ETIOLOGY, CLINICAL FEATURES AND
OCULOMOTOR NERVE PALSY
Dr. BHIMALA HASIKA
M.S.OPHTHALMOLOGY ( 2nd YR)
Ocular motor nerve palsies may be partial or
complete, congenital or acquired, isolated or
accompanied by signs of more extensive
They can result from lesions located anywhere
from the ocular motor nerve nuclei, along the
fascicular course within the brainstem, in the
subarachnoid space, in the cavernous sinus, to
the termination of the nerves in the extra-ocular
muscles within the orbit.
The diagnosis and management of ocular motor
nerve dysfunction varies according to the age of
the patient, characteristics of the ocular motor
nerve palsies, and presence of associated
Recent advances in noninvasive
neuroimaging facilitate earlier diagnosis
and appropriate management.
For a patient with a complaint referable to
cranial nerve dysfunction, the problem must
be approached in an orderly, logical, and,
above all, anatomic manner.
A N A T O MY
The oculomotor nerve (third cranial nerve)
supplies motor innervation for the superior
rectus, medial rectus, inferior rectus, inferior
oblique, and levator palpebrae superioris
muscles and also parasympathetic input to
the pupillary constrictor and ciliary muscles.
Cell bodies reside in the midbrain in a
nuclear mass straddling the vertical midline.
Each target muscle has a subnucleus devoted
exclusively to its function (the medial rectus has
Most rostral and dorsal are the visceral nuclei
(Edinger–Westphal nuclei and adjacent
structures) that supply parasympathetic
innervation to the pupillary sphincters and
ciliary muscles via the ciliary ganglia.
Caudal and dorsal, the ‘caudal central nucleus’
is a single midline structure that innervates the
levator palpebrae superioris muscles,
subserving upper lid elevation.
The cell bodies in the superior rectus
subnuclei send their axons directly across the
midline to join the contralateral oculomotor
The other subnuclei project ipsilaterally to
their individual extraocular muscles.
of third cranial nerve
fascicular fibers in a
rostrocaudal plane. IO,
inferior oblique muscle;
IR, inferior rectus
muscle; LP, levator
palpebrae; MR, medial
(subnuclei a, b, and c);
P, pupil; SR, superior
rectus muscle; CCN,
central caudal nucleus.
The oculomotor fascicles refer to the portion of
the nerve that travels through the brain stem
parenchyma to exit ventrally.
The fascicles pass through the substance of the
red nuclei and the medial cerebral peduncles.
On leaving the brain stem, the nerve enters the
subarachnoid space and courses forward and
laterally between the posterior cerebral artery
above and the superior cerebellar artery below
to run briefly alongside the posterior
At this level, the pupillary fibers are located
dorsally and peripherally.
Lateral view of the subarachnoid and intracavernous portions of the oculomotor nerve (III) and its vascular
supply. DMB, dorsal meningeal branches; MHT, meningohypophyseal trunk; ICA, internal carotid artery; IHB,
inferior hypophyseal branches; RB, recurrent collateral branches of the ophthalmic artery; IV, trochlear nerve;
V1, ophthalmic division of the trigeminal nerve; OC, optic chiasm; PG, pituitary gland.
The nerve then pierces the dura and enters the
Within the anterior aspect of the cavernous sinus, the
third nerve divides so that two divisions of the
oculomotor nerve pass through the superior orbital
fissure and enter the orbit.
The superior division contains axons destined for the
levator palpebrae superioris and superior rectus
The inferior division carries the motor fibers to the
medial rectus, inferior rectus, and inferior oblique
muscles, as well as the preganglionic parasympathetic
fibers to the ciliary ganglion.
A coronal section of the right cavernous sinus viewed anteriorly.
Orbital apex, superior and inferior orbital fissure. Note that the
trochlear nerve lies outside the muscle cone. n., nerve; a., artery;
v., vein; MR, medial rectus; IR, inferior rectus; LR, lateral rectus;
SR, superior rectus; L, levator; SO, superior oblique.
