Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |
|
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 |
1° No disc edema Disc margins sharp + clearly defined 2° 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 +
|