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Neuro-Ophthalmology > 7 - Abnormal Ocular Motility or Diplopia > Flashcards

7 - Abnormal Ocular Motility or Diplopia Flashcards

1
Q

History Points in Patients with Diplopia

A
  1. Patients with ocular misaligment may report double vision or blurred vision
  2. Helpful to determine if diplopia more bothersome at near or far fixation, particular position of gaze, hx of head pain, eye pain, eyelid swelling or redness, numbness or other neurological signs that could provide clues of possible orbital, cavernous sinus or CNS causes of diplopia.
  3. Helpful to ask about hx of malignancy, trauma, thyroid disease, generalized weakness
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2
Q

Physical Examination in Patients with Diplopia

A
  1. Movement of eyes should be checked in all positions of gaze — individually (ductions) and together (versions)
  2. Important to establish whether ocular misalignment comitant or incomitant. Comitant alignment present in congenital strabismus while incomitant misalignment evidence of an acute disorder, except in rare cases
  3. Formal measurement of amount of misalignment with prism and alternate cover test (PACT) to determine comitant or incomitant (objective)
  4. Maddox Rod Test can help reveal subtle cases of strabismus (subjective)
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3
Q

Maddox Rod Testing

A
  1. Dissociates 2 eyes thus patient with phoria will also report diplopia
  2. Typically red Maddox rod in front of RIGHT eye and light in front of left eye
  3. Double Maddox rod quantifies torsional misalignment when vertical diplopia present → red Maddox rod in front of right eye and white Maddox rod in front of left eye
    1. Qualitative method for detecting relative cyclotropia using horizontal line
    2. Patient asked whether both lines are parallel or if they converge to 1 side.
    3. Cranial Nerve 4 palsy typically associated with convergence of lines toward side of palsy
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4
Q

Maddox Rod Left Exodeviation

A
  1. Straight Gaze — Light hitting temporal L retina at baseline gives nasal white image AND normal R eye with light hitting centered fovea this gives CROSSED IMAGE
  2. Right Gaze — Light hitting PORTION of nasal L retina gives slightly temporal white image AND normal R eye with light hitting ALL temporal R retina giving more nasal red image thus deviation INCREASES
  3. Left Gaze — Light hitting ALL temporal L retina gives nasal white image AND normal R eye with light hitting ALL nasal R retina giving temporal red image thus images INTERSECT
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5
Q

Maddox Rod Right Esodeviation

A
  1. Straight Gaze — Light hitting nasal R retina at baseline gives temporal red image AND normal L eye with light hitting centered fovea thus UNCROSSED IMAGE
  2. Right Gaze — Light hitting PORTION temporal R retina gives slightly nasal red image AND normal L eye with light hitting ALL nasal L retina giving more temporal white image thus deviation INCREASES
  3. Left Gaze — Light hitting ALL nasal R retina gives temporal red image AND normal L eye with light hitting ALL temporal L retina giving nasal red image thus images INTERSECT
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6
Q

Maddox Rod Right Left Hypodeviation

A
  1. Straight Gaze — Light hits right foveal retina giving normal Red right image and light hits left inferior retina giving superior White left image
  2. Upgaze — Light hits right superior retina giving inferior Red right image and light hits some inferior inferior retina giving still some superior white image
  3. Downgaze — Light hits Inferior retinas EQUALLY
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7
Q

Monocular Diplopia Causes

A
  1. Uncorrected Astigmatism
  2. Corneal Irregularities — keratoconus
  3. Tear film abnormality
  4. Cataract
  5. Retinal pathology — maculopathy with retinal distortion by fluid, hemorrhage, fibrosis
  6. Cerebral monocular diplopia or polyopia RARE and bilateral

Characteristics of optical causes are seeing ghost images, haloes, more than 2 images

