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Neuro-ophthalmology
Blurring of Vision: A Practical Approach to Common Case Scenarios 13 February 2016
Sangtam Tiakumzuk MBBS, MMed (Ophth), FRCSEd (Ophth) Registrar, Ophthalmology & Visual Sciences
http://www.deviatingeye.com/graphics/textbook-illustrations/visual-pathway-from-the.html
History
• Laterality of the vision loss
• Time course of the vision loss
• Associated symptoms
Laterality of the vision loss
• Unilateral Versus Bilateral
• Ask specifically if they have checked each eye individually
• Binocular involvement may not be appreciated until the patient is examined
Laterality of the vision loss
Unilateral
• Lesion anterior to the chiasm
Bilateral
• Bilateral ocular, chiasmal, or retrochiasmal process
Time Course of Vision Loss
• Sudden onset to Rapid vision loss
• Days to weeks
• Over months
• Months or years
• (Caveat: Various etiologies exhibit considerable overlap
among the different time courses)
Time course Sudden to Rapid
Ischemic event or origin
Days to Weeks
Inflammation
(Caveat: Various etiologies exhibit considerable overlap among the different time courses)
Over months
• Typical of toxic lesions
Months to Years
• Most consistent with compressive causes
(Caveat: Various etiologies exhibit considerable overlap among the different time courses)
Associated Symptoms
• Globe tenderness or ipsilateral periorbital pain
• Increases with eye movement
• Optic neuritis
Associated Symptoms
• Diplopia, oscillopsia, hemiparesis, and hemisensory changes
• Demyelinating disease
Associated Symptoms
• Nonspecific pain, facial numbness, or diplopia
• Orbital or cavernous sinus lesions
Associated Symptoms
• Headache, jaw claudication, scalp tenderness,
• Systemic symptoms (weight loss, night sweats, malaise, myalgia)
• Giant Cell Arteritis
Examination
• Best-Corrected Visual Acuity (BCVA)
• Color Vision Testing
• Pupillary Testing
• Fundus Examination
• Visual Field Evaluation
BCVA
• BCVA obtained with refraction
• Improvement with pinhole: refractive component
• Worsening with pinhole: retinal or lenticular contribution
Color Vision Testing
• Complements VA
• Optic nerve disease: affect color vision>>VA
• Macular disease: VA=color vision decline correspondingly
Pupillary Testing
• Dim ambient lighting
• Fixate at distance
• Use a well-charged, bright, steady light source
Pupillary Testing
• Stimulate 1 eye for 2–3 seconds
• Quickly move across the bridge of the nose to stimulate the other eye for 2–3 seconds
• Do not rely on a single observation
Pupillary Testing
• If 1 pupil does not react (eg, iris trauma, synechiae, pharmacologic mydriasis or miosis)
Source: AAO-Neuro-Ophthalmology 2015-16
Fundus Examination
• 3CCC: Color, Contour, Cupping
• 3SSS: Shape, Size, Structures ±
Source: AAO-Neuro-Ophthalmology 2015-16
Fundus Examination
Structures
Source: AAO-Neuro-Ophthalmology 2015-16
Visual Field Evaluation • Examiner sits 1m from the patient @ same
level
• Patient covers 1 eye and fixates on the examiner’s nose
• Examiner asks the patient if specific portions of his face cannot be seen
• Ask to identify a target of 1, 2, or 5 fingers presented at the midpoint of each of the 4 Qs
• If cannot identify fingers, present progressively stronger stimuli such as HM, LP in each quadrant
https://www.youtube.com/watch?v=2-9FVywV2j4
Optic Neuritis
• Retrobulbar neuritis
• Papillitis
• Neuroretinitis
Source: AAO-Neuro-Ophthalmology 2015-16
http://www.slideshare.net/aravin8292/optic-neuritis-43175548
http://slideplayer.com/slide/4522455/
Clinical features of demyelinating optic neuritis
• Symptoms
Subacute monocular visual impairment
Usual age range 20–50 years (mean around 30)
Some patients experience tiny white or colored flashes or sparkles (phosphenes)
Clinical features of demyelinating optic neuritis
Discomfort/pain in or around the eye (>90%), typically exacerbated by ocular movement
May precede or accompany the visual loss and usually lasts a few days
