Third Nerve Palsy (Oculomotor Nerve Palsy)

Updated: Jan 06, 2022
Author: Fiona Costello, MD, FRCP; Chief Editor: Andrew G Lee, MD 



The oculomotor (third) cranial nerve plays an important role in the efferent visual system by controlling ipsilateral eye movements, pupil constriction, and upper eyelid elevation. Accordingly, damage to the third cranial nerve may cause diplopia, pupil mydriasis, and/or upper eyelid ptosis. The clinical manifestations of third cranial nerve dysfunction reflect its constituent parts. Outer parasympathetic fibers supply the ciliary muscles of the eye and the sphincter pupillae (sphincter muscles that cause pupillary constriction). The inner somatic fibers of the third cranial nerve supply the levator palpebrae superioris in the eyelid (controlling upper eyelid elevation), and four extraocular muscles that govern ocular motility (the superior, medial, and inferior recti muscles, and the inferior oblique muscle).[1, 2, 3, 4, 5]  Classically, third cranial nerve impairment is associated with a “down and out” appearance of the ipsilateral eye (Figure 1). This eye position reflects the unopposed actions of depression and abduction of the globe, which are governed by superior oblique (innervated by the fourth cranial nerve) and lateral rectus (innervated by the sixth cranial nerve) muscles, respectively. Localizing an isolated third cranial nerve palsy, particularly one that causes a “down and out” position of the ipsilateral eye is relatively straightforward when there is complete involvement of the levator palpebrae superioris (causing complete ptosis), complete paralysis of innervated extraocular muscles, and complete pupillary mydriasis. In reality, however, third cranial nerve palsies are often incomplete and result in partial deficits that may be relatively subtle and easily overlooked (Figure 2). For this reason, it is imperative to carefully establish a good history and perform a thorough examination to localize third cranial nerve lesions, which may herald vision and life-threatening problems. 

Illustration of a complete right oculomotor palsy Illustration of a complete right oculomotor palsy demonstrating the classic "down and out" appearance, complete ptosis and mydriasis of the right eye. Courtesy of Tyler Henry, MD, Medical Illustrator (


Illustration of a partial right oculomotor nerve p Illustration of a partial right oculomotor nerve palsy demonstrating incomplete ptosis, hypotropia and mydriasis of the right eye. Courtesy of Tyler Henry, MD, Medical Illustrator (



The third cranial nerve, alternatively known as the oculomotor nerve, has multiple important functions. Owing to its elegant anatomical organization and course, third cranial nerve deficits can be readily localised to specific site (nucleus, fascicular portion, cavernous sinus segment, or orbit), depending on the pattern of oculomotor dysfunction observed and associated clinical findings. Broadly speaking, nuclear third cranial nerve palsies may be isolated, or accompanied by other neurologic symptoms given the proximity of the oculomotor nucleus to other important structures in the midbrain tegmentum.[1, 2, 3, 4]  The fascicular portion of the oculomotor nerve courses ventrally from the nucleus in the midbrain, crosses through the red nucleus near the corticospinal tract, and emerges from the medial aspect of the cerebral peduncle (Figure 3).[4]  Its close proximity to other midbrain structures means that fascicular lesions often co-associate with neurological findings, in addition to oculomotor palsy.[4]  The cisternal portion of the third cranial nerve travels in the subarachnoid space anterior to the midbrain after exiting between the superior cerebellar and posterior cerebral arteries (Figure 3). Here, it is vulnerable to compressive effects from vascular lesions, such as aneurysms (Figure 4). The oculomotor nerve runs through the lateral wall of the cavernous sinus.[4]  Lesions of the cavernous sinus often produce third nerve palsies that are accompanied by one or more other neurologic findings including palsies of the fourth, fifth (first division), and sixth cranial nerves, with or without an associated Horner syndrome.[4]  Finally, the oculomotor nerve enters the orbit through the superior orbital fissure adjacent to the fourth cranial nerve. Usually, the third cranial nerve branches into superior and inferior divisions within the posterior orbit, but, occasionally, divisional branching occurs in cavernous sinus. The superior division of the third cranial nerve innervates the levator palpebrae and the superior rectus muscles.  The inferior division innervates all the other muscles innervated by the third nerve, and supplies the preganglionic parasympathetic fibers to the ciliary ganglion, which in turn innervate the iris sphincter.[4]  As a general rule of thumb, orbital lesions may be associated with other clinical signs such as proptosis, which can help in the localization process.  A more detailed description regarding how anatomical site of injury impacts third cranial nerve function is discussed in the sub-section ”Localizing Third Cranial Nerve Palsies: How Does Form Affect Function?”