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8
Q

Paretic Vs. Restrictive Diplopia

A
  1. Restrictive strabismus → TED and orbital trauma most commonly. Diplopia may be due to neural and restrictive components especially after trauma
    1. IR restriction → IOP 5 pts higher in upgaze than primary gaze
  2. Paretic and restrictive syndromes distinguished by assessing saccadic speed — paretic conditions reduce saccadic velocity whereas restrictive conditions DO NOT.
  3. If saccadic speed equivocal can perform forced duction test.
    1. Restrictive process produces limitation that can be felt by examiner when forceps used to advance limited eye movement. If abduction deficit then restriction will be due to restrictive MR thus should grab MR and pull towards direction of palsy.
    2. Chronic neural lesions may also cause mechanical limitation by gradual shortening unopposed antagonist muscle thus a tight muscle may give false positive result
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9
Q

Comitant and Incomitant Deviations

A
  1. Comitant deviation
    1. Characteristically found in patients with congenital or early-onset strabismus. Do not typically report diplopia 2/2 suppression which reduces responsiveness of visual neurons in occipital cortex to input from 1 eye
    2. Patients wth childhood strabismus may experience diplopia later in life if ocular misalignment changes — patients with long-standing exophoria, horizontal diplopia may develop in 5th decade when accomodation and convergence capacities wane
  2. Incomitant deviation
    1. May become comitant with passage of time. Spread of comitance may occur with restrictive or paretic incomitant deviation, i.e. CN4 palsy 2/2 recalibration of neural input.
    2. Usually acquired and causes diplopia
    3. If deviation small, fusion may align eyes and eliminate diplopia. Small misalignment may cause blurry vision rather than diplopia. Patients with subnormal vision may not recognize diplopia
    4. Congenital incomitant deviations though quite obvious typically do not produce diplopia
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10
Q

Localizing Lesions of EOM Dysfunction

A
  1. Brain
    1. Supranuclear
  2. Brainstem → usually with neurological deficits as well.
    1. Nuclear, cranial nerve segments aka fascicular pathways or intramedullary area
  3. Subarachnoid Space
    1. Between brainstem and cavernous sinus
  4. Cavernous Sinus
  5. Superior Orbital Fissure
  6. Orbit
  7. NMJ
  8. Muscle

Diffuse disease (inflammation or meningeal disease) may give false localization

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11
Q

Supranuclear Causes of Diplopia

A
  1. Most supranuclear disorders affect BOTH eyes equally and DO NOT cause diplopia
  2. Some supranuclear lesions HOWEVER may produce ocular misaligment and diplopia
    1. Convergence Insufficiency
    2. Divergene Insufficiency
    3. Ocular Tilt Reaction
    4. Skew Deviation
    5. Thalamic Esodeviation
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12
Q

Nuclear CN 3 Palsy

A
  1. Single caudal nucleus for BOTH LPS
  2. Paired subnuclei for Edinger-Westphal nuclei
  3. SR fascicles decussate just after emerging from nuclei and next to single LPS nucleus — lesions of CN3 complex affect or spare both upper eyelids and may affect contralateral superior rectus muscle
  4. Injury to CN3 nuclear complex while uncommon may occur 2/2 reduced perfusion through small blood vessels causing unilateral damage to 1 nuclear complex
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13
Q

Nuclear CN 4 Palsy

A
  1. Nuclear lesions rare given short course of nerve within brainstem → will give contralateral deficit given decussation of fibers from nucleus
  2. Lesion of CN4 nucleus identical to lesion of fascicle
  3. 2/2 ishemia, trauma, demyelination, neoplasia
  4. Occasionally CN4 palsy accompanied by Horner syndrome of contralateral side due to proximity of descending sympathetic pathway adjacent to CN4 nucleus
  5. RAPD may also be seen with CN4 palsy due to pupillary fibers running in nearby superior colliculus
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14
Q

Nuclear CN 6 Palsy

A
  1. Lesion of CN6 nucleus causes horizontal gaze palsy and NOT abduction deficit in 1 eye → may not see diplopia because CN6 nucleus controls ipsilateral lateral rectus muscle and contralateral medial rectus muscle
  2. Ipsilateral upper and lower facial weakness also present with a nuclear CN4 palsy due to adjacent facial nerve fascicle
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15
Q

