11. CNS (Motor) (1) Flashcards

1
Q
  • Neurone:
A
  • Neurone: consists of a cell body (soma), axon and presynaptic terminal Not a nerve
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2
Q
  • Nerve:
A
  • Nerve: group of axons usually consisting of varying combinations of sensory, motor, and autonomic neurones
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3
Q
  • Nerve:
A
  • Nerve: group of axons usually consisting of varying combinations of sensory, motor, and autonomic neurones
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4
Q
  • Sensory neurone:
A
  • Sensory neurone: a neurone with sensory receptors that when stimulated conveys sensory information to the brain
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5
Q
  • Sensory neurone:
A
  • Sensory neurone: a neurone with sensory receptors that when stimulated conveys sensory information to the brain
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6
Q
  • Motor neurone:
A
  • Motor neurone: a neurone that when stimulated produces a motor response (e.g muscle contracting)
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7
Q
  • Lower motor neurone (LMN):
A
  • Lower motor neurone (LMN): AKA anterior/ ventral horn cell, alpha motor neurone or gamma motor neurone —-> Neurone providing the presynaptic terminal at the neuromuscular junction
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8
Q
  • Upper motor neurone (UMN):
A
  • Upper motor neurone (UMN): neurones controlling LMNs. Found throughout CNS.
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8
Q
  • Upper motor neurone (UMN):
A
  • Upper motor neurone (UMN): neurones controlling LMNs. Found throughout CNS.
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9
Q
  • Efferent:
A
  • Efferent: refers to the direction of neuronal information travelling away from a point of reference e.g LMNs
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9
Q
  • Efferent:
A
  • Efferent: refers to the direction of neuronal information travelling away from a point of reference e.g LMNs
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10
Q
  • Afferent:
A
  • Afferent: refers to the direction of neuronal information travelling towards a point of reference e.g. sensory neurones
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11
Q
  • Afferent:
A
  • Afferent: refers to the direction of neuronal information travelling towards a point of reference e.g. sensory neurones
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12
Q
  • Interneurone:
A
  • Interneurone: a neurone that connects two other neurones and may be excitatory or inhibitory when stimulated
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13
Q
  • Agonist muscle:
A
  • Agonist muscle: muscle that produces a movement of interest when contracting e.g flexion at the elbow = biceps is the agonist —> Agonists can be antagonists for different movements
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14
Q
  • Antagonist muscle:
A
  • Antagonist muscle: muscle that opposes movement of interest when contracting e.g for elbow flexion = triceps is the antagonist —-> Antagonist can be an agonist for a different movement
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15
Q
  • Paresis:
A
  • Paresis: partial paralysis
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15
Q
  • Paresis:
A
  • Paresis: partial paralysis
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16
Q
  • Hemiparesis:
A
  • Hemiparesis: partial paralysis on one half of the body
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17
Q
  • Contralateral:
A
  • Contralateral: refers to opposite side of a region of interest
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18
Q
  • Ipsilateral:
A
  • Ipsilateral: refers to same side as region of interest
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19
Q
  • Ipsilateral:
A
  • Ipsilateral: refers to same side as region of interest
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20
Q
  • Tracts:
A
  • Tracts: groups of axons that convey similar sensory or motor information
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21
Q

Anatomical areas affecting motor function:
* Motor function refers…

A
  • Motor function refers to the smooth (coordinated) and effective movement in an autonomic fashion ( without thought )
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21
Q

Anatomical areas affecting motor function:
* Motor function refers…

A
  • Motor function refers to the smooth (coordinated) and effective movement in an autonomic fashion ( without thought )
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22
Q

Cerebrum=
Cerebellum=
Spinal chord=
Brain stem=

A
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22
Q

Cerebrum=
Cerebellum=
Spinal chord=
Brain stem=

A
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23
Q

Anatomical areas affecting motor function:
* Grey matter =
* Area where _______ movements are initiated
* Brainstem also has UMNs that control _____ muscle

A
  • site in motor strip of UMN
  • voluntary movements are initiated
  • postural
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24
Q
  • Brainstem and spinal chord have ____ either for cranial or somatic muscles in the body
A

LMNs

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25
Q

Midbrain:
Cerebrum:
Cerebellum:

A
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26
Q

What is the basal ganglia?