Anatomy of the oculomotor nerve. Courtesy of Tyler Anatomy of the oculomotor nerve. Courtesy of Tyler Henry, MD, Medical Illustrator (




In a recent population-based cohort study by Fang and colleagues[6] , 145 cases of acquired third cranial nerve palsy diagnosed over a 37-year period in Olmsted County, Minnesota were assessed. The age- and sex-adjusted annual incidence of acquired third nerve palsy was 4.0 per 100 000.[6]  Not surprisingly, the annual incidence was higher in older patients (aged greater than 60 years) relative to younger patients (12.5 vs 1.7 per 100 000; difference, 10.8 per 100 000; P < .001).[6]  This observation likely reflected the higher predilection for microvascular ischemic third nerve cranial nerve palsies in older versus younger adults.[6]  In this study, the most common causes of acquired third nerve palsy were presumed microvascular injury (42%), trauma (12%), compression (from neoplastic lesions) (11%), post-operative neurosurgical cases (10%), and aneurysmal compression (6%).[6]  Notably, 10 patients (17%) with microvascular ischemic third nerve palsies had pupil involvement, whereas pupil involvement was seen in not all, but only 16 patients (64%) with compressive third nerve palsies.[6] The findings from Fang et al [6]  bear careful consideration, because although compressive lesions had a higher likelihood of pupil involvement, pupil involvement did not exclude microvascular third nerve palsy; moreover, lack thereof did not rule out potentially life-threatening causes of compressive third nerve palsy. 


The morbidity and mortality caused by third cranial nerve palsies are intrinsically linked to etiology, the details of which are beyond the scope of this article. 

That said, several important causes of mortality and morbidity presenting with evidence of oculomotor dysfunction include: subarachnoid hemorrhage from a ruptured aneurysm of the posterior communicating artery, meningitis, and infiltrative meningeal processes.[4]


The overall prognosis of any oculomotor palsy depends on the etiology. Post-traumatic, post-infectious, post-inflammatory, and ischemic oculomotor palsies may spontaneously recover to a variable degree.[4]  Compressive lesions (including aneurysm or tumor) may also improve or resolve after appropriate surgical intervention.[4]  Cause notwithstanding, patients with chronic and stable ptosis or ophthalmoplegia due to oculomotor nerve palsy may benefit from reconstructive lid or strabismus surgery over the course of their follow up.[4]

Patient Education

Patients should be informed regarding potentially life-threatening causes of an acquired third cranial nerve palsy, appropriately weighted to the context of their case.  Accordingly, they should undergo appropriate evaluation and treatment of their third cranial nerve palsy in a manner that is tailored to their needs. Finally, patients should be provided information that facilitates a good understanding regarding the implications of their diagnosis and prognosis for recovery. 




Patients with third cranial nerve lesions may report anisocoria owing to the effects of dysfunctional pupillary constriction, and/or ptosis, yet mild ptosis and pupillary mydriasis are often asymptomatic findings noted on the clinical examination, and may not be problems that prompt patients to seek immediate medical attention. Diplopia (double vision), however, can be highly disabling and disruptive to activities of daily living such as driving.  Thus, patients with diplopia often present for evaluation. Since the third cranial nerve controls elevation (by innervating the superior rectus and inferior oblique muscles), adduction (medial rectus), and depression (inferior rectus) of the ipsilateral eye, patients may report symptoms of both binocular horizontal and vertical diplopia.  A carefully obtained history can help localize the cause of diplopia caused by third cranial nerve dysfunction, and also exclude potential clinical mimics (Table 1).

Table 1: Details from the Clinical History that Help Localize a Third Cranial Nerve Palsy (Open Table in a new window)


Clinical Relevance

Nature of Diplopia (Binocular versus Monocular; Horizontal versus Vertical or Oblique)

Binocular diplopia reflects ocular misalignment whereas monocular diplopia implicates an anterior segment issue, or retinal abnormality.  Ask the patient to alternately occlude each eye to localize the nature of the diplopia.


Third cranial nerve palsies can cause variable patterns of diplopia, and manifestations of horizontal and vertical misalignment will reflect to what extent elevation, adduction, and depression of the eye are impaired. Diplopia is typically worse in the gaze direction of weakest muscle action.

Intermittent or Constant

Intermittent diplopia may be gaze directional or reflect a breakdown of binocular fusional control. In the case of a neuromuscular junction mimicking a third cranial nerve palsy, the diplopia may be truly intermittent.

