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Neuro anatomy 2 > CN II > Flashcards

CN II Flashcards

1
Q

Function of CN III

A
  • GSE = SKELETAL MOTOR to upper eyelid and extraocular muscles

–> levator palpebrae superioris (LPS), Super, medial and inferior rectus, and inferior oblique

  • GVE = PARASYMPATHETIC visceral motor to internal muscles of eye

–> sphincter pupillae muscle and ciliary muscle

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2
Q

describe oculomotor nucleus (GSE)

A
  • Located ventral to periaqueductal gray in ROSTRAL MIDBRAIN
  • contains motor neurons whose axons gather to form the oculomotor nerve
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3
Q

describe Edinger-Westphal nucleus (EW-N)

A
  • Contains cell bodies of PREGANGLIONIC PARASYMPATHETICS
  • axons join the main oculomotor nerve to course to the orbit
  • fibers terminate in the CILIARY GANGLION with post ganglionic parasympathetic neurons
  • Postganglionic fibers terminate in eye bulb via short ciliary nerves

**INNERVATE ciliary muscles (LENS ACCOMMODATION for near vision) and SPHINCTER PUPILLAE MUSCLES (for pupillary constriction)**

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4
Q

oculomotor and trochlear nerve passes between what two structures

A
  • posterior cerebral artery and superior cerebellar artery
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5
Q

What are the muscular deficits resulting from damage to the oculomotor nerve?

A
  • IPSILATERAL LPS IS PARALYZED = Ptosis
  • Superior and inferior rectus paralyzed = inability to move eye vertically
  • Medial rectus paralyzed = inability to move eye medially
  • Inferior oblique paralyzed = Antagonist pulls eye DOWN AND OUT

**Since LR6SO4 are intact, the affected eye deviates DOWNWARD AND LATERALLY**

–> patient presetns with LATERAL STRABISMUS (lateral deviation) and the resulting MISALIGNMENT causes DIPLOPIA (double vision)

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6
Q

describe the parasympathetic deficits resulting from damage to oculomotor nerve.

A
  • Sphincter pupillae = nonfunctional - pupil on the affected side remains dilated (MYDRIASIS)

–> Pupil does NOT constrict in response to light

  • CILIARY MUSCLE = Nonfunction - cannot accommodate lens (cannot focus on near objects)

–> Lens is flat

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7
Q

what is the result on intracranial pressure on GVE fibers (which run with the GSE fibers)

A
  • Results in DILATED PUPIL unresponsive to light
  • May be confused with HORNER’s SYNDROME
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8
Q

compare and contrast Pressure/damage to CN III and Horner’s syndrome

A

CN III

  • Ptosis (due to paralysis of LPS)
  • DEFECTIVE EYE MOVEMENTS (eye is deviated DOWN AND OUT)
  • DILATED, LARGE pupil (Mydriasis) due to nonfunctional sphincter pupillae

HORNOR’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
  • ANHIDROSIS
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9
Q

describe the trochlear nucleus

A
  • contains GSE nerve cell bodies (SKELETAL MOTOR to superior oblique)
  • 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
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10
Q

describe tochlear nerve

A
  • Arises from the CONTRALATERAL tochlear nucleus
  • emerges from the POSTERIOR surface of the brainstem
  • Has longest intracranial course
  • is the thinnest
  • Function = intorsion, depression, abduction (DOWNWARD AND OUTWARD)
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11
Q

What is the result of Damage to trochlear nucleus

A
  • Paralysis or paresis of the contralateral SO = eye drift’s upward caused by unopposed action of the antagonist caused in ELEVATION known as HYPERTROPIA
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12
Q

Result of damage to trochlear nerve (after it exits brainstem)

A
  • Paralysis of paresis of the IPSILATERAL SO = eye drifts upward causing elevation (HYPERTROPIA)
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13
Q

When does HYPERTROPIA become WORSE

A
  • downward gase (when looking down) = becomes partially depressed by IR, but not completely (vertical diplopia)
  • Medial downward gaze
  • When tilting the head toward the affected side
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14
Q

Why does the eye Extort with a lesion to the trochlear nerve

A
  • caused by action of unopposed inferior oblique muscle (which extorts, elevates and abducts) and results in EXTERNAL STRABISMUS
  • eyes become misaligned, the patient experiences VERTICAL DIPLOPIA (double vision)
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15
Q

