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380 Cards in this Set
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What differentiate's a supranuclear lesion from bilateral orbit disease? (2)
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Bell's Palsy---will be absent in orbit disease, present in supranuclear lesion
Doll's head reflex |
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What is INO?
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Interruption of connection between III and VI for lateral gaze
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what connects III and VI?
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MLF
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PPRF
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horizontal gaze center
located near VI nucleus at pons sends info to III in midbrain |
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unilateral INO deficts
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No adduction
contralateral abduction nystagmus |
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where is the lesion of a unilateral INO?
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ipsilateral MLF in pons or midbrain
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what differentiates pons vs midbrain in unilateral INO or BINO?
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convergence:
intact in pons lesion impaired in MB lesion |
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Why is convergence impaired in MB MLF lesion?
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input to medial rectus in affected
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BINO deficits
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no adduction in either eye
only input to LR< no input to MR abduction nystgmus on both sides |
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how does BINO occur?
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MLF is near the midline
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WEBINO deficit
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large xt in primary gaze
no convergence |
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webino lesion
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HIGH--MR subnucleus is knocked out with IIIrd
rostral midbrain |
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one and ahalf synfdrome defcit
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ipsilateral gaze palsy and contralteral INO
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one and a half lesion
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MLF and PPRF
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skew deviation presentation
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vertical misalignment, may be comitant or not, may see nystag
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skew deviation lesion
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brainstem or cerebellar
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what is skew deviation eitiology
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prenuclear input problem, may see other neuro findings
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what does 'bobbing' indicate
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lower brainstem lesion
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CN III innervation(6)
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levator, SR, IO, MR, IR, sphincter
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CNIII palsy presentation (5)
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H and V dip
pupil ptosis XT N>>D reversing hypertropia |
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nuclear IIIrd palsy presentation
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some bilateral
brainstem lesion |
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CNIII fascicle path and assoc sx
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red nucleus (tremor)
cerbral peduncle (contra weakness) cerebellar peduncle (ataxia) |
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what do you test for for CNIII fascicular palsy
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R vs L strength
gait tremor cerebellar fnc |
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subarachnoid IIIrd presentation
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often involves pupil
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why are pupils involved in sucarach IIIrd?
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pupillary fibers run on superior medial portion of nerve. most vulnverable to compression
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fixed, dilated pupil
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IIIrd palsy, consider aneurysm
anything compressive |
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what is most common cuase of subarachnoid iiird
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aneurysm at bifrucation of internal crotid and posterior communicating artery
other cause: herniation |
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most likely cause of pupil sparing iiird
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ischemia
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what causes ischemic lesions
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DM, HTN, aging
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what are ishcmeic lesions
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infacrction and local demyelinization, reversible
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what passes through the cavernous sinus
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III, IV, V1, V2 (V1 is free floating)
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what systemic sx indicate a cavernous sinus lesion
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pain and numbness in trigemincal dicivsion, other palsies, horner's
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where will V-1 affect?
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forhead, perioribital area
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what are possible oribtail IIIn lesions? (2)
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superior: SR, levator
inferior: IR< IO, MR, pupil |
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possible aberrant regeneration sx for iiird n palsy
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lid retraction on downgaze or adduction
constrictuion on adduction globe retraction on vertical gaze |
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can DM cause aberrant regen?
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no, aberrant regen is never from ischemia
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most common cause IIIrd palsy in kids
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congential
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management for isolated and COMPLETE iiird
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monitor, r/o systemic sx
should resolve in 3 mos |
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management for incomplete isolated iiird w/o pupil
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assume it is evolving
IMMEDIATE REFERRAL |
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management of iiird c pupil involvement
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send to ER
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isolated iird with pupil
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anuerysm at PCA until proven otherwise
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hallmark of nuclear IIIrd
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some asymm bilateral ptosis
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hallmark of cogential iiird
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no diplopia
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where does trochlear leave bs
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dorsally
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when does trochlea decssate
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upon leaveing brainstem
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trochlear lesion sx
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torsional diplopia
ipsi hypertropia in primary gaze --worse on contra gaze --worse on ipsi head tilit |
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what can compress both L and R tochlear at same time
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enlarged pineal gland
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congential IVth
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no further workup req, confirm with old photos
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IV fascicular palsy
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IPSI horners (pass near oculosympathetics), contra IVth palsy
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where is the vertical gaze center (2 loc)
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dorsal near SC and inderior (deeper)
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cause of subarachnoid IVth
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trauma
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when might you see papilledema with a IVth?
