TRANSIENT VISUAL LOSS(TVL)
Chairperson
Dr.Biswanath Ghosh
Associate Professor and Head
Department of Neurophthalmology
Moderator
Dr.Tarzeen Khadiza Shuchi
Assistant Professor
Department of Cornea
Presenter
Dr. S. M. Hasanuzzaman
FCPS Part ll Student, NIO&H
What is TVL?
Transient visual loss is the sudden loss
of visual function –
either partial or complete
either monocular or binocular
lasts less than 24 hrs.
Epidemiology:
• TVL is a very significant clinical
symptom
• Most important underlying cause is
retinal ischemia
• TVL with atheromatous carotid artery
disease have a 1 year risk of
recurrent stroke is 2%
• Patient with severe internal carotid
artery stenosis , risk of stroke is 16%
in 3 years
Causes of transient monocular
vision loss(TMVL)
A.Ocular pathology( non
vascular)
Tear-film abnormality
Corneal disease( keratoconus)
Recurrent hyphema
Intermittent angle closure glaucoma
Vitreous debris
Macular disease
B. Vascular Disease:
• Embolic phenomenon
Carotid
Cardiac
Great vessels
• Carotid artery dissection
• Vasculitis(eg.GCA, SLE)
• Vasospasm
• Systemic hypotension
• Hyperviscosity/ Hypercoagulability
states
• Ocular hypoperfusion(eg. Ocular
ischemic syndrome)
C. Optic nerve disorder:
• Acquired or congenital disc
disease(eg. papilloedema, disc
drusen)
• Compressive lesion of the intraorbital
optic nerve
• Demyelinating disease
D. Nonorganic Visual Loss
Malingering:
Willful feigning or exaggeration of
symptoms
 Hysteria:
Subconscious expression of
nonorganic sign and symptoms
Transient Binocular Vision
Loss:
• Migraine
• Occipital mass lesion(Tumor,
arteriovenous malformation)
• Occipital ischemia(embolic,
vasculitic, hypoperfusion)
• Occipital seizures
Vascular anatomy of visual pathway
Anatomy of visual pathway
Clinical Approach:
Diagnosis is done by:
 Careful history taking
 Clinical examinations
 Lab investigations
History:
1. Monocular Vs Binocular:
 Monocular loss implies a
prechiasmal problem
 Binocular loss implies chiasmal or
retrochiasmal
Homonymous hemianopia is
misperceived by the patients as
monocular visual loss
Age:
 <50 yr migraine or vasospasm is
the most likely cause of TVL
 >50 yr cerebrovascular disease or
giant cell arteritis should be
considered
Duration of visual loss:
 TVL from papilledema typically lasts
for few seconds
 TVL from retinal emboli or transient
ischemic attacks lasts for several
minutes(< 15 minutes)
 TVL from migraine typically lasts >
15 minutes
Pattern of onset:
An altitudinal onset of TVL(like a
curtain or shed descending) may
indicate embolic arterial occlusion
Concentric onset of TVL may
indicate vasospasm or neurologic
cause
Binocular visual disturbance having a
geometric quality suggest occipital
lobe dysfunction( migraine, seizure)
Associated symptoms:
Headache and positive visual
phenomena associated with TVL may
suggest migraine
Persistent headache with intracranial
noise may suggest increased
intracranial pressure
TVL associated with
Headache
Weight loss
Fever
Malaise
Scalp tenderness may suggest
GCA
Global perfusion problems associated
with loss of consciousness, dizziness,
headache, diplopia ,dysarthria, focal
weakness
Skin, joint changes or Raynaud
phenomenon may suggest collagen
vascular disease
Precipitating factors:
TVL associated with postural
changes may suggest papilledema,
GCA and hypotension
Gaze evoked visual loss suggests an
orbital mass like hemangioma or
meningioma
Physical activity or elevated body
temperature with TVL may suggest
previous or current optic neuritis
Comorbidities:
 History of vascular risk factor
Hypertension
Diabetes Mellitus
Dyslipidemia
Smoking
Cardiovascular disease
Coronary artery disease
Valvular heart disease
Atrial fibrillation
Stroke
Clinical examination:
Ocular examination:
 BCVA
 Color vision
 Pupillary light reaction
 RAPD
 Confrontation test
 Photostress recovery test
Ocular motility test
Slit Lamp Examination
 Blepharitis
 Tearfilm
 Corneal edema
 Corneal dystrophy
 Hyphema
 Cells in AC
 Pigments
 Iris neovascularizaion
 Lens position
Glaucomflecken
Intra ocular pressure
Gonioscopy (if suspision of narrow
angle)
Dilated Fundus Examination
 Retinal hemorrhage
 Arterial narrowing
 Dilated vein
 Cotton wool spot
 Optic nerve head edema
Crowded optic nerve head
Glaucomatous cupping of optic disc
Vitreo macular traction
Emboli
It is a major cause of TMVL
It can be observed with an
ophthalmoscope
Three common types are
1) Cholesterol(Hollenhorst plaque)
2) Platelet fibrin
3) Calcium
Cardiac emboli may arise from
ventricular aneurysm
Hypokinetic wall segments
Endocarditis
Valvular heart disease
Atrial fibrillation
Clinical Aspects of Retinal Emboli
Type Appearance Source
Cholesterol Yellow-orange
or copper color
Common or
internal carotid
artery
Platelet-fibrin Dull grey white
color
Walls of heart
specially valves
Calcium Chalky white
color
From heart,
great vessels,
calcific aortic or
mitral valve
Examination techniques in
functional Visual loss:
Nonvisual task
Finger nose test
Optokinetic nystagmus drum
Mirror test
Confusion test
Fogging test
Duochrome test
Cardiovascular system:
Pulse: Arrhythmia
Radiofemoral delay
Radioradial delay
Blood pressure:
Postural hypotension
Cardiac auscultation:
Murmur
Carotid auscultation:
Carotid bruit
Nervous system:
All patient should receive a detailed and
documented neurological examination.
We should give emphasis on
Cognitive and language function
Cranial nerve function
Facial and limb strength
Sensory function
Deep tendon reflex
Coordination
Investigations:
TMVL: to reveal an embolic cause:
1. Non invasive imaging:
• Carotid Ultrasonography
• Magnetic Resonance Angiography
• Computed Tomographic
Angiography
2. Invasive:
Conventional Angiography(gold
standard)
3.Holter Monitoring:
Undetected Cardiac Arrhythmia
In suspected endocarditis:
blood culture
Diabetes Mellitus:
FBS, 2HABF, HbA1C
Vasculitis:
ESR, C-reactive protien,
pANCA, cANCA,TPHA
• Hypercoagulability / Hyperviscosity:
platelet count, protein C, Protein S,
Partial thromboplastin time, Anti
cardiolipin antibody, Serum protein
electrophoresis
• Other:
Color Fundus Photography
FFA
Visual field
B scan
• In TBVL:
MRI with contrast enhancement
MRA
CT scan
CTA
EEG
Simplified Clinical Approach:
History
Blood chemistry
Abnormal
Systemic
Disease
Normal
Risk factor
Non invasive
tests
Abnormal Normal
Rethink
Cardiac/hematologic/idiopathic
Angiogram
Eye consult
Normal
/occlusive retinal
finding
Non invasive
tests
Abnormal
ocular
Normal retina
Ocular
disease
Treatment:
• Treatment is according to cause
• Collaboration of ophthalmologist ,
internist, cardiologist and neurologist
may needed
Medical
Antiplatelet
Anticoagulant
Treatment of risk factor
Hypertension
Diabetes
Hypercholesterolemia
• Surgical:
Carotid artery stenting(CAS)
Carotid endarterectomy(CEA)
Surgical management criteria
1. Male
2. Age >75 year
3. Previous history of TIA or stroke
4. Intermittent claudication
5. Stenosis 80% to 94%
6. Absence of collateral vessels on
angiography
Amourosis Fugax
The term Amaurosis Fugax not always
interchangeable with TVL.
Greek Amauroun means “To Darken”
Latin Fugax means “Fleeting”
The term Amaurosis Fugax is used to
describe TMVL due to retinal emboli
Take Home Message:
• Transient visual loss may lead to a
disease condition that can endanger
our life.
• So first and foremost patient must be
evaluated.
• Therefore we must educate the public
and medical colleagues about the
importance of getting an
ophthalmologic evaluation.
