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160 Cards in this Set

  • Front
  • Back

Drugs that can cause AION

Viagra


Amiodorone


Nasal decongestants


Sumatriptan


Interferons


Dapsone

Pearl


Hemianopai never reduces visual acuity

If acuity impaired, look for cataract, AMD etc


Bilat hemifield defect that involve macular representation (occipital pole) can impair visual acuity to the same degree

Gaze evoked or postural induced transient visual obscurations and hallucinations can be a 1st sign of raised ICP

---

Cerebral visual loss


Causes - Name 5

1. Vascular (PCA stroke) anoxia, CVST, PRES


2. Head trauma


3. Occipital mass


4. Infection - CJD, PML


5. Toxic - cyclosporine, mercury


6. Migraine 7 Occipital seizures

Transient Monocular


Vision Loss - Causes

1. Vascular - TIA, orbital ischemia, Retinal ischemia, choroidal ischemia, retinal migraine


2. Optic N - Papifledema, drusen, compression (gaze evoked) Uhthoff's


3. Migraine aura, cc Fistual

Occipital Seizure


- Transient visual loss ictal or post ictal


- visual hallucinations, gaze deviation

---

Object agnosia


Localize

Bilateral mesial


temporal lobes



Anton's syndrome


Localize

Bilateral occipital lobes


(or) bilat optic radiations

Topographagnosia


- Localize

Rt medial occiptotemporal

Hallucinations associated with sleep - wake cycle

Peduncular


Narcolepsy


Normal

Charles Bonnet syndrome


- Patient's have insight and N cognition


Rx: anticholisesterase inhibitors, SSRI, haloperidol

---

Charles Bonnet Syndrome

Release hallucinations


less stereotypical


Normal cognition


Sensory deprivation of v. cortex


due to visual field defects in both eyes (cataracts, AMD, hemianopia)

Alexia without agraphia

Lt occipitotemporal and posterior splenium of cc

Alexia with agraphia

Lt occipitotemporal with Lt angular gyrus

Proopagnosia - Localize

Bilat occipitotemporal (bilat medial temporal or Rt medial temporal) (can see in semantic FTD)

Balint Syndrome


_triad_

Simultaneous agnosia


Optic ataxia


Ocular apraxia

Achromtopsia


Localize

Lingual and fusiform gyri of bilateral medial temporal lobe (or) unilateral in hemiachromatopsia

Akinetopsia


Localize

Bilateral occipito - parieto - temporal junction

Balint's Syndrome


- localize-

Bilateral occipitoparietal lobes

2 ND disorders associated with V. hallucinations

1. DLB


2 PD


Drugs that can cause hallucinations

LSD


L-dopa


Psilocybin


Mescaline


Scopolamine

Peduncular Hallucinosis

Rostral midbrain lesion cerebral peduncles involved (Patients have disordered sleep-wake cycles)

Visual Hallucinations


Classify

1. Ocular (Entopic phenomena)


2. Cerebral


- Sleep wake changes


- Altered mental status


- Normal sensorium/cognition

Blind sight in visual loss

Residual, degraded, unconscious perception of stimuli in their blind hemifield ? 2° to routes to extra striate cortex that bypass geniculostriate pathway

Seizures arising from occipital lobes have color and motion components (unlike migraine)

---

Migraine Visual aura


- geometric pattern


- Black and white


- slowly move/grow across one quadrant


- visual blurring/loss in the entire visual field or portion

---

OTR in lower pons/medulla lesion


Hypertrophic eye contralateral to the lesion in the lower pons + medulla

---

Duane's Syndrome


- Cause

? prenatal insult between 4th and 10th week of embryogenesis


? DURS2 gene on Chr2

Mechanism of retraction in Duane's syndrome

Co contraction of MR and LR during adduction


- Gives rise to pseudoptotic appearance or pseudo enophthalmic appearance


- Causes globe retraction

Duane's retraction syndrome


Pathology findings

Absent sixth N


Absent or hypoplastic sixth nuclei


Aberrant innervation of LR by axons from MR subnucleus


- Explains the co contraction of both MR and LR during adduction causing globe retraction