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compression or swelling near sylvian aqueduct
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doral IVth lesions
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lose upgaze first
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why is ischemic IVth rare?
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trochlear has low metabolic demand
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cavernous sinus IVth
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with Horners and IVth on SAME SIDE
V1 (facial pain and numbness) |
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most common causes IVth palsy
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undet and trauma
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IVth workup
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r/o GCA in elderly
no worjup if congentical or cl hx of trauma |
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what would a bilateral IVth look like
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hyper switches with gaze or tilt
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VIth nerve sx
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slow ABD
duction >version (-) foreced duction lid closure or face turn |
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Duane's cause
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no abducens or nucleus, congential
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Duane type I
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globe retraction on ADDUction
(+) foreced duction due to MR overaaction |
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orbital myositis
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swelling, restriction, hyperemic insertions
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how does oribtal myositis differ from graves
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orbital myositis is unilateral, painful, and acute
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near refelx spasm
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bilateral ADDuction deficit
blur and diplopia may break cycle with cycloplegic |
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where does VIth originate?
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lower BS at pontomedullary junction
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VIth course
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pontomedullar ujunction, skull base, crosses middle cranial fossa to cavernous sinus to orbit
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what other structures is VIth fascicle in proximity to? (7)
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facial nerve, assoc with ipsi facial palsy
also PPRF and desc motor path V, symps, VIII (hearing loss), verstibular nuclei (nystagmus) |
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things near VI at cerebellarpontine angle
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V, VI, VII, VIII (m to L)
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what might cause a cerebellarpontine VI?
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compression, neoplasm
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what causes a lesion of VI at the petrous apex
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severe otitis media
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what else is near VI at the petrous apex/
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facial and trigeminal
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what is the hallmark of a clivus/posterior fossa VI?
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BILATERAL, often due to inc in ICP, meningitis, or VERY severe trauma
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what is the middle crnail fossa VI near
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trigeminal
great superfiction perstsal nerve (to lacrimal gland--tearing) |
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which of VI lesions has worse prognosis
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middle cranial fossa
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what indicates a cavernous sinus VI
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no weakness
no nystagmus |
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VI due to inc ICP
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will have VI palsy and papilledema ONLY
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most common cause of VI in adults
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isch vasc due to systmic, second is neoplasm
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most commonc ause of VI in kids
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tumor
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most common cause VI in young adults
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trauma or idiopathic
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VI management-complicated
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imaging
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VI management isolated
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r/o GCA in elderly
monitor expect improvmenent in 3-4 months neuro consult for kids |
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bilateral VI manageeent
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worry about skull base--image and lumbar puncture
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Myasthenia gravis cause
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antibodies attack NMJ
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which muslces does MG effect
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voluntary
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nonocular MG sx
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orofacial weakness: snarl, swalloing, regurgitating liquids
proximal limb weakness, gait, getting up from chair diaphragm--breathing prob--EMERGENCY |
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what percent ocular MG progress to general
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80%, 20% spong remiss
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MG workup
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rule out AI disease
Ach receptor antibody tensilon EMG |
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Thymus and MG
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2/3 have thymus hyperplasia
1/3 thymoma |
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thymectomy prognosis for MG
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85% improve, 35% remiss
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where are the oculosympathetics in the cavernous sinus
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with the ICA then with the abducens
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what causes a carotid cavernous fistula
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ICA or branch rupture
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most common neoplasm invading cav sinus
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pituitary adenoma
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Tolosa Hunt syndrome
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painful opthalmoplegia
at oribtal apex new inflammation tx with steroids |
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what is the most common orbital problem
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graves
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when do eye signs in graves occur
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within first 18 months for 80%
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graves eye signs
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red eye--eom insertions
lid edema--jelly roll in am lid retraction persists on downgaze EOM restriction optic neuropathy (rare) proptosis (later) |
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why is IOP inc in vertical gazes in graves
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muselc restriction increases corneal tension which increases IOP
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why might optic neuropathy occur in graves
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swollen muscles choke ON
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which part of the muscle swells in graves
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belly only
NOT the tendinous insertion |
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how do you diff inflammation from graves?