Transient Visual Loss

Transient Visual Loss

  • 1.
  • 2.
    Chairperson Dr.Biswanath Ghosh Associate Professorand Head Department of Neurophthalmology Moderator Dr.Tarzeen Khadiza Shuchi Assistant Professor Department of Cornea Presenter Dr. S. M. Hasanuzzaman FCPS Part ll Student, NIO&H
  • 3.
    What is TVL? Transientvisual loss is the sudden loss of visual function – either partial or complete either monocular or binocular lasts less than 24 hrs.
  • 4.
    Epidemiology: • TVL isa very significant clinical symptom • Most important underlying cause is retinal ischemia • TVL with atheromatous carotid artery disease have a 1 year risk of recurrent stroke is 2% • Patient with severe internal carotid artery stenosis , risk of stroke is 16% in 3 years
  • 5.
    Causes of transientmonocular vision loss(TMVL) A.Ocular pathology( non vascular) Tear-film abnormality Corneal disease( keratoconus) Recurrent hyphema Intermittent angle closure glaucoma Vitreous debris Macular disease
  • 6.
    B. Vascular Disease: •Embolic phenomenon Carotid Cardiac Great vessels
  • 7.
    • Carotid arterydissection • Vasculitis(eg.GCA, SLE) • Vasospasm • Systemic hypotension • Hyperviscosity/ Hypercoagulability states • Ocular hypoperfusion(eg. Ocular ischemic syndrome)
  • 8.
    C. Optic nervedisorder: • Acquired or congenital disc disease(eg. papilloedema, disc drusen) • Compressive lesion of the intraorbital optic nerve • Demyelinating disease
  • 9.
    D. Nonorganic VisualLoss Malingering: Willful feigning or exaggeration of symptoms  Hysteria: Subconscious expression of nonorganic sign and symptoms
  • 10.
    Transient Binocular Vision Loss: •Migraine • Occipital mass lesion(Tumor, arteriovenous malformation) • Occipital ischemia(embolic, vasculitic, hypoperfusion) • Occipital seizures
  • 11.
    Vascular anatomy ofvisual pathway
  • 12.
  • 13.
  • 14.
    Diagnosis is doneby:  Careful history taking  Clinical examinations  Lab investigations
  • 15.
    History: 1. Monocular VsBinocular:  Monocular loss implies a prechiasmal problem  Binocular loss implies chiasmal or retrochiasmal Homonymous hemianopia is misperceived by the patients as monocular visual loss
  • 16.
    Age:  <50 yrmigraine or vasospasm is the most likely cause of TVL  >50 yr cerebrovascular disease or giant cell arteritis should be considered
  • 17.
    Duration of visualloss:  TVL from papilledema typically lasts for few seconds  TVL from retinal emboli or transient ischemic attacks lasts for several minutes(< 15 minutes)  TVL from migraine typically lasts > 15 minutes
  • 18.
    Pattern of onset: Analtitudinal onset of TVL(like a curtain or shed descending) may indicate embolic arterial occlusion Concentric onset of TVL may indicate vasospasm or neurologic cause Binocular visual disturbance having a geometric quality suggest occipital lobe dysfunction( migraine, seizure)
  • 19.
    Associated symptoms: Headache andpositive visual phenomena associated with TVL may suggest migraine Persistent headache with intracranial noise may suggest increased intracranial pressure
  • 20.
    TVL associated with Headache Weightloss Fever Malaise Scalp tenderness may suggest GCA
  • 21.
    Global perfusion problemsassociated with loss of consciousness, dizziness, headache, diplopia ,dysarthria, focal weakness Skin, joint changes or Raynaud phenomenon may suggest collagen vascular disease
  • 22.
    Precipitating factors: TVL associatedwith postural changes may suggest papilledema, GCA and hypotension Gaze evoked visual loss suggests an orbital mass like hemangioma or meningioma Physical activity or elevated body temperature with TVL may suggest previous or current optic neuritis
  • 23.
    Comorbidities:  History ofvascular risk factor Hypertension Diabetes Mellitus Dyslipidemia Smoking
  • 24.
    Cardiovascular disease Coronary arterydisease Valvular heart disease Atrial fibrillation Stroke
  • 25.