Internuclear Ophthalmoplegia

A
  1. Disruption of MLF that connects VN6 nucleus on one side of pons to medial rectus subnucleus of CN3 on contralateral side of midbrain
  2. Unilateral INO → slowed adduction saccadic velocity in 1 eye usually associated with abducting nystagmus of fellow eye. Eye with slowed adduction may have full or limited range of adduction. INO named for side with slowed adduction
    1. Convergence may be spared or affected
    2. May report horizontal diplopia
    3. May also experience ipsilateral vertical-oblique diplopia (hyperdeviation) due to skew deviation since MLF also receives vestibular input
    4. Episodic diplopia related to head-eye movements if partial lesion
    5. Difficulty tracking fast-moving objects due to mismatch in saccadic velocity
  3. Most common causes are demyelination (younger) and strokes (older)
  4. Infection, neoplasm, trauma, progressive supranuclear palsy also etiology
  5. Myasthenia Gravis can produce pseudo-INO
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16
Q

Bilateral Internuclear Ophthalmoplegia

A
  1. Bilateral INO → adduction lag (MLF affecting bilateral medial rectus), bilateral abducting nystagmus and vertical gaze-evoked nystagmus most noticeable in upgaze
    1. Vertical nystagmus from disruption of vertical vestibular pursuit and gaze-holding pathways which ascend from vestibular nuclei through MLF
  2. Large-angle exotropia may occur (“wall-eyed”) due to midbrain lesion near CN3 nucleus → WEBINO syndrome
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17
Q

One-and-a-Half Syndrome

A
  1. Due to LARGE pontine abnormality that involves CN6 and PPRF nucleus + ipsilateral crossed MLF (towards ipsilateral CN3)
    1. In essence — frozen eye on side of lesion and contralateral eye with half movements!!
  2. Eight-and-a-half syndrome
    1. One-and-a-half syndrome + CN 7 palsy
  3. Raymond-Cestan Syndrome = INO + contralateral hemiparesis from corticospinal tract damage
  4. 2/2 Stroke
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18
Q

Infranuclear Causes of Diplopia

A
  1. Intraxial aka fascicular CN palsies due to lesions distal to nucleus within confines of brainstem which tend to produce numerous deficits and affect many structures
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19
Q

Fascicular CN 3 Palsy

A
  1. CN3 fascicle palsy + contralateral hemiparesis (cerebral peduncle) = Weber syndrome (Weber is weak)
  2. CN3 fascicle palsy + contralateral tremor (red nucleus and substantia nigra) = Benedikt syndrome (Benedikt buzzes)
  3. CN3 fascicle palsy + contralateral ataxia ( superior cerebellar peduncle) = Claude syndrome (Claude is clumsy)
  4. CN3 nuclear palsy + fascicular palsy + ataxia + supranuclear eye movement dysfunction = Nothnagel syndrome
20
Q

Fascicular CN 4 palsy

A
  1. Rare to have fascicular involvement of CN4 in brainstem
  2. May have involvement of both CN4s from pineal tumors that compromise tectum of midbrain → dorsal midbrain syndrome
21
Q

Fascicular CN 6 palsy

A
  1. May also injure CN7 whose fibers course around CN6 nucelus
  2. CN6 fascicle palsy + CN7 fascicle palsy + CN5 descending tract = ipsilateral abduction + facial weakness + loss of taste over anterior 2/3 of tongue + facial hypoesthesia → Foville syndrome
  3. CN6 fascicle palsy + CN7 fascicle palsy + corticospinal tract = Millard-Gubler syndrome
  4. CN6 fascicle palsy + corticospinal tract → Raymond syndrome
22
Q

