1) A 78-year-old male presented with decreased vision and eye pain in the right eye. Examination found elevated pressure and signs of ischemia in the right eye consistent with ocular ischemic syndrome caused by over 90% blockage of the carotid artery. 2) A 42-year-old male presented with eye redness and blurry vision in the left eye. Examination found elevated pressure and inflammation in the left eye consistent with glaucomatous cyclitic crisis. 3) A 57-year-old male presented with difficulty focusing and jumping eye movements on right gaze. Examination found impaired right eye adduction and left eye nystagmus, consistent with right internuclear ophthal

1. OCULAR GRAND ROUNDS
2017
Steven Blausey, OD
Bloomberg Eye Center
October 19, 2017

2. CASE #1
78 year old male with decreased
VA in OD over 2 days
• Dull ache in OD
• Photophobia
• Red eye OD

3. Medical History
•HTN (medicated)
•no DM
•Pseudophakic OU
•Last examined 3 mos ago

4. EXAMINATION
• BVA
• OD 20/200 ------ 20/20 3 mos. Ago
• OS 20/25 ------ 20/25
• External *
• 2+ diffuse hyperemia OD
• Pupil (-) APD
• SLE OD
• corneal edema OD
• 1+ CELLS OD
• (+) NVI OD *
• PCIOL + open capsule
• IOP
• OD = 40mmHg
• OS = 15 mmHg
OS
UNREMARKABLE

5. • RULE OUT:
- Angle Closure
- Neo-Vascular
OS OD

6. DILATION
• C/D *
• OU 0.3
• Vessels OD
• narrowed arteries / veins normal caliber!
• Blot hemes both arcades
• no NVE or NVD
• Macula
• clear/flat OU
• Periphery *
• few scattered blot hemes
OS DFE
WNL
OD
OD
OS

7. DIFFERENTIAL DIAGNOSIS
• CRVO*
• Dilated and tortuous veins
• Flame hemes
• Disc edema
• Macular edema
• DR *
• Bilateral
• May be asymmetric
• CWS and blot hemes

8. DIFFERENTIAL DIAGNOSIS
• Hyper viscosity Syndrome
• Bilateral and tortuous
• Macroglobulinemia
• Multiple Myeloma
• Ocular Ischemic Syndrome!
• Unilateral
• (Carotid occlusive dx)
• Aortic Arch Disease
• Bilateral
• Large vessel granulomatous
vasculitis
• Takayasu's arteritis

9. Diagnosis and Discussion
OCULAR ISCHEMIC SYNDROME

10. Work up & Evaluation
• Hx of amaurosis fugax ? ( arterial blockage)
• IVFA*
• slowed filling of choroid in OD vs OS
• Retinal capillary non-profusion
• Reduced Choroidal profusion and Macular
ischemia (reduced VA)
14 secOS
OD

11. Work up (continued)
•Carotid duplex*
• >90% blockage
•BP (130/90) RAS
•Lab Tests
• CBC with Diff / Platelets (norm)
• FBGL (98 mg/dL) r/o DM
• ESR (30) r/o GCA and blood dyscrasias

12. DISCUSSION
• Arterial sclerosis of Internal Carotid
• lead to inadequate supply to ocular structures
• Ischemia (90% stenosis)
• Prolonged Ischemia
• NVI and NVG
• NVD
• NVE
• Ischemic Maculopathy
• lead to blind painful eye

13. SIGNS OF ANTERIOR SEGMENT ISCHEMIA
• Ciliary Injection
• d/t shunting of the
external carotid
• Iritis
• NVI

14. SIGNS OF ANTERIOR SEGMENT ISCHEMIA
• Rapid cataract development
• Reduced IOP (until NVG develops)
• Corneal edema

15. SIGNS OF POSTERIOR SEGMENT ISCHEMIA
• Dilation of retinal veins (not tortuous)
• Narrowing of retinal arteries
• Equatorial blot hemes
• CWS
• NVD
• NVE

16. MANAGEMENT of IOP
• Control IOP (difficult)
• Combigan
• Dorzolamide
• Diamox Sequel
• Avoid Pilocarpine
• NVI
• Trabeculectomy
(poor prognosis)
Note IOP may be reduced in earlier phase of ischemia

17. TREATMENT
• PRP
• reduces the metabolic demand
• reduces neovascularization
• Carotid endarterectomy
• not beneficial in advanced, may lead to emboli
• Cardiology Consult
• Evaluate significant systemic Dx

18. CASE #2
• 42 year old, white male
• Red eye and foggy vision this AM OS
• No refractive error
• Mild soreness around OS
• No discharge
• No Hx of Trauma

19. Corneal Edema

20. IOP
OD 18 mmhg
OS 54 mmhg

21. Rule out angle closure and NVG
Open OU
closed
Neo

22. 2-3+ CELL / FLARE &
KERATIC PERCIPITATES!

