Neuro-ophthalmology. MBBS, MMed (Ophth), FRCSEd (Ophth) Registrar, Ophthalmology & Visual Sciences

Transcription

1 Neuro-ophthalmology Sangtam Tiakumzuk MBBS, MMed (Ophth), FRCSEd (Ophth) Registrar, Ophthalmology & Visual Sciences Blurring of Vision: A Practical Approach to Common Case Scenarios 13 February 2016

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3 History Laterality of the vision loss Time course of the vision loss Associated symptoms

4 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

5 Laterality of the vision loss Unilateral Lesion anterior to the chiasm Bilateral Bilateral ocular, chiasmal, or retrochiasmal process

6 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)

7 Time course Sudden to Rapid Days to Weeks Ischemic event or origin Inflammation (Caveat: Various etiologies exhibit considerable overlap among the different time courses)

8 Over months Months to Years Typical of toxic lesions Most consistent with compressive causes (Caveat: Various etiologies exhibit considerable overlap among the different time courses)

9 Associated Symptoms Globe tenderness or ipsilateral periorbital pain Increases with eye movement Optic neuritis

10 Associated Symptoms Diplopia, oscillopsia, hemiparesis, and hemisensory changes Demyelinating disease

11 Associated Symptoms Nonspecific pain, facial numbness, or diplopia Orbital or cavernous sinus lesions

12 Associated Symptoms Headache, jaw claudication, scalp tenderness, Systemic symptoms (weight loss, night sweats, malaise, myalgia) Giant Cell Arteritis

13 Examination Best-Corrected Visual Acuity (BCVA) Color Vision Testing Pupillary Testing Fundus Examination Visual Field Evaluation

14 BCVA BCVA obtained with refraction Improvement with pinhole: refractive component Worsening with pinhole: retinal or lenticular contribution

15 Complements VA Color Vision Testing Optic nerve disease: affect color vision>>va Macular disease: VA=color vision decline correspondingly

16 Pupillary Testing Dim ambient lighting Fixate at distance Use a well-charged, bright, steady light source

17 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

18 Pupillary Testing If 1 pupil does not react (eg, iris trauma, synechiae, pharmacologic mydriasis or miosis) Source: AAO-Neuro-Ophthalmology

19 Fundus Examination 3CCC: Color, Contour, Cupping 3SSS: Shape, Size, Structures ± Source: AAO-Neuro-Ophthalmology

20 Fundus Examination Structures Source: AAO-Neuro-Ophthalmology

21 Visual Field Evaluation Examiner sits 1m from the 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

22 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

23 Retrobulbar neuritis Papillitis Neuroretinitis Optic Neuritis Source: AAO-Neuro-Ophthalmology

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26 Clinical features of demyelinating optic neuritis Symptoms Subacute monocular visual impairment Usual age range years (mean around 30) Some patients experience tiny white or colored flashes or sparkles (phosphenes)

27 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

28 Uhthoff phenomenon in MS (sudden worsening of vision or other symptoms on exercise or increase in body temperature) Wilhelm Uhthoff ( ) German ophthalmologist (Wikipedia)

29 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

30 Lhermitte sign in MS Jacques Jean Lhermitte French neurologist, neuropsychiatrist (Wikipedia)

31 Visual field defects

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34 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

35 Detailed history Monocular Lesion anterior to the chiasm binocular Bilateral ocular, chiasmal, or retrochiasmal process

36 Age < 50 years, Migraine Vasospasm Older patients CVA GCA (Important exception in pregnant women is eclampsia - harbinger of more serious and permanent visual loss, usually occurring within days of delivery)

37 Duration of visual loss Lasting only seconds UL or BL transient obscurations of vision Lasting several minutes (<15) Symptomatic ipsilateral ICA stenosis Often precipitated by a change in posture OD drusen or papilledema

38 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

39 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

40 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

41 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

42 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 minutes but can take up to 1 hour in some cases

43 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

44 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

45 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)

46 Kanski Cholesterol (Hollenhorst plaque) Yellow-Orange/Copper Refractile Globular or rectangular major bifurcation Source: CCA or ICA, rarely Aorta/Innominate artery AAO

47 Kanski Cholesterol (Hollenhorst plaque) Evaluation AAO 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)

48 Platelet-fibrin AAO Dull gray-white Long smooth shape Concave each ends Usually mobile Lodge along course of vessel Source: wall of atherosclerotic vv, heart (esp. valves) Kanski

49 Platelet-fibrin AAO Evaluation General medical examination Cardiac assessment, including Holter monitor and ECHO Noninvasive studies of carotid patency Hematologic studies Kanski

50 Calcium AAO Chalky white Large Round or ovoid Lodge in 1 st or 2 nd bifurcation May overlie optic disc Source: Heart/great vv, RHD, calcific aortic stenosis, calcification of mitral valve annulus Kanski

51 Calcium AAO Evaluation General medical examination Cardiac assessment, including ECHO Angiogram of aortic arch Kanski

52 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

53 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

54 Transient Binocular Visual Loss Migraine Occipital mass lesions: tumor, arteriovenous malformation Occipital ischemia: embolic, vasculitic, hypoperfusion Occipital seizures

55 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)

56 Source: AAO-Neuro-Ophthalmology Scintillating scotoma : blind region surrounded by a margin of sparkling lights Fortification spectrum : begins with a small scotoma, gradually expands into the peripheral vision

57 metry_of_war/geoamberina.php Source: AAO-Neuro-Ophthalmology 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

58 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

59 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

60 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

61 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)

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