C O MMO N C A U S E S O F
NUCL EAR AND F ASI CUL AR
T HI RD CRANI AL NERVE
PAL SI ES
- with neurological abnormalities
- with aberrant rennervation
- with cyclic oculomotor spasm
Vascular ( AV
S Y MP T O MS O F
O C U L O MO T O R
The classic presenting symptom of a patient with an abnormality
in 3 nerve function are E P A L S Y
Usually masked by drooping of the lid
Blurred monocular vision at near range (rarely)
Complains of enlarged pupil or difficulty in focussing with
involvement of accommodation
Horizontal and/or vertical binocular diplopia, may be recognized
only when the ptotic eyelid is elevated
Limitation of ocular movements
Associated symptoms :
headache, localized pain in the orbit, peri orbital region
Facial or body numbness or weakness
Hearing loss, tinnitus and loss of taste
S I GNS OF
O C U L O MO T O R
Pt osi sN E R ysi s of P A usclS Y
- par al V E LPS mL e.
2. D at i on – out , dow and i nt or t ed –
unopposed act i on of LR and SO
3. O ar m
ovem s :
Adduct i on – M
El evat i on – SR and I O
D essi on – I R
Ext or si on – I R and I O
4. Pupi l i s f i xed and di l at ed – par al ysi s of
sphi nct er pupi l l ae m
5. Accom odat i on i s com et el y l ost – par al ysi s
of ci l i ar y m
ead post ur e – i f t he pupi l l ar y ar ea
i s uncover ed, head t akes a post ur e
consi st ent w t h t he di r ect i ons of
act i ons of t he par al ysed
uscl es, i .e., head i s t ur ned on t he
opposi t e si de, t i l t ed t ow ds t he sam
si de and chi n i s sl i ght l y r ai sed.
DIFFERENTIAL DIAGNOSIS OF
ISOLATED THIRD NERVE PALSY
1. Vasculopathic infarction
2. Vasculitic infarction
3. Compressive lesion
5. Meningeal inflammation
6. Ophthalmoplegic migraine or demyelination
7. Myasthenia gravis
8. Early signs of thyroid disease
9. Generalised myopathic conditions
10. Congenital blepharoptosis
11. Type II Duane’s syndrome
The differential diagnosis of isolated third nerve
palsy is not so lengthy because of the many
structures innervated by the third nerve and the
Nonetheless, if no pain or pupil involvement exists,
myasthenia gravis must be considered.
Restrictive ophthalmopathy may mimic parts of a
third nerve paresis, but does not involve the pupil,
more often presents with lid retraction than ptosis
if thyroid ophthalmopathy is the cause, and often
has other orbital findings.
A supranuclear lesion may involve ptosis and an
elevation deficit, but usually has other associated
deficits that involve midbrain and diencephalic
The patient with a suspected ocular motor nerve
palsy must be observed for obvious ocular
deviation, ptosis, palpebral fissure asymmetry,
lagophthalmos, facial asymmetry, head tilt,
proptosis, conjunctival injection, or chemosis.
During visual assessment, binocularity of the
diplopia is verified by monocular occlusion.
Associated abnormalities of visual acuity, color
vision, or visual fields may be important localizing
If there is ptosis, one must look for lid fatigue or
lid twitch, because these might indicate
The pupils should be assessed for relative size
Special attention must be given to testing
corneal sensation, although several situations,
including chronic contact lens wear, aging,
previous cataract surgery, and concurrent use of
topical medications, may make interpretation
Symmetry of the sensory function of the three
divisions of the trigeminal nerve should be tested with
light touch and pinprick.
Sometimes, subtle asymmetry in sensory function can
be revealed by testing the perception of cold (the flat
side of a piece of metal such as the handle of a reflex
hammer or the end of a tuning fork is usually
First-, seventh-, and eighth-nerve function should
always be tested.
Olfactory pathways can be screened by using coffee
or other substances that have easily identified odors.
Facial nerve function is assessed by having
the patient smile, puff out the
cheeks, forcibly close the eyes, and wrinkle
Simple tests of hearing include the ticking of
a watch, finger rubbing, and whispering
common two-syllable words.
Ocular motility should be assessed monocularly
(ductions) and binocularly (versions and vergence) with
tests of saccadic and pursuit movements.
