oculomotor nerve anatomy ( third cranial nerve), clinical importance, treatment, emergency scenarios.

1. THIRD NERVE PALSY
DR. SAARANG HANSRAJ

2. • Dysfunction of the third cranial nerve (oculomotor nerve) can result from lesions
anywhere along its path between the oculomotor nucleus in the midbrain and the
extraocular muscles within the orbit.
• Third nerve palsy may herald a life-threatening intracranial process (tumor,
aneurysm).
• The diagnosis and management of third nerve palsy varies according to the age of
the patient, characteristics of the third nerve palsy, and the presence of
associated signs and symptoms
INTRODUCTION

3. • The third cranial nerve is a motor
nerve chiefly involved in execution
of movements of the eye.
• it supplies all the extraocular
muscles except for lateral rectus and
superior oblique.

4. • The chief muscles supplied by the third nerve are the Superior Rectus, Inferior
Rectus, Medial Rectus and Inferior Oblique which are responsible for the elevation,
depression, adduction and extorsion of the eye respectively.
• In addition, the ciliary muscle and the sphincter pupillae are supplied by the
parasympathetic fibres from the Edinger-Westphal nucleus and are responsible for
the accommodation and pupillary constriction.
• The levator palpebrae superioris (LPS) which elevates the eyelid is also supplied by
the oculomotor nerve.

5. • The palsy could be congenital or
acquired in nature.
• Complete or partial.
• Pupil-sparing or involving.
• Isolated or associated with other
neurological symptoms.

6. ANATOMY
• The nuclear complex of the
third cranial nerve extends
rostro-caudally near the
midline in the midbrain at
the level of the superior
colliculus, and it lies ventral
to the sylvian aqueduct.

7. • One unpaired column (the most dorsal, which contains the Edinger-Westphal nucleus
rostrally and the subnucleus of the levator palpebrae superioris caudally) and four
paired rostrocaudal columns can be distinguished in the nuclear complex.
Biittner-Ennever JA, Akert K: Medial rectus subgroups of the oculomotor rnucleus and their abducens internucleari nput in the monkey. J Comp Neurol 197:17-27,1981

8. • Of the four paired subnuclei, the
most medial innervate the
superior rectus muscles.
• Each medial subnucleus has axons
that extend to the opposite eye,
but the decussation occurs within
the nuclear complex, and the
decussating fibers actually
transverse the contralateral
subnucleus for the superior rectus
muscle.

9. • The lateral three oculomotor
subnuclei have axons that extend to
ipsilateral eye muscles; fibers of the
dorsal subnucleus extend to the
inferior rectus muscle, and fibers of
the intermediate subnucleus extend
to the inferior oblique muscle.
• Although the ventral subnucleus was
thought to innervate the medial
rectus muscle, recent studies have
demonstrated that neurons supplying
this muscle are distributed into three
separate areas of the oculomotor
nucleus.
Biittner-Ennever JA, Akert K: Medial rectus subgroups of the oculomotor rnucleus and their abducens internucleari nput in the monkey. J Comp Neurol 197:17-27,1981

10. NUCLEAR LESIONS
• Paresis of isolated muscles innervated by oculomotor branches
is almost always due to a lesion of their branches within the
orbit or to disease processes that affect the muscle or
myoneural junction.
• Pure unilateral lesions of the oculomotor nucleus are rare.

11. • Nuclear lesions, however, may cause isolated weakness of one of the muscles
innervated by the oculomotor nerve, except
• the superior rectus muscle (intra nuclear crossed innervation)
• the levator palpebrae superioris (a single caudal subnucleus innervates
the levators bilaterally)
• the pupillary constrictors (visceral nuclei are spread throughout the
oculomotor nucleus)
• the medial rectus muscle (three separate subnuclei).
Isolated unilateral palsies of the inferior rectus muscle have been associated with
lesions of the inferior rectus subnucleus.
Roper-HallG, Burde RM: Inferior rectus palsies as a manifestation of atypical IIIrd cranial nerve disease. AmOrthoptJ 25:122-130,1975
Pusateri TJ, SedwickLA, MargoCE: Isolated inferior rectus muscle palsy from a solitary metastasis to the oculomotor nucleus. Arch Ophthalmol 105:675-677, 1987

12. • More characteristic of nuclear involvement is unilateral palsy of the third cranial
nerve in conjunction with weakness of the ipsilateral and contralateral superior
rectus muscles and bilateral incomplete ptosis
• Occasionally, only the superior rectus muscle contralateral to the lesion is involved.
• Bilateral palsies of the third cranial nerve but with sparing of the levator muscles
of the eyelid may be caused by bilateral nuclear lesions that spare the central
caudal levator subnucleus.
• Conversely, isolated bilateral ptosis and sparing of the extraocular muscles and
pupils have been described with lesions that involve the levator subnucleus and
spare more rostral oculomotor subnuclei.
WarrenW, BurdeRM, KlingeleTG, Roper-HallG: Atypical oculomotorparesis. J Clin
NeuroOphthalmol 2: 13-18, 1982
Eustace P: Partial nuclear third nerve palsies. Neuro-ophthalmology 5:259-262, 1985
ConwayVH, RozdilskyB, SchneiderRJ, SundaramM: Isolated bilateral completeptosis. Can J
Ophthalmol 18:37-40, 1983.
GrowdonJH, WinklerGF, WraySH: Midbrainptosis: acase with clinicopathologic correlation. Arch
Neurol 30: 179-181,
1974

