Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Ophthalmology > neuro > Flashcards

neuro Flashcards

1
Q

Balint syndrome triad

A

ocular motor aprexia, simultagnosia, ocular ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Downbeat Nystagmus

A

cerebellomudllulary junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

LHON genetic

A

11778 (worse 4% VA recovery)
14484 (best 65% VA recovery)
3460

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

retrochiasmal VF loss causes in adult and children

A

adult: Stroke (60%), Hemorrhage (10%), trauma (10%)
children: trauma and tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Optic tract syndrome

A

contralateral APD, contralateral homonymous hemianopia, contraletral bowtie atrophty of ON , temporal pallor of the ipsilateral ON

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Visual function assessment

A

VEP shows gross deficits anywhere along the afferent visual pathway from the macula to the occipital lobe.
PAM is used to assess macular vision potential through hazy media (usually a cataract).
full field ERGis best at evaluating rod function although the stimulus frequency can be altered to evaluate gross cone function.
multifocal ERG: assess the focal retinal dysfunction within the macula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ADDA (Kjer syndrome)

A

first 10 years
+ve FH of vision loss
color vision defeciency (tritanopia)
VA 20/60 - 20/200
VF central / cecocentral scotoma or global depression
temporal excavation and pallor or diffuse pallor
OPA1 gene on chromosome 3
neuroimaging to rule out compressive lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

drug induced high ICP

A

Vitamie A, cyclosporin, tetracyclin, GH, OCP, prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CAR and MAR

A

Triad: progressive VA loss, nyctalopia, photophobia
CAR:cone and rod
MAR: only rod
CAR: small cell lungCA, uterus, cervix, breast
intially normal fundus» pale ON, attenuated BV, atrophy of RPE
+/- mild vitritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

neutritional /toxic neuropathy

A

temporal ON pallor
central/cecocentral VF scotoma
central VA loss
Chronic use of ethambutol, ethanol, chloramphenicol, hydroxyquinolones, penicillamine, cisplatin, and vincristine
B-12 / folate / thiamine defeciency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

risk of contralateral ON involvment in AION and NAION ?

A

AION: 55-95% within weeks
NAION: 15% in 5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute toxic neuropathy

A

Ethylene glycol / mythanol
acute bilateral diffuse VA loss
papilledema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Diabetic papillopathy

A

ON swelling with telangiectatic BV on the surface ( leak on FFA but not into vitreous), VF defect is enlargment of blind spot, VA is minimally affected , usually resolved after 2-10 months, if bilateral&raquo_space; MRI and LP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

time to have ON pallor after insult

A

4-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

optociliary shunt causes

A

chronic papilledema, chronic glaucoma, old CRVO, ON sheath meningioma, ON glioma (low grade),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute idiopathic blind spot syndrome

A

monocular , young women, enlargment of blind spot with adjacent photopsias, fundus normal
DD: MEWDS, AZOOR
do multifocal ERG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Heerfordt syndrome (aka uveoparotid fever)

A

uveitis, facial palsy (usually from parotid gland involvement / swelling as seen in this photo),and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lofgren syndrome

A

erythema nodosum, bilateral hilar adenopathy (usually diagnosed on chest imaging), and arthritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Raymond syndrome

A

a 6th nerve palsy with a contralateral hemiparesis due to a lesion in the mid pons affecting the 6th nerve fasciculus along with the corticospinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Claude syndrome

A

superior cerebellar peduncle and 3rd nerve fasiculus typically resulting in ipsilateral 3rd nerve palsy and contralateral ataxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Weber syndrome

A

Lesion of the cerebral peduncle: Contralateral hemiparesis due to involvement of the corticospinal tract within the cerebral peduncle + 3rd CNP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Benedikt syndrome

A

Lesion of the red nucleus and substantia nigra: Contralateral ataxia or tremor / involuntary limb movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Nothnagel syndrome

A

CN III fascicular lesion + ipsilateral ataxia +/- some features of dorsal midbrain syndrome (e.g., vertical gaze paresis, convergence retraction saccades, skew deviation, and lid retraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CAR is associated with which an auto-antibody?