Types of Duane's Syndrome

Type 1 - 80% limited abduction


Type 2 - 7% limited adduction


Type 3 - 15% add and Abd limited

Types of Infantile nystagmus

1. Congenital


2. Manifest latent nystagmus

INO and Lt 4th N palsy - localize the lesion

Rt IVth N nucleus and MLF lying anterior to it

Lt 4th N palsy


Rt Horner's syndrome


Rt limb ataxia


Lt spinothalamic deficit


localize the lesion

Rt 4th N fascicle pre-decussation = Lt 4th N palsy


Rt sympathetics - horners


Rt dentato rubro fibers = Rt ataxia


Rt spinothalamics - Lt body

Adult


3rd N


4th N


6th N palsy


Common causes


Top 3

3rd vascular, aneurysm, idiopathic


4th trauma, idiopathic, ischemic, cong


6th idiopathic

Pediatric 3rd


4th


6th N palsy


Common causes

3rd Congenital


4th Trauma, idio, neoplastic


6th Neoplastic

6th N palsy


+ Horners same side


- localize

Cavernous sinus


Pons

Difference between SOF and orbital apex syndrome

Optic N involved in orbital apex syndrome

CC Fistulas - types

1. High flow CCF - 2° to trauma, CEA complication, rupture of IC aneurysm


2. Low flow CCF - spontaneous

How would you investigate for CCF?

1. Orbital US


2. Color doppler


3. MR/MRA


4. Conventional angio

Findings in Fastigial N lesion

Hypometric contraversive sacc


Hypermetric Ipsi saccades

Findings in dorsal vermis lesion?

Hypermetric contra saccades


Hypometric Ipsi saccades


Ipsi saccadic sm. pursuit


Opsoclonus ( disinhibits fastigial N)

Gaze evoked Nystagmus


Pathophysiology

* 'leaky ' neural integrator


* Flocculus lesions


( NI = NPH-MVN complex)

Rx options for any nystagmus

1. Treat underlying disorder if possible (eg surgery)


2. Symptomatic Rx ( 4-AP, baclofen, gabapentin, memantine)


3. Base down prisms

5 Causes of Monocular Nystagmus (or) dissociated nystagmus

Superior oblique myokymia


Spasmus nutans


Amblyopia


Ictal nystagmus


IND


Nystagmus with absent one eye


Acquired monocular blindness


Brainstem infarction ( thalamus, upper midbrain)

Congenital Nystagmus


- Features


mnemonic CONGENITAL

C- Convergence + eye closure dampen nystagmus


O - Oscillopsia absent


N - Null zone present


G - Gaze position does not change direction of nystagmus


E - Equal amplitude and frequency of nystagmus


N - Near acuity is good


I - Inversion of OkN


T - Turning of head allows head to enter into null zone


A - Absent nystagmus during sleep


L - Latent nystagmus occurs

Cortical vision loss versus bilat ocular disease - differentiate

Cerebral


VA N


Pupillary Intact


VF Hemifield (vertical meredian)


Blindsight Present


Anton's Present


Ocular


VA Impaired


Pupillary Impaired


Reflexes


VF Horiz meridian


Blindsight Absent


Anton's Absent

Sudden onset headache decreased vision or VF loss


ophthalmoplegia


Altered LOC


Endocrine dysfunction


- Localize

Pituitary Apoplexy


Rx with high dose steroids for hypopituitarism


Medical emergency

Extrastriate visual processing - 2 streams

1. Occipito temporal (what) - object identify such as form and color


2. Occipito - parietal (where) - localization and preparation for action, motion stercopsis, spatial location

Achromatopsia


Localize

Fusiform and lingual gyri

insert pic here

Rt posterior occipital cortex sparring the unpaired nasal fibers representing 'temporal cresent'

Localize


insert pic

Rt Anterior occipital cortex involving the unpaired nasal fibres representing 'temporal crescent'

Localize


insert pic

Junctional scotoma

Localize


insert pic

Lt temporal lobe (Meyer's loop)

Localize


insert pic

Rt optic tract


Insert pic

Lt occipital (lower bank)

RADP with optic tract lesion - where and why?