Subarachnoid Space CN Palsy

A
  1. Subarachnoid segment of ocular motor CNs extends from brainstem to cavernous sinus where nerves exit dura and most ischemic neuropathies occur within this area
  2. Pain may or may not be present
  3. Ocular misalignment 2/2 ischemia with diplopia usually resolves within 6 months
    1. Patients require evaluation for risk factors — DM, HTN, serum lipids
    2. Progression of ocular misalignment beyond 2 weeks or failure to improve within 3 months should prompt search for other etiology
  4. Myasthenia Gravis may mimic any pattern of painless EOM dysfunction and should be included in ddx
  5. GCA also may present with diplopia from skew deviation, EOM ischemia, ischemic cranial neuropathy
  6. If patient has cancer and presents with EOM neuropathy then neuroimaging should be performed to rule out compressive or infiltrative etiology
23
Q

CN 3 Palsy - Introduction

A
  1. Complete CN3 palsy
    1. Down and Out deviation of eye + complete ptosis (LPS), inability to adduct/infraduct/supraduct; pupil may or may not be involved
  2. Partial CN3 palsy
    1. More common, variable limitation of supraduction/adduction/infraduction, variable ptosis; pupil may or may not be involved
  3. Most isolated unilateral CN3 palsies — microvascular injury in subarachnoid space or cavernous sinus. Less commonly aneurysmal, compression, tumor, inflammation, vasculitis, infection, infiltration, trauma
24
Q

CN 3 Palsy + Pupil Involving

A
  1. Mid-dilated pupil that responds poorly to light
  2. With variable dysfunction of EOMs and LPS
  3. Aneurysms arising at junction of PCoA and ICA juxtaposed to CN3 and can produce CN3 palsy with aneurysm expansion or rupture
  4. Pupillary involvement — pupillomotor fibers reside superficially in medial aspect of nerve adjacent to PCoA
  5. MRA or CTA can detect aneurysms up to 3mm in diameter. CTA faster, slightly better resolution and may show evidence of SAH. MRI with MRA more likely to show nonaneurysmal lesions.
  6. When neuroimaging normal — LP may show evidence of subarachnoid hemorrhage (xanthochromia of spinal fluid) or detect inflammatory or neoplastic cause.
  7. Catheter angiography used for diagnostic confirmation and definitive treatment of aneurysm but rarely for diagnosis.
  8. Isolated pupillary involvement (dilated and responds poorly to light) BUT exhibits normal eyelid and EOMs almost always benign disorder — Adies pupil, pharmacologically dilated, mechanically damaged.
    1. Must exclude subtle CN3 palsy and minor degrees of incomitant strabismus with prism alternate cover test OR maddox rod
  9. Pupillary dysfunction or progressive loss of function does not alwasy indicate aneurysm — vasculopathic form of CN3 palsy may produce pupillary defect in 20% of cases though pupillary involvement usually mild (<1mm anisocoria).
    1. HbA1c, Lipids, BP should be checked though even patients with these risk factors may develop aneurysms
  10. Pupillary involvement = Neuroimaging
25
Q

CN 3 Palsy Pupil-Sparing

A
  1. Pupillary function normal with complete/partial motor dysfunction
  2. Ischemic cranial neuropathy usual etiology and resolves within 6 months — HTN, HLD, DMT2. Usually pupil-sparing and complete!
  3. Acute isloated pupil-sparing and complete CN3 palsy in patients over 50 with known vascular risk factors and without hx of cancer does NOT necessarily require neuroimaging BUT general medical evaluation indicated to assess serum glucose, SBP, lipid levels. In older adults screening for vasculitis — GCA with ESR, CRP, platelets
  4. If other cranial neuropathies develop, progression occurs, no improvement within 3 months neuroimaging should be taken in search for a mass, infiltrative lesion at base of skull or within cavernous sinus. Lumbar puncture may be needed to detect carcinmatous meningitis, inflammation, or infection.
  5. Pupil-sparing and partial — NOT AS BENIGN as complete oculomotor paresis given that many other fibers within CN3 are also spared. Some partial CN3 palsies with normal pupillary function are due to compressive lesions, including aneurysm and may later progress to involve pupil. MRA/CTA indicated to exclude aneurysm. If MRA/CTA negative and CN3 palsy has progressed, MRI of Brain and Orbits with gadolinium contrast should be obtained to search for anatomic lesion
  6. Pain may be present in vasculopathic palsies or anuerysms
  7. Patients with partial CN3 palsy 2/2 aneurysm have better recovery of function than patients with complete CN3 palsy after undergoing same neurosurgery intervention
26
Q