Associated Symptoms (Pain and Other Systemic Complaints)

Inflammatory and compressive causes of third cranial nerve palsy may be associated with pain, whereas microvascular ischemic lesions are less commonly painful.  Patients older than 50 years may experience third cranial nerve palsies secondary to giant cell arteritis (GCA); therefore, asking about transient vision loss, headache, scalp pain, weight loss, muscle aches, and jaw claudication are important facets of the history to explore so as not to miss this vision-threatening/life threatening diagnosis.


Abrupt onset cranial third nerve palsies suggest a vascular etiology (pituitary apoplexy, subarachnoid hemorrhage) whereas compressive lesions may cause more insidious onset of deficits.

Progression and Course

Progressive worsening of third cranial nerve palsies may be seen with compressive lesions. Progressive improvement over weeks to months after acute onset symptomatology (diplopia) may implicate an ischemic cranial nerve palsy.


Prominent fatigue and variability with respect to ptosis and diplopia often implicate a neuromuscular junction abnormality in lieu of a third cranial nerve palsy.

Other Neurological Manifestations

Localizing brainstem findings such as a third cranial nerve palsy and contralateral weakness (Weber syndrome) can help localize a midbrain lesion such as stroke, whereas multiple cranial nerve palsies that are slowly progressive can implicate a chronic compressive lesion (aneurysm, meningioma) of the cavernous sinus. Multiple cranial nerve palsies with vision loss in the ipsilateral eye can implicate a lesion of the orbital apex.


Underlying diagnoses such as diabetes, pituitary macroadenomas, and multiple sclerosis can help localize the cause of third nerve palsies, when known. Systemic conditions such as Grave’s Disease can cause a restrictive orbitopathy which may mimic manifestations of a third cranial nerve palsy.


Some medications such as immune check point inhibitors (inflammatory), vaccinations (inflammatory), tumor necrosis factor alpha inhibitors (demyelinating), and bisphosphonates (inflammatory) may cause manifestations of third nerve palsies or, in the case of restrictive orbital lesions, mimic third nerve palsies.

Prior Strabismus

Patients with a prior history of strabismus with or without surgery might be interpreted to have an acquired third nerve palsy if they are symptomatic for loss of fusional control.


Patients with a history of  what was previously called "ophthalmoplegic migraine" may experience recurrent painful stereotyped third cranial nerve palsies over time.


It can be challenging for many physicians to localize a third cranial nerve palsy on examination, particularly when there is partial involvement of muscle, upper eyelid, and/or pupil. Thirty-five percent of neurological diagnosis are not rendered in acute care settings,[7, 8]  and ocular motility findings may be hard for non-eye care specialists to decipher. In emergency room settings, 59% of cases requiring an eye examination have significant omissions in terms of clinical evaluation as compared with only 8% of eye casualty (urgent ophthalmology) records.[7, 9]  To aid localization, it is first important to determine if a third cranial nerve palsy is isolated or part of a larger constellation of clinical manifestations. Table 2 outlines relevant examination findings that can help localize the cause of an acquired third cranial nerve palsy.


Table 2:  Examination Findings that Can Help Localize a Third Cranial Nerve Palsy (Open Table in a new window)

Examination Finding

Clinical Relevance

Afferent Examination

Visual Acuity

Evidence of vision loss with a third cranial nerve palsy may implicate a common underlying mechanism such as papilledema, or localize lesions in the sellar region (pituitary apoplexy) or orbital apex.

Pupils (Efferent and Afferent Functions)

Evidence of anisocoria, with a mydriatic pupil or tonic pupil with light near dissociation ipsilateral to the third cranial nerve palsy will help localize the lesion; the presence of a concomitant ipsilateral relative afferent pupil defect may implicate a lesion of the orbital apex.

Color Vision 

Color vision loss disproportionate to high contrast visual acuity deficits may implicate a third cranial nerve palsy and ipsilateral optic neuropathy.

Fundus Examination

Evidence of optic atrophy (compressive lesion) or optic disc edema (anterior ischemic optic neuropathy or papilledema) may help localize the lesion or mechanism causing the third cranial nerve palsy.


The presence of focal visual deficits ipsilateral to the third cranial nerve palsy might suggest an orbital apex syndrome, whereas enlarged blind spots might implicate raised intracranial pressure with papilledema. A bitemporal defect suggests a lesion of the sellar region (pituitary tumor) with cavernous sinus involvement.

Efferent Examination


Evidence of ptosis suggests a third cranial nerve palsy. Orbital signs such as proptosis and arterialized conjunctival vessels, might suggest an orbital process mimicking a third nerve palsy due to muscle restriction, including Grave’s Disease, orbital inflammation, orbital infiltration, or a carotid cavernous sinus fistula (CCF).