1. Contalateral eye


2. Because more nasal fibers cross (57:43) than temporal


Localize


insert pic here

Lt LGN


Quadruple setoranopia


(anterior choroidal artery)

Visual symptoms in Migraine vs Occipital Sz

Migraine


Shape: geometric lines


color: Black/white


Duration: 5-60 mins


Within Central visual field: frequent


Occip. Sz


Shape: Multiple circles, round spots


Color: Colors


Duration: 1-3- secs


Within Central visual field: Occasional

Localize


Insert pic here

Left LGN supplied by lateral choroidal artery


- Sectoranopia

Types of VF defects seen in ON

Altitudinal


Arcuate


Cecocentral


Central

Retrobulbar ON compression - Name 5 causes

1. Intraorbital tumors, (meningiomas, pit. adenomas, cranopharyngioma, chordoma)


2. Vascular - aneurysms


3. Thyroid disease


4. Bone lesions


5. Inflmm (paranasal sinus)

Pathognomonic finding in ONS meningioma

Optociliary shunt vessels - loops of veins that shunt venous drainage from blocked central retinal venous circulation to choroid circulation

Nutritional causes of optic neuropathy

Vitamin B12 deficiency


Thiamine


Niacin


Folate

Blood Supply of ON

Ophthalmic artery


Orbital course - post ciliary


Intracranial course - ICA, Superior hypophyseal arteries, A1 ACA and ACOM

3 segments of ON

1. Intra orbital


2. Intra canalicular (prone for trauma)


3. Intra cranial


Toxic optic neuropathy

1. Etoh


2. Methanol


3. Ethylene glycol


4. Organic solvents


5. Amlodorone


6. Ethambutol

Von Graefe's sign eyelid retractioin seen with downgaze in Grave's disease

Pseudo Von Grafefe's sign aberrant regeneration of 3rd N IR fibers rewire into levator therefore


downgaze causes eyelid elevation (retraction)


Can be seen with adduction

Bowtie atrophy


- Chiasmal lesions


- Optic tract lesions

3 group of ganghori cell fibers atrophy


A. nasal to macula


B. nasal retina


C. temporal


Results in bowtie atrophy

1° and 2° optic atrophy - differentiate


No disc edema


Disc margins sharp + clearly defined



Disc edema present somepoint


Disc margins


rough/poorly defined


Gliosis or water marks suggesting previous edema

Optic atrophy - timeline

takes 4-6 weeks to develop

Small c/d ration + Aion


c/d ratio = 0.4 discs with NAON tend to have small scleral openings and crowding of nerve fibers

PEARL


TMVL preceeded by diplopia is diagnostic of GCA

Types of optic atrophy

1° lesions that damage ganglion cells/axons in the absence of optic disc swelling


2° characterized earlier by disc edema some time during the course → 4-6 weeks → atrophy

Blook work in GCA

ESR


CRP


↑ platelets


Anemia


↑ fibrinogen

% of patients with normal ESR in GCA

12%


ONTT results


IV steroids hasten the recovery of vision loss but does not improve long term visual outcome

Therefore Rx with steroids should be bases on quality of life, risk to patient, vision in the fellow eye

ONTT results


IV steriods hastened visual recover only in the 1st 2 weeks


After 1 yr FU there was no significant differences among the groups in VA, VF, HRR

Oral prednisone increased the rate of recurrence


IV steriods lowered the risk of MS only in the 1st 2 yrs thereafter no effect.

Optic neuritis and risk of MS

10


All corners: 38%


Normal MR: 22%


> 1 or more MR lesion: 56%


15


All corners: 50%


Normal MR: 25%


> 1 or more MR lesion: 72%

ONTT


457 patients 18-45 yrs


Acute unilateral ON


< 8 days from onset

75% women


mean age 32 yrs


EOM pain 92%


Optic disc edema 35%


and normal in 65%

Visual recover in ON

Majority of the patients will notice improvement of vision in the 1st one month


6 months 94% 20/40


75% 20/20


12 months 90% 20/40 or better

Bilateral transient


vision loss


- 5 causes

Vascular - occiptial ischemia, bilat. carotid disease


Other - Papilledema


Occipital migraine aura


Occipital seizures


PRES, contrast dye

3 infectious causes of optic neuropathy

Syphilis


Cat scratch


Lyme

Why swing the light in testing for RAPD?