The extent of movement is ascertained for each of the
nine diagnostic positions of gaze as defined by the
primary actions of the 12 extraocular muscles
The nature and extent of the deviations of the eyes in
relation to each other may be assessed subjectively with
the red glass or Maddox rod and confirmed objectively
by the alternate-cover test.
The latter test with prisms can provide quantifiable
measurements that help to localize the underacting
muscles and allow careful follow-up.
The principal actions of the
extraocular muscles. SR, superior rectus; IO,
inferior oblique; LR, lateral rectus; MR, medial
rectus; IR, inferior rectus; SO, superior oblique.
For a patient with a complaint referable to
cranial nerve dysfunction, the problem must
be approached in an
orderly, logical, and, above all, anatomic
Localization of the lesion helps to determine
the differential diagnosis and subsequent
A B N O R MA L I T I E S I N
T H I R D -N E R V E
F U NCT I ON
Third-nerve palsies may be partial or
complete, congenital or acquired, isolated, or
accompanied by signs of more extensive
They can result from lesions anywhere along
the anatomic pathway from the nucleus to the
Oculomotor nerve palsies present at birth are
presumed secondary to maldevelopment,
intrauterine injury, or birth trauma.
Although relatively rare compared with acquired
lesions, they constitute nearly half of the third-nerve
palsies documented in children.
Typically, they are unilateral and isolated, although
bilaterality and accompanying neurologic signs are
Some degree of ptosis and ophthalmoplegia is the
The pupil is usually involved (either miotic, because of
presumed aberrant regeneration, or dilated), but
pupillary sparing has been noted in some cases.
The location of the lesion probably varies among cases.
The significant occurrence of aberrant regeneration
suggests that some of the lesions are along the
peripheral course of the nerve, but modern
neuroimaging has demonstrated more central loci.
Except in cases of obvious birth trauma in which some
recovery is expected, most congenital oculomotor
nerve palsies are permanent.
Congenital partial third-nerve palsy. Motility photographs (a)
show poor elevation of the right eye in both adduction and
abduction. MRI (b) revealed a lesion in the right midbrain
oculomotor nerve fascicles most consistent with an old
NUCLEAR THIRD NERVE PALSY
Lesions involving the oculomotor nucleus have a particular
constellation of clinical signs reflecting the unique
Although a unilateral, stereotactically placed experimental
lesion could conceivably result in bilateral ptosis,
contralateral superior rectus dysfunction, and
abnormalities of the remaining muscles ipsilaterally, the
clinical picture is more likely that of a complete ipsilateral
oculomotor nerve palsy with additional contralateral
ptosis and superior rectus dysfunction.
If the nuclear lesion is rostral, pupillary involvement is
likely and lid function may be spared.
Conversely, with caudal lesions, bilateral ptosis may
be a prominent or even an isolated finding.
The most common cause of lesions of the
oculomotor nucleus is infarction, usually a result of
thrombotic occlusion of small perforating vessels off
the basilar artery or embolic or thrombotic occlusive
disease of larger vessels (‘top of the basilar’
Other causes to consider include small
intraparenchymal hemorrhage resulting from
presumed vascular malformations, metastatic
neoplasms, and abscesses.
nucleus lesions. A 78year-oldman had
sudden onset of
notable for bilateral
complete ptosis and
no ocular motility
abduction of both
eyes. MRI revealed
bilateral infarction of
the midbrain and
thalami, involving the
region of the thirdnerve nuclei.
FASCICULAR THIRD NERVE
Classically, the feature differentiating fascicular from
peripheral nerve lesions has been the accompanying
neurologic signs reflecting the fascicles’ location within the
parenchyma of the brain stem.
Several syndromes have been recognized, although the
original descriptions and what are now included may differ :
Third-nerve palsy and ipsilateral cerebellar ataxia may
result from involvement of the fascicles and the
brachium conjunctivum (commonly called Nothnagel’s
Oculomotor palsy and contralateral tremor may reflect
a lesion in the region of the red nucleus (commonly
called Benedikt’s syndrome;
and third-nerve dysfunction plus contralateral
hemiparesis implicates involvement of the ipsilateral
cerebral peduncle (commonly called Weber’s
syndrome, but the eponym may actually have been
originally applied to a variant of the dorsal midbrain
Cross-section of the midbrain at the level of the
oculomotor nerves depicting the location of lesions responsible for
Weber’s syndrome (1) and Benedikt’s syndrome (2).