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inflamm processes will be PAINFUL, graves wont
tendinous insertions involved in inflamm processes inflamm uniltateral |
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diff graves from orbital tumor
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tumor is unillateral
eye can be displaced NO lid retraction |
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diff trauma from graves
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enophthalmos, IR and MR most affecgted by entrapment
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when is systemic tx used for graves
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only when thyroud fnc also affecfed bc it wont help the ocular
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ocular decompression
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tx for sudden drop in vision in graves
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can sx help graves
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yes, for cosmesis once inflmm is gone
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radiation for graves
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when steroids fail
can cause optic neuropathy |
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what ON function tests are used in evaluateing graves
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30-2
VA color vision RED CAP TEST constrast sensitivity |
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what is the best EOM eval for graves?
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hess lancaster
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when are immunosupressants recommended in tx of graves?
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rapid progression and threat to vision
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when is tarsorrhaphy done?
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to protect cornea in graves
AFTER other issues have been resolved--lid can be variable, and EOM restrictions change eye orientation |
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what is infilitrative dermopathy
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associated with graves, seen on shins most often
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toxic thyroid nodules
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benign nodules
cause hyperthyroid older patients |
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toxic multinodular goiter
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older pts
cause hyperthyroid |
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is goiter a sign of hyper or hypothyroid?
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both:
toxic goiters are hyper, nontoxic are hypo can also be normothyroid |
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hashimotos
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hypothyroid
autoimmune |
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who gets hashimotos
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women more than men
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ocular effects of hashimotos
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none
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how is TSH affected by hyper/hypothyroid
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high in hypo
low in hyper |
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synthroid
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treats hypothyroid
synthetic T4 |
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most common hyperthyroid tx
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radioactive iodine followed by synthroid
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when is surgery for hyperthyroid indicated
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large glands
pregnancy |
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ansiocoria due to symp lesion
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no dilation
worse in dark |
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anisocoria due to para lesio
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no constriction
worse in light |
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what is light near dissociation
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when the near reflex is better than the light reflex
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ptosis + mydriasis
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IIIrd palsy
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ptosis + mitosis
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symps
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dorsal midbrain syndrome
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lid retraction
pupils fixed to light, respond to near aka Colliers sign |
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how is neutral density filter used in APD eval
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will exaggerate APD
will not induce APDin normal use to quantify |
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when will a VF threshold indicate APD?
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3dB difference between eyes
30-2 |
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when to suspect APD
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dec VA, CV, VF, trauma
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inverse APD
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observe only reactive pupil
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right eye fixed and dilated, right APD
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OS does not constrict when OD stim
OS constricts when OS stim |
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left eye fiixed and dilated, right APD
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right contricts when OS is stim
OD does not constrict as much when it is stimulated |
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catarcts and APD
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may ehance APD, will never cause (like neutral density filter)
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ablyopia and APD
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75% AMBLYS have trace to gr 1 APD
no corr with vision loss, no other ON defects |
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how does anisocoria confoundresults
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pseudo APD on larger pupil
true APD on smaller possible--less light entering |
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oculosympathetic pathway (3 neurons)
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hypothalmus to synapse at C8/T1
secondary neuron leaves spinal cord and goes up symp chain to angle of jaw to superior cervical ganglion around ICA to cav sinus, to eye to muller's and pupil |
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inverse ptosis
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LL elevates
seen in horner's |
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miosis in horners