A

anti-recoverin antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MAR is associated with which an auto-antibody?

A

TRPM1 cation channel located on bipolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

both ON hypoplasia and morning glory syndrome associated with ?

A

basal encephalocele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

distinguishing PFK and FK

A

the type of visual field defect in the eye with disc edema; FK will show only an enlarged blind spot and PFK will show a visual field defect consistent with NAION (altitudinal defect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Riddoch phenomenon

A

ability to see moving targets for some patients with cortical
blindness who are unable to see any stationary targets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Anton syndrome

A

bizarre denial of blindness usually found in patients with cortical blindness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pulfrich phenomenon

A

illusion that an object moving perpendicular to a person’s line of sight is actually moving toward them or away from them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Charles Bonnet syndrome (CBS)

A

patients with severe bilateral visual loss of any type (often macular degeneration, glaucoma, or cortical blindness) see formed and unformed visual hallucinations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

target size in Goldmann perimetry

A

Every successive Roman numeral has an area 4 times the
previous such that target** size I = 1/4 mm2, II = 1 mm2, III = 4 mm2, IV = 16 mm2, and V = 64
intensity of the stimulus presented with 1 being the least intense and 4 being the most intense
letter represents the filter** used to dim the light with “a” being the darkest (or most dense filter) and “e” being the lightest filter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

extinction

A

inability to see a stimulus in one hemifield of an eye only when a target is simultaneously presented in both hemifields of that
eye.
parietal lobe lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

sign of a pituitary mass

A

Chiasmatic post fixational blindness
Hemifield slide
See-saw nystagmus
Bitemporal visual field defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Morning Glory syndrome

A

congenital , usually unilateral , more in female
leads to poor vision and APD
associated with
transsphenoidal basal encephalocele
moya moya disease
SRD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

posterior inferior cerebellar artery syndrome
Wallenberg syndrome (WS)
lateral madullary syndrome

A

loss of pain and temperature sensation on the contralateral side of the body (due to impairment of the lateral spinothalamic tract) and ipsilateral side of the face (due to impairment of the spinal trigeminal tract), ipsilateral** Horner syndrome **due to loss of ipsilateral descending sympathetic fibers, Damage to the inferior cerebellar peduncle as it enters the medulla results in ipsilateral ataxia (of the limbs) and ipsilateral axial lateropulsion (falling to the same side of the lesion when walking), Damage to the inferior cerebellar peduncle and the vestibular nuclei results in nystagmus. Other associated features include vertigo (from vestibular dysfunction), diplopia (from skew deviation), and uncontrollable hiccups (from vagal nerve dysfunction).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Amsler grid testing evaluates how many central degrees of the visual field?

A

central 20 degrees

38
Q

Optic nerve drusen VF

A

enlarged blind spot 75%-90% of cases
5%-10% have transient obsecuration of vision

39
Q

optic nerve drusen associated with ?

A

RP
alagile syndrome
PXE
caucasian

40
Q

color vision tests ?

A

Ishihara plates&raquo_space; red green
Lanthony tritan plates» blue yellow
Farnsworth Panel D-15 test, the Lanthony desaturated 15-hue test, or the Farnsworth-Munsell 100-hue test

41
Q

How to Differentiate supranuclear from nuclear and infranuclear lesions?

A

Oculocephalic (Doll’s eyes) reflex
Vestibulo-ocular reflex testing (COWS (cool, opposite, warm,
same)

42
Q

superior oblique myokymia

A

episodic paroxysmal contraction of the superior oblique on one side causing a “jumping” of vision in one eye and binocular diplopia. SOM is almost always unilateral.small amplitude episodic incyclotorsional and infraduction movements of the affected eye.
some cases of SOM demonstrate MRI findings of vascular
compression of the 4th nerve on the affected side.
Stressing the superior oblique muscle by head tilt towards the ipsilateral side or looking down can often trigger an event of SOM.

