Neuro-Ophtho Examination

Question 1

Optic Nerve - CN II
- exiting location
- axons stem from what cells
- function

Answer 1

• exits @ optic disc / optic foramen
• axons stem from the retinal ganglion cells
• function = to carry electrical signals from the retina to the brain (for vision)

Question 2

Where do CNs III, IV and VI exit from and what are their functions?

Answer 2

Question 3

Which CN helps you to look up, towards your nose, down, to centralize the pupils via conteracting the dorsal oblique, and to lift the upper eyelid?

Answer 3

CN III - Occulomotor

Question 4

Which CN counteracts the ventral oblique?

Helps centralize pupil

Answer 4

CN IV - Trochlear

Question 5

Deficit in what CN?

Answer 5

Occulomotor (III)

Question 6

Deficit in what CN?

Answer 6

Trochlear (IV)

Question 7

Which CN “sucks” the eye inwards passively, moving the third eyelid?

Answer 7

CN VI (Abducens)

Question 8

Deficit in what CN?

Answer 8

Abducens (VI)

Question 9

Where do each of the Trigeminal branches exit at?

Answer 9

Ophthalmic (V1 / VO) = oribtal fissure
Maxillary (V2 / VMax) = round foramen thru rostral alar canal
Mandibular (V3 / VMan) = oval foramen

Question 10

Functions of each of the trigeminal branches?

Answer 10

Question 11

Functions and exiting location of CN VII (Facial Nerve)?

Answer 11

• Innervation to orbicularis oculi mm. & the orbicularis ori m.
• parasympathetic innervation to the lacrimal glands and 3rd eyelid glands
• exits @ stylomastoid foramen

Question 12

Function and exiting location of CN VIII (vestibulococchlear)?

Answer 12

Question 13

CN X function with regards to the oculocardiac reflex and the importance of its monitoring during surgeries like enucleations?

Answer 13

CN VIII mediates the efferent parasympathetic signaling to the oculocardiac reflex. Manipulations to the eye and/or increases in IOP can lead to this reflex, resulting in sudden bradycardia.

DURING SX If this reflex is left unrecognized / untreated, the patient can develop hypotension 2º to bradycardia, which can be detrimental

Question 14

Ocular clinical manifestations of facial nerve deficits?

Answer 14

Neurogenic KCS (dry eyes) with xeromycteria (dry nose)

Question 15

What factors can cause inconsistencies in testing the menace response?

Answer 15

Age, stoic animals, pain (ocular or systemic), cats

Question 16

What tests assess vision?

Answer 16

Menace, cotton ball, maze

Question 17

What tests assess sensation?

Answer 17

Palpebral, corneal

Question 18

What test assesses movement?

Answer 18

Oculcephalic reflex

Question 19

What does the Dazzle Reflex test?

Answer 19

Blink and globe retraction via a bright light

Question 20

In species with double crossover (rostral axons decussate @ optic chiasm & again @ pretectal nucleus in midbrain), what type of response occurs in the PLR?

Answer 20

Direct & consensual (ipsilateral and contralateral pupil constriction)

direct is of greater magnitude than consensual

Domestic species: double crossover is NOT 50:50

Question 21

In species with 100% crossover (birds), what type of response is produced in PLR?

Answer 21

Direct ONLY! No consensual PLR

Question 22

Afferent lesions manifesting as abnormal PLR?

Answer 22

Question 23

Efferent lesions manifesting as abnormal PLR?

Answer 23

Question 24

End-Organ Lesions (Iris) manifesting as abnormal PLR?

Answer 24

Question 25

Identify the top & bottom afferent lesions

Answer 25

Top: image is thru the pupil. Lesion = retinal detachment (notice ballooning of the vessel)
Bottom: optic neuritis (optic nerve is “fuzzy” and edematous)

Question 26

Identify the end-organ lesion

Answer 26

Iris atrophy

Question 27

If PLR is absent with a cataracts patient, what is the actual inciting cause of the absent PLR?

Answer 27

retinal detachment and retinal degeneration

Question 28

If PLR is absent in a SARDS (sudden acquired retinal degeneration syndrome) patient, what is the actual inciting cause of the absent PLR?

Answer 28

Glaucoma and optic neuritis

Question 29

If PLR is absent in patient with central blindness, what is the actual inciting cause of the absent PLR?

Answer 29

multi-focal disease

Question 30

Describe the Marcus Gunn pupil // a positive swinging flashlight test

Answer 30

Swinging Flashlight Test

Normal eye: consensual pupillary constriction occurs (when light shone onto contralateral / non-diseased eye)

Diseased eye (unilateral retinal detachment or unilateral optic neuritis): consensual pupillary constriction occurs, but absent direct pupillary constriction occurs // immediate pupil dilation occurs (when light is shone directly onto diseased eye) = positive swinging flashlight test

Used to detect pre-chiasm optic nerve lesions, or unilateral (asymmetrical) retinal diseases

Question 31

What are the 4 classic signs of Horner’s Syndrome?

Answer 31

1. Enopthalmos (sunken eyes)
2. Ptosis (upper-eyelid drooping)
3. Protrusion of 3rd eyelid
4. Miosis

Question 32

What is Horner’s Syndrome?

Answer 32

Dysfunction of sympathetic innervation to the eyes & facial muscles

Question 33

How to confirm Horner’s Syndrome // localize the inciting lesion?

Answer 33

1 drop of 10% phenylephrine eye drop -> induces mydriasis in…
-** less than 20 minutes for 3rd-order lesions**
- 20-60 mintues for 2nd-order lesions
- 60-90 minutes for 1st-order lesions

It is helpful to consider that the sympathetic pathway is a three-neuron system, and as such Horner’s syndrome can be classified as first, second, or third order.

First-order Horner’s syndrome, or upper motor neuron Horner’s syndrome, may originate anywhere along the pathway from its origin in the hypothalamus through the lateral tectotegmentospinal system in the cervical spinal cord to its termination in the lateral gray column from T1-3. Typically, first-order Horner’s syndrome is accompanied by significant neurologic deficits and has reportedly been associated with neoplasia, trauma, infarctions, and meningoencephalomyelitis.

Second-order Horner’s syndrome (preganglionic) results from a lesion in the pathway beginning from T1-3, through the associated spinal roots and ramus communicans, and up the cranial thoracic and cervical parts of the sympathetic trunk. This trunk travels with the vagus nerve, forming the vagosympathetic trunk, located in the carotid sheath. Trauma, aggressive jugular venipuncture, bite wounds, mediastinal lymphoma, and brachial plexus avulsion have all reportedly been the cause of second-order Horner’s syndrome.28,63

Third-order Horner’s syndrome is most commonly recognized associated with otitis media and results from lesions rostral to the termination of the preganglionic axons in the cranial cervical ganglion, located at the level of the tympanic bulla.