Infarction causing Weber’s syndrome. The patient was a 70-year-old woman with sudden onset of
a right oculomotor nerve palsy and left hemiparesis. MRI (a) axial view; (b) coronal view; revealed a
hyperintense T2 lesion (arrows) in the right midbrain involving the oculomotor nerve fascicles and
the cerebral peduncle.
With the advent of more sensitive neuroimaging tests such
as magnetic resonance imaging (MRI), isolated and even
pupil sparing oculomotor nerve dysfunction has been shown
to result occasionally from fascicular lesions.
MRI has also demonstrated that a lesion of the fascicles can
cause isolated dysfunction of either the superior or inferior
division of the third nerve.
This suggests that functional organization of the oculomotor
nerve into divisions may occur before the anatomic
separation seen grossly within the anterior cavernous sinus.
The causes of fascicular oculomotor nerve
lesions are nearly identical to those of
lesions of the nuclear complex, with vascular
causes heading the list, followed by
infiltrative and inflammatory causes.
Because the fascicles are white matter
tracts, the diagnosis of multiple sclerosis
must also be considered
involving the right
midbrain and optic
tract. The patient, a 34year-old woman, had
including a right thirdnerve palsy, a left
hemiparesis, and a left
LESIONS IN SUBARACHNOID SPACE
Third-nerve involvement in the subarachnoid
space is more often presumed clinically than
demonstrated pathologically or with
The subarachnoid space is the most likely site of
injury in cases of isolated oculomotor palsies.
Involvement may be partial or complete,
although most commonly there is progression
to total involvement over time.
Because of the dorsal and peripheral location
of the pupillary fibers, a dilated pupil may be
the first sign of a compressive lesion in the
A common cause of an isolated oculomotor
nerve palsy with pupillary involvement in
adults is an intracranial aneurysm, typically
situated at the junction of the posterior
communicating and internal carotid arteries.
an aneurysm of
Posterior communicating artery aneurysm causing a third-nerve palsy.
The patient was an otherwise quite healthy 85- year-old woman who
presented with headache, diplopia, and ptosis and was found to have a
right pupil-involved oculomotor nerve palsy. MRI with and without
gadolinium was normal but magnetic resonance angiography (a)
revealed a posterior communicating artery aneurysm (arrow), which
was confirmed by cerebral angiography (b).
Almost without exception, there is pain (although
sometimes modest) and eventually other
evidence of oculomotor nerve involvement.
Other locations of aneurysmal dilatation that have
been shown to cause third-nerve palsies include
the top of the basilar artery and the junction of the
basilar and superior cerebellar arteries.
Diabetic ‘microvascular’ oculomotor palsies are
also commonly painful and can have pupil
involvement in 10–38% of cases, although usually
the degree of aniosocoria is 1 mm or less.
Other causes of oculomotor nerve dysfunction
in the subarachnoid space include compressive
or infiltrating neoplasms or inflammatory
lesions, meningitis (infectious, inflammatory,
or neoplastic), compression by large
dolichoectatic vessels or cerebral structures
shifted by expanding supratentorial lesions or
edema, and trauma.
With the advent of more sensitive neuroimaging, many cases of
idiopathic third nerve palsy, either permanent or recurrent, and
so-called ‘ophthalmoplegic migraine’, have been revealed to be
the result of intrinsic lesions of the oculomotor nerve, likely
benign schwannomas, cavernomas, inflammation and
The trauma necessary for third-nerve damage is typically severe
enough to have caused skull fractures and loss of consciousness.
Beware the oculomotor palsy apparent after minor trauma,
because it may reflect an underlying mass lesion or aneurysm.
Third-nerve dysfunction may be a component of a generalized
polyneuropathy or the Fisher variant of the Guillain–Barré
LESIONS IN CAVERNOUS SINUS
There are no specific distinguishing features of
third-nerve involvement in the cavernous sinus.
