Visual Fields and Gaze Palsies B&B + Vertigo

Question 1

what are the 2 projections of the LGN?

Answer 1

lateral geniculate nucleus (thalamus) is major termination site of retinal projections, sends fibers to the visual cortex via:
1. Meyer’s loop - temporal lobe
or
2. Baum’s loop - parietal lobe

Question 2

damage to which portion of the visual tract would cause anopia?

Answer 2

optic nerve compression OR retinal lesion

[for example, optic neuritis: demyelinating, associated with multiple sclerosis]

Question 3

amaurosis fugax

Answer 3

painless, transient vision loss in one eye (anopia) - classically described as “curtain shade” over vision

due to damage to optic tract or retina - may be a symptom of TIA (transient ischemic attack), often via embolism to retinal artery (common source is carotid artery)

Question 4

painless, transient anopia classically described as “curtain shade” over vision

Answer 4

amaurosis fugax

due to damage to optic tract or retina - may be a symptom of TIA (transient ischemic attack), often via embolism to retinal artery (common source is carotid artery)

Question 5

damage to which portion of the visual tract would cause homonymous hemianopsia? (2)

Answer 5

optic tract lesion or posterior cerebral artery (PCA) stroke (damages occipital lobe)

bilateral loss of one half of the visual field

[recall PCA strokes spare the macula due to dual blood supply by MCA!!]

Question 6

damage to which portion of the visual tract would cause “pie in the sky” vs “pie in the floor” quadrantic anopia?

Answer 6

damage to Meyer’s loop running through temporal lobe = “pie in the sky”

damage to Baum’s loop running through parietal lobe = “pie in the floor”

Question 7

explain how lateral conjugate gaze works - include the nuclei involved

Answer 7

1. PPRF (paramedian pontine reticular formation) signals to CN VI (abducens), which activates lateral rectus on one side
2. some CN VI also sends some fibers via medial longitudinal fasciculus (MLF) to CN III in opposite eye, which activates medial rectus one the other side

Question 8

where is the medial longitudinal fasciculus (MLF) found, and what is its function?

Answer 8

MLF is found in medial pons and is very important for conjugate gaze

PPRF —> CN VI, activating lateral rectus and also sending fibers along MLF —> CN III, activating contralateral medial rectus

lesion to MLF —> internuclear opthalmoplegia

Question 9

what is the cause of internuclear opthalmoplegia, and how does it present?

Answer 9

lesion of MLF (medial longitudinal fasciculus) required for conjugate gaze

—> horizontal gaze disorder with weak adduction of affected eye + nystagmus of abducted eye (lesioned MLF cannot communicate with adducting eye)

convergence spared (different neural pathway)

Question 10

Pt presents with inability to gaze horizontally. Their L eye cannot move towards their nose, and a nystagmus is noted in the R eye. However, convergence is intact. What is the diagnosis?

Answer 10

internuclear opthalmoplegia: lesion of MLF (medial longitudinal fasciculus) required for conjugate gaze

—> horizontal gaze disorder with weak adduction of affected eye + nystagmus of abducted eye (lesioned MLF cannot communicate with adducting eye)

convergence spared (different neural pathway)

Question 11

what is the most important clinical cause of MLF syndrome?

Answer 11

aka medial longitudinal fasciculus syndrome: MLF required for horizontal conjugate gaze, if lesioned, cannot communicate to opposite (adducting) eye

occurs commonly in multiple sclerosis because MLF is highly myelinated

Question 12

how does MLF syndrome differ in presentation from abducens (VI) palsy?

Answer 12

look at the eye that is stuck - is it trying to move medially or laterally?

if the eye CANNOT move MEDIALLY = internuclear opthalmoplegia (MLF syndrome)

if the eye CANNOT move LATERALLY = CN VI (abducens) palsy

Question 13

how would a PPRF lesion present?

Answer 13

PPRF = paramedian pontine reticular formation, signals to CN VI (abducens) to activate lateral rectus

lesion (such as by medial pons lesion) —> ipsilateral horizontal gaze palsy, can’t look to the side of the lesion (left PPRF coordinates left conjugate gaze)

convergence is preserved (separate neural pathway)

Question 14

damage to which neural structure would cause an ipsilateral horizontal gaze palsy (can’t gaze towards the side of the lesion)

Answer 14

PPRF = paramedian pontine reticular formation, signals to CN VI (abducens) to activate lateral rectus

lesion (such as by medial pons lesion) —> ipsilateral horizontal gaze palsy, can’t initiate horizontal gaze on side of lesion (left PPRF coordinates left conjugate gaze)

convergence is preserved (separate neural pathway)

Question 15

how would the presentation of an MLF lesion differ from that of a PPRF lesion

Answer 15

recall PPRF —> CN VI, activating lateral rectus and also sending fibers along MLF —> CN III, activating contralateral medial rectus

PPRF lesion (or abducens/CN VI nucleus lesion) = ipsilateral horizontal gaze palsy (affected eye can’t look laterally)

MLF lesion = contralateral gaze palsy (opposite eye can’t look towards side of lesion)

damage to both = one and a half syndrome

Question 16

Pt presents with complaint of diplopia. When asked to gaze to the right, their R eye gazes horizontally but their L eye remains fixed. When asked to gaze to the left, both eyes remain fixed. Where did the damage occur? (include side)

Answer 16

one and a half syndrome: damage to BOTH PPRF and MLF (close together in medial pons!)

—> internuclear opthalmoplegia (MLF syndrome, cannot tell opposite eye to move medially) + loss of lateral gaze to affected side (PPRF, cannot initiate lateral gaze on affected side)

in this patient affecting the LEFT (the side that cannot initiate/ is frozen in both directions)

convergence is spared (different neural pathway)

Question 17

frontal eye fields of the cortex are Brodmann area ___

how would a lesion present?