A
  • Produces automatic movement
  • Where cell bodies are located
  • Help motor cortex plan movement involved in automatic planning
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27
Q

Initiation of movement:
How are UMNs activated? (2)

A
  • UMNs when activated are the central signal to initiate muscle contraction and movement
  • Cell bodies of UMNs to the upper and lower limbs and trunk are found in the primary motor cortex of the frontal lobe In pre central gurus anterior to middle cerebral fissure
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28
Q

How do signals travel from axons to LMNs?

A
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29
Q

How are UMNs derived and how do they travel down the spinal cord? (5)

A
  • UMNs are derived from both sides of the cerebral hemisphere Left and right primary motor cortices
  • Axons cross/decussate in the medulla oblongata in the medullary pyramids (pyramidal tract = tracts in brainstem)
  • UMNs travel down spinal chord and terminate on LMNs on contalateral side
  • In spinal chord, they mainly travel in the lateral corticospinal tract
  • UMNs from one side of the brain control movement on the opposite side of the body
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30
Q

What happens when UMNs are damaged?

A
  • Damage to UMNs and tracts up and until medullary decussation cause weakness on the contralateral side and damage to tracts in the spinal chord cause weakness on the ipsilateral side
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31
Q
  • UMNs are very _____
  • They have long axons
  • Their cell bodies are located in the ____ _____
  • Axons —-> Motor cortex —-> Internal capsule —-> _____.
A

long
motor cortex
Brainstem

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32
Q

Where are upper motor neurons to the limbs and trunk found?

A
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33
Q

What are pyramidal pathways called?

A
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34
Q

Through brainstem via _____ ______.
Through spinal cord via ____ ________.

A

pyramidal tract
corticospinal tract

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35
Q

Details of upper motor neuron pathways to limbs and trunk: (6)

A
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36
Q

LMNs to limbs & trunk:
Where are the LMNs found? (2)

A
  • LMNs to the limbs and trunk are found int the anterior/ventral horn of the spinal chord gray matter
  • Axons exit the spinal chord via the ventral root where they meet with the dorsal root of the spinal chord containing sensory neurons to form the common nerve before exiting the vertebrae
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37
Q

What do UMNs in the spinal cord supply?

A
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38
Q
  • Dorsal root =
  • Ventral root =
A

purely sensory
purely motor

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39
Q
  • LMNs target ______ muscle and presynaptic terminal of LMNs is part of the neuromuscular junction.
  • LMNs are activated by _____ to produce movement but can also be controlled by sensory neurones
A

skeletal
UMNs

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40
Q
  • Only two neurones are required to produce contraction of muscle =
A

LMNs and UMNs

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41
Q

Where do the LMNs exit? (2)

A
  • They exit the spinal chord to form the ventral root and then join the dorsal root (sensory nerves) to form a common nerve
  • Common nerve then passes through the foramina to exit the vertebral column
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42
Q

Where do the LMNs exit? (2)

A
  • They exit the spinal chord to form the ventral root and then join the dorsal root (sensory nerves) to form a common nerve
  • Common nerve then passes through the foramina to exit the vertebral column
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43
Q
  • Vertebral disc ______ would damage the common nerves
A

lesions

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44
Q

LMNs & muscle tone:
True or False,
* While power may be reduced, tone may be increased.

A

True,
* While power may be reduced, tone may be increased.
* e.g power of the biceps is tested by flexing the arm against resistance (person examining will try and extend the arm while the patient flexes)

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45
Q

How can we assess tone?

A
  • To asses tone, the patient will be asked to relax the arm and the examiner will passively flex and extend the arm while feeling the biceps muscle tone.
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45
Q

How can we assess tone?

A
  • To asses tone, the patient will be asked to relax the arm and the examiner will passively flex and extend the arm while feeling the biceps muscle tone.
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46
Q
  • Muscle tone comes from a level of muscle contraction at rest —->
  • Muscle spindles fire at all times to provide position ______
A
  • Stimulus for contraction at rest is from muscle spindles constantly firing at rest
  • sensation
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47
Q

How do lower motor neurons influence muscle tone?

A
48
Q

Label the parts of the reflex. (10)

A
49
Q
  • Reflex movements can be _____/____ depending on the type of stimulus
  • Reflexes can also be ______ of our ability to have voluntary movement
A

simple/complex
independent

50
Q

What happens when UMNs are damaged in terms of reflexes?

A
  • Damage to UMNs may still allow reflexes to happen due to intact LMN
51
Q

How are simple muscle reflexes produced?

