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Clinical neuroscience > Lecture 9- The motor system- upper motor neurones and descending tracts > Flashcards

Lecture 9- The motor system- upper motor neurones and descending tracts Flashcards

1
Q

Major motor tract which descends through the spinal cord and controls activity of LMN

A

The corticospinal tract

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2
Q

The corticospinal tract is responsible for

A
  • Voluntary, precise movements
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3
Q

upper motor neurones supplying the upper limb

A
  • UMN originates in lateral aspect of the motor cortex (homunculus)
  • Axon of the UMN passes down through the corona radiata and into the internal capsule
  • It then descends down through the midbrain via the cerebral peduncle, then through the pons and then to the medulla
  • The medulla has medullary pyramids which carry corticospinal axons on their way down into the spinal cord
  • Once the corticospinal axons have left the medullary pyramids the axons decussates and descends via the lateral corticospinal tract in the spinal cord where it synapses with a lower motor neurone and supplies muscles in the upper limb
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4
Q

Upper motor neurone supplying the lower limb

A
  • UMN originates in medial aspect of the motor cortex (homunculus)
  • Axon of the UMN passes down through the corona radiata and into the internal capsule (discrete white matter pathway running between the thalamus and lentiform nucleus)
  • It then descends down through the midbrain via the cerebral peduncle, then through the pons and then to the medulla
  • The medulla has medullary pyramids which carry corticospinal axons on their way down into the spinal cord
  • Once the corticospinal axons have left the medullary pyramids the axons decussates and descends via the lateral corticospinal tract in the spinal cord where it synapses with a lower motor neurone and supplies muscles in the lower limb
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5
Q

internal capsule

A

discrete white matter pathway running between the thalamus and lentiform nucleus

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6
Q

somatotopic organisation of the lateral corticospinal tract

A
  • Axons destined for the upper limb are found more medially
    • Need upper limbs axons more medially so they can peel off and synapse in the ventral horn earlier on (as to not waste axon and myelin)
  • Axons destined for the lower limb are found more laterally
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7
Q

Not all axons cross at the decussation of the pyramids

A

15% remain ipsilateral and run down through the ventral corticospinal tract and cross over at the level where their LMN is

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8
Q

summary of the corticospinal system

A
  • System originates in the primary motor cortex
    • Lower limb= medial
    • Upper limb- laterally
  • Pathway descends through the corona radiata and condenses further to form the internal capsule
    • Fibres for the upper limb are found most anteriorly within the internal capsule
    • Fibres for the lower limb are found most posteriorly within the internal capsule
  • As we descend further we enter the brainstem via the cerebral peduncle (ears of mini mouse) of the midbrain
    • A number of fibres will leave the corticospinal system and synapsing within the brainstem (fibres of the corticonuclear pathway which supply LMN present within the cranial nerve nuclei)
  • The pathway then descend further through the ventral pons and then condense to form the medullary pyramids
    • Contain fibres of the corticospinal system which have not yet decussated
  • At the decussation of the pyramids the corticospinal fibres cross the midline forming the lateral corticospinal tract
    • Not all will cross the midline, some will run ipsilateral (15%)
    • These ipsilateral corticospinal fibres will form the ventral corticospinal tract
      • Only when they get to the level of the lower motor neurone will they synapse will they cross the midline
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9
Q

Fibres for the upper limb are found most …….. within the internal capsule

A

anteriorly

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10
Q

Fibres for the lower limb are found most…….. within the internal capsule

A

posteriorly

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11
Q

A number of fibres will leave the corticospinal system, synapsing within the brainstem and become the

A

corticonuclear pathway which supply LMN present within the cranial nerve nuclei

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12
Q

when do most corticospinal fibres decussate

A

at the decussation of the pyramis forming the lateral corticopsinal tract

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13
Q

what happens to the fibres which dont decussate after the medullary pyramids

A

these will stay ipsilateral forming the ventral corticospinal tract

  • Only when they get to the level of the lower motor neurone will they synapse will they cross the midline
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14
Q

Cortical spinal system is composed of 2 separate components:

A

Lateral corticospinal tract and Ventral corticospinal tract

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15
Q

features of the Lateral corticospinal tract

A
  • Much larger
  • Function: innervating muscle of the distal parts of the extremities e.g. arm, hand and leg, foot
    • E.g. fine movements
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16
Q

features of the Ventral (anterior) corticospinal tract

A
  • Much smaller and crosses at the level of the lower motor neurone
  • Function: innervating muscle of the proximal parts of the extremities e.g. limb girdle
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17
Q

Somatotopic organisation of the lateral corticospinal tract

A
  • Upper limbs = most medially
  • Lower limbs= most laterally
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18
Q

corticonuclear pathways

A
  • Cranial nerves can contain the axons of lower motor fibres
  • Corresponding upper motor neurones descend from the primary motor cortex and synapse upon on cranial nerve motor nuclei (e.g. trigeminal motor nucleus)
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19
Q

corticonuclear pathway of the trigeminal

A
  • Contains the axons of lower motor neurones
  • Cell bodies of lower motor neurones are found in the pons in the trigeminal motor nucleus
  • These LMN follow the course of the trigeminal nerve to muscles of mastication (mandibular branch)
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20
Q

cranial nerve motor nuclei (cell bodies of cranial nerve LMN) receive ……… innervation from the cerebral cortex

