16 - Cranial Nerves II Flashcards
CN III
Oculomotor nerve
Skeletal motor functional components
GSE: Skeletal motor to upper eyelid and extraocular muscles:
a. levator palpebrae superioris (LPS)
b. superior rectus
c. medial rectus
d. inferior rectus
e. inferior oblique
Parasympathetic functional components
GVE: Parasympathetic visceral motor to internal (smooth) muscles of the eye:
a. sphincter pupillae muscle
b. ciliary muscle
Two nuclei of CN III
- Oculomotor nucleus
- Edinger-Westphal nucleus
Oculomotor nucleus
Oculomotor nucleus (GSE) a. Is located ventral to the periaqueductal gray in the rostral midbrain.
b. It contains motor neurons whose axons gather to form the oculomotor nerve.
Edinger-Westphal nucleus (EW-N)
It contains the cell bodies of preganglionic parasympathetic neurons whose axons join the main oculomotor nerve to course to the orbit.
There, the preganglionic parasympathetic fibers terminate in the ciliary ganglion, where they synapse with postganglionic parasympathetic neurons whose axons terminate in the eye bulb via the short ciliary nerves of the trigeminal.
These parasympathetic fibers innervate the:
i. ciliary muscle (for lens accommodation, for near vision) and the
ii. sphincter pupillae muscle (for pupillary constriction)
Ipsilateral levator palpebrae superioris (LPS) is paralyzed
Ptosis (drooping of the upper eye lid)
Superior and/or inferior rectus is paralyzed
Inability to move eye vertically.
Medial rectus is paralyzed
Inability to move eye medially.
Inferior oblique is paralyzed
Now its antagonist, the SO causes deviation
of the eye “down and out”
Down and out deviation symptoms
• Since the LR6SO4 are intact, the affected eye deviates downward and laterally.
Eye deviates laterally (lateral strabismus),
eyes become misaligned resulting in:
combination horizontal and vertical diplopia (double vision)
Sphincter pupillae
Nonfunctional
The pupil on the affected side remains dilated (mydriasis)
Does not constrict in response to light
Ciliary muscle
Nonfunctional
Cannot accommodate lens (cannot focus
on near objects). Lens is flat
Intracranial pressure on GVE fibers (which run with the GSE fibers)
Dilated pupil, unresponsive to light. May be confused with Horner’s syndrome
Horner’s syndrome
Ptosis (due to loss of sympathetic
innervation to Muller’s muscle)
Constricted pupil (miosis) due to interruption of sympathetic innervation to the dilator pupillae
Now, compared to pressure or damage to CN III…
Ptosis (due to paralysis of LPS)
More pronounced
Defective eye movements
Eye is deviated down and out
Dilated, LARGE pupil (mydriasis) due to nonfunctional sphincter pupillae
CN IV
Trochlear nerve
CN IV function
GSE: Skeletal motor to the superior oblique muscle (SO4)
CN IV nucleus
Trochlear nucleus
- Contains GSE nerve cell bodies
- Located at the level of the inferior colliculus in the caudal midbrain
- Fibers leave nucleus, decussate posteriorly and exit the brainstem just inferior to the inferior colliculus
Trochlear nerve - UNIQUE characteristics
- arises from the contralateral trochlear nucleus
- emerges from the posterior surface of the brainstem
- has the longest intracranial course
- is the thinnest
The actions of the superior oblique (SO) are:
intorsion
depression
abduction
Normally, when it contracts, the SO actions cause the eye to look inferolaterally (downward and outward) : “down and out”. (“Salvation Army nerve”)
Damage to trochlear nucleus:
paralysis or paresis of the contralateral SO
Damage to trochlear nerve:
This means after is exits the brainstem
paralysis or paresis of the ipsilateral SO
Downward gaze is carried out by the joint effort of the
- SO and
* inferior rectus
How does this help to explain the deviation that occurs when the superior oblique (SO) is paralyzed?
Thus when the SO is paralyzed, the patient’s ability to depress the affected eye is impaired (experiences weakness — not total inability — of downward gaze with the affected eye). The eye drift’s upward caused by the unopposed action of its antagonist, the inferior oblique which extorts, elevates and abducts the eye. Upward deviation of the eye is known as hypertropia (hypertropia, G. hyper + tropein “turned”).
What three actions will make the hypertropia worse in this case?
- Downward gaze
- Medial downward gaze
- Tilting head toward affected side
Why does a downward gaze make it worse?
in downward gaze (when looking down) – as in going down steps.