A
  • Simple muscle reflexes are produced by activating muscle spindles found in intrafusal fibres of skeletal muscle.
51
Q

How are simple muscle reflexes produced?

A
  • Simple muscle reflexes are produced by activating muscle spindles found in intrafusal fibres of skeletal muscle.
52
Q

How are muscle spindles activated?

A
  • Muscle spindles are activated by increase in length and tension produced in intrafusal muscle
53
Q
  • This can be achieved by stretching muscle or transferring tension into the muscle by tapping the muscle-tendon with a _____ _____.
A

patellar hammer

54
Q

Reflex is independent of UMNs: (3)
LABEL the process.

A
55
Q

SImple patellar reflex (stretch reflex) monosynaptic (one synapse) as example (complete the diagram) :

A
56
Q

Which simple muscle reflexes tested clinically? (4)

A
57
Q

How is muscle contraction stimulated? (3)

A
  • When activated , muscle spindles send info via sensory afferents to the dorsal root ganglion where sensory neuronal soma are found
  • This sensory info will continue along the sensory neurone efferent axon and stimulate LMNs cause extrafusal muscle fibres to contract, shorten and movement occurs
  • Resting muscle tone and reflexes both depend on muscle spindle activation and require no UMN effects to produce muscle contraction
58
Q
  • Monosynaptic =
A

reflex only involves a single synapse between the proprioceptor neuron and the LMN

59
Q

What is the main problem with muscle spindle design?

A
  • Muscle spindles lie within intrafusal fibres and these are not used to produce movement when they contract Extrafusal fibres contract and shorten to produce movement
  • This means when an extrafusal muscle contracts and shortens, tension within the intrafusal fibre decreases and the muscle spindle is unloaded.
  • As tension in muscle spindle is now low, it will decrease its firing rate, which reduces the firing rate of the LMN and so muscle contraction will stop
60
Q

What is the solution to the problem with muscle spindle design? (7)

A
61
Q

What is the function of gamma motor neurons?

A
62
Q

What happens after UMNs activate gamma motor neurones? (5)

A
63
Q

2nd problem with muscle spindle design & solution: (4)

A
64
Q

What is the solution to the second problem with muscle spindle design? (5)

A
65
Q
  • Sometimes with patients with markedly increases reflexes, the ability of _____ _____ inhibition to inhibit the antagonist muscle will be ineffective
A

disynaptic reciprocal

66
Q

What are Golgi tendon organ reflexes? (5)

A
  • Some forces generated by human muscle contraction can be so great that damage can occur
  • Forceful movements need to be kept in check
  • This is mediated by Golgi tendon organs (GTO) found in the muscle-tendon and which primarily act as position receptors
  • GTO let’s us know if the force generated by muscle is too much for that muscle and it’s connection to the bone and tendon
  • Prevents us from over-contracting muscles and pulling the muscle out of the bone at its insertion
66
Q

What are Golgi tendon organ reflexes? (5)

A
  • Some forces generated by human muscle contraction can be so great that damage can occur
  • Forceful movements need to be kept in check
  • This is mediated by Golgi tendon organs (GTO) found in the muscle-tendon and which primarily act as position receptors
  • GTO let’s us know if the force generated by muscle is too much for that muscle and it’s connection to the bone and tendon
  • Prevents us from over-contracting muscles and pulling the muscle out of the bone at its insertion
67
Q

What happens when GTO is activated? (3)

A
  • When activated, GTO sends signals via the dorsal columns to the brain and sensory signals to interneurones which produce 2 effects
  • The signal inhibits LMNs to the agonist to stop the movement but stimulates LMNs to antagonist to cause contraction of opposing muscle forces and also stop movement
  • When damage to tendons occur, after repair, GTOs will not be replaces and through significant GTO loss, patients may experience repeated muscle injury
68
Q

Give the full process of the GTO reflex. (5)

A
69
Q

Flexor & crossed extensor reflexes:
What does the withdrawal reflex do?

A
  • Withdrawal reflex designed to allow us to move our limbs away from a noxious stimulus in response to mechanoreceptor activation
70
Q
  • Reflexes in the feet respond to light mechanical stimulation of the lateral plantar surface of the feet
    ——> ________ of toes and feet
A

Plantarflexion

71
Q

Clinical changes with LMN damage:
What happens when LMNs get damaged?