CN 3 Palsy Divisional

A
  1. CN3 branches into superior and inferior divisions within cavernous sinus and superior orbital fissure
  2. Isolated involvement of either division → anterior cavernous sinus lesion or posterior orbit
    1. Initial study should be cranial and orbital MRI with contrast and fat suppression + MRA. If normal, medical evaluation for HTN, BG, HLD, ESR, CRP, platelets (if necessary)
    2. Rare cases — divisional CN3 palsy may be secondary to brainstem disease from small-vessel stroke or demyelination. Aneurysms much less common. Rare causes include tumors, inflammation (sarcoid), vasculitis, meningitis, lymphoma, trauma
27
Q

CN 3 Palsy Young Patients

A
  1. May experience transient ophthalmoplegia after viral infection or vaccination
  2. Although aneurysms rare in children, pupil-involving CN 3 palsy necessitates workup to exclude aneurysm
  3. Recurrent painful oculomotor neuropathy term now in place of ophthalmoplegic migraine — presents as a CN3 palsy. Ophthalmoplegia develops after onset of head pain.
    1. MRI may show reversible thickening and enhancement of root exit zone of CN 3. CN 3 enhancement may persist after resolution of CN 3 palsy thus follow-up MRI indicated
28
Q

Aberrant Regeneration CN 3

A
  1. After nerve axons damaged, nerve fibers regrow to innervate muscles (of same CN) other than those they originally innervated. This produces synkinetic phenomenon — co-contraction of muscles normally not activated together. See eyelid retraction with adduction for example, or pupillary miosis with elevation/adduction/depression
  2. 2/2 normal development unlike usual synkinesis with abnormal miswiring that is congenital
29
Q

CN 4 Palsy

A
  1. Acute palsy causes diplopia worse in contralateral gaze, ipsilateral head tilt, downgaze
  2. Most cases show grossly normal EOMs with some showing limited downgaze in adduction
  3. Need to perform PACT or Maddox Rod tesiting to demonstrate hypertropia that worsens in contralateral gaze and ipsilateral head tilt
  4. Ipsilateral head tilt worsens vertical strabismus and patients may subconsciously tilt their head to opposite side to avoid diplopia
  5. Parks-Bielschowsky 3 step test for vertically acting muscles
    1. Find side of hypertropia in primary gaze
    2. Determine hypertropia is greater on L or R gaze
    3. Determine hypertropia greater on L or R head tilt
  6. Excyclotropia should be assessed by double Maddox rod testing
  7. Skew deviation may mimic CN 4 palsy → hypertropic eye intorted as opposed to extorted + patient in supine position reduces magnitude of hypertropia.
  8. Acquired vertical strabismus not from CN 4 often result of dysfunction of more than 1 muscle and will not generate positive 3 step-test — TED, MG, multiple CN palsies can produce variety of nonspecific patterns of ocular misaligment.
  9. Reliability of 3 step-test in identifying pattern of vertical strabismus lessens over time because of spread of comitance
  10. Bilateral CN 4 Palsy
    1. Should be considered if unilateral CN 4 palsy diagnosed especially in head trauma
    2. Crossed hypertropia — R eye higher on left gaze and L eye higher on right gaze
    3. Extorsion of > 10 degrees
    4. Large > 25 PD V pattern esotropia (greater esotropia in downgaze than upgaze)
    5. Chin-down posture (hypertropia decreases in down upgaze)
  11. Congenital CN 4 palsy
    1. Most common cause
    2. 2/2 anomalous SO tendon, anomalous insertion, defect in trochlea, schwannoma of nerve
    3. May be asymptomatic until adulthood when vertical fusion amplitudes diminish and diplopia develops
    4. Chronic head tilt seen on old phorographs
    5. Long-standing CN 4 palsy may have relatively large vertical fusional amplitudes > 3 PD
  12. Older patients — typically from microvascular ischemia. Usually function return in 6 months
    1. Assess vascular risk factors — HTN, HLD, DMT2, GCA.
  13. May also be 2/2 closed head trauma given dorsal midbrain crossing anatomy, disease within cavernous sinus or subarachnoid space, TED, skew deviation in atypical cases as well as MG or partial CN 3 palsy
  14. Diagnostic evaluation for isolated non-traumatic CN 4 palsy yields little information as most congenital, ischemic, idiopathic.
  15. Lack of improvement in 3 months should prompt neuroimaging at skull base to search for mass lesion
30
Q