23. DDx
•Glaucomatous Cyclitic Crisis
•Fuch’s Heterochromia
•Uveitic Glaucoma

24. Glaucomatous Cyclitic Crisis
(Posner-Schlossman Syndrome)
• Unknown etiology of TM inflammation and
degeneration (pos. Toxo or Herpetic)
• Minimal A/C inflammation
• Little Conjunctival Injection
• Raised IOP not proportionate to inflammation
• Recurrent
• Typically 20-50 years of age

25. Fuch’s Heterochromatic Iridocyclitis
• TRIAD
1. Asymmetry of iris color (lighter eye effected)
2. Cataract
3. Low Grade Iritis
• Pearls
– No synechia
– KP’s are stellate
– Steroids have little effect on a/c reaction
– Iris atrophy (moth eaten)
– No Hyperemia

26. Uveitic Glaucoma*
• Chronic Inflammatory raise in IOP
• WBC’s and Particular debris clog the TM
• Increase aqueous viscosity
• Potential for synechia
• Acute inflammation leads to lower IOP
• Reduced aqueous formation
• Increase uveal-scleral outflow
(prostaglandins)
• Commonly found with infectious causes
• Herpes (always dilate)
• Toxoplasmosis

27. Treatment for Uveitic Glaucoma
• Durezol q1hr
• Homatropine 5% bid
• Combigan bid
• Dorzolamide bid
• Diamox 250mg x2

28. TREATMENT
• Pilocarpine ?
• May lead to synechia
• Prostaglandin Analogs ?
• May potentiate inflammation
• May lead to CME

29. Case #3
• 57-year-old white male presented to ER
• Difficulty focusing and “jumping” eye
movements
• Diplopia worsening on right gaze
• Sudden onset and painless
• No hx of trauma
No adduction

31. Neuro-anatomical pathway for Horizontal Gaze
• Example: Left Lateral Gaze
• Initiated by the right frontal eye field
• Excitatory signal arrives at the left
Paramedial pontine reticular formation
(PPRF)
Internal capsule

32. Neuro-anatomical Pathways for Horizontal Gaze
• From Left PPRF, signal reaches left CN VI
(Abducens) nucleus
• A signal is sent to the left lateral rectus
resulting in abduction of the left eye
• Simultaneously , a signal ascends up the
MLF to activate the right CN III (Oculomotor),
resulting in adduction of right eye
s. colliculus

33. Medial Longitudinal
Fasciculus
• A heavily myelinated tract in the
brainstem, in the pons and
midbrain
• Allows conjugate eye
movements by connecting
abducens nucleus (VI n) to the
oculomotor nucleus (III n) of the
contra-lateral side
Internal capsule

34. Brain Stem Anatomy for Horizontal Gaze
3rd
6th

35. Internuclear Ophthalmoplegia
• Characterized by impaired
horizontal eye movement with
weak adduction of the affected eye
and nystagmus in the contralateral
eye
• Etiology: Lesion in the Medial
Longitudinal Fasciculus (MLF)
• “Left” or “Right” is defined
according to the side of the eye
with impaired adduction

36. Right Internuclear Ophthalmoplegia
• On left lateral gaze
• Abducting left eye moves laterally
• Adducting right eye remains
central
• Nystagmus is seen in the left
abducting eye
• Right lateral gaze and
convergence are normal

37. Anatomy of an Internuclear Ophthalmoplegia
• Example: Right INO
• Lesion in the right MLF
• Excitatory signal arrives at the left
PPRF as usual, activating the left
lateral rectus (LLR)
• Signal does NOT reach the right CN
III to activate the right medial
rectus (RMR)
OD OS
right left
Left gaze
R

38. Symptoms of INO
• Diplopia on horizontal gaze away from
the side of the lesion
(not present on convergence or
contra-lateral gaze)
• Neurological symptoms
• Visual confusion
• Oscillopsia
• Vertigo

39. Etiology of Internuclear Ophthalmoplegia
• Ischemic Stroke
• Older patients
• Usually Unilateral
• Multiple Sclerosis
• Younger patient
• Bilateral in most cases
• Rare causes
• Trauma
• Brainstem encephalitis
• Tumor

40. Differential Diagnosis
• Partial CN III Palsy
• No convergence
(MR)
• Myasthenia Gravis
• Miller- Fisher
variant of Guillian
Barre Syndrome

41. Associated Syndromes
• One-and-a-half-Syndrome
• Gaze palsy in one direction and
INO on opposite gaze
• Only abduction of contralateral eye
remains
• Convergence is spared (IIIn)
• Etiology is a lesion in the PPF and/or
abducens nucleus + MLF on the same
side
palsy
INO

42. One and a Half Syndrome

43. Associated Syndromes
• Walleyed Bilateral INO
• Bilateral INO (MLF from both VIn)
• Divergence of eyes (walleyed)
• Convergence retained if lesion is limited
to MLF
LESION
3rd and 6th spared

44. Binocular INO

45. Investigation of INO
• Studies
• MRI & MRA of brain
MRI Detection of MLF Lesions
Proton density>T2>Flair

46. Thank you for your attention