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due to dilator paresis
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light and near responses in horners
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intact
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dilation in horner's
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lag
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anhydrosis in horners
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primary: ipsi body
secondary: ipsi neck and face--pregang tertiary: ipsi brow--pregang |
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cocaine test for horners
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dilates normal pupils
36 hour urine trace no dilation in interrupted symps blocks norepi reuptake 2 drops 5 minutes apart OU |
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phenylepthinr 1% for horners
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affected eye will dilate more if lesion is POSTGANGLIONIC
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primary horerns cause
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brainstem
neuro |
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secondary horners cause
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SC injury
apical lung tumor neck injury/sx |
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thertiary horner's cause
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cav sinus
cluster HA otitis media |
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horners in kids
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if no hx trauma, 25% are neuroblastoma
heterochromia indicates congntical |
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when does eye color develop
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by 6 months
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horners management in adults
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image if primary or secondary
no testing if tertiary and no cav sinus signs recent neck injury--r/o carotid dissection |
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tonic pupils
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postgang dennervation
efferent L/N dissoc sluggish near response, slow redialtion, irreg puils, dec corneal sensitivity |
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pilocarpine and tonic pupils
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supersensitive
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stromal streaming
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in tonic pupils
innervated iris contricts and pulls denervated stroma |
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local tonic pupil
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unilateral
trauma, infection ciliary gang or cili nerves |
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neuropathic tonic pupil
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bilateral
ANS disase ie syphilis, DM, alcoholism, musc dystrophy |
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Adies pupil
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idiopathic
most common with absent or dec tendon reflexes in 90% |
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who gets adies
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20-50 yo
women |
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cholinergic sensitivity testing
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tonic pupil
fog c + lenses measure pupils 2 gtt 0.1% pilocarpine OU 30 sec apart remeasure 30-45 min later DO NOT let pt do nearwork postgang efferents v sens to o.1% pilo |
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causes of dorsal mb syndrome
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pineal tumor, stroke, bleed, hydrocephalus, infection
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dorsal MB signs (7)
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pupils round, slow, LN dissoc
suprneaclear vertical gaze palsy papilledema convergence retraction nystagmus IVth palsy bilateral lid retraction |
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argyll roberston pupil
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LN dissoc
syphillis (2 and 3) miotic, irreg pupil brisk near response |
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argyll roberston cause
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disruption of suprenealcular inhibitor fibers appraoching oculomotor nuclei
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argyll roberston workup
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FTA-abs, RPR, VDRL
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what must be ruled out in pharm blockade of pupil reflex
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IIIrd palsy secondary to aneurysm
herpetic infection of cili gang (look at AC) |
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1% pilo in pharm block pupil
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contricts normal and postgang IIIrd not pharm block
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who gets acute optic neuritis
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females
18-46 |
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VF defects in ONitis
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most are diffuse, then alt/arcuate/nasal step
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MRI abnormalities with ONitis
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59%
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how is VA affected by ONitis
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varies, wide spectrum
most improve to 20/40 or better within ayear |
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15 year MS risk in ONitis
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50%
25% with normal MRI 75% with abnormal MRI |
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what did the ONTT study tell us
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no MS at 15 yr follow up if:
normal MRI painless NLP severe edema hemorrhage exudate |
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atypical ONitis
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part of another problem
no pain bilateral and simultaneous continues to worsen past 14 days |
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typical ONitis
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sudden dec in VA, worsesn for 1 week, improvement begins in a month
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causes of atypical ONItis
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CT disease (lupus, sjogrens, behcets)
infection infitltrative |
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ONitis in kids
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bilteral
viral good prognosis |
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what is MS risk in kids with ONitis
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same as adults if UNILATERAL
better if BILATERAL |
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ONTT tx for ONitis
|
oral steroids inc risk of new attacks