Ocular Motility

An isolated third cranial nerve palsy may cause variable ipsilateral involvement of the superior, inferior, and medial recti muscles and/or inferior oblique muscle. Multiple cranial nerve palsies might indicate lesions of the brainstem, cavernous sinus, skull base, or a more generalized peripheral nerve process such as Miller Fisher Syndrome. 

Aberrant Regeneration

Signs of aberrant regeneration involving the lid, pupil, and muscles innervated by the third cranial nerve can be seen with chronic compressive lesions in the cavernous sinus, and in the setting of what has previously been called “ophthalmoplegic migraine”.

Lid Function

Ipsilateral ptosis is localizing for a third cranial nerve palsy. Weakness of eye closure can be seen with myasthenia gravis and in patients with multiple cranial neuropathies (ie, Miller Fisher Syndrome) 

Fatigue Testing

Evidence of fatigability and variability (and Cogan’s lid twitch sign) on the examination suggests a neuromuscular junction abnormality.

Ice Test

After ice application, improvement of ptosis suggests a disorder of the neuromuscular junction as a possible mimic of a third cranial nerve palsy


Blood Pressure

Systemic hypertension may implicate vascular risk factors linked to microvascular ischemic third cranial nerve palsy.

Physical Examination

Localizing Third Cranial Nerve Palsies:  How Does Form Affect Function?

As mentioned, the third nerve nucleus is located midline in the midbrain, at the level of the superior colliculus, where it lies ventral to the sylvian aqueduct, separated from it by the periaqueductal grey matter, and dorsal to both medial longitudinal fasciculi (Figure 3).[1, 2, 3, 4]  The nuclear complex is comprised of an unpaired dorsal column (containing the Edinger-Westphal nucleus which mediates pupillary constrictor function, and the subnucleus of the levator palpebrae superioris), and four paired columns.[1, 2]  The most medial of the four paired columns in the nuclear complex innervate the superior recti.[1, 2, 3]  The lateral three paired subnuclei of the oculomotor complex have axons that extend to ipsilateral eye to innervate the inferior rectus, medial rectus, and inferior oblique muscle.[1, 2, 3, 4]

The third cranial nerve traverses the red nucleus before leaving the midbrain anteriorly, medial to the cerebral peduncles.[1, 2, 3]  Once reaching the subarachnoid space, the nerve passes between the superior cerebellar and the posterior cerebral arteries,[1, 2]  where it is vulnerable to compression from vascular lesions such as aneurysms. The oculomotor nerve then courses near the medial uncus of the temporal lobe (where it is vulnerable to compression in cases of uncal herniation) and pierces the dura mater lateral to the posterior clinoid process to enter the lateral wall of the cavernous sinus.[1, 2]  Within the cavernous sinus, the oculomotor nerve lies superior to the trochlear and abducens nerves and medial to the ophthalmic branch of the trigeminal nerve.[1]  The oculomotor nerve reaches the orbit via the superior orbital fissure.[1, 2]  The superior division of the oculomotor nerve supplies the superior rectus and levator muscles.[1, 2]  The inferior division of the third cranial nerve supplies the medial and inferior recti, as well as the inferior oblique and the presynaptic parasympathetic outflow to the ciliary ganglion (sphincter pupillae muscle and ciliary muscle).[1, 2]  Understanding the elegant anatomical organization of the third cranial nerve, from its origin in the oculomotor nucleus through its course to the superior orbital fissure, is germane to localizing the site and nature of lesions that impede its function.