A

bilteralteral

  • Means that if there was a stroke in one hemisphere destroying one UMN, both nuclei would still have some innervation
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21
Q

the trigeminal nerve and bilateral innervation via the corticonuclear pathway

A

The trigeminal nerve

  • Trigeminal motor nuclei (collection of cell bodies of LMN that will distribute along the mandibular branch of the trigeminal nerve and innervate muscles of mastication)
  • How upper motor neurones stimulate lower motor neurones running alongside CNs:
    • Bilateral innervation
    • UMN descends from the primary motor cortex and synapses with LMN in the trigeminal motor nucleus on the ipsilateral side
    • There will also be projections from the same UMN that will innervate the contralateral trigeminal motor nuclei
    • Also have projections coming from the other cerebral hemisphere (contralateral and ipsilateral innervation
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22
Q

Effect on muscles of mastication if stroke affecting one hemisphere?

A

Although one UMN would be destroyed, each nuclei would still have some innervation i.e. from the contralateral UMN–> therefore muscles of mastication can still be used–> survival measure

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23
Q

the facial nerve and bilateral innervation

A
  • Facial motor nucleus (collection of cell bodies of LMN that will distribute along the facial nerve and innervate muscles of facial expression)
    • Split into two halves
      • Upper half- upper half of the face
        • Bilateral innervation
          • Think – stroke = forehead sparing
      • Lower half- lower half of the face
        • Only contralateral innervation
          • Stroke pts will have much worse set of signs affecting lower half than upper half of face
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24
Q

vagus nerve and bilateral innervation

A
  • Nucleus ambiguous (collection of cell bodies of LMN that will distribute along the vagus nerve and innervates muscles of the vocal cords and pharynx)
  • Bilateral innervation
    • Required because nucleus ambiguous controls swallowing necessary for survival
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25
Q

The internal capsule

A
  • White matter tract (not really a capsule) between the thalamus (medially) and the lentiform nucleus (laterally -globus pallidus and putamen) and caudate nucleus (laterally)
  • Basically the condensation of the corona radiata
26
Q

types of pathways which run through the internal capsule

A

Bidirectional pathway

  • Descending motor pathways (UMN)
  • Ascending sensory pathways (third order sensory neurones)
27
Q

Structure of the internal capsule

A
  • anterior limb
  • posterior limb
  • Genu (convergence of the anterior and posterior limb)
28
Q

posterior limb contains

A
  • Contains descending motor fibres (UMN axons)- Corticospinal tract
    • From anterior to posterior
      • Arms
      • Trunk
      • Lower limbs
29
Q

Genu (knee) contains

A

UMN supplying facial muscles are found at the genu- contains the corticobulbar (corticonuclear) tract–> CN 7

30
Q

Within the internal capsule is a discrete region called the thalamic radiation (both anterior and posterior) (light brown)

A
  • Posterior thalamic radiation
    • Contains 3rd order ascending sensory fibres form part of the somatosensory system
  • Anterior thalamic radiation
    • Contains projections going from the thalamus to the frontal lobes (not directly related to sensation)
31
Q

Outside regions of the internal capsule (dark brown) called corticofugal fibres

A
  • Go from the cortex away from the brain
  • Don’t worry to much about these
32
Q

midbrain mickey mouse anatomical orientation

A
33
Q

midbrain can be roated 180 degrees to make it more memorable

  • label
A

mickey mouse

34
Q

Mickey mouse ears = Cerebral peduncles

A
  • Connect the cerebral hemispheres to the midbrain
  • Contain descending motor fibres which will enter the corticospinal tract
  • Important motor structures
35
Q
  • Eyes = red nucleus
A
  • In fresh brain appears red
  • Involved in motor control
  • If damaged= corse tremor
  • Important landmark
36
Q
  • Eyebrows= Substantia nigra
A
  • Appears dark normally
  • produces dopamine for nigrostriatal pathway
37
Q
  • Tears = medial lemniscus
A
  • (part of dorsal column / spinothalamic system)
    • Parts of the sensory system
    • Ascending sensory fibres on their way to the thalamus
38
Q
  • Mouth= cerebral aqueduct
A

Channel connecting the third and fourth ventricles

39
Q
  • Lips= periaqueductal grey matter
A
  • Pain regulation
  • Micturition
40
Q
  • Nose= oculomotor nucleus
A
  • Cell bodies of LMN
  • Edwinger Westphal nucleus (cell bodies of parasympathetic neurones)
  • Fibres coming off the nose= fibres of the oculomotor
41
Q
  • Double chin= superior colliculus
A