IV with oral steroid--faster recovery but no improvement in outcome dec MS risk for 2 years, but no imrpovement past that placebo recovered slower but completely |
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ONItis workup
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CBC
ESR ACE chest xray FTAabs ANA CRP MRI lumbar puncture lyme titer |
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how is MS dx?
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MRI + clinical features
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MS pathology
|
T cells cross BBB and attack myelin/nerves
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MS presetation
|
ONitis
INO nystagmus babinski dysmetria tremor sensory impariment mood disturbance vertigo fatigue incontinence dysarthria menta disturb diplopia vision loss |
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MS dx criteria
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2+ MRI lesions
2+ episodes min 24h 1 month apart no other syst explanation |
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lumbar puncture and MS
|
inc IgG
oligoclonal banding on electrophoresis NOT diagnostic |
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most common type of MS
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relapsing remitting
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worst type of MS
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progressive relapsing
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MS tx
|
immune modulators with antiviral properties
avonex, betaseron, copaxone, reitt |
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gilenya
|
new ms drug
not for isolated events dequesters lymphocytes inc risk CME |
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progressive MS tx
|
tysabri--inc risk PML with viral titers
novantone--cardiotoxic |
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CHAMPS study and MS tx
|
tx after 1st demylinating event dec MS progression by 50%
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AION
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NON INFLAMMATORY
PAINLESS on swelling, flame hemes, dec VA, alt VF defect, macular star |
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AION cause
|
hypoperfusion --mechanical or atherosclerosis
worse at night worse with BP meds |
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inc AION risk
|
HTN
DM atherosclerosis smallnerve GCA (for arteritic) |
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how does viagra cause NA-AION
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dec ON perfusion
|
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Arteritic AION sx
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scalp tenderness
jaw pain fever arthalgia myalgias malaise |
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what is most predictive of arteritic AION
|
jaw pain
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NA AION prognosis
|
wont get better or worse
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arteritic AION prognosis
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poor, fellow eye involved within 24 hrs
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NA AION tx
|
none
|
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arteritic AION tx
|
IV steroids immediate to prevent other eye involvment
|
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who gets arteric AION
|
70+
caucasians |
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nerve in arteritic AION
|
pallid edema
|
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nerve in NA AION
|
sectoral edema
|
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NFL infacrts and AION
|
more common in arteritic form
|
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PION cause
|
retrolaminar infarction
|
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PION signs
|
NO disc swelling
acute VAS loss optic neuropathy |
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PION cause
|
GCA most comon
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VF in papilledema
|
enlarged blindspot
arcuate defect if axonal compromise |
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SVP in papilledema
|
absent
|
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CSF path
|
makde in lat ventrail, through intraventricular formaen to IIIrd ventrical to cerbral aqeuduct to IVth vetrnicle, abs in arachnoid granulations into veinous sinus into jugular beins
subrachnoid is continuous with ON meninges |
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papilledema progression
|
C shape edema (sup, inferior first)
then all boraders blurred, nasal elevation, peripap halo then inc NH diam, vessels obscured, halo has fingerprojections then entire ONH elevted then dome shaped disc, no cup |
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signs of acute papilledema
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hemes, exudate, hyperemia, NFL edema, nausea and vomiting
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signs of chornic papilledema
|
no hemes or exudates
telectangectatic vessels optociliary shunt end stage will not have swelling high water marks |
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papilledema sx
|
nonspecific HA due to meninge stretching
transient visual obscurations tinnitues (pulsatile) diplopia |
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why do you get tinnitus in papilledema
|
jugular passes near auditory canal
jusgular v impt in CSF drainage |
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retina in papilldema
|
choroidal doilds
macular star RPE distrubance |
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infection and papilledema
|
cerebral edeam
dec CSF abvs hypercoaguable state veinous sinus thrombosis |
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inflammatory causes of papilledema
|
sarcoid
behcet's |
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acute papilledema tx
|
send to ER
|
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chronic papilledmea workup
|
image
if normal--lumbar puncture if normal--dx as pseudotumor cerebri |
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pseudotumor cerebri causes
|
tetracyclins
nalilixic acid nitrofurantoin danazol steroids hypervitaminosis A endocrine nutritrialn lupus anemia HRN veinous sinus thrombosis sleep apnea |
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Foster Kennedy syndrom
|
papilledeama in 1 eye due to frontal lobe tumor impinging on ON
|
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who gets IIH
|
obese, childbearing females
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IIH mechanism
|
central obesity inc pleural pressure, inc cardiac P, impeded veinous return, inc ICP
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IIH tx
|
weigh management
CAIs if symptomatic Sx: CSF shunt, ON sheath fenestration |
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how does sleep apnea cause pseudotumor cerebri
|
sleep apnea cuases respiratory acidosis
CS/blood ratio altered capillary dilation and inc ICP |
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how is intracrainal veinus sinus thrombosis dx?
