S5) The Motor System Flashcards

1
Q

What is a lower motor neurone?

A

A lower motor neuron (LMN) is a multipolar neuron which connects the upper motor neurone (UMN) to the skeletal muscle it innervates

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2
Q

Where is a lower motor neurone found?

A

A lower motor neurone is located in either the ventral horn of the spinal cord or the cranial nerve nuclei of the brainstem

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3
Q

What do lower motor neurones do?

A

LMNs participate in spinal reflexes, particularly the deep tendon reflexes

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4
Q

What are primitive spinal reflexes and when are they seen?

A

Primitive spinal reflexes are reflexes which exist in babies but disappear as a baby grows due to maturation of descending upper motor neurone pathways

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5
Q

LMNs can be activated and inhibited.

Describe how they are activated

A

LMNs are activated by incoming impulses from sensory neurones that communicate with muscle spindles (muscle stretch reflex)

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6
Q

Describe the role of the interneuron in the reflex arc at the knee

A
  • Inhibitory interneuron inhibits the contraction of the flexor hamstring muscles
  • Stimulatory interneuron stimulates the contraction of the extensor muscles
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7
Q

What are the five principle features of LMN damage?

A
  • Fasciculations
  • Muscle atrophy
  • Hyporeflexia/ areflexia
  • Hypotonia/ atonia
  • Flaccid muscle weakness or paralysis
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8
Q

Explain the pathophysiology of the fasciculations seen in LMN damage

A

Fasciculations caused by uncoordinated muscle contractions due to up-regulation of muscle nAChRs to try to compensate for damaged motor neurones (denervation)

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9
Q

Explain the pathophysiology of the muscle atrophy seen in LMN damage

A

Muscle atrophy is caused by the loss of neurotrophic growth factors from the α-motor neuron to the muscle membrane (across neuromuscular junction)

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10
Q

Explain the pathophysiology of the hyporeflexia seen in LMN damage

A

Hyporeflexia/areflexia caused by disruption of the efferent portion of the reflex arc leading to decreased/absent reflexes

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11
Q

Explain the pathophysiology of the hypotonia seen in LMN damage

A

Hypotonia / atonia caused by loss of muscle activation due to loss of α-motor neurons

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12
Q

Explain the pathophysiology of the muscle weakness seen in LMN damage

A

Flaccid muscle weakness due to α-motor neuron damage, muscles receive a weakened/absent signal to contract

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13
Q

What is an upper motor neurone?

A

An upper motor neuron is a neuron whose cell body originates in the cerebral cortex or brainstem and terminates within the brainstem or spinal cord

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14
Q

Where is an upper motor neurone found?

A

An upper motor neuron originates either in the primary motor cortex (pre-central gyrus) / in the brain stem (CNS)

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15
Q

Where in the CNS are upper motor neurones absent?

A
  • Basal ganglia
  • Cerebellum

Hence, damage to these structures does not cause an UMN syndrome

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16
Q

What effect do UMNs have on LMNs?

A

The net effect of UMNs on LMNs is inhibitory (inhibition > stimulation)

17
Q

Describe the 8 structures which the descending axons of UMNs pass through

A

⇒ Corona radiata

⇒ Internal capsule

⇒ Cerebral peduncle in the midbrain

⇒ Pons

⇒ Medullary pyramids

⇒ Decussation of the pyramids (in the caudal medulla)

⇒ Ventral horn

⇒ Synapse (directly/via inhibitory interneurones) on LMNs

18
Q

What is the role of the lateral corticospinal tract?

A

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

19
Q

Describe the anatomical course of UMNs that innervate facial structures (i.e. structures innervated by cranial nerves not spinal nerves)

A

UMNs that supply facial structures leave the pathway in the brainstem and form the corticobulbar tract (aka corticonuclear tract) which innervates LMNs in the cranial nerve motor nuclei

20
Q

Explain how the facial motor nucleus differs from a usual cranial nerve motor nucleus

A

The facial motor nucleus is split into two halves – one supplies the superior face (mostly occipitofrontalis) and one the inferior face (most of the remaining muscles)

21
Q

Explain how the facial motor nucleus functions

A
  • The part of the facial motor nucleus that supplies the upper half of the face receives UMNs from both hemispheres
  • The part of the facial motor nucleus that supplies the lower face only receives a contralateral UMN input
22
Q

Explain how UMN lesions differ from true facial nerve palsies

A
  • UMN lesions involving the face will spare the forehead
  • True facial nerve palsies will affect all of the muscles of facial expression
23
Q

What are the four principle features of UMN damage?

A

When UMNs are damaged, the following signs are evident in the parts of the body supplied by the relevant UMNs:

  • Weakness
  • Hypertonia
  • Hyperreflexia
  • Extensor plantar reflexes
24
Q

Explain the pathophysiology of the weakness seen in UMN damage

A

Weakness due to loss of direct excitatory inputs onto LMNs from UMNs

25
Q

Explain the pathophysiology of the hypertonia seen in UMN damage

A

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

26
Q

Explain the pathophysiology of the hyperreflexia seen in UMN damage

A

Hyperreflexia due to loss of descending inhibition (an overactive reflex arc)

27
Q

Explain the pathophysiology of the extensor plantar reflexes seen in UMN damage

A

Extensor plantar reflexes due to the loss of the descending modulation of spinal reflexes (reversion to the situation in a baby)

28
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, following by hypertonia and thereafter hyperreflexia
29
Q

A motor homunculus represents a map of brain areas dedicated to motor processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.

Describe the layout of the motor homunculus

A
30
Q

A sensory homunculus represents a map of brain areas dedicated to sensory processing for different parts of the body. Sensory and/or motor loss can spread due to homunculus.

Describe the layout of the sensory homunculus

A