Although bifurcation of the nerve into its two
divisions typically occurs in the anterior cavernous
sinus, there is evidence that a functional bifurcation
occurs more proximally along the course of the
oculomotor nerve, probably within the brain stem,
making localization of a divisional paresis
To identify clinically a cavernous sinus location of an
oculomotor nerve palsy, one must note the
company it keeps.
Dysfunction of the trochlear and abducens nerves, the first
or second division of the trigeminal nerve, the
oculosympathetics, and the venous drainage of the eye and
orbit may be apparent.
Pain may be a prominent feature.
The pupil may be small or midsized and poorly reactive
because of concurrent oculosympathetic involvement.
Causes include neoplasms (pituitary
tumors, craniopharyngioma, meningioma , nasopharyngeal
carcinoma, schwannoma, metastatic
lesions), inflammations (Tolosa–Hunt, sarcoid), aneurysmal
compression, ischemia, cavernous sinus thrombosis, and
Cavernous sinus meningioma causing a partial third-nerve palsy. The patient was a 42
year-old woman who had left ptosis and both horizontal and vertical diplopia for 3
weeks. Examination revealed a partial left third-nerve palsy. MRI (a) axial; (b) coronal;
showed a uniformly enhancing mass of the left cavernous sinus, encasing the left
intracavernous carotid artery (arrow), consistent with a meningioma, which was
confirmed by biopsy.
LESIONS IN ORBIT
Orbital lesions may cause third-nerve palsies
that respect the anatomic bifurcation of the
nerve or that reflect individual muscle
Commonly associated clinical features include
proptosis and visual loss.
Causes include trauma, neoplasms, mucoceles,
vascular malformations, and inflammation.
Most studies reviewing the causes of oculomotor nerve
palsies do not distinguish isolated from nonisolated
palsies, nor do they list causes by location.
A large number of cases are recorded as of
‘undetermined’ cause and a still larger proportion, those of
presumed ischemic origin, remain of uncertain location.
Newer, more sensitive neuroimaging modalities, such as
MRI, are localizing more of these lesions and even
providing clues about pathogenesis, but most third-nerve
palsies remain poorly characterized.
Ischemic lesions causing oculomotor nerve
palsies were believed to occur most frequently
along the nerve’s subarachnoid or intracavernous
course, although fascicular involvement was later
demonstrated in some cases.
Conditions frequently associated with third-nerve
dysfunction include diabetes mellitus and
hypertension, and, more rarely hypertension,
giant cell arteritis, carotid occlusion and
dissection, systemic lupus erythematosus, and
The site of third nerve involvement in ‘viral’
syndromes remains unknown.
The phenomenon of ‘pupillary sparing’ bears special
True pupillary sparing implies that each of the
extraocular muscles innervated by the oculomotor
nerve is involved to some extent, but the pupil
remains of normal size and reactivity.
Oculomotor nerve palsies without dysfunction of all
of the muscles innervated by the third nerve that also
do not involve the pupil are not ‘pupillary sparing’.
The distinction becomes important in management.
The cause of most isolated pupil-sparing third-nerve
palsies is believed to be microvascular ischemia,
frequently associated with diabetes mellitus or other
vascular risk factors.
The explanation for this may be anatomic in that the
peripherally located pupillary fibers may receive more
collateral blood than the main nerve trunk.
Microvascular third-nerve palsies may be quite painful
but usually resolve after 2–4 months.
Rarely, isolated pupilsparing oculomotor nerve palsies
may be secondary to compressive lesions, although the
majority of these cases have incomplete palsies.
Cy c l i c a l
This is an uncommon but dramatic condition typically
O c u l o mo t o r
seen in patients with congenital third-nerve palsies.
Pa r e s i s
The classic scenario is that of baseline paresis alternating
with episodes lasting seconds of miosis, increased
accommodation, elevation of the ptotic upper lid, and
adduction of the eye.
In some cases, the spasms can be brought on by
voluntary efforts in the direction of paretic muscles.
