Clinical Case Challenges In Neuro
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Transcript Clinical Case Challenges In Neuro
Clinical Case
Challenges In NeuroOptometry I
Thomas J. Landgraf, O.D.,
F.A.A.O.
“Clinical Case Challenges in
Neuro-Optometry”
Thomas Landgraf, O.D., F.A.A.O.
Clinical Associate Professor, UMSL College of Optometry
My Background
Graduate of ICO…Chicago
Residency at PCO…Philadelphia
SCO x 15 years…Memphis
Now at UMSL College of Optometry
In terms of Neuro-Eye…
Dr. Lawrence Gray at ICO & PCO
My Background
At SCO…Chief of
Ocular Disease
Goals for this lecture
Not an expert
Share patient care
experiences
Share “optometric
legal consultant”
experiences
Resources
Journals and Internet
Review of Optometry
Review of Ophthalmology
Handbook of Ocular Disease
Management
Clinical Guide To Ophthalmic Drugs
Neuro-Optometry
Why spend 3 hours
on it?
Conditions are both:
Vision threatening
Life threatening
“True” ocular
emergencies
Case #1: ONH Edema?
Always A Tough
DDx (Differential
Diagnosis)
S:
52 yo Caucasian
male referred to
me
Tentative
diagnosis of
CRVO OS
Case #1: ONH Edema?
Always a Tough DDx
S:
Painless vision loss OS x 2 weeks
Prosthetic OD due to trauma
No significant medical or ocular conditons
Low daily dosage of methadone
Nicotine patch
Case #1: ONH Edema?
Always a Tough DDx
O:
BVA OS: 20/400
OS pupil round and reactive to light
Normal SLX
Tonometry 17 mm Hg
BP: 280/170 RAS: not done at previous
visit
Case #1: ONH Edema?
Always a Tough DDx
O:
DFE OS:
Optic nerve head edema
Accompanied by flame
hemes, exudates, cotton
wool spots, and macular
edema
Normal peripheral retina
Case #1: ONH Edema?
Always a Tough DDx
A: Malignant Hypertension and Resultant
Retinopathy OS
P:
Immediate referral to medical center
For lowering of BP
Referral to retinal specialist
Level Of Comfort
Confirmation
Case #1: ONH Edema?
Always a Tough DDx
Follow-up 4 months later
Current meds: minoxidil, norvasc,
coumadin
HTN and its complications
Noted improved vision
But some glare, distortion, “wavy lines” in
central vision
Case #1: ONH Edema?
Always a Tough DDx
Follow-up 4 months
later
BVA OS: 20/20
BP: 160/85
DFE OS: exudative
macular star, healthy
ONH (.2/.2), normal
peripheral retina
Case #1: ONH Edema?
Always a Tough
DDx
Follow-up 4
months later
Resolving
Malignant
Hypertensive
Retinopathy
Improved Blood
Pressure
Educated on
compliance
Case #1: ONH Edema?
Always a Tough DDx
Bottom Lines
Primary Care OD’s need to take BP’s
Especially on those with retinal vascular
disease
Consider typically bilateral retinal
conditions
In monocular patients
Case #1: ONH Edema?
Always a Tough DDx
Timely diagnosis for malignant HTN
Can significantly reduce morbidity and mortality
Like Neuro-Eye Disease: sight and life
threatening
Pseudotumor Cerebrii
(PTC)
Background
“false brain tumor”
Increased intracranial pressure
without an intracranial mass
Major diagnosis of exclusion: a
true intracranial tumor
All patients with papilledema must
have neuro-imaging studies
PTC: Why?
Poor CSF absorption
By meninges surrounding brain
and spinal cord
Increased intra-abdominal
pressure
From obesity
elevated intrathoracic pressure
decreased venous drainage from
the brain
PTC: Diagnosis
Who?
Obese women of childbearing
age
Secondary
Obstruction to venous drainage:
cerebral venous thrombosis
Exongenous agents: tetracycline,
vitamin A, corticosteroids, BCP’s
Medical conditons: lupus,
sarcoidosis, anemias, blood
dyscrasias
PTC: Diagnosis
Symptoms
Bad HA’s: frontal, around the
eyes, pressure-like, throbbing
Transient visual loss
Intracranial noises: heartbeat or
whooshing sound in ears, tinnitus
Vision loss: blur, temporal VF
defect
PTC: Diagnosis
Signs
Optic disc edema
Unilateral, bilateral,
asymmetric
VA, pupils, EOM’S
usually normal
VF: blind spot
enlargement,
inferonasal loss,
generalized
constriction
PTC: Differential
Diagnosis
Intracranial mass
Meningitis: abrupt onset,
fever and chills, stiff neck
Bilateral inflammatory
optic neuropathy: early
and central vision loss,
pain on eye movement,
retrobulbar
PTC: Differential
Diagnosis
Pseudopapilledema: optic
disc drusen or tilted discs,
ultrasound may aid
Neuroretinitis: macular
exudate, early central vision
loss
Bilateral ION: older, vascular
risk factors, painless, early
vision loss
PTC: Ancillary Tests
Optometric In-Office:
VF
B scan ultrasound
Photos or optic nerve
imaging
PTC: Ancillary Tests
Neurologist or neuro-eye doc referral
Neuroimaging before lumbar puncture
Standard MRI of the brain
CT scan with contrast if patient markedly obese
Neuroimaging
Major Scans Used To Evaluate NeuroEye Disease
CT (Computerized tomography)
MRI (Magnetic Resonance Imaging)
Neuroimaging
CT
Good to view bony abnormalities,
calcifications, acute hemorrhages
Valuable to diagnosis of orbital processes
Test of choice for thyroid eye disease
Neuroimaging
MRI
Far better at characterizing soft tissues
Preferable for most intracranial processes
Not subject to bone artifact
Contrast media and special studies can
sharpen
Gadolinium is a contrast material that can
increase signal intensity
PTC: Ancillary Tests
Lumbar Puncture
Required for the diagnosis of
PTC
Neurologist, radiologist or ER
physician
Usually > 200 mm
Lumbar Puncture
Procedure
Patient positioned on side in fetal position with
back fully flexed
18 g needle inserted at L4-L5 interspace
Opening pressure measured when needle
penetrates subarachnoid space
HA is most common complication
Lumbar Puncture
Opening pressure
Normal: 60-80 mm of H20
Borderline elevated: 180-210 mm of H20
Lumbar Puncture
CSF evaluation
Color
Clear and colorless is normal
Cloudy: infection
Xanthochromic (yellow): subarachnoid
hemorrhage
Cell count and differential, cytology,
chemical analysis, serologic analysis,
microscopy, culture
PTC: Management
“Comanage” with neurologist
Initial LP improved signs and sxs
VF, DFE, photos or optic nerve imaging
every month x 3 months
Every 2-3 months thereafter for about a
year
Individual case variability
PTC: Management
“Comanage” with neurologist
Other options for some persistent signs
and sxs
CAI’s : acetazolamide
Other diuretics
Weight loss
HA management
PTC: Management
Diamox
Not just for angle closure
Decreased CSF production up to
50%
1-3 grams qd
500 mg bid, tid, qid
Side effects: taste alteration,
nausea, fatigue, diarrhea, tingling
Not with sulfa allergies, kidney
disease
PTC: Management
Headache management
Topamax (topiramate)
Migraine prophylaxis and
epilepsy
PTC: HA relief and mild
inhibition of carbonic
anhydrase, also causes
weight loss
Recently: development of
angle closure glaucoma
from choroidal expansion
PTC: Management
For signs and symptoms unresponsive
to LP, severe vision loss
Corticosteroids
Surgery
Optic nerve sheath fenestration
CSF diversion (shunt)
PTC: My Clinical
Experience
Relatively rare condition?
Not at SCO
“Comanagement” turns into
MANAGEMENT
Optometrists take the time
Need to be familiar with ancillary
diagnostic tests and treatment
options
Case #2: Monocular
Acute Vision Loss In A
Golden Girl
S:
85 yo Caucasian female
Cx: acute vision loss OD
2 weeks earlier
Earache
Sore temporal veins
Jaw claudication
Past medical hx: non-contributory
Case #2: Golden Girl
O:
BVA
LP OD, 20/30 OS
+APD OD
BP: 150/100
No carotid bruits
SLX: NS consistent with 20/30 VA
Case #2: Golden Girl
O:
DFE: pallid swelling of the
optic nerve OD
Othewise normal retina
and posterior pole OU
Case #2: Golden Girl
A:
Provisional Diagnosis: Giant Cell
Arteritis OD
P:
FLAN:
increased arterial filling time OD
Choroidal nonfilling defect OD
80 mg Prednisone po daily
Case #2: Golden Girl
P: R/O all causes of Anterior Ischemic
Optic Neuropathy
CBC:
Elevated monocyte and platelet counts
ESR: 44
FTA-ABS and VDRL non-reactive
Case #2: Golden Girl
One week later…..
Right temporal artery
biopsy
Ear pain and
temporal HA
resolved
Case #2: Golden Girl
Two weeks later…..
ESR: 4
Plan:
Monitor with ESR
And for prednisone side effects
Case #2: Golden Girl
Eventually…..
VA did not improve OD
But remained stable OS
Anterior Ischemic Optic
Neuropathy (AION)
Arteritic
Or…..
Giant Cell Arteritis
Nomenclature following vision loss
Temporal Arteritis
AION-artertic
Background
Granualomatous vasculitis of mediumsized arteries
“True” ocular emergency
The Goal: Prevention of contralateral vision
loss
AION-arteritic
Background
Contralateral vision loss
2/3 if untreated
Within weeks if untreated
AION-arteritic
Why
Granulomatous vasculitis of temporal
artery
Occlusion of short posterior ciliary
arteries (supply anterior optic nerve)
AION-artertic
AION-arteritic
Diagnosis: Who?
Rose Nylen on the Golden Girls
Average age of onset = 70 years
Female and Scandanavian
Lower incidence rates
Tennessee & Israel
AION-arteritic
Diagnosis: symptoms
Unilateral decreased VA,
temporal HA, scalp
tenderness
VA usually < 20/200
Amaurosis fugax
Anorexia, fever, malaise,
depression
Onset is variable
AION-arteritic
Clinical Features
Vasculitis of coronary arteries: MI, CHF,
angina pectoris
Neurologic: peripheral neuropathies,
ischemic brain damage
Polymyalgia Rheumatica: pain and
stiffness of the neck, shoulders, hips
AION-arteritic
Diagnosis: signs
AION-arteritic
Optic nerve edema, hemes, cotton wool
spots
APD
VF defects: central, altitudinal, arcuate
AION-arteritic
Diagnosis: signs
AION-arteritic
Pallor described as chalky
white
CRAO in up to 10% of patients
Disc eventually glaucoma-like
with cupping BUT with pallor
AION-arteritic
Differential Diagnosis
Vs. non-arteritic AION
Worse VA
Worse VF
HA and scalp tenderness
Constitutional symptoms
Older
Worse ESR, CRP, CBC
variables
AION-arteritic
Ancillary Tests
Optometric In-Office
VF
Optic nerve imaging
Photos
FLAN considered to check for
choroidal perfusion defects
AION-arteritic
Ancillary Tests
Referral
ESR (erythrocyte sedimentation rate)
CRP (C-reactive protein)
Westergren
15% of GCA patients: normal ESR
Elevated in > 91%
Also elevated WBC, platelet counts; IgG
anticardiolipin antibodies
AION-arteritic
Ancillary Tests
Referral
Temporal artery biopsy
Should be performed on all
suspects
> 95% sensitive, 100% specific
Can be done shortly after
steroid treatment
Inflammatory cells in the
muscular walls of the artery
AION-arteritic
Diagnosis:
Summary
History and clinical
impression
ESR and CRP
Confirm with
temporal artery
biopsy
AION-arteritic
Management
Referral: neurologist, internist (PCP),
rheumatologist
For suspects or diagnosed:
Systemic steroids
AION-arteritic
Management
Systemic steroids
Hospital admission
1-2 gm IV methylprednisone x 2-3 days
60-100 mg of oral prednisone: tapered very
slowly
AION-arteritic
Management
Systemic steroids
Anecdotal vision recovery?
Poor prognosis?
No solid support for anti-steroid medications
(Rheumatrex aka methotrexate)
AION-arteritic
My Clinical Experience
This is rare?
Most important from an
educational perspective
Presume the worst if suspect
Vs. glaucomatous optic
neuropathy
Combination of AION + OAG in
my patients