43
Q

Volitional nystagmus

A

The nystagmus is bilateral, conjugate and marked by high-frequency, low amplitude nystagmus that is typically horizontal. Usually patients can’t sustain the nystagmus for more than a few seconds (although exceptions exist) and there are typically associated eyelid fluttering and convergence movements.

44
Q

ethambutol toxicity

A

estimated 1.5% of patients who use it. result in severe, permanent vision loss. The mechanism of vision loss in Ethambutol toxicity is related to mitochondrial toxicity of the retinal ganglion cells (RGCs). visual fields often show a cecocentral predominate pattern of vision loss with early decreased color vision and visual acuity. optic nerves appear normal until late in the course of vision loss (months after onset).
Ethambutol toxicity have a bitemporal pattern of visual field loss on formal visual fields in addition to a cecocentral pattern.

45
Q

cocaine in horner syndrome

A

no or poor dilation in the affected eye
(block the reuptake of norepinephrine from presynaptic fibers)

46
Q

Apralclonidine in horner syndrome

A

reverse anisocoria (the affected pupil will dilate (upregulation of A 1 receptor agonist ) and the normal pupil will constict (A 2 receptor agonist )

pre-synaptic alpha-2 receptors which act to decrease release of norepinephrine to the dilator muscle

47
Q

anhidrosis in horner according to the level of injury ?

A

1st» ipsilatral body
2nd» ipsilateral face
3rd» moy or moy not present ( limited to the ipsilateral brow)

48
Q

using pilocarpine in dilated unreactive pupil

A

tonic pupil&raquo_space; constrict with diluted pilo 0.125%
normal pupil and 3rd CNP» will constrict to full strength pilo 1%
pharmacologically dilated pupil&raquo_space; will not respond

49
Q

DDx of dilated unreactive pupil?

A

Trauma
tonic pupil
3rd CNP
pharmacologically dilated

50
Q

DDx of heterochromia in children

A

Horner syndrome ( birth trauma)
wardenburg syndrome ( NSD, dystopia canthorum, forelock white hair , heterochromia)
fuchs heterochormic iridocyclitis
neuroblastome (horner syndrome)

51
Q

Adies syndrome

A

damage to the ciliary ganglion or the postganglionic short ciliary nerves that innervate the iris sphincter and ciliary muscles
Tonic dilated oval shaped pupil» chronically become constricted
females (70% of cases) and are usually unilateral at onset
(80%)
nea-light dissociation
decrease corneal sensation
loss of accommodation (improved with time)
segmental contraction of pupil (“vermiform” spontaneous segmental oscillations of the iris musculature)
risk of other pupil 1- 4% / year
sometime associated with hypo reflexia (holmes aides syndrome)

52
Q

causes of a tonic pupil?

A

1.** Adie tonic pupil: a syndrome consisting of a tonic pupil and absent deep tendon reflexes.
2. Local damage to the ciliary ganglion or short ciliary nerves: trauma, viral infiltration, orbital tumors, sarcoidosis, and ischemic processes such as giant cell arteritis.
3. As a presentation of autonomic dysfunction: neurosyphilis, advanced diabetes, dysautonomia syndromes, Guillain-Barré syndrome / Miller fisher syndrome among many others.
4. Idiopathic**

in elderly&raquo_space; syphilis testing or ESR/CRP in elderly patients should be considered in the workup of tonic pupils as neurosyphilis and giant cell arteritis may be the underlying cause

53
Q

tadepole pupil

A

sectoral dilation or spasm of pupil
monocular
associated with Hx of migraine headache