Frontal headache and tenderness of the globe may also be present
Uhthoff phenomenon in MS (sudden worsening of vision or
other symptoms on exercise or increase in body temperature)
Wilhelm Uhthoff (31.7.1853 – 21.3.1927) German ophthalmologist (Wikipedia)
https://mmcneuro.wordpress.com/category/ms/
Clinical features of demyelinating optic neuritis
• Signs
VA is usually 6/18–6/60, but may rarely be worse
Other signs of optic nerve dysfunction - particularly impaired colour vision and a RAPD
Optic disc is normal in the majority (retrobulbar neuritis); the remainder show papillitis
Jacques Jean Lhermitte 20.1.1877 – 24.1.1959French neurologist, neuropsychiatrist (Wikipedia)
Lhermitte sign in MS
Visual field defects
Transient Visual Loss (TVL)
• Sudden loss of visual function (partial or complete) in 1 or both eyes <24 hours
• MC of monocular TVL is retinal ischemia due to carotid artery disease
• MC cause of binocular TVL is migraine
Detailed history
• Monocular • Lesion anterior to the chiasm
• binocular • Bilateral ocular, chiasmal, or
retrochiasmal process
Age
< 50 years,
• Migraine
• Vasospasm
• (Important exception in pregnant
women is eclampsia - harbinger of more serious and permanent visual loss, usually occurring within days of delivery)
Older patients
• CVA
• GCA
Duration of visual loss
Lasting only seconds
• UL or BL transient obscurations of vision
• Often precipitated by a change in posture
• OD drusen or papilledema
Lasting several minutes (<15)
• Symptomatic ipsilateral ICA stenosis
Pattern of visual loss and recovery
• Descending curtain in 1 eye - classic description of TMVL from retinal emboli
• Altitudinal visual loss strongly suggests carotid artery disease, sometimes vasospasm
• Visual loss precipitated by exercise also suggest vasospasm
Pattern of visual loss and recovery
• Posterior circulation ischemia typically causes: complete BL visual loss (ie, cortical blindness) homonymous hemianopia (often associated with brainstem and
cerebellar symptoms or deficits)
• BL geometric quality-hexagonal “chicken wire” pattern strongly suggests occipital lobe dysfunction
• Whiteout of vision or gradual “closing in” of peripheral vision may also signal occipital lobe ischemia
Associated symptoms and additional signs
• Positive visual phenomena and headache accompanying TVL suggest migraine
• Persistent headaches and intracranial noises are typical for increased intracranial pressure
• Elderly with headaches, wt. loss, fever, malaise, and scalp tenderness strongly suggest GCA
Associated symptoms and additional signs
• LOC, dizziness, diplopia, dysarthria, or focal weakness
• Suggest global perfusion problems, often involving the brainstem or cortex
• Skin or joint changes or Raynaud phenomenon may accompany collagen vascular disease
Transient Monocular Visual Loss (TMVL)
• Amaurosis fugax (“fleeting blindness”) is TMVL due to retinal emboli
• Abrupt, painless, and descends (or ascends) like a curtain over part or all of the visual field in 1 eye
• Usually resolves in 10–15 minutes but can take up to 1 hour in some cases
Transient Monocular Visual Loss (TMVL)
• At resolution, the curtain may either retract or dissolve like a clearing fog
• Amaurosis fugax is not associated with other neurologic deficits
• Ocular examination is often normal
Transient Monocular Visual Loss (TMVL)
• Emboli that cause TMVL usually travel to and lodge in blood vessels that supply the retina
• Ophthalmoscopically appear distinctive, their probable site of origin can often be inferred
• Such an inference may be crucial in directing appropriate patient evaluation
Transient Monocular Visual Loss (TMVL)
• 3 most common types of emboli:
Cholesterol (Hollenhorst plaque)
Platelet-fibrin
Calcium
Other less common: cardiac tumors (myxoma), fat (long-bone fractures,
pancreatitis), sepsis, talc, air, silicone, and depot drugs (corticosteroids)
Cholesterol (Hollenhorst plaque)
