Transcript Back to Basics: Diplopia

Back to Basics: Diplopia
Michael Dollin
PGY2 University of Ottawa Eye Institute
University of Ottawa Meds Year 4 LMCC review course
April 2, 2009
Outline
• What is diplopia?
• Important questions to ask
• Important causes of diplopia
• Monocular
• Binocular
• Investigations
• Management
• Summary
What is diplopia?
Double vision
Important questions
(1) Does the diplopia resolve when 1 eye is
covered? (i.e. monocular vs. binocular)
(2) Is it the same in all fields gaze (comitant) or
does it vary with gaze direction (incomitant)?
(3) Is it horizontal, vertical, or oblique?
(4) Is it constant, intermittent, or variable?
Causes of diplopia
• Monocular causes
• Binocular causes
Start with question #1:
Does the diplopia resolve when 1 eye
(either eye) is covered?
(If not, the diplopia is monocular)
Monocular causes
(1) Abnormalities of
the refractive media
• High astigmatism
• Corneal irregularity
(e.g. scar, k’conus)
• Lens opacities
(e.g. cataract)
(2) Retinal pathology
• Maculopathy
(fluid, Hgb, fibrosis)
The diplopia will persist when the unaffected
eye is covered, but resolve when the
affected eye is covered
Binocular causes
Binocular diplopia will resolve by covering
either eye
Now question #2:
Is the diplopia the same in all fields gaze
(comitant) or does it vary with gaze direction
(incomitant)?
Comitant deviations
• Characteristic of congenital or early-onset strabismus
• Typically do not cause diplopia although diplopia may
develop later in life
• e.g. patient with long-standing exophoria whose accommodation
and convergence capacities wane in 5th decade of life
• Divergence insufficiency
• Manifests as esodeviation greater at distance than at near;
comitant in right and left gaze
• Benign syndrome, resolves spontaneously
• Rule out incipient or resolving U/L CN6 palsy or highly symmetric
B/L CN6 palsy (consider MRI)
Incomitant deviations
• More likely acquired and usually cause diplopia
• Think of…
• Paretic etiologies
• Neural (CN 3, 4, and 6 palsies)
• Neuromuscular junction (MG)
• Restrictive etiologies
• Trapped or fibrotic EOM
Incomitant deviations
• Approach to these etiologies…
• Question #3:
• Is it horizontal, vertical, or oblique?
• Tells you which extra-ocular muscle(s) might be
involved
• Question #4:
• Is it constant, intermittent, or variable?
• Constant: paretic (neural) or restricted
• Intermittent, variable: paretic (neuromuscular; MG)
Way back to basics!
Let’s review the actions and innervations of
the extra-ocular muscles (EOM)
EOM
• 4 rectus muscles
• Lateral (LR), Medial (MR), Superior (SR), Inferior (IR)
• 2 oblique muscles
• Superior (SO), Inferior (IO)
• Innervation:
• CN3  SR (+ levator), MR, IR, IO
• CN4  SO
• CN6  LR
“LR6SO4”
AAO, Neuro-Ophthalmology
EOM
10 action
20 action
30 action
LR
MR
SR
IR
SO
IO
ABduction
ADduction
Elevation
Depression
Intorsion
Extorsion
None
None
Intorsion
Extorsion
Depression
Elevation
None
None
ADduction
ADduction
ABduction
ABduction
Back to incomitant deviations…
Neural (paretic) causes
• Oculomotor nerve palsies
• CN3 (Oculomotor)
• CN4 (Trochlear)
• CN6 (Abducens)
• Internuclear ophthalmoplegia (INO)
AAO, Neuro-Ophthalmology
CN3 palsy
• Exits ventrally from midbrain
• Motor innervation to levator, SR, IR, MR, IO
• Parasympathetic innervation to pupillary
sphincter (constrictor) and ciliary muscles
Reference 3
• Causes of 3rd nerve palsy
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Ischemic (DM, HTN) – most common
Brain stem lesion (infarct, MS)
Compression (P comm aneurysm, uncus)
Tumour
Inflammation (Sarcoid, vasculitis)
Infection (meningitis)
Infiltration (lymphoma, carcinoma)
Trauma
• Complete 3rd nerve palsy
• Severe ptosis
• Eye positioned “down and out”
• Dilated pupil that responds poorly to light
AAO, Neuro-Ophthalmology
• Partial 3rd nerve palsy
• Mild or moderate limitation
Always check pupils!
• “Pupil-involving”
• Dilated pupil that responds poorly to light
• Due to loss of parasympathetic input
• These fibers travel along the medial superficial
surface of CN3
• Susceptible to direct compression by an aneurysm of
the posterior communicating artery (P comm)
• Assumed to be secondary to an aneurysm until
proven otherwise  must image
• Gold standard is catheter angiography
• CTA or MRA can reliably detect 2-3 mm aneurysms
AAO, Neuro-Ophthalmology
Always check pupils!