13. • Within the substance of the midbrain, the
fascicular portion of the oculomotor nerve
crosses the medial longitudinal fasciculus
and decussating fibers of the superior
cerebellar peduncle.
• The axons then diverge widely to
transverse the red nucleus before exiting
the anterior aspect of the midbrain,
medial to the cerebral peduncles.

15. FASCICULAR LESIONS
• Oculomotor fascicular lesions often accompany nuclear lesions because
the paramedian branches near the top of the basilar artery often feed
both structures.
• Complete fascicular lesions cause ipsilateral involvement of all the
oculomotor innervated muscles and sparing of the contralateral eye.
• A fascicular localization for an oculomotor nerve palsy is suggested by
concomitant damage of neighboring mesencephalic structures and
pathways.

16. • Most fascicular third nerve lesions have vascular causes (hemorrhage, infarction).
Metastatic or infiltrative disease is less common; demyelinating disease is rare, even
in patients with known multiple sclerosis.
• Because fascicular third nerve palsies are typically ischemic in nature, they may have
varying degrees of recovery. Aberrant regeneration, however, does not occur.
• Patients who have aberrant regeneration after an acquired third nerve palsy must be
considered to have a compressive lesion of the third nerve.

17. • Classically, fascicular third nerve palsies were thought to affect all functions of the
third nerve equally, with the degree of pupil involvement (anisocoria increasing in
bright light) being proportional to the lid and motility defects.
• Recently, however, it has been recognized that isolated extraocular muscle paresis
can result from fascicular third nerve lesions.
• Divisional oculomotor paresis also can occur.
• The ‘isolated’, pupil-sparing third nerve palsy seen in adults with vascular disease
may also result from fascicular damage.

19. CLAUDE SYNDROME

20. • Fascicular lesions may cause palsies of the oculomotor nerve limited to specific
muscles.
• Rarely, fascicular lesions of the third cranial nerve develop in isolation without other
ocular motor or neurologic involvement present to suggest a mesencephalic site of
damage. Eg Mesencephalic lymphoma
• Although superior and inferior divisional palsies have classically been localized to
anterior cavernous sinus or posterior orbital lesions, reports support the contention
that a divisional oculomotor nerve pattern may occur from damage at any location
along the course of the oculomotor nerve, from the fascicle to the orbit.
Ksiazek SM, Repka MX, Maguire A, Harbour RC, Savino PJ, Miller NR, Sergott RC, Bosley TM: Divisional oculomotor nerve paresis caused by intrinsic brainstem disease. Ann Neurol 26:714-718,1989

21. • Other manifestations of mesencephalic
lesions that cause fascicular oculomotor
palsies include disorders of gaze and
convergence, somnolence, peduncular
hallucinosis, and paucity of speech or even
mutism.
• Contralateral abduction may be impaired
("pseudo-abducens palsy) perhaps because
of excessive convergence.
Elliott RL: Encephalitiswith ophthalmoplegia. Confin Neuro 31:194-197,1969
Selhorst JB, Hoyt WF, Feinsod M, Hosobuchi Y: Midbrain corectopia. Arch Neurol 33:193-195,
1976
Masdeu J, Brannegan R, RosenbergM, Dobben G: Pseudo abducens palsy with midbrainlesions. Ann Neurol
8:103,1980

22. • Upon reaching the subarachnoid
space, each oculomotor nerve passes
between the superior cerebellar and
the posterior cerebral artery, courses
near the medial uncus of the temporal
lobe, and then pierces the dura mater
just lateral to the posterior clinoid
process to enter the lateral wall of the
cavernous sinus.

23. In the cavernous sinus,
the oculomotor nerve is
superior to the trochlear
nerve and the abducens
nerve and medial to the
ophthalmic branch of
the trigeminal nerve.

25. • The oculomotor nerve then reaches the superior orbital fissure, which it
transverses to enter the orbit.
• Within the anterior cavernous sinus, superior orbital fissure, or posterior orbit,
the oculomotor nerve divides into a superior ramus, which supplies the superior
rectus muscle and the levator muscle of the eyelid, and an inferior ramus, which
supplies the medial and inferior rectus muscles, the inferior oblique muscle, and
the ciliary ganglion (parasympathetic fibers to pupillary constrictors).
• Segregation of fibers into superior and inferior groups may occur before
anatomic division in the cavernous sinus-perhaps even at a fascicular level.