Reflex actions related to the visual system

42
Q

summarise the motor neurone route

A
  • Cell body within the primary motor cortex
  • Sends axon down via the corticospinal tract/ Corticonuclear tract where it synapses on the cell body of a lower motor neurone
  • LMN then send sits axon out through the peripheral nervous system until it reaches its target muscle
43
Q

causes of lesions to UMN

A
  • Stroke
  • Spinal cord injury
  • Motor neurone disease
44
Q

causes of lesions to LMN

A
  • Peripheral neuropathy
  • Motor neurone disease
  • Spinal cord injury
  • Disc prolapses
45
Q

clinical features of UMN and LMN lesions

A
46
Q

why is power, tone and reflexes decreased in LMN lesions

A

muscle is deprived of nervous supply- No ACH release therefore wont move

–> atrophy ‘dont use it lose it’

47
Q

why is power decreased in UMN lesion

A

because LMN deprived of input

48
Q

why does tone increase in UMN lesion

A

most influence of UMN is inhibitory

therefore if lesion, inhibition will be lost, therefore amount of activity of LMN increases

49
Q

why do reflexes increase in UMN lesions

A
  1. intitial phase of decreased reflex activity (spinal shock)
  2. however after some time reflexes increase due to loss of descending inhibition
  3. therefore reflexes more reactive
50
Q

Fasciculations and fibrillations

*

A

Both features seen in LMN lesion (pathophysiology not fully understood)

  • Fasciculations
    • Visible
    • May be caused by aberrant activity in the distal portion of the LMN axon
      • Fibrillations
    • Only detectable using electromyography
    • May be caused by increased sensitivity of muscles fibres to ACh (changes in localisation of nicotinic receptors)
51
Q

why does atrophy occur in all LMN and some UMN lesions

A
  • Growth factors (as well as AP) are delivered to the muscle via the LMN0
  • If you damage the LMN nucleus or transect the axon you decrease the amount of GF getting to the muscle–> atrophy
52
Q
  • Spasticity= due to
A

hypertonicity

53
Q

Monosynaptic reflex arc can help us understand pahtophysiology of hypertonia and spaticity

e.g. in a healthy person

A
  • Sensory neurone receptor within spindle brings info into cord via the dorsal root ganglion
  • Enters ventral horn and synapses with lower motor neurone
    • Lower motor neurone also synapses with excitatory corticospinal tract neurone
      • Important for voluntary movement in this particular muscle i.e. you decide to move a muscle and it cause that motor neurone to cause muscle movement
      • Also other tracts will descend down the cord and terminate on inhibitory interneurons which inhibits the lower motor neurone
        • Most of the time it is in a state of inhibition
        • Controlled by the cortex
  • Motor neurone sends axons via the ventral root to the muscle of interest
  • Muscle twitch
54
Q

Monosynaptic reflex arc can help us understand pahtophysiology of hypertonia and spaticity

e.g. in someone who has had a stroke

A
  • Cortical lesion e.g. stroke destroys excitatory corticospinal tracts and the descending inhibitory inputs
  • Initially lower motor neurone will go into a state of ‘spinal shock’
    • Frequency of AP running along LMN will decrease significantly
    • Therefore tone of muscle supplied by this LMN will increase
  • As time goes on the LMN starts to wake up
    • Realises it still has the excitatory input of the muscle spindles (sensory afferents)
    • However, loss of CST- therefore no voluntary movements
    • Lost descending inhibitory influences
    • Therefore breaks have been taken off LMN, therefore it will fire off more frequent AP, leading to more frequent muscle contracts = increased muscle tone
      • Loss of net inhibition therefore increase excitation
55
Q

why if someone has a strpke affecting the upper limb, will the arm and hand be held in a flexed position

A
  • The flexor and extender muscles will be affected equally, but in the upper limb the flexors are more powerful
    • Flexed arm, wrist and fingers (think cerebral palsy)
56
Q

Following the diffusion of water pathway along the corticospinal tract

A
  • can see that motor cortex axon found mostly in the precentral gyrus
  • yellow fibres= trunk
  • blue fibres= lower limb
  • red fibres= face
57
Q

why do lacunar infarcts affect the brain, upper and lower limb equally

A
  • This is due to fibres from the corticospinal tract showing less somatotopic organisation in the internal capsulee.g. face and lower limb fibres mixes
58
Q
A
59
Q

Visualising the internal capsule

A
60
Q

Basal ganglia model

A
  • Key components
    • Thalamus
    • Internal capsule
    • Lentiform nucleus
      • Putamen- superficial
        • Putamen and caudate nucleus (C shaped) closely related
        • Connected to each other- same ancestral nucleus  together referred to as the striatum
        • The striatum receives input from the cortex
      • Globus pallidus- further subdivided
        • External
        • Internal
        • Sends output back to the cortex via the thalamus
    • Substantia nigra (part of the midbrain)
      • Dopaminergic neurones which sends axons up to striatum (putamen)via the Nigro striatal pathways
61
Q

somatotopic organisation in the ventral horn of the spinal cord

A
  • ventral (anterior) cotricospinal tract supplying the axial musculature and limb gurdles
  • lateral corticospinal tract supplying the intrinsic limb muscles and distal portion of the limbs

Clinical neuroscience (30 decks)

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