    Clinical examination: Ocular examination: BCVA  Color vision  Pupillary light reaction  RAPD  Confrontation test  Photostress recovery test Ocular motility test
  • 26.
    Slit Lamp Examination Blepharitis  Tearfilm  Corneal edema  Corneal dystrophy  Hyphema  Cells in AC  Pigments  Iris neovascularizaion  Lens position
  • 27.
  • 28.
    Dilated Fundus Examination Retinal hemorrhage  Arterial narrowing  Dilated vein  Cotton wool spot  Optic nerve head edema Crowded optic nerve head Glaucomatous cupping of optic disc Vitreo macular traction
  • 29.
    Emboli It is amajor cause of TMVL It can be observed with an ophthalmoscope Three common types are 1) Cholesterol(Hollenhorst plaque) 2) Platelet fibrin 3) Calcium
  • 30.
    Cardiac emboli mayarise from ventricular aneurysm Hypokinetic wall segments Endocarditis Valvular heart disease Atrial fibrillation
  • 31.
    Clinical Aspects ofRetinal Emboli Type Appearance Source Cholesterol Yellow-orange or copper color Common or internal carotid artery Platelet-fibrin Dull grey white color Walls of heart specially valves Calcium Chalky white color From heart, great vessels, calcific aortic or mitral valve
  • 33.
    Examination techniques in functionalVisual loss: Nonvisual task Finger nose test Optokinetic nystagmus drum Mirror test Confusion test Fogging test Duochrome test
  • 34.
    Cardiovascular system: Pulse: Arrhythmia Radiofemoraldelay Radioradial delay Blood pressure: Postural hypotension Cardiac auscultation: Murmur Carotid auscultation: Carotid bruit
  • 35.
    Nervous system: All patientshould receive a detailed and documented neurological examination. We should give emphasis on Cognitive and language function Cranial nerve function Facial and limb strength Sensory function Deep tendon reflex Coordination
  • 36.
    Investigations: TMVL: to revealan embolic cause: 1. Non invasive imaging: • Carotid Ultrasonography • Magnetic Resonance Angiography • Computed Tomographic Angiography
  • 37.
    2. Invasive: Conventional Angiography(gold standard) 3.HolterMonitoring: Undetected Cardiac Arrhythmia
  • 38.
    In suspected endocarditis: bloodculture Diabetes Mellitus: FBS, 2HABF, HbA1C Vasculitis: ESR, C-reactive protien, pANCA, cANCA,TPHA
  • 39.
    • Hypercoagulability /Hyperviscosity: platelet count, protein C, Protein S, Partial thromboplastin time, Anti cardiolipin antibody, Serum protein electrophoresis
  • 40.
    • Other: Color FundusPhotography FFA Visual field B scan
  • 41.
    • In TBVL: MRIwith contrast enhancement MRA CT scan CTA EEG
  • 42.
    Simplified Clinical Approach: History Bloodchemistry Abnormal Systemic Disease Normal Risk factor Non invasive tests Abnormal Normal Rethink Cardiac/hematologic/idiopathic Angiogram Eye consult Normal /occlusive retinal finding Non invasive tests Abnormal ocular Normal retina Ocular disease
  • 43.
    Treatment: • Treatment isaccording to cause • Collaboration of ophthalmologist , internist, cardiologist and neurologist may needed
  • 44.
    Medical Antiplatelet Anticoagulant Treatment of riskfactor Hypertension Diabetes Hypercholesterolemia
  • 45.
    • Surgical: Carotid arterystenting(CAS) Carotid endarterectomy(CEA)
  • 47.
    Surgical management criteria 1.Male 2. Age >75 year 3. Previous history of TIA or stroke 4. Intermittent claudication 5. Stenosis 80% to 94% 6. Absence of collateral vessels on angiography
  • 48.
    Amourosis Fugax The termAmaurosis Fugax not always interchangeable with TVL. Greek Amauroun means “To Darken” Latin Fugax means “Fleeting” The term Amaurosis Fugax is used to describe TMVL due to retinal emboli
  • 49.
    Take Home Message: •Transient visual loss may lead to a disease condition that can endanger our life. • So first and foremost patient must be evaluated. • Therefore we must educate the public and medical colleagues about the importance of getting an ophthalmologic evaluation.