What makes symptoms of a trochlear nerve lesion better

A
  • Diplopia is minimized when:

–> tilting the head TOWARD the NORMAL side = causes normal eye to rotate inward (intort) and become aligned with affected eye which is rotated OUTWARD (extorted)

–> Pointing chin Downward (chin tuck) which rolls normal eye upward = compensates for the hypertropia of the affected eye

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16
Q

describe abducens nucleus

A
  • Located in the CAUDAL PONS
  • cell bodies of motor neurons (GSE - skeletal motor to lateral rectus)
  • contains cell bodies of internuclear neurons whose axons CROSS the midline and join the medial longitudinal fasciculus (MLF) and ASCENDS to the rostral midbrain to terminate in the oculomotor nucleus and synpase with LMN that innervate medial rectus muscle
17
Q

describe abducent nerve

A
  • emerges from the brainstem at the pontomedullary junction
  • PROJECTS to the IPSILATERAL EYE where it innervates the LATERAL RECTUS MUSCLE
  • ABDUCENT ABDUCTS the eye (moves the eye laterally)
18
Q

describe damage to abducent nerve

A
  • ONLY motor neuron axons are damaged (LMN lesion)
  • Lateral rectus is paralyzed (flaccid, with no muscle tone) = CAN NOT move the affected eye LATERALLY (NO ABDUCTION)
  • Medial deviation of the eye = MEDIAL STRABISMUS, ESOTROPIA
  • eyes become misaligned which results in HORIZONTAL DIPLOPIA
19
Q

describe damage to the abducen nucleus

A
  • Lateral rectus is paralyzed and cannot move the affected eye laterally = medial strabismus, esotropia)
  • In addition, accompanied by INABILITY to move the CONTRALATERAL EYE medially as individual attempts to look toward the side of the lesion

–> ADDUCTION DEFICIT of the contralateral eye

  • IPSILATERAL LATERAL (horizontal) GAZE PARALYSIS/PALSY
20
Q

describe the mechanisms of internuclear opthalmoplegia (INO)

A
  • INO is caused by a lesion to MLF that connects Abducen nucleus to the CONTRALATERAL oculomotor nucleus
  • Causes Horizontal eye movement disorder
  • becomes apparent ONLY during CONJUGATE HORIZONTAL EYE MOVEMENT = windshield wiperrs or moving from side to side
21
Q

define conjugate horizontal eye movement

A
  • movement from side to side
  • lesion to MLF segment disrupts the movement due to disconnection of abducen and oculomotor nuclei
22
Q

Describe a lesion to the right MLF

A
  • Disconnection between Left abducen nucleus from the Right oculomotor nucleus
  • Produces Lateral gaze deficit to the left
  • The RIGHT EYE will ahve ADDUCTION deficit (only during conjugate horizontal eye movement, but NOT during CONVERGENCE of the eyes)
  • right medial rectus is NOT flaccid and has not lost its muscle tone, because its innervation provided by one of the branches of oculomotor nerve is intact
23
Q

Describe a lesion to the Right Abducen nucleus

A
  • Results in IPSILATERAL LATERAL (horizontal) gaze paralysis/palsy (loss of ipsilateral horizontal conjjugate gaze of inability to move both eyes simultaneously, TOWARD the side of the lesion (to the right))
  • 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 by relaxing the right medial rectus, however it WILL NOT ABDUCT PAST MIDLINE
24
Q

Describe One-and-a-half syndrome

A
  • Lesion in the vicinity of the abducens nucleus which involves the

–> ENTIRE ABDUCEN NUCLEUS of one side = results in IPSILATERAL LATERAL (horizontal) gaze paralysis/palsy when looking to side of the lesion

–> IPSILATERAL MLF fibers (of internuclear neurons) arising from CONTRALATERAL ABDUCEN nucleus = results in INTERNUCLEAR OPTHALMOPLEGIA when looking AWAY from side of the lesion (causes ADDUCTION deficity and nystagmus on abduction)

  • opposite eye can only abduct with nystagmus

Neuro anatomy 2 (10 decks)

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