Because you are comparing the relative strength of the light signals reaching the Edinger-Westapl N therefore NO light swing you can miss RAPD

Arterial supply of eye


Ophth art - CRA


- Ciliary arteries

CRA supplies - inner retinal layers


Cilicary ( posterior) - choroid, out retinal layers, optic nerve head

RAPD


When there is an unilateral afferent pathway defect, the pupils show subnormal response to light with decreased force and amplitude of constriction

The combination of subnormal direct pupillary light response and a normal indirect consensual light response is termed RAPD or Marcus- Gunn pupillary abnormality

Causes of raised ICP and papilledema - Name 5

1. tumor


2. hydrocephalus


3. pseudotumor


4. CVST


5. meningeal process ( lymphoma, sarcoid, meningitis)

Effect of severe carotid stenosis on retinal vessels

Venous statis retinopathy


Neovascularization of retina

Define supranuclear ocular motility disorder

Condition that results from damage to cerebral or vestibular pathways descending on ocular motor N

Post ganglionic parasympth innervation


- fibers to ciliary muscle out number that if iris sphincter muscle


RATIO 30:1

---

Adie's syndrome


- Adie's pupil + absent reflexes in LE


aka Holmes-Adie syndrome

---

Causes of Ll-N dissociation


Name 5 locations and etiologies for each?

insert diagram here


Superior oblique myokymia


Rx

1. Responds well to carbamzepine


Can also try propramolol, Gabapentin, Phenytoin


2. Harado-Ito procedure: weaken cyclotersion

Superior Oblique myokymia


- 2° to spontaneous discharge of trochlear N motor units


- Can be idiopathic or 2° to vascular loop compression

---

Superior oblique myokymia

1. Monocular oscillopsia, cyclovertical diplopia


2. Lasts seconds/occurs in clusters


3. Triggers - looking down and back to midposition, blinking, head tilt

Localization of ocular bobbing

1. Pontine ICH or infarct in typical OB


2. Metabolic encephalopathy and cerebellar hematoma in atypical OB

Pharmacologic dialted pupils do not respond to pilocarpine (due to lack of ACh in the nerve endings - they have blocked by anticholingergic)

---

NEAR TRIAD


mnemonic CAM (or) MAC

M - miosis


A - accomodation


C - Convergence

Ocular Bobbing - types

1. Typical - associated with paralysis of horizontal eye movements


2. Atypical - associated with intact horizontal eye movements

Pathogenesis of Opsoclonus

1. Dysfunction of omnipause neurons in the pons


2. Disinhibiton of fastigial N 2° to loss of purkynje cells in the dorsal vermis

Rx of opsoclinus in childran with neuroblastoma

1. Surgery - fails to respond


2. ACTH


Corticosteroids


IVIG

Painful loss of vision


F- functional


A - Aion (carteritic)


C - Corneal ulcer


E - Endophthalmitis


G - Glaucoma


O - Optic neuritis


D - Dissection

Painful loss of vision


H -


A - AION (non-arteritic)


D - Detachment


F- Functional


O - Occlusion (CRAO, BRAO, Venous)


A - Amaurosis fugax


M - Migraine

Painless vision loss


Name 5 causes

CRAO


N- AION


BRAO


RVO


TIA


Vitreous hemorrhage


Retinal detachment


Ocular migraine, FVL

Painful vision loss


5 Causes

Optic Neuritis


A - AION


Optic neuritis


Angle closure glaucoma


endophthatlmitis


Corneal ulcer


FVL

Artery of Percheron supplies what structures?

Medial inferior thalamus


Rostral midbrain


including ri MLF


(can cause selective paresis of down gaze)

Other name for artery of Percheron

PTSP


Posterior thalamo - subthalamo- paramedian artery of percheron

Eyelid signs in PSP

Blepharospasm


Apraxia of eyelid opening


↓ blink rate

Oculomotor findings in PD

Visual hallucination ↓ blink, blepharospasm , aprixia of eyelid opening


Convergence insufficiency


Saccades - ↑ latency, ↓ speed, hypometric (Horizon)


Sm. pursuit ↓


Square wave jerks (asymptomatic)

*Pearl


RiMLF involved in vertical saccades and torsional quick phases of nystagmus

---

*Pearl


INC - Vertical gaze integration


- takes part in vertical sm. pursuit vertical VOR

---

riMLF bilat lesioins cause selective loss of downward saccades - Why?