26. SUBARACHNOID LESIONS
• Pupillary dilatation and unresponsiveness, with variable paresis
of extraocular muscle function, are characteristic of
compression of the third cranial nerve in the subarachnoid
space, usually by uncal herniation or by an aneurysm of the
internal carotid artery or posterior communicating artery.
• Involvement of nerve at this level may be idiopathic in 25% of
the cases.
• Rarely, aneurysmal partial oculomotor nerve paresis may be
transient and clear spontaneously.
Bartleson JD, Trautmann JC, Sundt TM Jr: Minimal oculomotor nerve paresis secondary to unruptured intracranial aneurysm. ArchNeurol 43:1015-1020,1986

27. • Compressive subarachnoid lesions may
occasionally spare the pupil, perhaps
because even distribution of the pressure
of the lesion allows the relatively pressure-
resistant, small caliber pupillomotor fibers
to escape injury or because the lesion
compresses only the inferior portion of the
nerve and thus spares the dorsally situated
pupillomotor fibers.
• Ptosis has been described in isolation as
the sole manifestation of oculomotor
compression by an aneurysm of the
posterior communicating artery.
Kissel JT, Burde RM, Klingele TG, Zeiger HE: Pupil-sparing oculomotor palsies with internal carotid-posterior communicating artery aneurysms. Ann Neurol 13:149-154, 1983
Good EF: Ptosis as the sole manifestation of compression of the oculomotor nerve by an aneurysm of the posterior communicating artery. J Clin Neuro Ophthalmol 10:59-61, 1990

28. • The downward herniation of the uncus in the temporal lobe by
extradural or subdural hematoma caused by head trauma or an
expanding supratentorial mass can stretch or compress the
third nerve against the tentorial edge, initially causing irritative
miosis followed by pupillary dilatation (Hutchinson’s pupil) and
later total oculomotor nerve palsy.
• “The rule of the pupil” suggests that if a compressive lesion
causes a third nerve palsy, the chances of pupil involvement are
95-97%.
• In 32% cases of ischemic lesions pupil involvement may be seen.

29. LESIONS OF THE CAVERNOUS SINUS
• In the cavernous sinus, compressive lesions often involve the other ocular motor
nerves and the ophthalmic branch of the trigeminal nerve. The clinical findings are
similar when the region of the superior orbital fissure is involved; however, with
space-occupying lesions, proptosis strongly indicates localization to the superior
orbital fissure.
• Combined oculomotor paresis and sympathetic denervation (Horner's syndrome) are
virtually pathognomonic of a lesion of the cavernous sinus.
Greenberg HS, Deck MDF, Vikram B, Chu FCH, Posner JB: Metastasis to the base of the skull: clinical findings in 43 patients. Neurology 31:530-537,1981

30. • Compressive lesions of the cavernous sinus may also spare the pupil because they
often preferentially involve only the superior division of the oculomotor nerve that
has no pupillomotor fibers or the superior aspect of the nerve anterior to the point
where the pupillomotor fibers descend in their course near the inferior oblique
muscle.
• Pupil sparing occurs in 14% of patients of compressive third nerve palsy!
• Concomitant injury of nerve fibers to both the pupillary sphincter and the dilator can
result in a mid-position, fixed pupil.
Trobe JD, Glaser JS, Post JD: Meningiomas and aneurysm of the cavernous sinus: neuro-ophthalmologic features. Arc Ophthalmol 96:457-467, 1978
Kissel JT, Burde RM, Klingele TG, Zeiger HE: Pupil-sparin oculomotor palsies with internal carotid-posterior communicatin artery aneurysms. Ann Neurol 13:149-154, 1983

31. • Lesions of the medial cavernous sinus may affect only the
ocular motor nerves but spare the more laterally located
ophthalmic branch of the trigeminal nerve and thus result in
painless ophthalmoplegia. An isolated oculomotor palsy may be
the initial or sole sign of a pituitary tumor; indeed, ptosis may
be the initial manifestation of such a lesion.
Spoor TC, Hartel WC, Harding S, Kocher G: Aspergillosi presenting as a corticosteroid-responsive optic neuropathy. J Clin Neuro Ophthalmol 2:103-107,1982

32. ORBITAL LESION
• Orbital lesions are characterized by muscle paresis associated with
proptosis and, at times, optic neuropathy.
• Orbital masses may cause progressive unilateral visual failure associated
with swelling of the optic disk (followed by atrophy) and the occurrence
of opticociliary shunt vessels.
• Although proptosis is characteristic of orbital masses, it may also occur
with lesions of the cavernous sinus and may rarely even be due to an
intracranial lesion.
Boschetti NV, Smith JL, Osher RH, Gass JDM, Norto EWD: Fluorescein angiography of optociliary shunt vessels J Clin Neuro Ophthalmol 1:9-30,1981

33. ABERRANT REGENERATION
• This usually occurs in congenital third nerve palsy or following trauma, compression
of the nerve by slow growing tumour (meningioma) or aneurysm. The breached
myelin sheath and the perineurium cause misdirection of the regenerating axons and
innervate the surrounding muscles such as the LPS, superior oblique and occasionally
iris sphincter muscle.
• Clinical manifestations such as
• elevation of the eyelid during attempted adduction (Inverse Duane syndrome) or depression (Pseudo-Von
Graefe’s sign)
• miosis in an otherwise non-reactive pupil (Pseudo-Argyll-Robertson pupil).

