M Neuroanatomy > Week 6 Lecture 13: Descending pathways > Flashcards

Week 6 Lecture 13: Descending pathways Flashcards

1
Q

What does an ascending pathway do? give 2 examples

A

pathways that bring information to the brain e.g DCML, spinothalamic tract

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2
Q

What are the lateral corticospinal and ventral corticospinal tracts responsible for?

A

carrying our descending motor information controlling voluntary movement

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3
Q

What are the features of upper motor neurones?

A
  • originate in the cerebrum and subcortical structures e.g basal ganglia
  • influence LMN activity
  • motor local reflex activity
  • superimpose more complex patterns of movement
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4
Q

How are UMNs that supply the head and neck different?

A

they don’t travel through the spinal cord - they travel a short distance until they reach the cranial nerve nuclei and from there they synapse and contact with LMN which sends its axon via a cranial nerve

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5
Q

Where do LMNs originate?

A
  • from the brainstem if they are going to innervate structures in the head and neck
  • ventral grey horn of spinal cord if they send their axons peripherally to innervate body muscles
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6
Q

How do LMNs leave the spinal cord to go to specific muscle?

A

via the ventral root

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7
Q

What are the 3 main types of descending motor pathways?

A
  1. corticospinal
  2. corticonuclear/ corticobulbar
  3. extrapyramidal
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8
Q

How are the extrapyramidal pathways different to corticonuclear and corticospinal pathways?

A
  • they don’t initiate movement, they fine tune movement
  • don’t take origin in the cortex
  • do not pass through the medullary pyramids (which is why their called extrapyramidal?
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9
Q

Where does the corticospinal tract travel from and to?

A

from cortex to spinal cord

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10
Q

Where does the corticonuclear tract travel from and to?

A

from the cortex to the cranial nerve nuclei

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11
Q

What structures does the corticospinal/corticonuclear tract pass through in the brain before reaching the brainstem/spinal cord?

A
  1. cerebral cortex
  2. pre-central gyrus
  3. internal capsule
  4. brainstem/ spinal cord
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12
Q

Explain the pathway of fibres in the corticonuclear tract

A
  • UMNs originate in pre-central gyrus in cerebral cortex
  • travel through IC
  • stops at specific nucleus of a cranial nerve
  • make contact with LMN and the axon of LMN leaves the brainstem via a specific cranial nerve to innervate muscle
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13
Q

Explain the pathway of fibres in the corticospinal tract

A
  • UMNs originate in pre-central gyrus in cerebral cortex
  • travel through IC
  • makes its way through the medullary pyramids and cross the midline at the decccusation of pyramids
  • fibres enter the ventral grey horn and make contact with LMNs
  • LMNs use specific spinal nerves to innervate skeletal muscle
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14
Q

Where would you find UMNs that innervate the face, arms, trunk and leg in the pre-central gyrus?

A

face is most lateral
arm
trunk
leg is most medial

(somatotopic organisation)

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15
Q

How do descending fibres retain somatotopic representation as they pass through the internal capsule?

A

anterior limb–>
genu –> face
posterior limb –> arm, trunk, leg

from lateral to medial is anterior to posterior on a horizontal section

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16
Q

Fibres of the corticospinal tract use which part of the internal capsule?

A

posterior limb

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17
Q

What is the crus cerebri?

A
  • anterior portion of the cerebral peduncle
  • internal capsule connects to crus cerebri
  • there is continuity between the fibres of the internal capsule and cerebral peduncles
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18
Q

How is somatotopic representation still present at the level of the cerebral peduncle?

A

fibres that innervate the face are most medial and the fibres that innervate the legs are most lateral

19
Q

Explain the corticospinal pathway (8 steps)

A
  1. UMN in the pre central gyrus sends its axon via the posterior limb of the internal capsule
  2. Fibres continue descending - continuous with cerebral peduncles
  3. Fibres then make their way through the ventral pons
  4. In the caudal medulla they connect with the pyramids then cross the midline at the decussation of pyramids
  5. These fibres then join the lateral corticospinal tract: this is contralateral descending motor fibres (started in the opposite hemisphere)
  6. At a specific spinal cord level, the UMN makes contact with a LMN in the ventral grey horn
  7. Exit of the lower motor neuron
  8. OR some fibres do not cross at the pyramids and remain ipsilateral and join the anterior corticospinal tract (15%) and innervates LMNs on both sides of the cord, providing bilateral innervation
20
Q

How can fibres provide contralateral OR bilateral innervation?

A
  1. For limb musculature: 85% of fibres cross at decussation of pyramids, then enter the lateral corticospinal tract –> contralateral innervation

so 85% of UMNs contact cell bodies of LMNs in contralateral ventral grey horns

  1. For axial musculature: 15% of UMNs descend cord ipsilaterally (entering anterior corticospinal tract) –> bilateral innervation
21
Q

Which corticospinal tract is responsible for contralateral innervation?

