2. Introduction
Anatomy
Sixth NervePalsy
o Incidence
o Etiology
o Differential Diagnosis
o Clinical Signs& Symptoms
o Optometric Assessment & Investigation
o Other Clinical Assessment & Investigation
o Optometric Management
o Other Managements
o Prognosis
3. The sixth cranial nerve is a somatic efferent nerve that
innervates ipsilateral lateral rectus (LR) muscle to elicit eye
abduction.
o Effector organ : LR muscle
o Action: Eye abduction
Also called as abducens nerve or abducent nerve or CNVI.
Function:
o Solely to innervate the lateral rectus muscle and abduct the eye.
(Goodwin, 2006)
4. The sixth nerve nucleus is located in the
pons.
[Just ve ntralto the flo o r o f the fo urth ve ntricle and just
late ralto the m e diallo ng itudinalfasciculus (MLF)]
The sixth nerve contains only somatic
efferent fibers.
Runs a long course from the brainstem to
the lateral rectus muscle, through the
superior orbital fissure and into the orbit
through the annular ligament (annulus of
Zin) then to the lateral rectus.
Functioning to abduct the eyes.
5. 6th
nerve- The longest
subarachnoid course of all the
cranial nerve
The long course of the 6th nerve
between the brainstem and the eye
makes it vulnerable to injury at many
levels.
Close association between 6th
nerve
and 7th
nerve (facial) in the midbrain
Facial muscle also been involved in
some 6th
nerve palsies.
7. What?:
o Limited ability of the affected eye to turn out (abduct) due to 6th
nerve
lesion.
Why?:
Classified under neurogenic-cause of incomitant strabimus
It can be congenital (rare) or acquired (common).
Can be unilateral or bilateral 6th
nerve palsy.
8. Right gaze: Complete RE lateral rectus palsy Left gaze: Complete LE lateral rectus palsy
Primary gaze: Mild bilateral esotropia
Bilateral 6th nerve palsy
(Adapted from Hamidon et al. 2012)
9. Sixth nerve
palsy
Total palsy
(paralysis)
Partial palsy
(paresis)
Presence of abduction past
the midline
Presence of abduction past
the midline
Failure of abduction past
the midline
Failure of abduction past
the midline
Sclera is visible
on L gaze
HOW TO DIFFERENTIATE????HOW TO DIFFERENTIATE????
10. The sixth cranial nerve is the most commonly affected of
the ocular motor nerves based on some studies.
But ranking second following fourth nerve palsy according
to other reports.
11. Most patients who develop acute CN VI palsy are older than 50 years
of age. This group often has a concurrent history of hypertension
and/or diabetes.
(Acaroglu et al., 2008 & Richards et al., 1992)
Children are also prone to develop CN VI palsy. The causes may range
from benign (e.g., viral illness or trauma) to malignant etiologies.
(Janssen et al. 2008)
Young adults aged 20 to 50 years also can have CN VI palsy due
to neurologically complicated CN VI palsies involving additional cranial
nerves (such as III and IV) or other neurological signs (such as ataxia or
intention tremors).
(Brinar et al., 2007)
12. Lesions can affect any part of the nerve’s pathway.
o Usually due to direct damage of the sixth cranial nerve, encephalon
nuclei or less frequently diffuse axonal damage.
(Hamidon et al. 2012)
It can be congenital (rare) or acquired (common).
Identifying the causative factor is important for further
management.
The four most common causes were idiopathic (26%),
hypertension alone (19%), coexistent diabetes and
hypertension (12%), and trauma (12%).
(Patel et al., 2004)
13. (Patel SV, Mutyala S, Leske DA, et al. Incidence, associations, and
evaluation of sixth nerve palsy using a population-based method.
Ophthalmology. 2004 Feb;111(2):369-75)
14. More common Less common
Idiopathic Multiple sclerosis
Vasculopathic
(diabetes, hypertension, atherosclerosis)
Increased intracranial pressure
Trauma Sarcoidosis/vasculitis
Stroke (usually not isolated)
Lumbar puncture
Myasthenia Gravis
Giant cell arteritis
o Acquired
15. o Acquired
• Traumatic
• Tumour
• Idiopathic
• Infection
o Congenital
• Very rare
• If occurs as an isolated finding in the first week, usually
resolves spontaneously. (Reisner et al.