|
radiographic veinography--magnetic resonance veinography
|
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|
CVT
|
10-30% mortaltity due to pulmany emblosism or vasc accident
|
|
|
nutritional optic neuropathies
|
painless
bilat symmetric |
|
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most common nutriical optic neuropathies
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B1, B12, folate
cynaide buildup |
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alcholol-related nutritiaonl defict
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B1/thiamine
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B12 deficienty
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years to develop
pernicious anemia |
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tobacco relted optic neuropathies
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accum of cyanide
demyleniantion of fibers folate also implicated |
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carribean optic neuropathy
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cassava--bilat ON, cyanide if not processed properly
bush tea less of a problem--prob nutritional |
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where are deficits in toxic neuropathies seen
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papillomacular bundle
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methanol toxicity
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rapid, irev, bilateral
metabolic acidosis disc edema, dec conscious, parkinsonian |
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ethambutol toxicity
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anti TB med
slow pregoression after several mos tx continues to dec vision even after DC |
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who gets lebers optic neuropathy
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males, around age 28
hereditary |
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lebers optic neuropathy
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uni for bilateral
spared pupillary reflexes*** no FA leakage hyperermic disc c dialted capillaries |
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dominant optic neuropathy inheritance
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AD
appears by age 10 |
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dominant optic neuropathy signs
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VA loss to 20/200
bilat, symmetric trian color defct assoc with hearing loss |
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recessive optic neuropathy
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more severe
earlier onset |
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compressive optic neuropathy
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progressiv,e unilatera, contra field, ON edema, orbital signs, amy be asx
assoc with graves, menigioma, gliaoma, pit adenoma |
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hypoplasia of disc
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dec number of axons
may appear with APD small disc dec fnc severe with nystagmus VF loss common |
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assocated features with dev disc anomoly
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short
dev delay hypertelorism strab unusual refractive error swollen ONH aniridia microphthlamos |
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what causes ONH hypoplasia
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exaggerated apoptosis at 16-17 wks devel
can be infections, toxic, ischmic, or injury assoc with anterior midline abnorm |
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fetal alchohol syn
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ONH hypoplasia
hypertelorism elong philthrum poor devel nose bridge MR dev delay |
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septo-opto dysplasia
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assoc w hypoplastic disc
midline abnormality no septum, chiasmal hypoplasia |
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ON coloboma
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nerve or ocular
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ON only coloboma cause
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primary optic papilla closure impaired
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ON pits
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small partial colobomas
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ON pit/coloboma management
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monitor, no progression unless fluid accum in pits
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megallopapilla
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GLC appearance
pale appearance bc more visble lamina cribrosa |
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megallopapilla defect
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rare
enlarged BS only |
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dysplastic megallopapilla assoc
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basal encephalocele--potential breaks in meninges--infection
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morning glory syn
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assoc with basal encephalocele
elev choroiret ring funnel shaped spoke vessels |
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titled discs
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situs inversus
hi myopic astig |
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VF in tilted discs
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temporal defect
mimics chiasmal but does NOT repsect vertical meridian should be stable |
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pseudopapilledema
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inc risk drusen/hyaline bodies
axonal crowding |
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is pseudopapilledema hypoplastic of dysplastic
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neither
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pseudopapilldema VF
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arcuate--GLC like
progressive central sparing |
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pseudopapilledmea manageent
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monitor VF IOP
lower IOP over 20mmHg risk factor for NAION |
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how does swelling differ in papilledema and pseudo
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pap: where rim tissue is thickest, obscures vessels
pseudo: central, cl vasc and NFL |
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how does vasculature differ in pap and pseudopap
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pap: optociliary shunt, veinous engorgement
pseudo: multiple bifurcations, loops, coils, no microvasc changes, no shunts |
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how does cup differ in pap and pseudo
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pap: present when ICP > veinous P
pseudo-none |
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SVP in pap vs psdueo
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pap: absent
pseudo: present |
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hemes in pap vs pseudo
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pap: no flames, possible deep hemes decondary to disc drusn
pseudo: flames |
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inheritance of pap vs pseudo
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pap; acquired
pseudo-familial |
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how far is chiasm from pituiary
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10mm
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what separates chiam and pit
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diaphragma sella
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chiasaml vision loss
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painless, progressive
uni or bil |
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HA in chiasaml disease
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80% pit adenoma pts due to diaphrgma sella stretching and CNV innervation
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what are other signs of chiasmal disase
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APD, CV, endocrine
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anterior von willebrands knee
importance in chiasmal disease? |
inferior nasal fibers dip anteriorly at chiasm
causes superior temporal defect if there is a post-fixed chiasm (atnerior chiams syndrome0 |
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posterior chiasm syndrome
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post fixed chiasm
nasal macular fibers affected tract is involved |
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optic atrophy prognosis
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poor
more atrophy= worse |
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optic atrophy progression
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early band pallor--chiasmal fibers affected first (nasal and central)
later--dffuse pallor APD if aysmm VF |
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ant pit hormones
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prolactin
GH TSH ACTH LH FSH |
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cushing's disease
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excess ACTH
inc cortisol levels |
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hypothalamus lesion
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cause hypopituitary
also dec ADH (diabetes insipidus) dec gonadotropin |