A
  • With damage to LMNs, axons are destroyed, the amount of Ach release into the synapse decreases and the receptors attempt to compensate by upregulating ——> Denervation hypersensitivity
72
Q
  • Less axons and Ach available at NM junction =
A

muscle power, tone, and reflexes are reduced

73
Q

What happens when a muscle is less active? (2)

A
  • As muscle is less active, it undergoes disuse and develops atrophy (wasting) —–>
    Reduced muscle bulk
  • Ach from remaining axons will act on sensitised receptors and cause small muscle contractions —–> Fasciculations
74
Q

Tests of muscle function:
- Muscle strength
- Muscle tone
- Muscle reflexes
- Muscle atrophy

A
75
Q

Disuse atrophy in LMN disease:

A
75
Q

Disuse atrophy in LMN disease:

A
76
Q

Disuse atrophy (wasting of muscle) in LMN disease:
Motor neuron disease vs polio

A
76
Q

Disuse atrophy (wasting of muscle) in LMN disease:
Motor neuron disease vs polio

A
77
Q

LMN damage:
Ankle reflex -
Patellar reflex -
Biceps reflex -
Trcieps reflex -

A
77
Q

LMN damage:
Ankle reflex -
Patellar reflex -
Biceps reflex -
Trcieps reflex -

A
78
Q

What are the effects of UMN damage? (4)

A
  • Although UMNs are damaged, muscle spindle afferents still remain.
  • Muscle power decrease, but muscle tone and reflexes are not lost.
  • There is less neurotransmitter (glutamate) at the synapse between afferents and LMNs, denervation hypersensitivity occurs at the LMN (not the NM junction).
  • Consequently, normal muscle spindle afferent activity will result in enhanced LMN response and muscle tone and reflexes will increase.
78
Q

What are the effects of UMN damage? (5)

A
  • Although UMNs are damaged, muscle spindle afferents still remain.
  • Muscle power decrease, but muscle tone and reflexes are not lost.
  • There is less neurotransmitter (glutamate) at the synapse between afferents and LMNs, denervation hypersensitivity occurs at the LMN (not the NM junction).
  • Consequently, normal muscle spindle afferent activity will result in enhanced LMN response and muscle tone and reflexes will increase.
79
Q

When does a sustained increase in muscle tone occur?

A
  • A sustained increase in muscle tone may occur in flexor muscle and this causes spasticity of muscle and contractures
80
Q

In UMN damage, does disuse atrophy occur?

A
  • Disuse atrophy does not occur since muscle contraction is even higher than normal at rest
  • A positive Babnski sign also occurs
80
Q

In UMN damage, does disuse atrophy occur?

A
  • Disuse atrophy does not occur since muscle contraction is even higher than normal at rest
  • A positive Babnski sign also occurs
81
Q

In UMN damage, the reflex is not described as brisk. Why? (2)

A
  • In UMN damage, there is no activation of gamma motor neurones and hence the reflex is not only increased in amplitude, but through the inability to overcome muscle spindle unloading, the reflex is short duration —-> Reflex is NOT described as brisk
  • Sometimes reflex is so pronounced that disynaptic reciprocal inhibition is insufficient to prevent reflexes in antagonist muscles occurring during Pendular reflexes (repeated reflexes called clonus)
82
Q

Summation of the effects of UMN damage:

A
83
Q

Clinical changes with UMN damage
Muscle strength:
Muscle tone:
Muscle reflexes:
Muscle atrophy:

A
84
Q

What is the motor homunculus?

A
  • UMNs are distributed in the motor cortex in a somatotopic order —> Motor homunculus (UMNs for regions of the body are found together)
84
Q

What is the motor homunculus?

A
  • UMNs are distributed in the motor cortex in a somatotopic order —> Motor homunculus (UMNs for regions of the body are found together)
85
Q
  • UMNs for the legs and feet are found _______ and the rest laterally
A

medially

86
Q
  • Since the anterior cerebral artery supplies medial parts of the frontal lobe, strokes involving this artery may cause…
A

weakness of just the foot and leg on one side

87
Q
  • Since the middle cerebral artery supplies the remaining part of the motor cortex and internal capsule, strokes involving this artery result in…
A

complete hemiparesis

88
Q

What is the function of the motor homunculus?

A
  • Area of cortex dedicated to a limb is not proportional to the size of the limb but to the complexity of movement that the limb carries out
89
Q
  • UMNs for the hands, face, mouth, and tongue are as extensive as that for the _______________.
A
  • UMNs for the hands, face, mouth, and tongue are as extensive as that for the legs, feet, and trunk
90
Q

Motor homunculus:
* This is a reflection of human dependence for survival on verbal communication, facial expression, and manual ______.

