Clinical Case Challenges In Neuro

Download Report

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