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craniopharyngioma
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benign
from ebryonic ectoderm--young pts dec hypothal fnc interefere with IIIrd ventricle |
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meningioma affecting chiasm
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benighn
sella or adj tissue |
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trauma and chiasm ds
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v severe trauma can prolapse chiasm or cause bleed
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aneurysm and chiasm
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in cavernous sinus
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glioma and chiasm
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INFILTRATIVE
early childhood assoc with neurofibromatosis |
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infection and chiasm
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from sphenoid sinus
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chiasmal ds workup
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VF monitoring for life
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pituitary apoplexy
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pit tumor becomes necrotic
internal hemorhage rapid onset SEVERE HA high mortality emergent |
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causes ot retrochiasmal VF loss in adults
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ishemic/stroke
truama hemorrhagic stroke |
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cuaes of retrochiasmal VF loss in kids
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trauma
neoplasm |
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who gets optic tract defects and why
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kids
tumor prevalence |
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why is there an APD in tract lesions
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afferent pupillary fibers branch to pretectal nuclei
field is larger temporaally than nasally--more ifbers |
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where will the APD be relatieve to a tract lesion
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contra
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a L tract lesion willcause
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R homonymous hemianopa
R APD |
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optic tract VF
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partial incongruous hom hemianopia
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optic tract optic atrophy
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bilateral
ipsi temporal pallor contra band pallor |
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tract + chiasm lesion
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posterior chiasmal syn
IPSI APD |
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tract + ON lesion
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IPSI APD
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tract + cerebral peduncle lesion
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contra hemiparesis
contra homon hmemianopia |
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LGN VF patterns
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horiz homonymous sectoranopia
upper and lower homonyhoy sectoranopia |
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inferior fascicle of optic radiation
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loops anterior and inferior before going back
through temporal lobe |
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superior fascicle of optic radiation
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deep in parietal lobe
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where do optic radiations project to
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calcarine fissure
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temporal lobe VF defect
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pie in sky, does not approach hor meridian
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other temporal lobe defects
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internal capsule
hemiparesis hemianesthesia aphasia uncinate fit--seizure with taste/smell componenent incongruous |
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parietal lobe VF
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more congruous defect
denser inferiorly |
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other parietal lobe problems
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hemineglect
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dominant parietal lobe lesion defects
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finger agnosia
agrpahia, alcalculia RL dominant ractile agnosia |
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nondom pariteal lobe lesion defects
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hemineglect, memory loss, apraxias, polyopsia
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occipital love VF
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homonympus hemianop
temporal crescent sparing absolute congruity macular sparing |
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what is most common cause homon hemianopia
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occipital love lesion
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what is most likely lesion to present to optometrist
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occipital lobe
neuro assoc rare |
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carotid branches to visual syst
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middle cerebral a
anterior cerebral a ophthalmic a |
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middler cerbral supplies
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frontal
parietal temporal internal capsule--post limb |
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anter cerebral supplies
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medial cortex surface
corpus callosum int capsule--ant limb |
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opth a supplies
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ocular struct
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vertebrovasilar supplies
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brainstem, cerebellum, occip lobe
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what connects carotid and vertebrobasilar syst
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circle of willis
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stroke causes
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80% ishemic
20% hemorrhagic |
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lacunar infarction
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small, deep
affects basal ganglia, int capsule, BS, thalamus can present like MS |
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TIA
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less than 24 h, complete reversal
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amaurosis fugax
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transient
monocular 10 min or less ocular TIA |
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transient monocular blindness
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same as amaurosis fugx
caused by pletelt or emboli from carotid or heart |
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stroke risk assoc with transient monocular blindness
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10% 3 year stroke risk
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BRAO cause
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embolus until proven otherwise
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BRAO stroke risk
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10% in 3 yrs
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CRAO cause
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local atherosclerosis unless you see plaque
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CRAO stroke risk
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low, unless you see embolus, then same as BRAO
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hollenhorst plaques
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cholesterol from carotid or heart
dont block perfusion can move easily stroke risk unkown |
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vertical diplopia worse at distance--most likely muscle?
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IO or SR
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vertical diplopia worse at near--most likey EOM?
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SO or IR
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why do you see bilateral involvment in a pure nuclear IIIrd palsy?
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a single subnuclei controls both lids
SR subnuclei also innervates the contralateral SR |
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XT in IIIrd palsy
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worse at near
worse in contra gaze |
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what are systemic signs of fascicular IIIrd N
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tremor
weakness ataxia CONTRALATERAL |
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IIIrd nerve pasly aneurysm location
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bifurcation of internal carotid and posterior commisural a
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other than aneurysm, what else might cause a subarachnoid IIIrd?