The cause is unknown, but most authors speculate some
element of aberrant regeneration after nerve or nuclear
damage, similar to proposed mechanisms of ocular
Ab e r r a n t
Re g e n e r a t i o n
Although this phenomenon has been demonstrated or
suspected in virtually every peripheral nerve that has had partial
damage, the oculomotor nerve is particularly interesting in this
regard because of its many branches and target structures.
Signs include elevation of the upper lid with attempted
downgaze (pseudo-Graefe’s sign), upgaze, or adduction;
segmental constriction of the pupil with movement in the
direction of action of muscles innervated by the third nerve;
retraction of the globe with attempted vertical gaze
(presumably secondary to co-contraction of the superior and
inferior rectus muscles); and adduction of the eye with
attempted up- or downgaze.
Rarely, when both oculomotor and abducens
nerves are damaged, aberrant regeneration
may be of the abducens fibers into the
oculomotor nerve pathways.
Oculomotor synkinesis is generally believed
to reflect the misdirection of regenerating
fibers after partial damage to the peripheral
portion of the nerve.
However, other theories involving more
central mechanisms have been proposed.
A pseudo-Graefe sign is
shown in a patient with a
right cavernous sinus
aneurysm and aberrant
regeneration of branches of
the third nerve. On attempted
downgaze (bottom), the
right lid elevates.
Oculomotor nerve synkinesis is most commonly
seen 2–3 months after injury to the nerve by
trauma or compression resulting from
aneurysms or tumors. Ischemic lesions (i.e.,
secondary to diabetes) rarely if ever result in
aberrant regeneration, and the presence of
synkinesis requires a careful search for a
Slowly growing mass lesions are likely to be
responsible for the phenomenon of ‘primary’
oculomotor nerve synkinesis, in which a
recognizable paretic phase does not precede
development of the aberrant movements.
N e u r o my o t o n i a
Episodic involuntary contractions of the muscles
innervated by the oculomotor nerve have been
described in patients with and without baseline ocular
The contractions are brief and myotonic and can
sometimes be brought on by looking in the direction of
action of the involved muscle.
Most of these patients have a history of radiation
therapy to either the parenchymal or the peripheral
course of the ocular motor nerves.
Neuromyotonia of the fourth and sixth cranial nerves
has also been reported.
Neuromyotonia may respond to membrane-stabilizing
agents, such as carbamazepine.
An evaluation of the patient with a third-
nerve palsy depends on the associated
symptoms and signs, the pattern of
oculomotor nerve involvement, and the age
of the patient.
Ev a l ua t i on of Thi r dNe r v e Dy s f u n c t i o n
If the patient has findings localizable to the nerve’s nuclear
or fascicular course within the brain stem, MRI or at least
high-resolution computed tomography(CT) is indicated .
Accompanying meningeal signs (e.g., global headache, stiff
neck, and depressed level of consciousness) or other cranial
nerve involvement, especially if bilateral, should prompt
cerebrospinal fluid examination.
Localization to the cavernous sinus warrants neuroimaging,
preferably MRI with gadolinium.
High-resolution CT with thin coronal and axial views, after
the administration of a contrast agent, or MRI with fat
suppression techniques without and with gadolinium, is
indicated if an orbital locus is suspected.
Hemorrhage into a midbraincavernous hemangioma. A 30year-old man had sudden onset of diplopia, incoordination,
and poor tandem gait and was noted to have a partial
oculomotor nerve palsy in the right eye involving primarily the
inferior rectus. MRI (a) axial; (b) sagittal; revealed a
hemorrhage in the right midbrain.
The approach to the patient with an isolated third-nerve
palsy differs among clinicians, and some of the issues
The sudden onset of a painful third-nerve palsy with
associated meningeal signs demands an emergent
neurologic evaluation, regardless of the patient’s age or
the extent of third-nerve involvement, including those that
spare pupillary function.
The work-up should include CT without contrast (looking
for blood in the subarachnoid space), followed by CT with
intravenous contrast or, preferably, MRI with gadolinium
(looking for an intracranial aneurysm or alternative cause
of oculomotor nerve palsy).
If no cause for the third nerve palsy is found, one
must proceed in this setting to vascular imaging.