• “Pupil-sparing”
• Normal pupillary function but complete loss of
lid and ocular motor function
• Almost always ischemic (DM)
• May be painful
• Resolves within 3 months (if not  image)
• If partial w/o pupillary involvement or young
and no ischemic risk factors  follow closely
(may evolve)
• Older patients  consider GCA
CN4 palsy
• Crosses in the
brainstem
• Nucleus innervates
contralateral SO
• Exits dorsally
• Longest intracranial
course
Reference 3
• Palsy typically causes diplopia that is
worse in downgaze
• “Double vision is worse while reading”
• Motility testing often appears normal
• Identify using Parks-Bielchowsky 3-step test
• Look for: ipsilateral hypertropia and
compensatory contralateral head tilt
Left 4th nerve palsy
• Causes of 4th nerve palsy
• Congenital
• Asymptomatic until 40-60yo (↓ fusional amplitudes)
• Chronic head tilt – check old photographs
• Ischemic
• Patients older than 50yo with ischemic risk factors
• Expect resolution within 3 months
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Trauma
MS, tumour, hydrocephalus, aneurysm
Idiopathic
Consider Graves and Myasthenia
• Investigations
• Neuroimaging
• Usually of little diagnostic value
• Lack of recovery after 3 months  MRI
• Medical work-up
• Patients in vasculopathic age group
• BP, fasting BG, lipid profile
CN6 palsy
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Exits brainstem at ponto-medullary junction
Travels ventrally up the clivus
Crosses over the apex of the petrous bone
Enters the cavernous sinus
Reference 3
• Typically presents as horizontal diplopia
that worsens on ipsilateral gaze and when
viewing at a distance
AAO, Neuro-Ophthalmology
• Patient appears esodeviated
• Causes of 6th nerve palsy
• Ischemic – most common
• Patients older than 50yo with ischemic risk factors
• Expect resolution within 3 months
• CPA tumours (e.g. acoustic neuroma)
• CN 5, 6, 7, and 8 usually also affected
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Trauma
Raised intracranial pressure
Gradenigo syndrome (mastoiditis)
Consider leukemia or brain stem glioma (children)
Consider MS (adolescents and young adults)
• Investigations
• Adults > 50yo
• Medical work-up (BP, fasting BG, lipid profile)
• Lack of recovery after 3 months  MRI
• Patients < 50yo
• Rarely ischemic  must image (MRI/FLAIR)
• Consider LP, Tensilon test
INO
• Secondary to brainstem
lesion of the medial
longitudinal fasciculus
(MLF)
• Bundle of fibers
connecting 6th nerve
nucleus on one side to
the MR (3rd nerve)
subnucleus on the
opposite side
• Cardinal feature: slowed ADducting
saccadic velocity in eye ipsilateral to lesion
• INO = Insufficient Nasal Output
• Associated ABducting nystagmus of
contralateral eye
AAO, Neuro-Ophthalmology
• Most common causes:
• Adults: MS, brain stem stroke
• Children: post-viral, brain stem tumour
• Myasthenia gravis: pseudo-INO
Neuromuscular (paretic) causes
• Problem at the neuromuscular junction
(e.g. Myasthenia Gravis)
www.colorado.edu
Myasthenia Gravis
• Immunologic disorder characterized by weakness which
worsens with use (end of day) and improves with rest
• Pathophysiology: anti-acetylcholine receptor antibodies
• Hallmark features: fluctuation and fatiguability
• Common clinical presentation:
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Ptosis (worsens with sustained upgaze)
Diplopia (especially changing pattern of diplopia)
Cogan eyelid twitch
Pseudo-INO
Absence of pupil or sensory abnormalities
• Why is this diagnosis important to make?
• Systemic involvement:
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Dyspnea, dysphagia  life-threatening!
Muscle weakness (masticators, extensors)
Hoarseness
Dysarthria
Diagnosing MG
• Clinical exam
• Tensilon test
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Edrophonium chloride (Ach-esterase inhibitor)
Document baseline deficit (e.g. ptosis)
2 mg test dose (observe 60 sec) 4 mg  4 mg
Positive response dramatic if deficit was severe
Potential side effects: bradycardia, respiratory arrest,
bronchospasm, syncope, cholinergic crisis
• Pulse and BP monitoring; Atropine and crash cart ready
• Alternatives: sleep test, ice test
• Other diagnostic tests:
• Serology:
• Anti-Ach receptor antibodies
• Anti-muscle specific kinase
• Test for thyroid dysfunction (5%) and Lupus
• Single fiber EMG: decremental response
• CT chest: malignant thymoma (10%)
• Treatment:
• Mestinon (Pyridostigmine)
• +/- Thymectomy
Restrictive causes
• Most common causes:
• Thyroid-Associated Orbitopathy (Graves)
• Orbital trauma (blow-out fracture)
• Other causes:
• Orbital inflammation (myositis)
• Orbital infection (orbital cellulitis)
• Orbital tumour (EOM infiltration or metastases)
Thyroid-Associated Orbitopathy
(Graves’ disease)
• Autoimmune inflammatory disorder
• Usually hyperthyroid (can be euthyroid)
• Eye disease does not necessarily parallel
thyroid gland activity
• Clinical signs:
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Eyelid retraction
Lid lag
Proptosis (exophthalmos)
Restrictive EOM ( diplopia)
Compressive optic neuropathy
Orbital wall (blow-out) fracture
• Typically orbital floor or medial wall
• Mechanism: blunt trauma
• Diplopia 20 EOM or fascia entrapment
• Check motility (esp. up and lateral gaze)
• Other signs:
• Enophthalmos (affected eye sunken in)
• V2 numbness (over cheek bone)
• Subcutaneous emphysema
Summary
• Remember the 4 questions
• Determine onset and course
• Check pupils in CN3 palsy
• Pupil-involving needs imaging (CTA or MRI)
• Other indications for imaging
• Non-resolving (presumed ischemic) CN palsy
• Younger patients (< 50yo)
• Value of a Tensilon test in MG
• In older patients, consider GCA (ESR, CRP)
References
(1) AAO BCSC 2007-2008 Section 5, NeuroOphthalmology.
(2) Kanski JJ. Clinical Ophthalmology: A
Systematic Approach, 6th ed.
Philadelphia, PA: Elsevier Limited; 2007.
(3) Patel V. Efferent Neuroanatomy. NeuroOphthalmology teaching block, 2009,
University of Ottawa Eye Institute.
(4) www.colorado.edu (March 17, 2009)
Thank you
Any questions?
Good luck on the exam!
(Enjoy your summer)