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herniation due to bleeding elsewhere in brain
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congential ptosis likely cause
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developmental problem of superior division of III
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primary vs secondary IIIrd n aberrant regeneration
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primaryis SUBTLE, due to slow compression
secondary is only seen in trauma, compressive, congenital, NEVER ischemia |
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why do you often see an associatd Horners in acquired IVth palsies?
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trochlear fascicles pass near to descending oculosympathetics
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when IVth and oculosymps are damaged in the BS, what will you see?
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CONTRA IVth
IPSI Horner's |
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which is the only crossed CN?
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IV--crosses upon exiting BS
will see contra defects in nuclei and fasciular lesions |
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where would you see a IVth palsy with pupil involvement and why
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at lesion upon exiting BS
due to proximity to SC fibers |
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When would you see Horners and IVth on the SAME side?
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cavernous sinus lesion
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what are signs of a dorsal midbrain IVth
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convergent retraction
nystagmust with vertical upgaze palsy vertical upgaze palsy papilledema (due to proxmity to slvian aqueduct, compression) fixed pupils |
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what else would you see with a cavernous sinus IVth
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IPSI Horners
facial pain and numbness from V1 |
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what would you see with bilateral IVth
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swtiching hyper deviation
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is duction or version better in VIth N palsy
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version
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is there diplopia in duanes
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no, it is congenital
pts often asymptomatic |
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forced duction testing in duanes
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(+)
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would you expecct (+) forced duction in graves?
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yes, muscle restriction
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why do you see an IPSI facial palsy in a fascicular VIth palsy
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V wraps around IV in the pons
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what type of motor deficit do you expect with a fasciular VIth and why
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CONTRA hemiplegia
descending motor path is close by |
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do you expect hearing loss with a VIth?
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yes if its fasicular or at cerebellarpontine angle
VIII is near VI |
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what are other gaze complications with VIth
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in fasciular VI, PPRF often affected--horizontal gazy palsy
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where is the petrous apex
what is it vulnerable to and what nerve is here |
inner ear
ear infections VI, V, VII |
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where would you expect nystagmus with a VIth palsy
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fasicular lesion
cerebellopontine angle |
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what is at the cerebellopontine angle
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V, VI, VII, VIII
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where would a lesion be for a bilateral VI
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at the clivus because R and L are close together
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most common cause of a bilteral VI
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increased ICP
presents with papilledema or meningitis |
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where might a lesion to VI also affect lacrimal gland function
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middle cranial fossa
greater superfical pertrosal nerve is here |
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if there is a VI, and lacriaml gland dysfunction, what else might you expect?
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facial pain
(CN V is also here) |
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a VIth palsy WITHOUT weakness or nystagmus would indicate a lesion where
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cavernous sinus
only III, IV, v1 and oculosymps here |
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what is most likely cause of complicated VI
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tumor
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what is least likely cause of a complicated VI
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ischemic or vascular
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which muscles does generalized MG affect
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proximal
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where does tolosa-hunt occur
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orbital apex
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tolosa hunt characterisitcs
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painful
ophthalmoplegia idiopathic |
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what increases risk of eye signs in graves
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smoking
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other eye signs in graves
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lid retraction
jelly roll red eye optic neuropathy (in 5%) |
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explain cocain testing
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blocks norepi reuptake
dilates normal pupils no dilation if sympathetics are interrupted no dilation in primary, secondary, OR tertiary horners |
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PE testing
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postganglionic lesions: the affected eye will dilate more due to denervation sensitivity
dilation only in tertiary horners |
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supersensitivity to dilute Pilocarpine indicates
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tonic pupils--POSTGANGLIONIC
deficit of efferents due to increased ACh sensitivty |
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what type of tonic pupils are associated with an inabiltiy to relax accomodation
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Adie's
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is herpes zoster tonic pupil usually unilateral or bilateral
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unilateral
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is argyll robertson unilateral or bilateral
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always BILATERAL
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what differentiates argyll robertson pupils from neuropathic pupils 2^ to syphillis
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neuropathic pupils are regular
argyll robertson pupils are IRREGULAR |
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what type of pupils does syphilis cause
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local tonic
neuropathic or argyll robertson |
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a present babinski reflex may indicate
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MS
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what is seen in lumbar puncture of MS patients
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increased IgG
oligoclonal banding on electrophoresis |
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basal encephalocele is assocated with:
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megalopapillae
monrning glory syndrome |
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APD in optic tract lesion
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CONTRALATERAL
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