34. • Dissociation of the light and near reflexes of the pupil often occurs, and the pupil
may constrict on adduction or downward gaze.
• Aberrant regeneration to the iris sphincter may be too weak to constrict the pupil,
but on slit-lamp examination, clear segmental contraction of the sphincter may be
seen when movement of the eye in any oculomotor mediated direction is attempted
(Czarnecki's sign)
• This gaze-evoked segmental constriction of the pupil may occur in portions of the
sphincter that are unreactive to light, and other segments of the pupil have normal
reactions to light without Czarnecki's sign.
Cox TA, Goldberg RA, Rootman J: Tonic pupil and Czarnecki's sign following third nerve palsy. J Clin Neuro Ophthalmol 11:55-56,1991

35. • Aberrant regeneration may occur after oculomotor damage due to trauma,
aneurysm, and other causes, but it is seldom caused by ischemic (for example,
diabetic) neuropathy.
• Rarely, aberrant regeneration of the third cranial nerve may develop without a
history of oculomotor palsy (primary aberrant regeneration).
• Primary aberrant regeneration has occurred unilaterally in patients with
intracavernous meningioma, aneurysm, or trigeminal neuroma and bilaterally in a
patient with abetalipoproteinernia (Bassen-Kornzweig syndrome)
• Combined Oculomotor-Abducens synkinesis has been described after severe head
trauma that resulted in misdirection of nerve fibers to the right medial rectus and
right lateral rectus muscles. On attempted adduction, the right eye slightly
abducted, but it adducted on attempts at abduction; in addition, attempts at
abduction resulted in pupillary constriction.
Cohen DA, Bosley TM, Savino PJ, Sergott RC, Schatz NJ: Primary aberrant regeneration of the oculomotor nerve: occurrence in a patient with abetalipoproteinemia. Arch Neurol 42:821-823,1985
Packer AJ, Bienfang DC: Aberrant regeneration involving the oculomotor and abducens nerves. Ophthalmologica 189:80-85, 1984

38. ETIOLOGY IN ADULTS
• Etiologies of acquired third nerve palsies are specific to the location. These include
a wide variety of pathologies, including structural lesions, cerebrovascular disease,
inflammatory or infectious conditions, and trauma.
• Isolated oculomotor nerve palsy is idiopathic in 25% of the cases and is commonly due
to basilar lesions.
Ganger A, Yadav S, Singh A, Saxena R. A Comprehensive Review on the Management of III Nerve Palsy. Delhi J Ophthalmol 2016;27;86-91.

39. • Intracranial aneurysm — The most dreaded cause of a third nerve palsy is
compression by an enlarging intracranial aneurysm.
• The most common site of an aneurysm causing a third nerve palsy is the posterior
communicating artery; however, aneurysms involving the internal carotid artery
and basilar artery are reported to produce third nerve palsies as well.
• In the setting of an acute third nerve palsy, the aneurysm is believed to be
acutely enlarging and therefore at risk of imminent rupture. In this setting,
subarachnoid hemorrhage can occur within hours or days of initial presentation of
the third nerve palsy.
• The mean age of presentation of aneurysmal subarachnoid hemorrhage is 55
years; however, aneurysms have been reported in young children and in the
elderly.
Green WR, Hackett ER, Schlezinger NS. Neuro-ophthalmologic evaluation of oculomotor nerve paralysis. Arch Ophthalmol 1964; 72:154–67.

40. • The aneurysms in the posterior part of the Circle of Willis, posterior communicating
and basilar tip aneurysms have the highest rates of ruptures between 2.5-50%
depending upon their size.
• Risk of rupture is 1% per year.
(0.05% for anterior circulation, 0.5% for posterior circulation)
• These aneurysms are the most commonly associated with isolated third nerve palsy.
• The most common cause of a SAH is trauma, however 80-90% of non traumatic SAH
are due to aneurysms.
• Kissel JT, Burde RM, Klingele TG, Zeiger HE. Pupil- sparing oculomotor palsies with internal carotid-posterior communicating artery aneurysms. Ann Neurol 1983; 13:149–54. Wiebers DO,
Whisnant JP, Huston J 3rd, Meissner I, Brown
• RD Jr, Piepgras DG, et al. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003; 362:103–10.

41. • Ischemia — Ischemic third nerve palsies, also called diabetic third nerve palsies, are
the most common etiologic subset of third nerve palsy in adults. The pathogenesis is
felt to be microvascular; hypertension and advanced age are also risk factors. While
some isolated ischemic third nerve palsies are due to midbrain infarction, most are
peripheral.
• Pupil-sparing third nerve paresis in an elderly patient with known systemic vascular
disease can be considered to be ischemic mono neuropathy, which is a common
cause.
Talebnejad MR, Sharifi M, Nowroozzadeh MH. The role of Botulinum toxin in management of acute traumatic third- nerve palsy. J AAPOS 2008; 12:510-3.

