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Semester 4 - Clinical Neuroscience > 7. Motor system > Flashcards

7. Motor system Flashcards

1
Q

What is the main tract for the motor system?

A

Lateral corticospinal tract

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2
Q

what are lower motor neurones and what can activate them

A

They are the ‘final common path’, and when activated will cause muscle contraction

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3
Q

what are LMNs controlled by?

A

controlled by upper motor neurones, which descend through the cord or brainstem and synapse on LMNs

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4
Q

where are the cell bodies of LMNs found?

A

ventral horn and in cranial nerve motor nuclei (brainstem)(oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus etc)

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5
Q

Where are lower motor neurones found?

A

Both CNS and PNS

  • Cell body and first part of the axons is found in the CNS (projecting out from the ventral horn)
  • Rest of the axons in the PNS
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6
Q

Considering where LMNs are located, lesions where can affect them?

A

Lesions in the PNS or CNS can affect the lower motor neurones

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7
Q

what do LMN participate in?

A

spinal reflexes, particularly the deep tendon reflexe

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8
Q

describe what activates and inhibits LMNs

A

They are typically activated by incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex), but can also be inhibited (best example is inhibition of antagonist muscles such as hamstrings following patellar reflex activation)

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9
Q

give examples of ‘Primitive’ spinal reflexes that exist in babies

A

up going plantars, Moro reflex and palmar grasp

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10
Q

why do the ‘Primitive’ spinal reflexes that exist in babies disappear?

A

due to maturation of descending upper motor neurone pathways which are inhibitory on the LMN

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11
Q

Describe the monosynaptic reflex.

A
  • stretch of muscle spindle
  • activation of afferent first order sensory fibres
  • synapse with LMN in ventral horn
  • activation of LMN causing contraction reflex
  • sensory fibres also ascend/descend and synapse with inhibitory interneurones which inhibit LMN of the antagonistic muscle causing relaxation
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12
Q

what is the influence of the brain in reflexes?

A

Inputs descending from brain have modulatory role on reflexes and if these modulatory fibres are damaged eg in a stroke, the way these reflexes manifest themselves may be changes.

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13
Q

What is the main action of descending UMN on LMN?

A

major inhibitory role but also some excitatory effect.

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14
Q

what signs can be seen in the muscles supplied by a damaged LMN?

A

o Weakness (due to denervation) (reduced power)
o Areflexia (due to denervation)
o Wasting
o Hypotonia (due to loss of muscle activation)
o flaccid
o Fasciculation (due to up-regulation of muscle nAChRs to try to compensate for denervation)

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15
Q

Why does wasting/atrophy occur in LMN lesions?

A

due to loss of trophic support to the muscle from the LMN across the neuromuscular junction

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16
Q

Define fasciculation.

A

visible uncoordinated contractions

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17
Q

What is the net innervation of the LMNs?

A

Net inhibition of the LMNs by UMNs via inhibitory interneurones

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18
Q

where are upper motor neurones found?

A

In the CNS

  • cell body in the primary motor cortex
  • axons projecting to the spinal cord and synapse onto LMNs directly (or indirectly) in the ventral horn or cranial nerve motor nuclei
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19
Q

are neurones in the basal ganglia and cerebellum considered to be UMN?

A

NO - damage to these structures does not cause an UMN syndrome, but something completely different

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20
Q

through which structures do UMN descend through from the PMC?

A
  1. Corona radiata
  2. Internal capsule
  3. Cerebral peduncle in the midbrain
  4. Pons
  5. Medullary pyramids
  6. Decussation of the pyramids (in the caudal medulla)
  7. Lateral corticospinal tract (in the lateral funiculus of the cord)
  8. Ventral horn
  9. Synapse (directly but usual indirectly via inhibitory interneurones) on LMNs
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21
Q

what is The lateral corticospinal tract involved in

A

involved with fine motor control in the limbs, primarily the distal extremities (but all of limb can be affected by a UMN lesion)

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22
Q

what is different in the pathway of UMNs that supply facial structures?

A

UMNs that supply facial structures (i.e. structures innervated by cranial nerves not spinal nerves) leave the pathway in the brainstem and form the corticobulbar (aka the corticonuclear) tract, which innervates LMNs in the cranial nerve motor nuclei

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23
Q

List the cranial nerve motor nuclei

A

trigeminal motor nucleus
facial motor nucleus
nucleus ambiguous

and CN 3, 4, 6, 9, 10, 11, 12

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24
Q

what is special about the facial motor nucleus?

