CN 13 pt 1 Flashcards
Nuclear and infranuclear pathways
CN III, IV, and VI nuclei, their peripheral nerves, and the extraocular muscles
Supranuclear pathways
Brainstem and forebrain circuits that control eye movements
• Connect with CN III, IV, and VI nuclei
Extraocular muscles that do horizontal movement
Lateral rectus
• Medial rectus
Extraocular muscles producing vertical movement
Superior rectus
• Inferior rectus
Extraocular muscles origin and insertion
Common tendinous ring at apex of orbit
Muscles insert into the sclera
Oblique muscles
Torsional movements
• Eye is slightly rotated about its axis
Superior oblique
• Inserts on superior surface
• Produces primarily intorsion
• Movement of the upper pole of the eye inward (nasally)
Inferior oblique
• Inserts on inferior surface
• Produces primarily extorsion
• Movement of the upper pole of the eye outward (temporally)
Movement produced by an extraocular muscle depends on…
the direction the muscle pulls relative to the main axis of the eye
Ie. With the eye adducted, the superior oblique causes depression
Innervation of extraocular muscles
(LR6 SO4)3 …LR by CN VI, SO by CN IV, the rest supplied by CN III
CN III has two major branches
Superior division
- Innervates levator palpebrae superior (elevates eyelid)
- Innervates superior rectus (SR)
Inferior division
-Contains parasympathetic fibers to pupillary constrictor muscles and
ciliary muscles of the lens
-Innervates the other extraocular muscles (except LR and SO)
CN III, CN IV, and CN VI all travel through
cavernous sinus and enter the orbit via the superior orbital fissure
Table 13.1
Go look at it on slide 7
CN III: oculomotor nuclei
In upper midbrain (level of superior colliculi and anterior to PAG) CN III exits anteriorly between posterior cerebral artery and superior cerebellar artery
CN III: oculomotor nuclei parasympathetic fibers
run in the superficial and medial portion of CN III
• Susceptible to compression from PComm aneurysms
CN IV: trochlear nuclie
In lower midbrain (level of inferior colliculi and anterior to PAG)
CN VI
Cross over each other before exiting the brainstem dorsally
• Susceptible to compression from cerebellar tumors
• Very thin and easily damaged by shear injury from head trauma
CN VI: abducens nuclei
In mid/lower, posterior pons (floor of fourth ventricle) CN VI exits at the pontomedullary junction
CN VI
Ascends and exits the dura to enter Dorello’s canal
• Has a long, ascending, vertical course to reach the orbit
• Highly susceptible to downward traction injury produced by
elevated ICP
Diplopia
Double vision
caused by abnormalities in several locations
Mechanical problems
• Orbital fx with muscle entrapment •
The extraocular muscles
• Orbital myositis
The neuromuscular junction
• Myasthenia gravis (MG)
CN III, IV, VI and their central pathways
The supranuclear ocular pathways
• Ingestion of toxins
• Anticonvulsant medications
Dysconjugate gaze
strabismus
Visual input normally helps maintain the eyes yoked in the same direction
Occurs when an extraocular muscle is not working properly, and
the result is diplopia
Diplopia in kids
Conventional muscle weakness can produce dysnconjugate gaze
Over time will cause suppression of one of the images and result in amblyopia (decreased vision in one eye)
Early intervention!!
Diplopia worse when
Looking at objects that are near because the medial rectus has been affected, need adduction of both eyes for near vision
Common causes of oculomotor palsy (CN III)
Diabetic neuropathy • Head trauma (shearing forces) • Aneurysms (junction of PComm and ICA) • Infection • Tumor • Infarct of the nucleus • Herniation of temporal lobe (over edge of tentorium cerebelli) • Lesions of CN III fascicles
Oculomotor palsy (CN III)
Superior oblique and lateral rectus are left intact so the remaining movements are ABduction, In torsion, and depression.
The eye will rest in a “down and out” position
Levator palpabrae has been affected so eye lid closed
Loss of PS fibers that constrict pupil lead to dilation
PComm aneurysm
Suspected w/ pts w/ painful CN III palsy involving pupil
Diagnosis until prove otherwise
Emergency CT angiogram needed immediately
Trochlear palsy (CN IV)
Eye will rest hypertrophic and extortion
Vertical diplopia
Diplopia can be improved by
Tucking chin and tilting head away from affected eye because these movements produce the movements that the eye muscles would normally do
Common causes of trochlear palsy (CN IV)
Head trauma
• Very commonly injured CN with head trauma
• Neoplasm • Infection • Aneurysms • Microvascular damage (DM)
Rln b/n compensatory head positions and eye movement abnormalities
Head movement is always in the direction of the action normally
produced by the affected muscle
• E.g. In a right CN IV palsy, the head down/chin tucked, and head tilted
to the left (CN IV actions are normally depression and intorsion)
Abducens palsy (CN VI)
Horizontal diplopia because lesion to CN VI which normally causes eye abduction
Worse when looking at objects that are far because the lateral rectus cannot abduct both eyes
Common causes of abducens palsy
Downward traction from elevated ICP
• Infection
• Neoplasm
• Aneurysms
• Microvascular damage (DM)
• Pontine infarcts can damage CN VI fascicles (affecting ipsilateral eye)
• Lesions of CN VI nucleus in pons will not produce a simple abducens
palsy, but instead a horizontal gaze palsy (movements of both eyes in one direction are decreased)
Which way will your pt turn head in attempt to compensate for horizontal diplopia?
Toward the affected eye (lateral rotation of head)
Light shown in one eye causes
- Pupillary constriction (direct response) in that eye
2. Pupillary constriction (consensual response) in the other eye
Light entering one eye activates
CN II which projects to the optic
tracts
• Extrageniculate fibers project to
the pretectal area of the
midbrain
• Synapse occurs at the pretectal
nuclei
Fibers then project bilaterally to synapse at the Edinger-Westphal nuclei
• Most fibers cross at the
posterior commissure
Preganglionic parasympathetic fibers arise bilaterally from the Edinger-Westphal nuclei and travel with CN III
Synapse occurs at the ciliary ganglia in the orbit
Postganglionic parasympathetic fibers then target pupillary constrictor muscles
Pupillary light reflex review
Light entering one eye activates CN II, which then projects to both optic tracts to the pretectal area of the midbrain. After synapsing at the pretectal nuclei, fibers project bilaterally to the Edinger-Westphal nuclei, where preganglionic parasympathetic fibers will exit bilaterally to travel w/ CN III to synapse at the ciliary ganglion. After synapse, the post - ganglionic parasympathetic fibers project to the pupillary constrictormuscles of the iris.
