Motor Neurones Flashcards

1
Q

What are motor neurones

A

Nerve cell that provides efferent response of CNS

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2
Q

How do you classify motor neurones

A

Upper motor neurones

Lower motor neurones

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3
Q

Where are the cell bodies of UMN located

A

In the brain:
Cerebral cortex - pyramidal motor neurones/cortical efferents

Sub-cortical areas - extra-pyramidal motor neurones/brainstem and bulbar efferents

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4
Q

Where are cell bodies of LMN located

A

Spinal cord: ventral horn lamina IX

Brainstem: cranial nerve nuclei

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5
Q

What are the key properties of LMNs

A

Have cell body in CNS - so CNS lesions can present with LMN signs
Project into peripheral nervous system
Spinal LMNs innervate skeletal muscle (link UMN w muscle)
Cranial nerve LMNs innervate eyes, face, tongue
Receive descending inhibition from cortex by UMNs

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6
Q

What are the signs of LMN lesion

A
Paralysis 
Weakness
Wasting
Hyporeflexia
Hypotonia 
Fasciculations
Fibrillations 
Negative Babinskis sign
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7
Q

What is fasciculation

A

Rapid Uncoordinated contraction of group of muscle fibres, that is visible
Caused by increased expression of nAChR to compensate for lack of innervation

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8
Q

What is fibrillation

A

Rapid uncoordinated contraction of individual muscle fibre, not visible

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9
Q

Why do you get hypotonia with LMN lesion

A

LMNs send tonic stimulatory signal to muscle

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10
Q

Why do you get hyporeflexia in LMN lesions

A

LMNs are the efferent fibre of spinal reflexes

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11
Q

What is a spinal reflex

What are the components of spinal reflex arc

A
Involuntary and automatic reaction to stimulus that does not require the brain 
Receptor (in skin, muscle, tendon) 
Afferent fibre (to posterior horn)
Integration centre (lamina IX) 
Efferent fibre (LMN, anterior horn to effector) 
Effector (skeletal muscle)
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12
Q

What is a stretch reflex

A

Monosynaptic reflex of muscle contraction in response to stretch

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13
Q

List the steps of patellar reflex

A
  1. Muscle spindle detects stretch in muscle fibre (stretch receptors that detect change in length of muscle)
  2. Signal transmitted down afferent fibres to L3 L4 spinal roots
  3. Afferent fibres synapse with efferent motor neurones in spinal cord
  4. Motor neurone causes contraction of quadriceps muscle - knee extension
  5. Afferent fibres descend in spinal cord to level of antagonist muscle innervation. Stimulate inhibitory interneurones to inhibit motor neurone of antagonist muscle. This inhibits tonic stimulation of muscle and facilitates knee extension.
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14
Q

What is withdrawal reflex

List steps of the plantar reflex

A

Spinal reflex to withdraw part of body from noxious stimuli

  1. Nociceptor of S1 dermatome stimulated
  2. Afferent fibres enter nerve root L5 S1 and synapse with motor neurones
  3. Motor neurones of L5 S1 nerve roots elicit plantar flexion response
  4. There is descending pyramidal control of reflex arc to inhibit extensor response. Loss of descending inhibition in UMNL causes extensor/dorsiflexion - +ve Babinski sign
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15
Q

What are the key properties of UMNs

A

Cell body in CNS: cortex, brainstem
Located entirely within CNS: UMNL always indicates CNS pathology
Synapse with LMNs in spinal cord: descending tracts are all UMNs
Net Inhibitory effect on LMNs: majority synapse via inhibitory interneurones

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16
Q

What are the signs of UMN lesion

A
Weakness
Hypertonia
Hyperreflexia 
Spasticity
Clasp knife reflex 
\+ve Babinski sign
17
Q

Why do you get hypertonia in UMNL

A

Loss of descending tonic inhibition of LMN, continuous contraction

18
Q

What is spasticity

A

Combination of skeletal muscle paralysis, hyperreflexia, hypertonia
Muscles are fixed in position by the more powerful muscle of antagonist pair : UL flexed LL extended

19
Q

Why do you get hyperreflexia in UMNL

A

Loss of descending inhibition of LMNs, LMNs become hyperexcitable in spinal reflex

20
Q

What is clasp knife response

A

Sudden decrease in resistance when attempting to flex a joint
Mediated by Golgi tendon organs: stretch receptors only stimulated by extreme stretch
Sign of UMNL: muscles are hypertonic so initial resistance to flexion. Sudden drop in resistance with activation of GTO and stimulation of inhibitory interneurones that inhibit LMN, causing relaxation.