42. • However the possibility of vascular inflammation such as giant cell arteritis should be
kept in mind in elderly patient and may be excluded by
• history
• complete hemogram,
• erythrocyte sedimentation rate (ESR) and
• C-reactive protein (CRP). These patients can be managed conservatively and
• Reassess after a week to rule out pupil-involvement or increase in pain. Weekly
follow-ups initially followed by monthly evaluation are important to document
recovery and plan any intervention accordingly.
• Ischemic mono neuropathies usually start recovering by 8-12 weeks.
• Acute palsy in individuals less than 40 years of age suggests need for
neuroimaging and a complete neurological workup.
Ganger A, Yadav S, Singh A, Saxena R. A Comprehensive Review on the Management of III Nerve Palsy.
Delhi J Ophthalmol 2016;27;86-91.

43. • Trauma — Traumatic third nerve palsy usually arises only from severe blows to the
head, with skull fracture and/or loss of consciousness.
• Trivial trauma without loss of consciousness should suggest the possibility of pre-
existent mass lesion at the base of skull.
• Thus, a third nerve palsy associated with mild head trauma should prompt evaluation
for associated pathology.
• When diurnal variation or fluctuations in clinical findings are associated with a pupil-
sparing palsy, myasthenia gravis should be excluded.

44. • Migraine — Ophthalmoplegic 'migraine,' a condition affecting children and young
adults, was reclassified as a cranial neuralgia in 2004. This most commonly affects
the third cranial nerve, sometimes with permanent deficits.
• Several cases have been reported in which ophthalmoplegic 'migraine' is associated
with MRI (magnetic resonance imaging) gadolinium enhancement suggesting that the
condition may be a recurrent demyelinating neuropathy.
• A 3rd nerve palsy of unknown cause must have a work up for Tuberculosis, Sarcoidosis,
Multiple Sclerosis to rule out these rare causes.
Ophthalmoplegic migraine: a recurrent demyelinating neuropathy? Lance JW, Zagami Cephalalgia. 2001;21(2):84.
Magnetic resonance imaging in ophthalmoplegic migraine of children. O'Hara MA, Anderson RT, Brown D J AAPOS. 2001;5(5):307

45. LOCATION OF
LESION
ASSOSCIATED SIGNS/SYMPTOMS MOST COMMON CAUSE
Nucleus
Complete ipsilateral third plus contralateral ptosis and contralateral superior rectus weakness
Infarction
Hemorrhage
Tumor
Fascicles
Contralateral hemiparesis (Weber's syndrome)
Contralateral tremor (Benedikt's syndrome)
Ipsilateral ataxia (Nothnagel's syndrome)
Infarction
Hemorrhage
Tumor
Demyelination
Subarachnoid space
Typically isolated
May present with headaches or orbital pain
ICA/Pcom A/Basilar/PCA Aneurysm
Microvascular (ischemic)
Tumor (pituitary, carcinomatous
meningitis)
Meningitis
Herniation
Trauma
Cavernous sinus
Cranial nerves IV, VI, V1, V2
Oculosympathetic dysfunction (Horner)
Pain may be prominent
Tumor
Inflammation
Carotid aneurysm
Microvascular (ischemic)
Thrombosis
Arteriovenous fistula
Orbital apex
Proptosis
Visual loss
Cranial nerves IV, VI, V1, V2
Oculosympathetic dysfunction (Horner)
Pain may be prominent
Trauma
Tumor
Inflammation
Infection (fungus)

46. ETIOLOGY IN CHILDREN
• Third nerve palsy is uncommon in children and often assosciated with
other neurological abnormalities. A population-based study in Minnesota
identified 36 cases over a 15-year period; the age- and sex-adjusted
annual incidence was 1.7 per 100,000 county residents under the age of
18.
• One review at the Wilmer Eye Institute identified 41 children younger
than eight years of age with third nerve palsy. The most frequent causes
were congenital (39 percent), traumatic (37 percent), and neoplastic
(17 percent).
Pediatric third, fourth, and sixth nerve palsies: a population-based study. Holmes JM, Mutyala S, Maus TL, Grill R, Hodge DO, Gray DT Am J Ophthalmol. 1999;127(4):388.
Ophthalmologic outcome after third cranial nerve palsy or paresis in childhood. Mudgil AV, Repka MX J AAPOS. 1999;3(1):2.

47. • Third nerve palsy in children often is congenital (intrauterine or birth-
related events) but may occur after postnatal trauma, infection,
inflammation, tumor, arteriovenous malformation or childhood migraine.
• Aberrant regeneration is common, which, if present, argues against a
nuclear lesion.
• Loewenfeld and Thompson speculated that perinatal damage to the
third nerve causes retrograde degeneration of the oculomotor nucleus,
which then is re innervated haphazardly.
• In a few rare cases congenital 3rd nerve palsy is assosciated with cyclic
oculomotor spasms with alternating paretic and spasmodic phase. This
persists throughout life and is not seen with acquired lesions.

