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Six Steps of Sixth Nerve Palsies
Kelly A. Malloy, OD, FAAO, Diplomate, Neuro-Ophthalmic Disease
Kelly A. Malloy has no financial interests to disclose.
Course Description: This is a step-wise approach to abduction deficits, focusing on identification,
restrictive vs. neurogenic causes, and anatomic localization. A case-based approach shows how
multiple causes have similar clinical presentations, and how appropriate work-up determines the
correct etiology. Treatment and prognosis are discussed for each case.
Course Learning Objectives:
1. To understand the definition of an abduction deficit vs.a cranial nerve VI palsy.
2. To differentiate a restrictive from a neurogenic abduction deficit.
3. To understand anatomic localization in regard to a cranial nerve VI palsy.
4. To become familiar with the necessary work-up for abduction deficit / cranial nerve VI
palsy.
5. To understand the possible etiologies of cranial nerve VI palsies as well as other
abduction deficits.
6. To get a better understanding of the treatment / prognosis of an abduction deficit / cranial
nerve VI palsy.
Course Outline:
I.
Is This An Abduction Deficit?
A.
Horizontal Diplopia Greater at Distance and Toward Side of Abduction Deficit
B.
Measure at Distance with Cover Testing or Maddox Rod in ALL Positions of Gaze
C.
Pattern: Esodeviation Increasing in the Action of the Palsied Eye
D.
Causes of Abduction Deficit
1. muscle
a. lateral rectus damage
b. enlargement of medial rectus (thyroid disease)
2. neuro muscular junction
a. myasthenia gravis
3. nerve – CN VI palsy (isolated)
4. brain – CN VI palsy (not isolated)
5. others, including
a. loss of fusional reserves
b. spasm of the near reflex
c. Duane’s retraction syndrome
d. idiopathic inflammatory orbital pseudotumor
e. orbital mass
II.
Is This A Restrictive or Neurogenic Process?
A.
Duction vs. Version
1. restrictive process: ductions = versions
2. neurogenic process: ductions > versions
B.
Speed of Saccades
1. restrictive process: saccades normal speed, just stop short
2. neurogenic process: slowed saccades (glissades)
C.
Optokinetic Nystagmus
1. restrictive process: symmetric OKN
2. neurogenic process: abnormal, asysmmetric OKN due to slowed saccade
D.
Forced Duction Testing
1. restrictive process: positive forced duction test (eye cannot be moved into
full abduction)
2. neurogenic process: negative forced duction test (eye can be moved into
full abduction)
III.
If This Is A CN VI Palsy, Can Anatomic Localization Be Determined?
A.
Abducens Nucleus Lesion Causes Gaze Palsy, NOT Abduction Deficit
B.
Fascicular – Pons
1.
C.
Subarachnoid
1.
D.
Mastoid Infection, Petrous Bone Fracture, Schwannoma, Lumbar Puncture,
Spinal Anesthesia
Cavernous Sinus / Superior Orbital Fissure
1.
IV.
Increased Intracranial Pressure, Meningitis, Trauma, Subarachnoid
Hemorrhage, Clivus Tumor
Petrous
1.
E.
Accompanied by CN VII / Contralateral Hemiplegia
Tumor (Meningioma), Aneurysm, Thrombosis, Fistula, Tolossa-Hunt
What Is The Necessary Work-Up?
A.
CN VI Palsy Work-UP (may include)
1.
Laboratory Testing –
a. CBC with Platelets, FBS, Hemoglobin A1C, ESR, C-reactive Protein,
Lyme titer, RPR, FTA-ABS, ANA, ACE
2.
Neuro-Imaging –
a. MRI of Brain and Orbits With and Without Gadolinium Contrast
3.
Lumbar Puncture (NEVER done prior to neuro-imaging!)
a.
B.
Infectious / Inflammatory / Increased Intracranial Pressure
Other Abduction Deficits
1.
Myasthenia Gravis –
a. Lab Testing : Acetylcholine Receptor Antibody Testing (binding, blocking &
modulating)
b. EMG (single fiber)
2.
Thyroid Orbitobathy –
a. MRI / CT of orbits
b. TSH, T3, T4, Anti-thyroid Antibodies (Anti-thyroglobulin & Antithyroperoxidase, Thyroid Stimulating Immunoglobulin
V.
What Are The Possible Etiologies Of An Abduction Deficit? (Case Examples Used)
A.
Case-Based Examples to Demonstrate Previously Mentioned Concepts
B.
For Each Case, the Differential Diagnosis and Diagnostic Clues are Discussed
C.
Photographs, Videos, Neuro-Images, and Laboratory Test Results are Presented and
Analyzed Where Appropriate
D.
The Following are Among the Etiologies to be Considered:
1. thyroid orbitopathy, myasthenia gravis, idiopathic orbital inflammatory pseudotumor,
vasculopathic CN VI palsy, aneurysm, mass lesions, metastatic disease,
infectious/inflammatory processes, increased intracranial pressure
VI.
What Is The Treatment /Prognosis of CN VI Palsy?
A.
Vasculopathic - Improvement in 3 Months / 90 Days
B.
Chronic CN VI Palsy is Indicative of Serious Disease !
(Treat DM / HTN)
(Treat the Cause – Specific Treatments to be Discussed for Each Presented Case)