CT alone misses many cerebral aneurysms, and
MRI is more sensitive than CT but is still not
adequate to rule out the presence of a clinically
Magnetic resonance angiography (MRA) provides a
more sensitive noninvasive means of screening for
intracranial aneurysms With the appropriate
techniques, especially in combination with
conventional MRI, aneurysms of a size sufficient to
cause third nerve compression and to be at risk of
rupture will be detected more than 98% of the
However, small aneurysms can rupture, and the consequences of
missing even 1.5% of intracranial aneurysms are potentially grave.
Computed tomographic angiography (CTA), if performed and
interpreted by a skilled neuroradiologist, will detect most
aneurysms large enough to cause third nerve palsies, and the
combination of well-performed and wellinterpreted MRA and CTA
may be sufficient to replace catheter angiography in the
investigation of cerebral aneurysms.
Although most aneurysms are seen by angiography of the
ipsilateral carotid circulation, the basilar circulation must also be
studied to exclude a more posterior location.
The contralateral carotid circulation should also be evaluated,
because ~20% of patients have more than one aneurysm.
All patients younger than 50 years who present with
an isolated third-nerve palsy of any extent should
also have a complete neurologic evaluation,
including a cerebral angiogram if CT or MRI does not
reveal the etiology.
There is some controversy about the application of
this rule to children younger than 10 years, in whom
aneurysms are extremely rare.
Patients older than 50 years who present with an
isolated, pupil-sparing, but otherwise complete
third-nerve palsy, even in the presence of pain, can
usually be assumed to have an ischemic neuropathy.
Minimal work-up for the known diabetic patient
would consist of a measurement of systemic blood
pressure, serum glucose, erythrocyte sedimentation
rate and C-reactive protein.
If there is no history of diabetes, a glucose tolerance
test or a serum hemoglobin A1c level should be
These patients must be observed closely for the next
week for evidence of pupillary involvement.
Some authors argue that even these patients require
some form of initial neuroimaging, preferably MRI.
The patient older than 50 years with an isolated complete
oculomotor nerve palsy with some pupillary involvement or
a partial third-nerve palsy presents the most difficult
All of these patients should have at least the minimal blood
work-up outlined earlier and a neuroimage
obtained, preferably MRI of the brain without and with
The majority of these patients will need vascular
imaging, MRA or CTA or both.
Whether to pursue catheter angiography will depend on the
level of suspicion for an aneurysm and the quality of the
noninvasive vascular imaging and the skill and experience
of its interpreter.
The majority of ischemic third-nerve palsies resolve
within 3 months.
Compressive or traumatic oculomotor nerve palsies
may take longer to improve, and incomplete
recovery with or without synkinesis is more likely.
Despite rare reports of continued improvement in
third-nerve palsies years after onset, once the deficit
has stabilized (usually within 6 months after injury),
further recovery is unlikely.
The chronic oculomotor palsy, especially in younger
age groups, requires serial neuroimaging over the
years, especially as the sensitivity of the techniques
Diabetic third-nerve palsy . The patient was a 62-year-old man with insulindependen
diabetes mellitus and new-onse diplopia and complete left ptosis. Examinatio 2
weeks after symptom onset (a) showe resolution of the ptosis, but nearly complet
deficits of adduction, elevation and depressio of the left eye, and equal and reactive
Six weeks later (b) his motility had become completely normal.
Microvascular third-nerve palsies, especially in
diabetics, may be exquisitely painful during the
acute phase. Intense pain may require
analgesics for 1–2 weeks.
Various surgical procedures have been used to provide binocular
fusion in at least primary position after third-nerve palsy and to
correct vision-limiting or cosmetically annoying upper lid ptosis.
However, complete oculomotor nerve palsies rarely allow a
completely satisfactory surgical result.
The Scott procedure (transposition of the insertion of the superior
oblique tendon to a point anterior and medial to the insertion of the
superior rectus muscle without trochleotomy) combined with large
recessions of the lateral rectus muscle and, occasionally, recessionresection procedures of horizontal rectus muscles of noninvolved
eyes can result in a satisfactory cosmetic outcome and alignment in
primary position in some cases.
The role of botulinum toxin injection in the management of acute or
chronic third-nerve paresis has not been adequately investigated.