Because the normal eye becomes depressed, but the affected eye becomes partially depressed only by the IR (since the SO is paralyzed). The eyes are misaligned resulting in vertical diplopia.
A lesion to the trochlear nerve with resultant paralysis of the SO muscle causes the eye to…
Extort
What causes this extortion?
This is caused by the action of the unopposed inferior oblique muscle (which extorts, elevates, and abducts), and results in external strabismus. Since the eyes become misaligned, the patient experiences vertical diplopia, which is most apparent when looking down as one does when going down stairs, or reading a book
How does the diplopia cause the patient to see “double”?
The diplopia causes the patient to see “double”.
Imagine going down steps, with each (real) step appearing to have an overlapping (diplopic / false) step above it, or reading words that appear to be overlapping (a diplopic word above the real word).
What makes the symptoms of a trochlear nerve lesion better?
- Tilting head to the normal side
- Pointing chin downward
Why does tilting the head to the normal side help?
Tilting of the head toward the normal side, causes the normal eye to rotate inward (intort) and become aligned with the affected eye which is rotated outward (extorted). This head tilt, compensates for the extorsion of the affected eye
Why does pointing the chin downward help?
pointing chin downward (“chin tuck”) which rolls normal eye upward. This compensates for the hypertropia of the affected eye.
CN VI
Abducent nerve
Function of CN VI
GSE: Skeletal motor to the lateral rectus muscle (LR6)
Nucleus of CN VI
Abducens nucleus
contains the cell bodies of motor neurons (GSE) whose axons gather to form the abducent nerve.
What else does the abducens nucleus contain?
also contains the cell bodies of internuclear neurons (interneurons) whose axons cross the midline, join the medial longitudinal fasciculus (MLF) and ascend to the rostral midbrain to terminate in the oculomotor nucleus where they synapse specifically, with the cell bodies of the neurons (LMN’s) that innervate the medial rectus muscle.
Where is the abducens nucleus located?
In the caudal pons
Pathway of the abducent nerve
- Emerges from the brainstem at the pontomedullary junction
- It projects to the ipsilateral eye where it innervates the lateral rectus muscle
- Abducent Abducts the eye (moves the eye laterally)
Damage to the abducent nerve
Only the motor neuron axons running in the nerve are damaged (LMN lesion).
Results of abducent nerve damage
- The lateral rectus is paralyzed (flaccid, with no muscle tone) and cannot move the affected eye laterally (affected eye cannot abduct).
- Results in medial deviation of the eye (medial strabismus, esotropia).
- The eyes become misaligned which results in horizontal diplopia.
- Individual is able to move the affected eye from the nose to the midline, but not past it. This is accomplished by relaxing the medial rectus.
Damage to abducens nucleus
- Results in the same deficits as the nerve damage.
- In addition, it is accompanied by the inability to move the contralateral eye medially as individual attempts to look toward the side of the lesion.
- This is referred to as ipsilateral lateral (horizontal) gaze paralysis / palsy
Why is the abducent nerve and its nucleus UNIQUE?
The abducent nerve and its nucleus are unique because it is the only cranial nerve where a lesion of the nucleus and a lesion of the nerve do not produce the same clinical signs.
- A lesion of the abducent nerve results in LMN loss to the ipsilateral LR muscle with consequent medial strabismus.
- A lesion to the abducens nucleus results in the same deficit as a lesion to the nerve and in addition, an adduction deficit of the contralateral eye.
Describe what occurs when one abducens nucleus is stimulated by higher brain centers via the reticular formation (RF).
NORMALLY, the eyes move as a pair. Higher brain centers stimulate the RF which in turn projects to and stimulates the abducens nucleus.
When the right abducens nucleus is stimulated, horizontal gaze is evoked ipsilateral to the stimulated (right) abducens nucleus, so gaze will be to the right.
Conjugate horizontal eye movement
The simultaneous movement of the two eyes to one side (to the right in this case), is referred to as conjugate horizontal eye movement (eyes move in unison, horizontally), so they both look in the same direction (to the right) and at the same object.
How does the abducens nucleus relate to conjugate horizontal eye movement?
The abducens nucleus is the center of conjugate horizontal eye movement.
Horizontal gaze involves the coordinated and simultaneous contraction of which two muscles?