Because burst neurons for downward saccades project only IPSILATERALLY from riMLF to IR and SO

Localize the lesion


1. Paresis of downgaze

Selective loss of downward saccades - bilateral ri MLF


loss of all forms of vertical eye movements = PC and INC

Localize the lesion


Paresis of upgaze

1. loss of all forms of vertical eye movements: INC or PC


2. Convergence - retraction nystagmus with upward saccades: PC

Localize the lesion


complete V. gaze palsy

Selective loss of vertical saccades: bilat riMLF


INC or PC

One-and-a-half syndrome localize

Ipsi abducens N or PPRF Ipsi MLF


(only preserved eye movement is contralateral abduction)

Millard-Gubler Syndrome

6th N fascicle (intra axial) + 7th N + contralateral hemiparesis


(lesion in the pontic tegmentum)

Dorsal midbrain syndrome - localize

Involvement of PC (INC fibers cross in the PC - reason behind upgaze paresis)


Also nucleus of PC involvement

Each ri MLF projects unilaterally to motor neurons for downgaze and bilaterally for upgaze.


Therefore ri MLF lesions have greater effect on downgaze than upgaze.

---

Structures innervated by 3rd N

SR, MR


IR, IO


Levator


Iris sphinctor


Ciliary muscle

Superior division of 3rd N supplies?

Levator


Superior rectus


(parasympathetics carried in the inferior division)

Nuclear 3rd N lesion findings

Bilat SR


Bilat ptosis


Bilat mydriasis


Plus other muscle weakness innervated by 3rd N

Anisocoria in bright light


6 causes

1. IIIrd N palsy


2. Adie's pupil


3. Iris trauma


4. Acute glaucoma


5. Siderosis


6. Pharmacologic

Dilated pupil - How would you differentiate pre ganglionic vs post ganglionic in the acute setting based on exam

Post ganglionic = segmented involvement of iris sphincter


Pre ganglionic = symmetrical involvement of iris sphincter

Horner's syndrome with ipsilateral facial pain


DDx

1. Carotid dissection


2. Cluster headache


3. Raeder's paratrigeminal neuralgia

Ocutomotor abnormalities in Chiari Malformations

I INO


R - Rebound N


A - Alternating N


C - Convergence N


E - Evoked gaze N


D- Downbeat


I - Increased VOR gain


N - Nystagmus


S - Skew deviation


I - Impaired OkN


P - Paralysis of divergence


I - Impaired pursuit/VOR cancell


D - Dysemtrica of saccade

2 egs of supranuclear diplopia

INO


Skew


Neimann Pick C


PSP


Whipple's

Name 3 conditions causing supranuclear motility problems

1. PSP


2. PD


3. Skew deviation


4. Niemann - Pick type C


5. Parinaud's


6. Thalamic estropia

L-N dissociation locations

1. Anterior visual pathway


2. Midbrain, tectum


3. Ciliary ganglion


4. Long ciliary N


5. 3rd N

Anisocoria in dim light


- Name 6 causes

1. Sympth. denervation (Horner's)


2. Mechanical - posterior synechial


3. Sympth stimulation - tadpole pupils in migraine, cocaine


4. Pharmocologic - cocaine


5. Parasymp stimulation


6. Physiologic

Large Rt hemispheric stroke


- Findings on EOM exam

Loss of Rt sm. pursuit


Loss of Lt horiz saccades

Occipitoparietal ( where) syndromes

Akinetopsia


Balint's triad


Hemineglect

Occipitotemporal (what) syndromes)

Achromatopsia


Prosopagnosia (R or bilat)


Alexia (L)


Topographagnosia

Extrastriate visual syndromes


1. Occipito temporal (what)


2. Occipito parietal (where)

What - Object recognition


Where - Object localization

Parinaud's syndrome features


mnemonic CLUES

C - Convergence retraction nystagmus


L - Light near dissociation


U - Upgaze paresis


E - Eyelid retraction (Collier's)