A

lateral corticospinal tract

22
Q

Which corticospinal tract is responsible for bilateral innervation?

A

anterior corticospinal tract

23
Q

What mechanisms of injury could cause LMN lesions and where would the lesion be?

A

mechanisms: peripheral nerve injury (crush or cut), infection (poliomyelitis), IV disc herniation

occurs due to lesion to ventral gray horn cells of the spinal cord/brainstem or their axons

24
Q

What are the clinical consequences of LMN lesions?

A
  • flaccid (soft/weak) paralysis of muscles involved
  • dimished (hypoeflexia) or absent (areflexia) tendon reflexes at the level of lesion
  • muscle wasting
  • muscle weakness (paresis)/ reduced power
  • hypotonia - decreased muscle tone
  • fasciculation (spontaneous muscle twitches)/ fibrillation (rapid spontaneous muscle contractions)
25
Q

What would be the initial symptoms of damage to UMN only? (due to lesion to cerebral hemisphere or asthey descend down corticospinal tract to lateral white column of SC)

A
  • flaccid paralysis of opposite limbs
  • loss of tendon reflexes
  • motor function slowly recovers (because other pathways appear to ‘take over’ most corticospinal functions) but hypertonia
26
Q

If there was an UMN lesion on one side, why would axial muscle groups be spared?

A

axial muscles are supplied bilaterally - other side can compensate to innervate the muscles

27
Q

How can you detect an UMN lesion?

A

Babinskis sign:

  • sole of foot is stroked with sharp object from front to back
  • normal plantar response is for toes to bend down
  • if there is a UMN lesion and the foot is stroked, the toes extend outwards and separate called the extensor plantar response
28
Q

Why might lesions int he corticonuclear pathway be less severe than in the corticospinal pathway?

A
  • innervations of LMNs is largely bilateral
  • this means that fibres from the right hand side of the pre-central gyrus innervate the right and left side so lesions are not as severe
29
Q

Which head and neck muscles are NOT bilaterally innervated - i.e what are the exceptions?

A
  • lower facial
  • extrinsic tongue muscles
  • under contralateral control
    e. g the right hand side of the pre-central gyrus innervates the left lower facial nucleus
30
Q

What part of the internal capsule do UMNs in the corticonuclear tract travel through?

A

the genu

31
Q

What is the facial colliculus?

A
  • bump at the level of the floor of the 4th ventricle

- motor fibres of the facial nerve loop around the nucleus of the abducens which forms the FC

32
Q

Explain the corticonuclear input to innervate the upper and lower face?

A
  • right side of the pre-central gyrus supplies both sides of the upper face
  • right side of pre-central gyrus supplies contralateral lower face i.e left side
  • fibres travel using facial nerve
33
Q

What is the consequence of unilateral damage to corticonuclear fibres?

A
  • deprives the lower half of the opposite facial motor nucleus of corticonuclear input
  • results in paralysis of the lower half of the face on the opposite side to the lesion
  • paralysis of the whole of one side of the face indicates damage to the facial nerve itself
34
Q

How can you differentiate between an UMN lesion and LMN lesion?

A

with an UMN lesion, the upper face is spared because both hemispheres contribute to movement of the upper face, and the unaffected hemisphere can compensate. with a LMN lesion, the entire face is affected on one side

35
Q

Summarise the features of an UMN lesion

A
  • contralateral lower quadrant weakness
  • angle of mouth
  • opposite side
36
Q

Summarise the features of an LMN lesion

A
  • ipsilateral half of face
  • orbicularis oculi muscle and facial muscles involved
  • unable to close eyes
  • weakness of angle of mouth
  • cannot elevate eyebrows
  • same side
37
Q

Where will the tongue deviate if we lesion the left hypoglossal nerve?

A

the tongue will deviate to the left (ipsilateral to the side of lesion) –> deviates to the same side as lesion

38
Q

Where do you think the tongue will deviate if we lesion the fibres coming from the right side of the internal capsule?

A

The tongue will deviate to the left (contralateral to the lesion) – because the left hypoglossal nerve will not receive innervation from the right pre-central gyrus

39
Q

Summarise the affect of a UMN lesion to the extrinsic tongue?

A

deviation is contralateral to the lesion

40
Q

Summarise the affect of a LMN lesion to the extrinsic tongue?

A

deviation ipsilateral to the lesion

41
Q

What is the reticulospinal pathway and what is its function?

A
  • reticular formation (pons and medulla) to spinal cord

- contributes to fine tuning voluntary movement/breathing/consciousness

42
Q

What is the vestibulospinal pathway and what is its function?

A
  • vestibular nuclei (pons and rostral medulla) to spinal cord
  • controls posture
43
Q

What is the rubrospinal pathway and what is its function?

A
  • red nucleus (midbrain) to spinal cord

- controls muscle tone

C&M Neuroanatomy (44 decks)

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