Transcript Slide 1

Neurology Case Presentation
MARCH 23, 2012
LORI NOOROLLAH
Chief Complaint
 Double Vision
 HPI:
 53 yo F who reports that during the first week in December she
woke up with blurry vision and pain in her right eye
 Week before Xmas – woke up with double vision
Binocular, vertical and horizontal
 Worse on right gaze
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First week in February – woke up with blurry vision in left eye
and left orbital pain
More History
 PMH:
 HTN, Anxiety, chronic pain, GI bleed due to diverticulosis
 Meds:
 Clonidine 0.2mg qHS
 Metoprolol 50mg BID
 Diazepam prn
 Diltiazem qAM
 Losartan 100mg qHS
 hydrocodone prn
 SH:
 Smokes 3-4 cigarettes daily for 25 years
 No EtOH or illicit drug use
General Exam
 Alert, oriented, no acute distress
 CV: RRR, no carotid bruit
 Chest: CTAB
 Visual Acuity:
 OD: 20/60
 OS: 20/25
 +relative APD on right
 red-green dyschromatopsia on right
Neurological Exam
 Mental status and speech normal
 CN:
 PERRL
 APD on right
 Visual Fields –
Inferior arcuate defect on Right
 Enlarged blind spot on Left
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normal facial sensation and movement, symmetric palate
elevation, tongue midline
EOM:Limited abduction and slightly limited upgaze bilaterally
 Motor, Sensory, Reflexes, Coordination – within
normal limits
Visual Fields
Inferior arcuate defect in right eye
Enlarged blind spot in left eye
?Where?
?What?
Differential Diagnosis
 Anterior Ischemic Optic Neuropathy (AION) +
cranial nerve infarcts
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AAION vs. NAION
 Optic Neuritis
 Ocular Myasthenia gravis
 Acetylcholine receptor antibodies negative
NAION
Non-arteritic Anterior Ischemic
Optic Neuropathy is an
“idiopathic” ischemic insult of
the optic nerve head
 Most common optic neuropathy
 Annual incidence for people > age 50 is
2.3 – 10.2 /100,000
 95% of cases occur in Caucasian population
NAION
 Clinical presentation:
 Sudden monocular visual loss
 Blurring or cloudiness
 Often noticed upon awakening (73%)
 Most often painless
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12% have ocular pain or headache
A lot of pain more suggestive of optic neuritis
or AION
 Exam:
 Reduced visual acuity to varying degrees
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Dyschromatopsia proportional to reduction in visual acuity
Afferent pupillary defect
Fundoscopic Exam:
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Not ruled out by normal visual acuity
Optic disc swelling
Disc hyperemia with splinter or flame hemorrhages
Small optic cup (nerve fiber crowding) in unaffected eye
Visual field defect – relative inferior altitudinal defect and absolute inferior nasal
defect
NAION – Fundoscopic Exam
Hayreh SS (2009) Ischemic optic neuropathy. Progress
in retinal and eye research 28: 34-62
NAION
 Vascular supply to optic nerve head
 15-20 short posterior
ciliary arteries, supplied
by ophthalmic artery
NAION
 Pathogenesis:
 Different than Ischemic CVA
No clear relationship with HTN, HLD, smoking
 Not associated with embolism or large vessel occlusion
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Transient hypoperfusion of posterior ciliary arteries
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Vasospasm vs. nocturnal hypotension vs. impaired autoregulation
of microvasculature vs. vasculopathic occlusion vs. venous
insufficiency
Hypoxia/Ischemia  optic disc swelling (in setting of
physiologically crowded optic nerve head) 
infarction
 Treatment = Modify risk factors, vision therapy
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Early therapy shown to have better recovery
Questionable role for steroids
NAION and OSA
 Nocturnal Hypotension
 Normal physiologic occurrence
 Autoregulation
 OSA
 Loss of autoregulation
 Non-dipping status
 Hypoxic-ischemic insult to optic nerve head
 Anti-hypertensive medications at night may also
disrupt autoregulation
OSA and NAION
 Stein, 2011 – American Journal of Ophthalmology
 Retrospective cohort study
 Review from managed care database looking at patients > 40
with at least 1 eye-care visit
 N=2,259,061
 Compared incidence of NAION in population with and without
OSA
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Compared NAION in treated vs. untreated OSA
OSA and NAION
 Results:
 After adjusting for confouding variables:
 Untreated OSA patients had 16% increased hazard of
experiencing NAION (HR 1.16, CI 1.01-1.33) compared with
non-OSA patietns
 Treated OSA patients had no difference in hazard (HR 1.38,
CI 0.76-2.5) compared with non-OSA patients
NAION – Future Studies
 Implications:
 Do patients with NAION need screening for OSA?
 Do patients with OSA need evaluation?
 Consider avoiding anti-hypertensive medications at night,
especially in patients “at risk” for NAION
 Future Studies:
 Treatment options/Intervention/Prevention
 Further investigation into the pathophysiology of NAION
References
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Anterior Ischemic Optic Neuropathy:Part II: a discussion for physicians. Sohan Singh
Hayreh, MD, MS, PhD, DSc, FRCS, FRCOphth
http://webeye.ophth.uiowa.edu/component/content/article/118-aion-part2
Atkins, EJ Nonarteritic Anterior Ischemic Optic Neuropathy. Current Treatment Options in
Neurology. 2011; 13: 92-100
Hayreh SS (2009) Ischemic optic neuropathy. Progress in retinal and eye research 28: 34-62
Kerr NM, Etal. Non-arteritic ischaemic optic neuropathy: A review and update. Journal of
Clinical Neuroscience. 2009; 16: 994-1000.
Stein JD, Etal. The Association between Glaucomatous and other causes of Optic
Neuropathy and Sleep Apnea. Am J Ophthalmol. 2011; 152: 989-998.
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