CN 6 Palsy

A
  1. May see divergence insufficiency or diolopia worse at distance as less abduction required on near vision
  2. Most common cause is ischemic mononeuropathy
  3. Cerebellopontine angle lesions (acoustic neuroma) may involve CN 6 + other CNs such as CN 5 (decreased facial sensation), CN 7 (facial paralysis), CN 8 (decreased hearing with vestibular signs).
  4. Chronic inflammation of petrous bone may cause an ipsilateral abducens palsy and facial pain especially in children with recurrent middle ear infections → Gradenigo syndrome.
  5. Susceptible to injury from shearing forces of head trauma or elevated ICP — injury in these situations occurs where nerve enters the cavernous sinus through Dorello canal (the opening below the petroclinoid ligament).
  6. Vulnerable to meningeal processess such as meningioma, nasopahryngeal carcinoma, chordoma, chondrosarcoma
  7. Palsy after seemingly minor trauma — should raise concern for preexisting pathology such as tumor compression that makes nerve more suceptible to injury.
  8. Congenital CN 6 palsy almost never occurs in isolation — abduction paresis that is present early in life usually manifests as Duane syndrome (with narrowing of palpebral fissure)
  9. Older adults > 50 — usually ischemic, and resolves within 6 months. Some people recommend neuroimaging. Medical evaluation important. MRI mandatory if no improvement after 3 months.
    1. May require LP, chest imaging, hematologic studies to identify underlying systemic process such syphilis, sarcoidosis, collagen vascular disease, GCA. Recovery does not always indicate a benign process.
  10. Younger < 50 — requires careful scrutiny with neuroimaging. May be presenting sign of posterior-draining CCF (white eye syndrome).
    1. Negative results — assess for MG, TED, LP to look for meningeal disease
    2. Leukemia and brainstem glioma important to consider in young children while demyelination may be seen in adolescents and young adults (MRI with FLAIR).
  11. Mimics — Duane Type 1, spasm of near reflex, MG, TED, medial orbital wall fracture with entrapment
31
Q

Ocular Neuromyotonia

A
  1. Rare cause of episodic diplopia
  2. Prior skull-based radiation therapy for neoplasm most common. Months to years postradiation, patients experience episodic diplopia lasting 30-60 seconds
  3. May affect any of the oculomotor nerves
  4. Diplopia triggered by activation of affected nerve in eccentric gaze with resultant sustained muscle contraction producing ocular misalignment (CN 6 neuromyotonia — produces sustained lateral rectus muscle spasm).
  5. Disorder responds well to carbamazepine
32
Q

Multiple Cranial Nerve Palsy

A
  1. Benign microvascular disease rarely causes simultaneous involvement of more than ocular motor CN.
  2. Simultaneous involvement of unilateral CNs 3, 4, 5, 6 and sympathetic nerves then strongly suspect cavernous sinus lesion
  3. Bilateral involvement of CNs — suggests diffuse process such as infiltrative disease (carcinoma, leukemia, lymphoma) or midline mass that extends bilaterally (chondroarcoma, nasopharyngeal carcinoma, chordoma), meningeal based process, inflammatory polyneuropathy (GBS or Miller-Fisher, sarcoidosis), MG
  4. Neuroimaging should be done — if normal then LP with cytopathology should be considered. Special testing for cancer-associated protein markers may be helpful.
  5. Idiopathic multiple cranial neuropathy syndrome should be considered after neuroimaging, CSF analysis, extendend observation have excluded neoplastic, inflammatory, infectious causes
33
Q