54
Q

1st order neuron in sympathatic pathway

A

posterior lateral hypothalamus and descends through the brainstem to the intermediolateral cell column between C7 and
T2.
cuases of horner: Wallenberg (or lateral
medullary syndrome), thalamic hemorrhage / stroke and tumors,
cervical disc disease, demyelination, and other pathology of the cervical spinal cord

54
Q

3rd order neuron in sympathatic pathway

A

superior cervical ganglion and pass superiorly into the
cranial cavity with the internal carotid artery (ICA) in a fine web of nerves along the wall of the artery known as the carotid plexus.&raquo_space; cavernous sinus. While in the cavernous sinus1» the abducens nerve before joining the nasociliary branch of V1. The
sympathetics then travel with the nasociliary branch of V1 into the orbit and through the ciliary ganglion (without synapsing) to extend to the dilator muscle of the eye.

causes of horner:internal carotid artery pathology (including
dissection), cavernous sinus compressive / inflammatory lesions, and trigeminal autonomic cephalgia type headaches (e.g. cluster headache, SUNCT)

54
Q

2nd order neuron in sympathatic pathway

A

intermediolateral cell column between C7 and T2 to the paravertebral sympathetic chain where fibers ascend to the superior cervical ganglion

causes of horner: apical lung malignancies (“Pancoast syndrome”), thoracic aortic aneurysms, brachial plexus injuries, and thoracic surgery with disruption of the superior portion of the paravertebral sympathetic chain.

55
Q

physiologic anisocoria

A

almost always less than 1 mm difference in pupillary diameter in physiologic anisocoria.
20% of general population
physiologic anisocoria (PA) is the same in light and dark conditions

56
Q

Hydroxyamphetamine 1% in horner syndrome

A

pre-ganglionic lesion (1st or 2nd order Horner syndrome),
the pupil will dilate whereas in a post-ganglionic lesion (3rd order) it will not dilate

57
Q

Adrenaline 1:1000 in horner syndrome

A

preganglionic lesion, the pupil will fail to dilate whereas in a
postganglionic lesion it will dilate.

58
Q

Dilute phenylephrine (1%) in horner syndrome

A

Much like apraclonidine 0.5% or 1% testing this may lead to a reversal of anisocoria.

59
Q

smaller than average pupils

A

opioid narcotic ingestion, increasing age, chronic tonic pupils (initially large but “shrink” over time), parasympathomimetic agents (such as pilocarpine), sleep, and pontine hemorrhages.

60
Q

larger than average pupils

A

young age, seizures,arousal (fight or flight response), sympathomimetic medications, and anoxic brain injury (possibly due to midbrain ischemia)

61
Q

Anisocoria which is greater in dark (miotic pupil)

A

Horner’s syndrome, old chronic Adies pupil, pharmacologic miosis, or posterior synechiae.

62
Q

differential diagnosis for paradoxical pupillary reaction

A

congenital stationary night blindness
* congenital achromatopsia
* Best disease
* dominant optic atrophy
* optic nerve hypoplasia
* Leber congenital amaurosis
* Albinism
* retinitis pigmentosa
immediate pupillary constriction instead of dilation upon turning the exam room lights off.

63
Q

Color vision loss can be acquired in association with

A

Macular Disease
parital lobe lesions
optic neuropathy

64
Q

GCA ocular presentation

A

The majority of GCA cases present with arteritic anterior ischemic optic neuropathy although less common presentations include posterior ischemic optic neuropathy, central retinal artery occlusion, branch retinal artery occlusion, choroidal
infarction, and diplopia from ischemia of the extraocular muscles and/or ocular motor nerves.