Answer 17

Brodmann area 8

normally, both eyes are being pushed towards the middle by each side… if there is a lesion, the “tug of war” is lost and both eyes deviate towards the lesioned side

Question 18

how can you differentiate central vs peripheral vestibulopathy?

Answer 18

peripheral = unilateral, causes hearing loss, horizontal nystagmus only (fast component towards normal ear), postural instability without falls

central = bilateral, hearing unaffected, can cause horizontal (direction-changing) or vertical or rotational nystagmus, postural instability + falls, focal deficits (depending on location of lesion)

Question 19

are the following consistent with peripheral or central vestibulopathy?
a. hearing loss
b. direction-changing nystagmus
c. fast component towards normal ear
d. postural instability + falls
e. focal deficits

Answer 19

peripheral = unilateral, causes hearing loss, horizontal nystagmus only (fast component towards normal ear), postural instability without falls

central = bilateral, hearing unaffected, can cause horizontal (direction-changing) or vertical or rotational nystagmus, postural instability + falls, focal deficits (depending on location of lesion)

Question 20

with peripheral vestibulopathy, there is unidirectional peripheral-type nystagmus with a fast corrective component - to which side is this corrective movement (normal or lesioned)?

Answer 20

fast component towards NORMAL ear

Question 21

will peripheral or central vestibulopathy present with a positive head impulse?

Answer 21

positive head impulse = corrective saccade with head turned towards side of lesion (will take longer for eyes to readjust back to middle)

presents with peripheral vestibulopathy

Question 22

what vestibulopathy symptoms will present with vertebrobasilar stroke vs vestibular neuritis?

Answer 22

both spontaneous causes of continuous vestibulopathy

vertebrobasilar stroke —> postural instability + falls, sudden persistent hearing loss, facial numbness + weakness, dysarthria/dysphagia, Horner’s syndrome, central-type nystagmus (direction-changing, vertical), negative head impulse

vestibular neuritis —> association with viral prodrome, gradual resolution, mild gait impairment (NO falls), positive head impulse (catch-up saccade toward injured side), peripheral type nystagmus (unidirectional, beats away from affected side), absent focal deficits

Question 23

how does Meniere Disease vs vestibular migraine present?

Answer 23

both causes of spontaneous episodic vestibulopathy

Meniere Disease: 20mins-3 hours, unilateral, fluctuating hearing loss + tinnitus preceding vertigo, drop attacks (Tumarkin falls), peripheral-type nystagmus

vestibular migraine: hours-days, sensory hypersensitivities + motion sickness, associated with migraine

Question 24

which 2 types of nystagmus indicate a central lesion?

Answer 24

1. direction-changing
2. vertical

Question 25

how does BPPV present?

Answer 25

benign positional paroxysmal vertigo: 10-30 second episodes triggered by positional change, gait instability but no falls

positive Dix-Hallpike test (delayed, remitting up-beating nystagmus with torsional component toward the downward/affected ear)

Question 26

patient chart describes: 20mins-3 hours lasting episodes of unilateral, fluctuating hearing loss + tinnitus preceding vertigo, drop attacks, and peripheral-type nystagmus

Is the cause of their vestibulopathy most likely:
a. vertebrobasilar stroke
b. Meniere disease
c. vestibular neuritis
d. benign paroxysmal positional vertigo (BPPV)

Answer 26

b. Meniere disease - cause of spontaneous episodic vestibulopathy

Question 27

lesions to which 7 components of the vestibular system can produce vestibulopathy (vertigo)?

Answer 27

1. inner ear
2. CN VIII
3. vestibular nuclei in medulla
4. cerebellar peduncles and pons
5. cerebellum
6. red nucleus in midbrain
7. thalamus

Question 28

paralysis of rightward gaze in R eye ONLY + esotropia of R eye with forward gaze = lesion where?

Answer 28

lesion of right abducens (CN VI) nerve —> CN VI palsy

[esotropia = medial strabismus on forward gaze, occurs in affected eye when there is CN VI nerve OR nucleus lesion]

Question 29

paralysis of rightward gaze in BOTH eyes + esotropia of R eye with forward gaze = lesion where?

Answer 29

lesion of right abducens nucleus —> right lateral gaze palsy

[esotropia = medial strabismus on forward gaze, occurs in affected eye when there is CN VI nerve OR nucleus lesion]

Question 30

how does presentation of a CN VI nerve vs nucleus lesion present?

Answer 30

BOTH present with esotropia of the affected eye on forward gaze (medial strabismus)

CN VI nerve lesion —> CN VI palsy: affected eye cannot abduct, normal eye CAN

CN VI nucleus lesion —> lateral gaze palsy: neither eye can abduct TOWARD the affected side

Question 31

how can you differentiate between a CN VI nucleus lesion vs a PPRF lesion?

Answer 31

CN VI nucleus lesion —> lateral gaze palsy: neither eye can abduct toward the affected side + ESOTROPIA of affected eye (medial strabismus on forward gaze)

PPRF lesion —> lateral gaze palsy: neither eye can abduct toward the affected side (NO esotropia)

Question 32

right lateral gaze palsy with NO esotropia present = lesion where?

Answer 32

lesion of right PPRF - can’t initiate rightward lateral gaze

[esotropia only presents with lesion of CN VI nucleus OR nerve]

Question 33

left lateral gaze palsy + R eye nystagmus with right lateral gaze and no movement of L eye + L esotropia on forward gaze = lesion where?

Answer 33

left MLF AND left abducens nucleus lesion —> 1 1/2 syndrome

esotropia = medial strabismus on forward gaze, occurs in affected eye when there is CN VI nerve OR nucleus lesion

[if PPRF was lesioned, there would be NO esotropia]