Cavernous Sinus and Superior Orbital Fissure CN Palsy

A
  1. Ipsilateral CN dysfunction involving combination of CN 3, 4, 5, 6, and sympathetic fibers hallmark of ophthalmoplegia secondary to cavernous sinus lesion
  2. If only 1 CN involved then usually CN 6 which is only CN NOT protected within lateral dural wall of cavernous sinus → Abducens Bathed in Blood!!
  3. Aggressive lesions of cavernous sinus — may cause engorgment of ocular surface vessels from compromised venous outflow, orbital venous congestion, increased intraocular pressure, increased ocular pulse pressure
  4. Difficult to distinguish cavernous sinus lesions from those involving superior orbital fissure — sometimes called sphenocavernous syndrome or parasellar syndrome
  5. If offending lesion extends toward optic canal into orbital apex and optic nerve compromised then —- orbital apex syndrome applied
34
Q

Tolosa-Hunt Syndrome

A
  1. Idiopathic, sterile inflammation affecting cavernous sinus
  2. Severe boring pain almost always present + ophthalmoplegia
  3. Neuroimaging may show enhancing mass within cavernous sinus
  4. Pain responds rapidly to corticosteroid therapy but may also be seen in a neoplastic process especially lymphoma
  5. Sometimes found that painful ophthalmoplegia in patients initially diagnosed with Tolosa-Hunt syndrome due to neoplasm
  6. Diagnosis of exclusion
  7. Other causes of cavernous sinus lesions — aneurysm, meningioma, lymphoma, schwannoma, pituitary adenoma, CCF, metastasis, sarcoidosis, cavernous sinus thrombosis
35
Q

Carotid-Cavernous Sinus Fistula (CCF)

A
  1. Abnormal connection between cavernous sinus and carotid artery or its branches introduce high arterial pressure into normally low-pressure venous circulation of cavernous sinus. Causes reverse blood flow within SOV and produces venous congestion within orbit.
    1. See arterialization of conjunctival vessels
  2. Direct high-flow connections between ICA and cavernous sinus
    1. 2/2 severe head trauma with cranial bruit
  3. Dural low-flow connections between small arterial feeders off ICA or ECA and cavernous sinus
    1. Spontaneously and usually in older woman
  4. Cannot distinguisn between high-flow or low-flow besides cranial bruit
  5. MRA, CTA or cerebral angiography necessary to make diagnosis
  6. See elevated IOP and proptosis and other signs:
    1. Diplopia from CN palsy or orbital congestion
    2. Arterial or venous compromise to retina and eye
    3. Ischemic optic neuropathy
    4. Choroidal effusions
    5. Ocular Pain (may be partly from dry surface from proptosis)
    6. Cerebral Venous infarction resulting from venous hypertension
    7. Pulsatile tinnitus
  7. Compression of CN 6 due to posteriorly draining fistula can cause an isolated CN 6 palsy
  8. Dural fistula may close spontaneously
  9. CCF either high/low flow may be treated with IR techniques
36
Q

Myasthenia Gravis and Diplopia

A
  1. Produces variable diplopia, variable ptosis with pupil-sparing painless ocular misalignment
  2. Never produces sensory symptoms, pain or pupil dysfunction
37
Q

Thyroid Eye Disease and Diplopia

A
  1. Most common cause of restrictive strabismus in adults
  2. Most commonly Inferior Rectus and Medial Rectus
    1. Will see hypotropia worse on upgaze and esodeviation that increases on lateral gaze
  3. Forced duction testing may provide support for diagnosis
  4. Diagnosis of TED straightforwards if associated with proptosis, chemosis, eyelid retraction, lid lag
  5. Neuroimaging reveals enlargement of EOM bellies with sparing of tendons
38
Q

Posttraumatic Restriction and Diplopia

A
  1. Blowout fractures of orbit may cause diplopia
  2. Especially orbital floor with entrapment of inferior rectus
  3. Paretic swelling from swelling may also occur in acute phase — as swelling resolves so may diplopia thus decisions about surgery for orbital fractures must be made judiciously
39
Q