65
Q

common DVST associated hypercoaguable
states include

A

pregnancy (and the peripartum period), oral contraceptive use, lupus, inherited coagulopathies, infection, dehydration, and acute head injury

66
Q

oculopharyngeal muscular dystrophy

A

middle age
AD
bilateral progressive ptosis and dysphagia
external ophthalmoplegia , facial weakness, proximal limb weakness, slowed saccades, and ocular misalignments
(PABPN1 gene)
filamentous intranuclear inclusion in affected muscles

67
Q

CPEO

A

sporadic Mitochondrial DNA deletion
slowly progressive symmetric ptosis and ophthalmoplagia
no diplopia or pupil invlovment
asymptomatic orbicularis, neck, and limb weakness
KSS ( heart block, ophthalmoplagia, pigmentary retinopathy, SNH loss, dementia,CSF protein above 100 mg/dl, or ataxia), <20 y
regged red fiber

68
Q

miller fisher syndrome

A

ocular variant of Guillain-Barré Syndrome
ataxia, ophthalmoplegia, and areflexia
90% of patients with Miller Fisher syndrome will have** GQ1b IgG autoantibodies **in the serum
excellent prognosis over months with IVIG and plasmapheresis
diplopia. pupillary involvement facial nerve dysfunction cytoalbuminal dissociation in the CSF, and an antecedent C. jejuni infection can be present

69
Q

myotonic dystophy

A
  • AD
  • ophthalmoplegia, ptosis, pigmentary retinopathy, miotic poorly reactive pupils, “Christmas tree” cataracts.
  • atrophy of the muscles of the face “hatchet face”and extremities with distal muscle weakness predominating initially.
  • continued contraction of muscles despite attempted relaxation.
  • cognitive delay, testicular atrophy, cardiac abnormalities/arrhythmias, and heart failure.
70
Q

Melkersson-Rosenthal syndrome

A

recurrent facial paralysis (~30% of cases), orofacial edema (usually the lips; “cheilitis”), and lingua plicata (i.e. fissured tongue)
typical granulomatous infiltration.

71
Q

apraxia of eyelid opening DDx

A

extrapyramidal disease including
* Parkinson disease
* Huntington disease
* Wilson disease
* progressive supranuclear palsy.

72
Q

Progressive supranuclear palsy Vs Parkinson disease

A

PSP»to affect vertical saccades first

73
Q

combination of uveitis and facial nerve palsy

A

sarcoidosis (loves 2 and 7 CN)
Lyme Disease

74
Q

Millard-Gubler syndrome

A

affect the ventral pons
7nth CNP
6th CNP
contralateral hemiplagia

75
Q

types of diplopia?

A

binocular : misalignment
monocular: optical problem
bilateral monocular: optical problem or functional (stoke , epilepsy, migraine)

76
Q

One-and-a-half syndrome

A

internuclear ophthalmoplegia (INO) with an ipsilateral horizontal gaze palsy.
RIGHT one-and-a-half syndrome :
impaired adduction OD (due to the right INO) + impaired abduction OD + impaired adduction OS (due to the right gaze palsy).
The only horizontal eye movement left (“the half”) is abduction of the LEFT (contralateral) eye.
This contralateral eye would classically display
an** abduction nystagmus** as typically occurs in an INO
Vertical gaze is unaffected in this syndrome.
stroke or other lesion of the pontine region which contains the medial longitudinal fasciculus (MLF) and paramedian pontine
reticular formation (and CN VI nucleus).

77
Q

direct, high flow
carotid-cavernous fistula (CCF)

A

arterialization of the conjunctival vessels, chemosis, elevated intraocular pressure (IOP), proptosis, cavernous sinus cranial neuropathies (CN III, IV, VI, V1, V2), optic disc swelling, and venous stasis retinopathy.
vision loss can be due to glaucoma, venous stasis, or corneal exposure.