48. • Aneurysms are rare, but certain children are at increased risk (e.g.,
those with polycystic kidney disease, coarctation of the aorta, or Ehlers-
Danlos syndrome).
• Traumatic third nerve palsy usually arises only from severe blows to the
head.
• Thus, third nerve palsy associated with mild head trauma should prompt
evaluation for associated pathology.
• Both complete and incomplete palsy has been reported post MMR
vaccine. In cases with no apparent cause an IgG titre for Rubeola, Mumps
and Rubella is warranted.
Oculomotor nerve palsies in children. Ing EB, Sullivan TJ, Clarke MP, Buncic JR J Pediatr Ophthalmol Strabismus. 1992;29(6):331
Manzotti, F., Menozzi, C., Porta, M.R. et al. Partial third nerve palsy after Measles Mumps Rubella vaccination. Ital J Pediatr 36, 59 (2010)

49. CLINICAL FEATURES
• Adults with an acute acquired third nerve palsy usually complain of the sudden onset
of binocular horizontal, vertical, or oblique diplopia and a droopy eyelid.
Infrequently, the patient is aware of an enlarged pupil.
• Patients with chronic third nerve palsies (especially with primary aberrant
regeneration) may be asymptomatic.
• Pain accompanying the onset of third nerve palsy is common, except in midbrain
lesions, and is not useful to distinguish among etiologies.
Relative pupil-sparing third nerve palsy: etiology and clinical variables predictive of a mass. Jacobson DM Neurology. 2001;56(6):797.

50. • Sudden, severe pain ("the worst headache of my life") might suggest subarachnoid
hemorrhage due to a ruptured aneurysm as the cause of the third nerve palsy.
• Severe pain may also be present in inflammatory lesions or pituitary apoplexy, but
mild or moderate pain is also common in ischemic lesions.

51. • On examination, patients with a complete third nerve palsy have ptosis,
a large unreactive pupil, loss of accommodation and paralysis of
adduction, elevation, and depression. The eye rests in a position of
abduction, slight depression, and intorsion "down and out”
• Concurrent paralysis of the levator palpebrae and unopposed tonus of
the orbicularis muscle will cause ptosis of the upper lid, and general
relaxation of tonus of four of the six extraocular muscles may produce a
small degree of proptosis.
• The motility of the affected eye will be limited to abduction, to small
degrees of depression in abduction (which is limited by the minor
contribution of the superior oblique muscle to depression in that
position), to incycloduction, and to an adduction movement of the eye
that does not go beyond the primary position.

52. • In partial lesions, the pupil may be of
normal size and normally reactive, dilated
and poorly reactive or dilated and non-
reactive to light and near stimulus
(complete internal dysfunction).
• The asymmetry of pupil size is greater in
the light than in the dark.
• There may be complete or incomplete
involvement of the extraocular muscles
(external dysfunction) innervated by the
third nerve, producing varying degrees of
ptosis as well as weakness of ipsilateral
adduction (medial rectus), elevation
(superior rectus, inferior oblique), and/or
depression (inferior rectus).

53. • If the elevator muscles (superior rectus or inferior oblique muscles) are involved, an
ipsilateral hypotropia in primary gaze occurs with excyclo and incyclotorsion
respectively.
• If the deficit of adduction is significant, a primary position exotropia worse in gaze
toward the paretic medial rectus muscle occurs. Head posture is towards the paretic
muscle
• If the inferior rectus muscle is involved, an ipsilateral hypertropia with incyclotorsion
occurs. Torticollis is not diagnostically significant.

56. • Children with congenital third nerve palsies may not complain of diplopia because
they ignore or suppress the second image or because they have superimposed
amblyopia; often they are brought to medical attention by their parents, who have
noticed ptosis or strabismus.

57. RUPTURED ANEURYSM !!!
1. Vasospasm is the most common cause of death.
2. 10 percent die before receiving medical attention.
3. 50 percent die within a month.
4. 50 percent of survivors have residual neurological defects.
5. If untreated 25 percent rebleed within 2 weeks.

58. OTHER EMERGENCIES WITH IIIrd NERVE DYSFUNCTION

59. PARTIAL 3rd NERVE PALSY - ALWAYS GO
FOR NEURO-IMAGING!

60. MANAGEMENT
• Treatment initially involves medical management of systemic predisposing factors
and conservative measures to obviate symptoms followed later by surgical
intervention in non-resolving oculomotor nerve palsy. The patient should be
evaluated at each follow up with a complete squint work- up, diplopia charting and
Hess-charting.

62. • Ischemic neuropathies usually resolve in 6 weeks to 12 weeks and can be
treated conservatively. Underlying systemic conditions should be
adequately controlled and managed to prevent further ocular morbidity.
Ptosis in a complete oculomotor palsy usually limits the diplopia.
Occlusion of the normal eye during the period of observation if ptosis is
not present eliminates the troublesome diplopia and past pointing
associated with acute palsies.

63. • Botulinum toxin injection to the only functioning rectus muscle, lateral rectus has
been described to prevent contracture during the period of conservative
management.
• The exotropia shows marked recovery early in the course.Though temporary it
provides short term diplopia free vision. It could provide an alternative treatment
modality in a patient who is unfit for neurosurgical intervention or strabismus surgery.
• An alert patient may notice anisocoria and increased light sensitivity resulting due to
pupil involvement. Pilocarpine can be used if there are no other contraindications.
• Diminished accommodation, can also occur in pupil involving oculomotor palsy, and
the clinician should consider near vision addition in optical prescriptions.
Kubatko-Zielińska A1, Krzystkowa KM, Madroszkiewicz A, Wójcik E, Filipowicz E. Principles and results of treatment in acquired paralysis of III, IV and VI nerves. Klin Oczna 1995; 97:147-51.
Talebnejad MR, Sharifi M, Nowroozzadeh MH. The role of Botulinum toxin in management of acute traumatic third- nerve palsy. J AAPOS 2008; 12:510-3.

64. • Mono neuropathies with aneurysmal compressions or other
compressive lesions require neurosurgical referral and
intervention.
• In non-recovering or residual third nerve palsies surgical
intervention may be considered in cases with stable deviation
and minimum follow-up of 6-12 months.
Ganger A, Yadav S, Singh A, Saxena R. A Comprehensive Review on the Management of III Nerve Palsy. Delhi J Ophthalmol 2016;27;86-91.

65. SURGICAL
MANAGEMENT
Ganger A, Yadav S, Singh A, Saxena R. A Comprehensive Review on the
Management of III Nerve Palsy. Delhi J
Ophthalmol 2016;27;86-91.

66. • The surgical correction of large angle exotropia and hypotropia in the oculomotor
nerve palsy is a formidable challenge.
• It varies according to the number of extraocular muscles involved, their recovery and
the presence or absence of aberrant regeneration.
• The goals and limitations of the surgery should be clearly understood by the patient
to avoid disappointment. Several staged procedures are required to achieve an
optimal correction, to assess the results prior to considering further options and to
avoid anterior segment ischemia.

67. • Surgical outcome is often better and predictable in partial oculomotor nerve palsy.
• Paralysis of the upper division of the oculomotor nerve can be corrected by Knapp
procedure
• In large angle hypotropia (>15Δ) the above can be combined with recession of the
contralateral superior rectus muscle.
Flanders M, Hasan J, Al-Mujaini A. Partial third cranial nerve palsy: clinical characteristics and surgical management. Can J Ophthalmol 2012; 47:321–5.

68. KNAPPS PROCEDURE
• Transposition of medial and lateral
rectus adjacent to the insertion of
the superior rectus on the affected
eye

69. • Isolated palsy of the inferior division of the oculomotor nerve is rare.
• A procedure has been described by Kushner that involves simultaneous transposition
of the superior rectus muscle to lie adjacent to the medial rectus and of the lateral
rectus muscle toward the insertion of inferior rectus muscle, with tenotomy of the
ipsilateral superior oblique.
• Isolated palsy of the medial rectus is even rarer. Lateral rectus disinsertion and
periosteal fixation to the lateral wall with or without medial globe anchoring.

70. • Complete oculomotor palsy
is difficult to correct
because of involvement of
most of the extraocular
muscles. Several surgical
options are available with
acceptable results.

71. 1. Large Recession and Resection –
• A forced duction test for adduction should be performed by which the passive
mobility of the globe is determined to rule out mechanical restriction of ocular
motility.
• If significant medial rectus muscle function is present so as to cause adduction of the
eye past midline, the eye may be aligned in the primary position with a
supramaximal recession of the lateral rectus muscle and resection of the medial
rectus muscle.
• It is usually combined with posterior tenectomy of the superior oblique (PTSO).
Von Noorden GK, Campos EC. Paralitic Strabismus. Binocular Vision and Ocular Motility. 6th ed. St Louis: Mosby; 2002:414- 57.

72. 2. Globe anchoring Procedures –
• In the absence of significant medial rectus muscle function, even supramaximal
recession of the lateral rectus muscle and resection of the medial rectus muscle will
almost always result in recurrence of the strabismus.
• In such a case, an active force generation test and saccadic velocities are useful in
assessing the function of apparently paretic medial rectus muscle in the presence of
contracture of the lateral rectus.
• When no or minimal force is generated, a globe fixation procedure to the medial wall
of the orbit at the anterior lacrimal crest can be performed.
• This can be achieved by using either 5-0 nonabsorbable polyester suture, fascia lata,
orbital periosteal flap, superior oblique tendon or silicon bands through a skin
incision or through a precaruncular approach.
• The suture/T- plate anchoring platform system anchors the globe by sutures to a
titanium T-plate screwed to the orbital wall, advantages being reduced risk of
anterior segment ischemia and fewer re-operations, with likely longer durability of
the system.
Sharma P1, Gogoi M, Kedar S, Bhola R. Periostal fixation in third nerve palsy. J AAPOS 2006; 10:324-7. K. A. Sadagopan and B. N. Wasserman. Managing the patient with oculomotor nerve palsy. Curr Opin
Ophthalmol 2013; 24:438-47.