Postsurgical Restriction and Diplopia

A
  1. May see binocular diplopia from injury or inflammation to inferior rectus or other muscles after retrobulbar or peribulbar injection for cataract or other ocular surgery. Onset of diplopia immediately following surgery suggests nerve damage or nyotoxicity from local anesthetic.
  2. Over time, initiial paretic or myotoxic effect evolves into extraocular muscle fibrosis leading to overaction or a restricted eye movement.
    1. ​If inferior rectus affected — involved eye transitions from hypertropic (paretic) to hypotropic (restricted)
  3. Restrictive diplopia may also be seen in: pterygium excision, SB placement, episcleral plaque brachytherapy, tube shunt procedures
40
Q

Orbital Myositis and Ophthalmoplegia

A
  1. Idiopathic inflammation of 1 or more EOMs may produce ophthalmoplegia and pain often with associated conjunctival hyperemia, chemosis, sometimes proptosis
  2. Pain may be intense and exacerbated by eye movements
  3. If inflammation confined to posterior orbit, eye may appear to be white and quiet
  4. CT or MRI may show enlargement of 1 or more EOMs with tendon involvement with extension of inflammation into orbital fat
  5. Pain responds to corticosteroids whereas diplopia may take longer to resolve
  6. Usually an isolated phenomenon but may be associated with systemic disease:
    1. GPA, SLE, sarcoidosis, IgG4, lymphoma, metastatic disease
  7. EOM Bx should be done in cases of recurrent orbital myositis with steroid taper
41
Q

Neoplasia and Ophthalmoplegia

A
  1. If cancer infiltrates orbit from surrounding paranasal sinuses, eye movements may be impaired either due to muscle infiltration or involvement of ocular motor CNs.
42
Q

Brown Syndrome and Ophthalmoplegia

A
  1. Restrictive ocular motor disorder = limited upgaze when eye adducted
  2. Usually congenital (short SO tendon) but may be acquired
  3. Acquired → RA, idiopathic orbital inflammatory disease, trauma, iatrogenic trauma, focal neoplastic metastasis to superior oblique muscle
43
Q

Heavy Eye Syndrome and Ophthalmoplegia

A
  1. AKA strabismus fixus
  2. Results in progressive esotropia and hypotropia in high myopes (limited abduction and limited supraduction) → superotemporal shift of staphylomatous globe posteriorly with medial displacement of SR and inferior displacement of LR. Intervening connective tissue band also degenerates
  3. Neuroimaging required to confirm muscle slippage
  4. Initial treatment is bilateral loop myopexy between SR and LR to restore normal anatomy
44
Q

Sagging Eye Syndrome and Ophthalmoplegia

A
  1. Can be seen in older patients without myopia
  2. Presents with mild-moderate angle esotropia at distance (divergence insufficiency), full lateral gaze, minimal hypotropia with limited supraduction
  3. LR-SR band degenerates → inferior displacement of LR with NO globe prolapse.
  4. Often with degenerative changes that can cause deep superior sulci, high lid crease, prosus from levator aponeurosis dehiscence.
  5. Usually etiology of divergence insufficiency in elderly.
45
Q

Refractive Procedure-Induced Diplopia

A
  1. In patients with childhood strabismus, diplopia may be induced by refractive procedures that cause a change in fixation preference to the nondominant eye (monovision correction, cataract surgery on an amblyopic eye prior to dominant eye, noncycloplegic refraction leading to undercorrected hyperopia and fixation with amblyopic eye) → “Fixation switch diplopia” resolves with appropriate optical correction to reestablish fixation with dominant eye
46
Q

Foveal Displacement Syndrome

A
  1. Foveal displacement syndrome from macular disease or surgery can result in typically vertical or oblique binocular diplopia that cannot be corrected with prisms
  2. May be 2/2 to ERM
47
Q

Congenital Fibrosis Syndrome

A
  1. LPS and SR congenital agenesis of nuclei

Neuro-Ophthalmology (14 decks)

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