78
Q

Cavernous sinus thrombosis

A

same as C-C fistula + pt is septic and has miningitis symptoms
direct or heamtogenous spread of sinusitis, otitis media, facial furancle infection or dental abscess
+ve bllod culture and CSF
VA loss (15%) due to arterial occlusion, venous stasis, glaucoma , corneal exposure
Rx: broad spectrum AB +/- anticoagulent
complication: cerebral infarction , meningitis

79
Q

Gradenigo’s syndrome

A

Inflammation in the petrous portion of the temporal bone can affect the 5th, 6th and 7th cranial nerve

80
Q

ocular tilt reaction

A

(1) a head tilt towards the hypotropic eye; (2) a skew deviation; and (3) bilateral torsional deviations
(the hypertropic eye is usually incyclotorted to a lesser degree than the hypotropic eye is excyclotorted).

81
Q

Skew deviation

A

supranuclear disorder due to distruption of vistibular input to brainstem area resposnible of vertical eye movment (4th and 3rd)
due to cerebellar or brainstem insult
can cause comitant/ incomitant vertical deviation
unkmown cuase of SD requires neuro imaging and stroke work up
diffrentiate it from 4th CNP:
1- hypertropic eye incyclotorte
2- upright -supine test: hypertropia is measured in the upright position and then again in the supine position using alternate cover testing. In patients with a SD, there will often be a
profound reduction in the hypertropia measurement (> 50%) when laying supine while** there is no hypertropia reduction in patients with 4th nerve palsy.**

SD often manifests as weakness of the inferior rectus
muscle(s). Skew deviation presenting with bilateral inferior rectus weakness presents with alternating hypertropia (in which a right hypertropia is seen in right gaze and a left hypertropia is
seen in left gaze) often localizes to the cervicomedullary junction, and can be associated with downbeat nystagmus.

lesion of the MLF often causes a skew deviation in addition to an
INO.

82
Q

divergence insufficiency

A

normal motility and a comitant esotropia that resolves with convergence.
if presented acutly or associated with other neurological symptoms consider ordering MRI brain ans acetylcholine receptor antibodies
usually resolved spontaneously and treated temporarly with pris od SX if stable for at least 3-9 MONTHS

83
Q

Tolosa-Hunt syndrome

A

severe ipsilateral periorbital pain along with deficits of any or all of the nerves passing through the affected cavernous sinus (CN 3,4,V1,V2,6 and the sympathetics).

84
Q

Congenital fibrosis of the extraocular muscles

A

caused by congenital agenesis of the 3rd nerve central levator palebrae superioris subnucleus and the bilateral
3rd nerve superior rectus subnuclei.

85
Q

Mobius syndrome

A

agenesis of the 6th and 7th cranial nerves producing failure of
abduction bilaterally, esotropia, and facial diplegia

86
Q

Raymond-Cestan syndrome

A

damage to MLF and corticospinal tracts; leads to
INO + contralateral hemiparesis

87
Q

Eight-and-a-half syndrome

A

one-and-a-half syndrome + ipsilateral facial
palsy (i.e. 1.5 + 7)

88
Q

alternate hypertropia DDX

A

SD:in which a right hypertropia is seen in right gaze and a left hypertropia is seen in left gaze
bilateral 4th CNP:hypertropia of the adducting eye (not abducting eye) so that there is a right hypertropia in left gaze and a left hypertropia in right gaze.
partial CN III palsy with superior and inferior rectus weakness
can result in a hypertropia that alternates with up-gaze and down-gaze. With a partial right CN III palsy, for instance, there may be a left hypertropia on up-gaze and a right hypertropia on down-gaze.
Bilateral inferior rectus restriction can occur with thyroid associated ophthalmopathy and would cause a left hypertropia on right gaze and a right hypertropia on left gaze.

89
Q

Horizental Gaze palsy

A

A gaze palsy to one side means that BOTH eyes have
limited motility to that side.
MLF with either 6 CNP or PPRF will cuase ipsilateral gaze palsy

90
Q

3rd nerve nuclear lesion

A

bilateral ptosis, bilateral superior rectus dysfunction, ipsilateral mydriasis, and ipsilateral dysfunction of the medial rectus, inferior rectus, and inferior oblique muscles.

Ophthalmology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions