Neurotutorial

15 October
2015

Cranial neuropathy part

I
Neuroopthalmology

Cranial neuropathy

Exclude Apraxia, NMJ, Muscle

Mononeuropat
hy

Multiple
neuropathy

With long
tract sign

Monocular
visual loss

Cavernous sinus
syndrome
et.al

Weber
syndrome
et al

Horner
syndrome
Isolated 3,4,6
palsy
Vestibular palsy

Cerebellopontin
e angle
syndrome
et.al

Millard Gruber
syndrome
et.al

Trigeminal
neuralgia
Facial n palsy

Jugular foramen
syndrome
et.al

Wallenberg
syndrome
et al

 Female 40 year old with UD hypertension com

plaints progressive Rt.eye pain on eye movem
ent for 5 days with central blurry vision. Exami
nation found pupil 2 mm both eyes but poorly
react Rt.side. Rt. VA 20/60, Lt VA 20/20. Eye g
round exam have no papilledema or exudate.
MRI with gad of brain is normal. What is the m
ost appropriate management.
A. ASA 300 mg
B. Oral prednisolone
C. Observe and FU 3 weeks.
D. Intravenous methyprednisolone

Optic neritis
Monocular visual loss
Anterior to optic chiasm
Impaired VA
Impaired light reflex
Binocular visual loss
Retrochiasm
Not impair VA (unless bilat lesion)
Not impair light reflex
( Retrogeniculate body)

Blurr disc hard to

diff from papilledema
( usualy bilat
involve)

Acute monocular visual loss

Clinical,
Eye ground
Typical for
MS*

Atypical for
MS

MRI brain
+/- LP

Normal

Demyelinatio
n

IVMP: if VA worse than 20/40,

disabling scotoma,severe pain
Low risk for
MS. (20%)

High risk for

MD
(60-90%)

Work up for
mimicker
LP, Serology,
CT/MRI
NMO (more bilat, less pain,less
recover)
Ishemic : AION
Inflamatory : esp Giant cell
arthritis
Infiltrative : Malignancy
Infection : Syphilis, CMV
neuroretinitis
Hereditarty

Adapted from Bermel RA, Continuum .2013 Aug;19(4 Multiple

Typical sign and

symptom of MS optic
neuritis

Unilat
Pain on movement
Partial : color, contrast, scotoma
Normal disc (most) or mild
swelling
Progressive days to weeks

IVMP in optic neuritis

IVMP 250 mg, 6 hourly
3 days,
followed by Oral pred (1 mg\kg\d) 11 days
tapering of prednisolone within
3 days
The optic neuritis ONTT -compares oral placebo,
IVMP, Oral stearoid
IVMP
-> Faster recovering vision (but no long term
impact)
-> Slower progress to be definite MS

Male 70 years-old complain shoulder and headache for 1 day

The eye examination as the picture. The Lt. pupil is reactive but
delayed dilatation after dimmed light. Other wise examination
is normal
What would be investigation of choice.

A.
B.
C.
D.
E.

Chest X-ray
US carotid a.
CT brain angiogram
CT brain with contrast
Refer ophthalmologist for cocain test

Horner syndrome
Sympathetic paralysis -> look lazy
- Mild ptosis
- Mild anisocherea :dilate lag in
the dark
- May anhidrotic : 1st and 2nd
order

Anisochorea = Inequal pupil

Sympathetic -> dilate eye in the dark
Defect side -> dilation lag
Aniso in the dark
Parasympathetic -> constrict in light
Defect side -> Non react dilated
Aniso in the light
Physiology = no change

Anisochorea
Anisochorea never caused by optic
nerve
due to consensual reflex
: if optic n. defect -> smaller pupil bo
th

Aniso in the dark: Sens 70% Spec

95%

After mydriasin drop

Aniso in the light + Non reactive

pupil

No change

Horner
syndrome
1st : Descending
tract from
hypothalamus
3

:intermediolat corlumn
near corticosponal tract

2nd :
Preganglionic
apical lung - ciliospinal
center of budge C8

3rd : Post
ganglionic

Any combination of ptosis, miosis or

anhidrosis -> suspect Horner
syndrome (HS)
Delayed
dilation in
the dark
Acute onset ,
Painful,
Trauma, UD
Malignancy
With long
tract sign
1 order HS
-> MRI brain
E.
st

Without long
tract sign

Chronic

Confirm by
Cocain &
Methylphenidate

2nd or 3rd HS
-> CTA/MRA
E:
HS protocal

Adapted from Davagnanam I ,Eye (Lond).2013 Mar;27(3):291-8

Pharmacologic test

Specificity
100%
But need 24
hrs for testing

Female 50 years-old underlying diabetes complain painless

diplopia when look to the right side for 1 week. The eye
examination in primary position as the picture. EOM limited
adduction 60%, upgaze 80% downgaze 80%. The Rt pupil is 3
mm while Lt. 4 mm sluggish react to light. Other wise
examination is normal.What would be investigation of choice.

A.
B.
C.
D.
E.

FBS
Ice pack test
CT brain angiogram
CT brain venogram
CSF for NMO antibody

Isolated 3rd nerve palsy

Oculomotor n. go along with

parasym
- Ptosis
- Opthalmoplegia
- May dilated and non react to
the light
: 20% of vasculopathy
80% of compressive -> severity of
pupil involvement usually correlate with severity
of opthalmoplegia

PC
O
an M
ys eu
m r

3rd nerve palsy almost always consider imaging R/O PCOM

pupil sparing in partial ophthalmoplegia cannot R/O
only pupil sparing in complete opthalmoplegia likely R/O

Isolated 4th nerve palsy

Oculomotor n. go along with

parasym
- Ptosis more obvious
- Opthalmoplegia
- May dilated and non react to
the light
: 20% of vasculopathy
80% of compressive -> severity of
pupil involvement usually correlate with severity
of opthalmoplegia

Isolated 6th nerve palsy

Oculomotor n. go along with

parasym
- Ptosis more obvious
- Opthalmoplegia
- May dilated and non react to
the light
: 20% of vasculopathy
80% of compressive -> severity of
pupil involvement usually correlate with severity
of opthalmoplegia

Binocular diplopia

Isolated CN 3
palsy
With long
tract sign
1 order HS
-> MRI brain
E.
st

Isolated CN 4
palsy

Without long
tract sign

DM, HT
FU 3-6 mo

Isolated CN 6
palsy
WU focused
malignancy

2nd or 3rd HS
-> CTA/MRA
E:
HS protocal

Adapted from Davagnanam I ,Eye (Lond).2013 Mar;27(3):291-8