- lateral rectus of the ipsilateral (right) abducting eye (supplied by CN VI) and the
- medial rectus of the contralateral (left) adducting eye (supplied by III)
Actually, its the (left) MLF that connects the (right) abducens nucleus to the contralateral (left) oculomotor nucleus, which in turn stimulates the (left) medial rectus
What is the mechanism of internuclear ophthalmoplegia (INO)?
The (right) MLF connects the (left) abducens nucleus to the contralateral (right) oculomotor nucleus.
Internuclear ophthalmoplegia (INO)
A lesion to one MLF will “disconnect” these two nuclei.
When these two nuclei are disconnected, the resulting deficit is referred to as internuclear ophthalmoplegia (INO). INO is a horizontal eye movement disorder.
What signs and symptoms would you see with INO
The function of the MLF comes into play during conjugate horizontal eye movements: (think of windshield wipers (eyes), and how they move from side to side – in unison). So a lesion involving the MLF segment connecting the abducens and oculomotor nuclei, becomes apparent only during conjugate horizontal eye movement.
A lesion to the right MLF
- will disconnect the (left) abducens nucleus from the (right) oculomotor nucleus producing a lateral gaze deficit (to the left).
- On gaze to the left, the left eye abducts normally, however, due to the (right) MLF lesion, the right eye will not adduct.
- This is disconjugate gaze, and the side of the INO is ipsilateral to the MLF lesion.
- The right eye will have an adduction deficit (only during conjugate horizontal eye movement, but NOT during convergence of the eyes).
Is the right medial rectus flacid in this condition?
The right medial rectus is not flaccid and has not lost its muscle tone, because its innervation provided by one of the branches of the oculomotor nerve is intact
A lesion to the (right) abducens nucleus
- affecting both types of neurons enclosed in this nucleus, results in an ipsilateral lateral (horizontal) gaze paralysis / palsy (loss of ipsilateral horizontal conjugate gaze, or the inability to move both eyes simultaneously, toward the side of the lesion (to the right):
- The left eye will not adduct (to look to the right).
- Due to the paralyzed right lateral rectus, the right eye will be deviated medially (medial strabismus).
- On attempt to gaze to the right, the right eye will roll from its adducted position to the midline (at best) by relaxing the right medial rectus, however it will not abduct past the midline.
What do you expect to see if you ask a patient who has INO or a lesion to one abducens nucleus to look at a pencil placed 5 - 6 inches in front of his/her eyes?
If the supranuclear connections to the reticular formation and the oculomotor nuclei and nerves are intact, but there is ONLY a lesion to one MLF or one abducens nucleus, the individual maintains the ability to adduct both eyes, so the eyes WILL converge normally, to look at the pencil.
Why will the eyes converge normally?
The reason why this is possible is as follows:
- If both oculomotor nuclei and oculomotor nerves are intact, then the individual does not have an adduction palsy.
- Both medial recti will contract, the eyes will converge and the individual can look at the pencil.
- This eye movement (convergence of the eyes) occurs independent of the MLF, thus a lesion to one (or both MLF’s) will not affect convergence of the eyes!
Key point regarding conjugate horizontal eye movement
Note that during conjugate horizontal eye movement the LMNs that innervate the medial rectus are driven by the MLF, but during convergence of the eyes, the LMN’s to the medial rectus are driven by higher brain centers via the RF
What is “One-and-a-Half” Syndrome?
A rare condition that results following a lesion in the vicinity of the abducens nucleus which involves
One (the entire abducens nucleus)
and
A Half (the ipsilateral MLF fibers of internuclear neurons)
Describe the “one” of “One-and-a-Half” Syndrome
One
The entire abducens nucleus of one side (containing LMN’s to the lateral rectus and the internuclear neurons to the contralateral oculomotor nucleus).
This results in ipsilateral lateral (horizontal) gaze paralysis / palsy when looking to the side of the lesion.
Describe the “half” of “One-and-a-Half” Syndrome
“Half”
The ipsilateral MLF fibers (of internuclear neurons) arising from the contralateral abducens nucleus.
This results in internuclear ophthalmoplegia (INO) when looking away from the side of the lesion. This causes adduction deficit and nystagmus on abduction (etiology is speculative).
What are the characteristics of “One-and-a-Half” Syndrome?
Is characterized by a combination of an ipsilateral lateral (horizontal) gaze paralysis / palsy and INO.
That is, the eye ipsilateral to the lesion has no horizontal movement (note that this eye is medially deviated).
The opposite eye can only abduct with nystagmus.