73. 3. Superior oblique transposition procedures-
• Transposition of the superior oblique muscle, with or without trochleotomy, along
with horizontal recti surgery, has been the mainstay of treatment in achieving ocular
alignment in third nerve palsy.
• Scott described the disinsertion and shortening of the superior oblique tendon
without trochleotomy and its insertion at the superior end of the medial rectus
insertion to improve the alignment.
• However it is associated with paradoxical movements of the globe and induced
hypertropia.
• Cosmetically satisfactory results with
Scott’s procedure when combined
with recession of the lateral and
superior recti have been reported by Maruo et al.
Scott AB. Transposition of the superior oblique. Am Orthopt J 1977; 27:11-4. Maruo T, Kubot N, Iwashige H. Transposition of the superior oblique tendon for paralytic exotropia in
oculomotor palsy in 20 cases. Binocular Vision 1988; 3:203-13.

74. 4. Lateral Rectus Transposition Procedures –
• Complete transposition of the lateral rectus muscle to the medial globe to facilitate
the medial rotation of the eye uptil the primary gaze was described by Taylor et al.
• Y-splitting of the lateral rectus and its transposition to retro equatorial points 20 mm
posterior to the limbus near the nasal superior and the inferior vortex veins or to
points 1mm posterior to the superior and inferior borders of the MR insertion without
or with posterior fixation sutures have been described.
Taylor JN. Surgical management of oculomotor nerve palsy with lateral rectus transposition to the medial
side of the globe. Aust NZJ Ophthalmol 1989; 17:27-31.
Kaufmann H. “Lateralis splitting” in total oculomotor paralysis with trochlear nerve paralysis.
Fortschr Ophthalmol 1991; 88:314-16.
Gokyigit B1, Akar S, Satana B, Demirok A, Yilmaz OF. Medial transposition of split lateral rectus muscle
for complete oculomotor nerve palsy. JAAPOS 2013; 17:402 10.
Saxena R, Sharma M, Singh D, Dhiman R, Sharma P. Medial transposition of split lateral rectus
augmented with fixation sutures in cases of complete third nerve palsy. Br J Ophthalmol 2016;0:1–3.

75. • Management of ptosis depends on the presence or absence of Bell’s phenomenon and
aberrant regeneration.
• Complete ptosis with poor Bell’s phenomenon can be managed with crutch glasses.
• Frontalis sling procedures for the ptosis can be done, however keeping in mind that
overcorrection can lead to corneal exposure.
• Levator resection may be inadequate as the levator muscle is paralysed to some
extent and may show variable response to the procedure.

76. • In patients with aberrant regeneration, ptosis can be corrected by performing a
recession-resection procedure in the contralateral eye.
• Similarly, in a case of partially recovered oculomotor nerve palsy with residual
Superior rectus function, the ptosis can be corrected using the concept of ‘Fixation
duress’ in the non-involved eye.
• The fixation duress is proposed to decrease the elevation of the normal eye thereby
creating similar forces of duress in both eyes when fixation takes place.

78. Worths Four Dot Test :
EOM
• Extraocular movements in BE were limited except for BE abduction, LE
depression and LE levodepression.
• Ductions Versions
-3 -3 -2 -3 -3 -2
0 -3 -3 0 0 -3 -2 0
-2 0 -1 -2 -2 0

79. Diplopia charting
Diplopia was seen in primary position, elevation, depression and on
levoversion, levoelevation and levodepression

80. Procedure done:
• RE squint correction with
supramaximal LR recession
(16mm) - MR resection(9mm)
was done and ptosis surgery
planned in the next stage.

81. • Post operatively BE were
orthotropic with central HCRT.
• Patient was doing well in
subsequent visits till date.

82. A CHRONIC CASE OF
INCOMPLETE PUPIL SPARING
ISCHEMIC 3RD NERVE PALSY
ON DEXTRO-ELEVATION
(LE) UNABLE TO ELEVATE AND
UNABLE TO CROSS MIDLINE
ALSO LID MARGIN ELEVATES
S/0 RECOVERED/SPARED (?)
SUPERIOR RECTUS
(LE) LATERAL RECTUS IS
SPARED. S/O SINGLE NERVE
INVOLVEMENT
PRELIMINARY DIAGNOSIS OF (LE) CHRONIC AQUIRED ISOLATED INCOMPLETE THIRD
NERVE PALSY INVOLVING THE INFERIOR DIVISION SPARING THE PUPIL

83. ACUTE AQUIRED COMPLETE ISOLATED 3RD NERVE PALSY INVOLVING
THE PUPIL

84. THANK YOU