A

The facial motor nucleus is a special case of a cranial nerve motor nucleus, in that it is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)

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25
Q

what is the significance of the splitting of facial motor nucleus into two halves in an UMN lesion?

A

o The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres, whereas the part that supplies the lower face only receives a contralateral UMN input
3. Hence UMN lesions involving the face will spare the forehead (as opposed to true facial nerve palsies which affect all of the muscles of facial expression)

26
Q

Where do the UMNs deccusate?

A

At the medullary pyramids

27
Q

What percentage of UMNs deccusate at the medullary pyramids?

A

85%

28
Q

What tract do the UMNs that don’t deccusate at medullary pyramid form?

A

Ventral corticospinal tract - remain ipsilateral and descend in the ventral
funiculus

29
Q

What muscles are the ventral corticospinal tracts important for controlling?

A

Proximal parts of muscles and postural muscles (muscles of the trunk)

30
Q

Where do UMNs of the ventral corticospinal tract deccusate?

A

At the spinal level they innervate

31
Q

What are the cerebral peduncles?

A

White matter on ventral midbrain, which contains Axons of the UMNs.
Peduncle: connects a peduncle to the brainstem (cerebral or cerebellar)

32
Q

What is the corticonuclear tract?

A

Composed of the upper motor neurons of the cranial nerves

33
Q

Where do the UMN of the corticonuclear tract terminate?

A

In the brain stem (at the CN nuclei)

34
Q

Do the UMNs in the corticonuclear tract deccusate?

A

Some do, some don’t, some have both ipsilateral and contralateral fibres

35
Q

Describe the UMN innervation to the facial nerve nuclei.

A
  • Upper part of the facial nerve nuclei get innervation from motor cortex of both hemispheres
  • Lower part of the facial nerve nuclei get innervation only from the contralateral motor cortex
36
Q

What is the deficit in a lesion to the UMNs of the facial nerve?

A

‘Forehead sparing’

  • forehead gets innervation from both sides, so no paralysis of the forehead
  • contralateral side of the lower part of the face is paralysed
37
Q

describe the close affiliation between spinal cord and brainstem

A

dorsal horn extends into brainstem to form a series of sensory nuclei

ventral horn extends into Brainstem to form a series of motor nuclei

38
Q

how are axons destined for upper limb and lower limb positioned in the lateral corticospinal tract?

A

axons for upper limb found more medially and for lower limb found more laterally

39
Q

What are the signs of UMN lesion?

A
  1. Weakness (due to loss of direct excitatory inputs onto LMNs from UMNs)
  2. Hypertonia (due to loss of descending inhibition – remember that the net effect of UMNs on LMNs is inhibition)
  3. Hyperreflexia (same as hypertonia – an overactive reflex arc)
  4. Extensor plantar reflexes (this is a reversion to the situation in a baby, due to loss of descending modulation of spinal reflexes)
  5. spasticity - increased rigidity so increased muscle tone
  6. small amount of atrophy
40
Q

what is spinal shock?

A

Spinal shock is a phenomenon that occurs in the days immediately following a UMN
lesion. Initially there is flaccid paralysis with areflexia (like in LMN lesions) but then tone increases (becoming hypertonia) and reflexes become exaggerated (hyperreflexia). The mechanism of this is unclear, but is related to neuroplasticity in the spinal cord

41
Q

In an UMN lesion, why is the hypereflexia and hypertonia?

A

LMN are. normally held in an inhibitory state due to inhibitory influence of UMN so only stimulated when excitatory input form UMN or sensory neurone. when UMN are damaged, there is a loss of inhibitory and excitatory influence but there is continued unapposed excitatory input from afferent sensory neurones which leads to increased tone and hypereflexia.

42
Q

why is there a small amount of atrophy in UMN lesion?

A

LMN are still able to transport growth factors to muscle fibres but disuse atrophy as lack of voluntary movement induced by UMN

43
Q

in and UMN lesion explain why the arm may be held in a flexed position?

A

all muscles are effected but flexors are stronger in upper limb - vice versa for lower limb

44
Q

What is the internal capsule?