S - Skew deviation

Areas involved in control of smooth pursuit

MT, posterior parietal


MST


FEF/SEF


Dorsolateral pontine N


Flocculus


Fastigial N, MVN

Regions of brain involved in control of saccades

Frontal eye fields


Supplementary eye fields


DLPFC


Posterior parietal


Superior colliculus


PPRF, Caudate, SNpr

RAD - Vertical recti are adductors so, obliques are adbuctors


Inferiors are extortors so, superiors are intortors


Vertical recti exert greatest vertical action in abduction


Obliques exert greatest vertical action in adduction

---

Extracranial arteries involved in GCA - Name 4

1. ECA


2. Subclavian artery


3. Axillary artery


4. Vertebral artery at its origin

Oculomotor findings in PSP

Supranuclear gaze palsy


Slow saccades vertically esp. downward


decreased v. sm pursuit


loss of slow phase of OkR - V


Convergence insufficiency


Square wave jerks > 16/min


Horiz saccades/sm. pursuit affected later: VORS lost later

Hemianopia plus optic atrophy


- Where is the lesion?

Optic tract


* Mass lesion suspected unless otherwise proven

Anton syndrome


TRIAD

1. Cerebral blindness


2. Denial of blindness (anosoagnosia)


3. Confabulation

Fastigial N in EOM

1. Accelerates contraversive saccades


2. Involved in coordination of smooth pursuit

Function of Nodulus and uvula in EOM

1. Decreases duration of vestibular responses


2. Inhibits "velocity storage mechanism" of vestibular neurons

Dorsal vermis in EOM

Tonic inhibitory control of fastigial nucleus

Function of cerebellar floculus - paraflocculus in EOM

Aids in generation of smooth pursuit and maintains eccentric gaze; Calibrates step-pulse ratio of saccades

Acute causes of vision loss


Name 5

CRAD


Branch RA occln


AION


Migraine


Occipital sz


Papilledema

Subacute causes of vision loss


Name 2

Demyelinating


Infectious

Chronic causes of vision loss - Name 5

Compressive lesions


Neoplastic


Infiltrative


Hereditary


Toxic

Vision Loss


Seconds = 3 causes


Minutes = 2 causes


Hours = 3 causes

Seconds - Sz, papilledema optic drusen


Mins = TIA, migraine aura


Hours = Optic neuritis, PRES, Occipital infarct

Ocular hypoperfusion syndrome

Critical carotid stenosis


Light induced amanrosis/postural


Impaired dark adaptation


Positive visual phenomenon


Transient or prolonged vision loss


Ocular neovascularization observed

Ocular causes of TMVL

Kertatoconus


Hyphema


Angle closure glaucoma


Retinal detachment

Pearl


Optic N edema can cause photopsias or phosphenes cause by irritation of the surrounding retina by the edema

---

Anton's Syndrome

Blind individuals insist that they can see, confabulate visual experience


Anosognosia - denial

Diplopia


- levels of localization

1. Supranuclear ( eg skew)


2. Ocular motor N


3. Infra nuclear


4. Inter nuclear


5. NMJ


6. Muscle

Horizontal diplopia


- 5 Causes

6th N palsy


Duane's


Myopathy


MG


Spasm of near reflex

Vertical diplopia


5 Causes

3rd N palsy


4th N palsy


Skew deviation


MG


Myopathy

Alternating skew deviation seen in which condition?

Arnold-Chiari malformation


Abducting eye is usually hypertropic

3 Components of saccade


testing = Velocity or speed


Accuracy


Latency

Accuracy and Latency impaired in cerebral lesions


Speed impaired in pontine/ cerebellar lesions

Neural integrator


- Name structures involved in horizontal and vertical neural integrator?

1. Horizontal neural integrator nucleus prepositus hypoglossi, nucleus intercalatus, ventral N of roller, MVN


2. Vertical neural integrator INC

1 test to differentiate skew from IVth N palsy

Vertical deviation that decreases greater than or equal to 50% from upright to supine position suggests skew deviation

Differentiate skew deviation from 4th N palsy

4th N


Hypertropia in 1°


Incomitant


Hypertropia worse with ipsi head tilt


Compensatory head tilt to opp side


Excyclotorsion of hypertropic eye


No other neuro signs


Skew


Hypertropia in 1°


Incomitant, comitant, alt


No change


Pathologic head tilt to opp side


Incyclotorsion of hypertropic eye


other signs +