• Yellow-Orange/Copper
• Refractile
• Globular or rectangular
• Usually @ major bifurcation
• Source: CCA or ICA, rarely Aorta/Innominate artery
AAO
Kanski
Cholesterol (Hollenhorst plaque)
• Evaluation
General medical examination Noninvasive studies of
carotid patency Angiography, including
Aortic arch Cardiac assessment (not for
source of embolus but because these emboli increase the risk of cardiac disease and death from cardiac dysfunction)
AAO
Kanski
Platelet-fibrin
• Dull gray-white
• Long smooth shape
• Concave meniscus @ each ends
• Usually mobile
• Lodge along course of vessel
• Source: wall of atherosclerotic vv, heart (esp. valves)
AAO
Kanski
Platelet-fibrin
• Evaluation
General medical examination
Cardiac assessment, including Holter monitor and ECHO
Noninvasive studies of carotid patency
Hematologic studies
AAO
Kanski
Calcium
• Chalky white • Large • Round or ovoid • Lodge in 1st or 2nd
bifurcation • May overlie optic disc • Source: Heart/great vv,
RHD, calcific aortic stenosis, calcification of mitral valve annulus
AAO
Kanski
Calcium
• Evaluation
General medical examination
Cardiac assessment, including ECHO
Angiogram of aortic arch
AAO
Kanski
Medical treatment
• TMVL due to carotid artery stenosis (ie, retinal TIA) begins with aspirin
• Clopidogrel bisulfate is useful for patients who are intolerant of or allergic to aspirin
• Cilostazol, may be more protective than either aspirin alone or clopidogrel
Medical treatment
• Once antiplatelet therapy is maximized, consider adding a statin or increasing the dose of a statin if already taking
• There is some evidence that high doses of statins can reduce plaques and the frequency of stroke
• Finally, ACE inhibitors and ACE receptor blockers may be useful for their favorable effects on endothelial tissue
Transient Binocular Visual Loss
• Migraine
• Occipital mass lesions: tumor, arteriovenous malformation
• Occipital ischemia: embolic, vasculitic, hypoperfusion
• Occipital seizures
Migraine
• MC cause of binocular TVL is the homonymous hemianopic defect caused by migraine
• Migraine with aura (classic migraine-30% of migraine): typical visual aura have a hemianopic distribution
• Migraine aura without headache (acephalgic migraine-5% of migraine)
Source: AAO-Neuro-Ophthalmology 2015-16
“Scintillating scotoma”: blind region surrounded by a margin of sparkling lights “Fortification spectrum”: begins with a small scotoma, gradually expands into the peripheral vision
Fortification spectrum (Teichopsia-Greek word teichos-”town wall”) so-named because of the resemblance of the zig-zag margin to the ground plan of town fortifications in Europe
Source: AAO-Neuro-Ophthalmology 2010-11 http://clements.umich.edu/exhibits/online/geometry_of_war/geoamberina.php
• Aura lasts <60 minutes and is typically followed by a throbbing headache on the contralateral side of the head
• Most experience associated nausea, photophobia, and phonophobia
• When untreated, migraine attacks typically last from 4 hours to 72 hours
• Abnormal excitatory activity followed by a wave of depressed neuronal function
• Some experience “Alice in Wonderland effect” (micropsia/macropsia)
• Heat waves, cracked glass, kaleidoscopic vision, or fragmented vision
Walsh & Hoyt’s Essential Neuro-Ophthalmology 2016
Who need Evaluation?
• Typical history with normal neurologic and ophthalmic exam
• Neuroimaging studies unlikely to show an intracranial abnormality
• Occasionally, mass lesion/large vascular malformation (often residual-visual field defects)
Source: AAO-Neuro-Ophthalmology 2015-16
Who need Evaluation?
• Following findings may suggest additional evaluation of patients presumed to have migraine:
Headache or aura always occurring on the same side
Headache preceding the aura
Neurologic deficit, including visual field defect, persisting after aura resolves
Atypical (>1 aura occurring in a single day, lack of expansion of/change in aura, duration <5 min or >60 min)