A

dexterity

91
Q

Where are the intrinsic neural plans for movement found?

A
  • The intrinsic neural plans for movement are found in areas of the frontal lobe anterior to middle and lateral components of the primary motor cortex.
92
Q

Motor homunculus:
* The supplementary motor cortex lies…
* The premotor cortex lies…

A
  • The supplementary motor cortex lies medially in front of the UMNs for legs and feet
  • The pre motor cortex lies laterally in front of UMNs for the rest of the body
93
Q

How is motor control of the head and neck initiated?

A
  • Motor control of head and neck is also initiated by UMNs in primary motor cortex and LMNs (in the brainstem NOT the spinal chord)
93
Q

How is motor control of the head and neck initiated?

A
  • Motor control of head and neck is also initiated by UMNs in primary motor cortex and LMNs (in the brainstem NOT the spinal chord)
94
Q

Where are the LMNs for the head and neck found?

A
  • The LMNs for head and neck are found in cranial nerve nuclei in the midbrain, pons, and medulla
95
Q
  • LMNs controlling head and neck generally have UMNs influencing their function derived from both left and right motor cortices —–>
  • LMNs for the limb and trunk —–>
A
  • Bilateral UMN supply
  • Contralateral UMN supply
96
Q

What happens if one motor cortex is damaged? (2)

A
  • Even if one motor cortex is destroyed, motor function to the head and neck will not be lost because LMNs still receive UMN info from Contralateral/ ipsilateral cortex
  • However, motor function for the limbs and trunk will be lost on the Contralateral side
97
Q

When do abnormalities of cranial nerve function occur? (2)

A
  • In general, abnormalities of cranial nerve function can only occur if damage to the brainstem or the cranial nerves themselves has occurred
  • Damage to both motor cortices or pathways will also cause abnormalities on both sides of head and neck
97
Q

When do abnormalities of cranial nerve function occur? (2)

A
  • In general, abnormalities of cranial nerve function can only occur if damage to the brainstem or the cranial nerves themselves has occurred
  • Damage to both motor cortices or pathways will also cause abnormalities on both sides of head and neck
98
Q
  • Two cranial nerve nuclei are exceptions to the rule regarding bilateral UMN supply —>
A

Facial (VIIth) and hypoglossal (XIIth)

99
Q

Facial (VIIth) and hypoglossal (XIIth):
* These only receive _______ UMN supply (as with limbs and trunk)
* Facial nerve supplies the lower half of the face and hypoglossal nerve controls tongue _______

A

Contralateral
movement

100
Q

Extraocular muscles (II, IV and VI), which nerves control one’s ability to look up and then down, left and then right?

A
101
Q

What happens if there is loss of innervation to the following nerves: IIIrd, IVth and VIth cranials nerves (CN)

A
102
Q

How can we test for damage to the oculomotor nerve on the right side?

A
103
Q

How can we test for damage to the trochlear (IVth cranial) nerve?

A
104
Q

How can we test for damage to the abducent nerve?

A
105
Q

How can we test for damage to the VIIth (facial) cranial nerve?

A
106
Q

How can we test for damage to the trigeminal nerve?

A
107
Q
  • LMNs to the upper half of the face receive ______ UMN supply while LMNs of lower half of the face receive ______ UMN supply only.
A

Bilateral
Contralateral

108
Q
  • Damage to UMNs to the facial nerve occurs —->
  • Damage to LMNs (nucleus or nerve) —->
A
  • Only lower half of the face will be weak
  • Weakness to both the upper and lower half of the face
109
Q

How do we test for the corneal reflex?

A
110
Q

Is this an upper or lower motor neuron VIIth CN palsy?

A
111
Q

Is this an upper or lower motor neuron VIIth CN palsy?

A
112
Q

What does the left vagus nerve elevate?

A
113
Q
  • The UMN supply to the LMNs supplying the tongue muscles, is from only one motor cortex Contralateral
  • With damage to the motor cortex or internal capsule on one side =
A

= an inability to show facial expression in the lower half of the face, inability to move the leg and arm and deviation of the tongue to the side of weakness on protrusion

114
Q

What is the function of the XIth (accessory) cranial nerve?

A
115
Q

What is the function of the XIIth (hypoglossal) cranial nerve?

A