A

A bidirectional white matter pathway connecting the cerebral hemisphere with the rest of the CNS

45
Q

what is the internal capsule superiorly and inferiorly continues with?

A

o Superiorly continuous with the corona radiata

o Inferiorly continuous with the cerebral peduncle of the midbrain

46
Q

what two structures is the internal capsule found between?

A

thalamus medially and lentiform nucleus laterally

47
Q

what does the internal capsule contain?

A

Primarily contains descending axons of upper motor neurones (condensation of corona radiata)but also
has ascending axons of third order sensory neurones

48
Q

what are the three anatomical divisions visible on a transverse section of the internal capsule

A

o Anterior limb - between lentiform nucleus and caudate nucleus
o Genu (knee)
o Posterior limb - between the lentiform nucleus and the thalamus

49
Q

What are the 2 parts of the lentiform nucleus?

A

Putamen and globus pallidus

50
Q

what does the anterior limb of internal capsule contain?

A

Contains axons connecting the motor cortex with the

cerebellum

51
Q

what is the genu of the internal capsule and what does it contain?

A
  • The ‘bend’ in the internal capsule

* Contains axons of upper motor neurones supplying the face

52
Q

what does the posterior limb of internal capsule contain?

A

• Contains axons of upper motor neurones supplying upper limb, trunk and lower in that order from anterior to posterior
• Also contains third order sensory axons connecting thalamus to postcentral gyrus
o Like the UMN axons, these fibres run in the order fac0arm-trunk-leg from front to back

53
Q

which arteries supply the internal capsule?

A

lenticulostriate arteries

54
Q

describe the spinal cord at the cervical enlargement

A

• The cord is wide at the cervical enlargement
o This correlates with the presence of the brachial
plexus at these levels
o There are many LMN cell bodies and second order
sensory neurone cell bodies at these levels to
supply the upper limbs

55
Q

describe the spinal cord at the thoracic levels

A

• Narrow at the thoracic levels
o Narrow since there are relatively few LMN cell
bodies and second order sensory cell bodies due to relatively small dermatomes and myotomes at thoracic levels
o However, remember that these levels of the cord (as well as down to about L2) have the lateral horn which contains sympathetic preganglionic cell bodies)

56
Q

describe the spinal cord at the lumbosacral enlargemen

A

• Wide at the lumbosacral enlargement
o This correlates with the presence of the lumbosacral plexus
o There are many LMN cell bodies and second order sensory neurone cell bodies at these levels to supply the lower limbs

57
Q

describe the spinal cord at the sacral levels

A

Narrow at the lower sacral levels (aka the conus medullaris)
o Relatively few muscles that need supplying and small area of skin
o However, don’t forget that S2-S4 contains parasympathetic preganglionic cell bodies (in a region homologous to the lateral horn) as well as the cell bodies of LMNs that distribute to the perineum in the pudendal nerve

58
Q

what does the amount of grey matter at each level depend on?

A

upon the presence/absence of limbs

59
Q

what does the amount of white depend on?

A

o At the top of the cord (C1) there is the maximum amount of white matter since it contains UMN axons yet to be distributed as well as the convergence of all sensory axons from levels below
▪ As we descend the cord the UMN axons are distributed to LMNs in the cord grey matter (hence as we descend number of UMN axons decreases)
▪ As e ascend the cord from the bottom sensory axons are gradually added
▪ The net effect of the above is a gradual increase in total white matter as we ascend the cord

60
Q

if the dorsal and ventral horns can be thought of as cell
columns running the length of the cord and Within these columns we have subdivisions containing groups of LMN cell bodies, which cell bodies will be found most medially?

A

o Sitting most laterally in the ventral horn are LMNs supplying distal muscles
▪ This makes sense as they sit closest to the lateral CST which supplies distal muscles

61
Q

if the dorsal and ventral horns can be thought of as cell
columns running the length of the cord and Within these columns we have subdivisions containing groups of LMN cell bodies, which cell bodies will be found most laterally?

A

o Sitting most medially in the ventral horn are LMNs supplying proximal muscles
▪ This makes sense as they sit closest to the anterior/ventral CST which supplies proximal muscles

Semester 4 - Clinical Neuroscience (19 decks)

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