TVL is a very important issue for Ophthalmologists and Neurologists. In this presentation i want to make simple analysis to make a possible conclusion. I hope it will help the students.

1. TRANSIENT VISUAL LOSS(TVL)

2. 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

3. 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.

4. 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

5. 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

6. B. Vascular Disease:
• Embolic phenomenon
Carotid
Cardiac
Great vessels

7. • Carotid artery dissection
• Vasculitis(eg.GCA, SLE)
• Vasospasm
• Systemic hypotension
• Hyperviscosity/ Hypercoagulability
states
• Ocular hypoperfusion(eg. Ocular
ischemic syndrome)

8. C. Optic nerve disorder:
• Acquired or congenital disc
disease(eg. papilloedema, disc
drusen)
• Compressive lesion of the intraorbital
optic nerve
• Demyelinating disease

9. D. Nonorganic Visual Loss
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 of visual pathway

12. Anatomy of visual pathway

13. Clinical Approach:

14. Diagnosis is done by:
 Careful history taking
 Clinical examinations
 Lab investigations

15. 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

16. Age:
 <50 yr migraine or vasospasm is
the most likely cause of TVL
 >50 yr cerebrovascular disease or
giant cell arteritis should be
considered

17. 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

18. 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)

19. Associated symptoms:
Headache and positive visual
phenomena associated with TVL may
suggest migraine
Persistent headache with intracranial
noise may suggest increased
intracranial pressure

20. TVL associated with
Headache
Weight loss
Fever
Malaise
Scalp tenderness may suggest
GCA

21. 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

22. 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

23. Comorbidities:
 History of vascular risk factor
Hypertension
Diabetes Mellitus
Dyslipidemia
Smoking

24. Cardiovascular disease
Coronary artery disease
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. Glaucomflecken
Intra ocular pressure
Gonioscopy (if suspision of narrow
angle)

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 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

30. Cardiac emboli may arise from
ventricular aneurysm
Hypokinetic wall segments
Endocarditis
Valvular heart disease
Atrial fibrillation

31. 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

33. Examination techniques in
functional Visual loss:
Nonvisual task
Finger nose test
Optokinetic nystagmus drum
Mirror test
Confusion test
Fogging test
Duochrome test

34. Cardiovascular system:
Pulse: Arrhythmia
Radiofemoral delay
Radioradial delay
Blood pressure:
Postural hypotension
Cardiac auscultation:
Murmur
Carotid auscultation:
Carotid bruit

35. 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

36. Investigations:
TMVL: to reveal an embolic cause:
1. Non invasive imaging:
• Carotid Ultrasonography
• Magnetic Resonance Angiography
• Computed Tomographic
Angiography

37. 2. Invasive:
Conventional Angiography(gold
standard)
3.Holter Monitoring:
Undetected Cardiac Arrhythmia

38. In suspected endocarditis:
blood culture
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 Fundus Photography
FFA
Visual field
B scan

41. • In TBVL:
MRI with contrast enhancement
MRA
CT scan
CTA
EEG

42. 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

43. Treatment:
• Treatment is according to cause
• Collaboration of ophthalmologist ,
internist, cardiologist and neurologist
may needed

44. Medical
Antiplatelet
Anticoagulant
Treatment of risk factor
Hypertension
Diabetes
Hypercholesterolemia

45. • Surgical:
Carotid artery stenting(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 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

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.