1971)
• May represent one of following: Duane syndrome, infantile
esotropia, nystagmus blockage syndrome (Ansons & Davis,
2014)
16. DIFFERENTIAL DIAGNOSIS WHY
Duane’s retraction
syndrome
Difficulty on ABD & ADD with eyelid retraction
Grave’s orbitopathy (TED) Proptosis + decreased ability of eye movement + diplopia
Orbital trauma Orbital fracture + Muscle swelling + eye restriction ABD & ADD
+ diplopia
Infantile esotropia Esotropia + limit in ABD (improve after doll’s head maneuver) +
IO overaction + nystagmus + vertical deviation
Spasm of the near reflex Triad of intermittent : conv. strabismus + acc. Spasm + miosis
Myasthenia Gravis Muscle restriction, diplopia & ptosis
High myopia Can lead to progressive loss of abduction
(Ansons & Davis, 2014)** ABD: abduct & ADD: adduct
17.
18.
19.
20.
21. Patient adopt face turn towards the
affected eye (Right side)
Control
diplopia
Maintaining
BSV
24. Abduct to R
gaze
Abduct to L gaze
LE sixth nerve palsy
Source: Kirtpatrick, C. Cranial Nerve 6 (Abducens Nerve) Palsy Secondary to Schwannoma
25. Abduct to R
gaze
Abduct to L gaze
Bilateral sixth nerve palsy
Source: Kirtpatrick, C. Bilateral Cranial Nerve VI (Abducens Nerve) Palsies Secondary to Retroclival Hematoma
26.
27.
28. Diagnosis:
RE 6th
nerve palsy
•The constricted RE field demonstrates LR underaction.
•Contralateral MR overaction.
•The central point is shifted in both eyes indicating
diplopia in primary gaze.
35. Binasal occlusion
o Type of sector occlusion
o Not as a permanent treatment
o Indication: Esotropia, amblyopia, diplopia, CE, DI
o Why recommended :
• Reduce double vision and direct patients to use their
peripheral system, helping them to locate objects and
judge distances more accurately
o Material : Translucent material (opaque) , clear
nail polish, black tape
o Sector size measurement:
• Pt wear the glasses, focus at distant target
•
36. Monocular occlusion
o Method of full patch
covering affected eye.
o Purpose: Remove diplopia
in lateral gaze
o Material: Occluder with
different grades (Bangerter
foils)
40. Approximately half of all 6th
nerve palsies recover
spontaneously approx. 3 months after onset. (Goodwin, 2006)
Patient with vasculopathic 6th
nerve palsy have a better
chance of recovery (69% to 86%) & recover more rapidly (4
to 6 weeks) than pt with 6th
nerve palsy from other causes.
(Goodwin, 2006)
A report of over 2000 patients with 6th
nerve palsy of
unknown etiology found that 36% recovered in 8 weeks (2
months) and 84% recovered in 4 months.
(King et al. 1995)
41. 1. Acaroglu G, Akinci A, Zilelioglu O. Retinopathy in patients with diabetic ophthalmoplegia.
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Ophthalmic & Vision Research, 8(2), 160–171.
3. Bagheri, A., Babsharif, B., Abrishami, M., Salour, H., & Aletaha, M. (2010). Outcomes of Surgical and
Non-Surgical Treatment for Sixth Nerve Palsy.Journal of Ophthalmic & Vision Research, 5(1), 32–
37.
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1985
5. Goodwin, D. (2006). Differential Diagnosis and Management of Acquired Sixth Cranial Nerve Palsy.
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6. Holmes JM, Leske DA, Christiansen SP: Initial treatment outcomes in chronic sixth nerve palsy. J
AAPOS 5:370–376, 2001
7. Janssen K, Wojciechowski M, Poot S, et al. Isolated abducens nerve palsy after closed head trauma:
a pediatric case report. Pediatr Emerg Care. 2008 Sep;24(9):621-3.
8. Patel SV, Mutyala S, Leske DA, et al. Incidence, associations, and evaluation of sixth nerve palsy
using a population-based method. Ophthalmology. 2004 Feb;111(2):369-75.
9. Richards BW, Jones FR Jr, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the
oculomotor, trochlear, and abducens cranial nerves. Am J Ophthalmol. 1992 May;113(5):489-96.
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