Nuclear and Brainstem Lesions

The oculomotor nucleus and/or fascicles can be damaged with brainstem lesions. Notably, pure unilateral nuclear lesions are quite rare, and less commonly manifest as isolated muscle weakness relative to lesions of the muscle or orbit.[1, 2]  Lesions of the oculomotor nucleus could cause isolated weakness of a muscle innervated by the third cranial nerve, with the exception of the super rectus muscles, levator palpebrae, or pupillary constrictors.[1, 2]  These muscles are often affected bilaterally even with discrete lesions within the oculomotor nucleus.[1, 2] Classic teaching is that nuclear third nerve lesions lead to bilateral variable ptosis (reflecting involvement of the subnucleus of the levator palpebrae superioris), a supraduction deficit of the contralateral eye, and limited adduction and infraduction of the ipsilateral eye with pupillary mydriasis (partial third cranial nerve dysfunction).[1, 2, 10]  These clinical findings reflect the fact that the motor neurons of each subnuclei innervate their corresponding ipsilateral extraocular muscles, except for the superior rectus subnuclei, which innervate the contralateral superior rectus muscle.[11]  The levator palpebrae subnuclei innervate the ipsilateral and contralateral levator palpebrae muscles. Notably, isolated palsies of the inferior rectus have been associated with nuclear lesions affecting the inferior rectus subnucleus.[1, 2]  Moreover, bilateral palsies of the third cranial nerves with sparing of levator function may arise from bilateral nuclei lesions that spare the central caudal levator subnucleus.[1, 2] Isolated ptosis with sparing of the pupillary function and intact ocular motility are features that have been reported with nuclear lesions involving the levator subnucleus, but sparing the rostral oculomotor subnuclei.[1, 2]  Margolin and Freund[10]  have reported that the most common motility deficit in patients with nuclear third nerve palsy is an ipsilateral adduction palsy. Pupillary involvement and bilateral ptosis are less frequently observed.[10]  Nuclear third cranial nerve palsies may manifest with ipsilateral ptosis and contralateral eyelid retraction (Plus Minus Syndrome).[1, 2]  This syndrome is caused by a lesion of the paramedial mesencephalon involving ipsilateral levator function (causing ptosis) and damaging inhibitory fibers to the contralateral levator (causing retraction).[1, 2]  Notably, many patients with nuclear third nerve palsies will have other localizing symptoms and signs of midbrain dysfunction. The most common etiology of the nuclear/fascicular third cranial nerve lesions is ischemia in the territory of the medial mesencephalic branches of the posterior cerebral artery, albeit neoplasms and demyelination are other causative mechanisms.[10]

In clinical practice, third cranial nerve palsies caused by midbrain lesions may co-associate with other neurological deficits. For example, “top of the basilar artery” syndrome (caused by occlusion of the basilar artery resulting in damage to the midbrain, thalamus, and portions of the temporal and occipital lobes) may result in paralysis of vertical gaze, “pseudoabducens” nerve palsies, convergence retraction nystagmus, lid retraction, skew deviation, and pupil abnormalities caused by third nerve nucleus or fascicle involvement. These patients may also manifest hemianopia, cortical blindness, and altered level of consciousness.[12]  Parinaud’s syndrome is caused by lesions of the dorsal midbrain, damaging the superior colliculus, as well as the oculomotor and Edinger Westphal nuclei.[12]  In the setting of Parinaud’s syndrome, third cranial nerve dysfunction may be accompanied by lid retraction, pupillary light near dissociation, upgaze palsy, and convergence retraction nystagmus.[12]  In cases of Weber syndrome, damage to the cerebral peduncle arising from vascular compromise of the paramedian branches of the basilar artery or posterior cerebral artery, may cause ipsilateral third cranial nerve dysfunction with contralateral hemiparesis.[1, 2, 12]  Claude syndrome is caused by posterior cerebral artery occlusion affecting the third cranial nerve, red nucleus, and superior cerebellar peduncle. This results in an ipsilateral third cranial nerve palsy and contralateral ataxia and tremor.[1, 2, 12]  Nothnagel syndrome is akin to Claude syndrome by involving third cranial nerve fascicles and the superior cerebellar peduncle, and causes ipsilateral third cranial nerve palsy and ipsilateral cerebellar ataxia.[13] Finally, Benedikt’s syndrome causes ipsilateral third cranial nerve dysfunction and contralateral involuntary movements; these findings are caused by damage to the third cranial nerve, red nucleus, and substantia nigra due to vascular compromise of the posterior cerebral artery.[1, 2, 12]

Lesions of the Third Nerve Fascicle 

The fascicles of the third nerve exit oculomotor nucleus ventrally (Figure 1) and pass through the red nucleus and cerebral peduncle.[1, 2, 9]  Here, fascicular third nerve involvement is accompanied by localizing brainstem neurologic findings as outlined previously in descriptions of Weber, Nothnagel, Claude and Benedikt syndromes.[12, 13]  Fascicular syndromes occur in concert with nuclear involvement because paramedian branches near the top of the basilar artery supply both the third cranial nerve and its nucleus.[2]  That said, fascicular third nerve palsies due to midbrain infarction are relatively uncommon, compared with other types of fascicular lesions.[14]  Since third cranial nerve fascicles fan out as they course through the midbrain, it is possible to cause dysfunction to certain muscles and spare others.[15]  

Oculomotor nerve damage along its fascicular course can produce varied presentations.[15]  Third nerve palsies with a partial or completely dilated pupil for example, can implicate compressive lesions since pupillo-constrictor fibers occupy a peripheral location in the nerve.[15]  Notably, patients who suffer a subarachnoid hemorrhage from rupture of a posterior communicating artery or superior cerebellar artery aneurysm (Figure 4) often manifest altered level of consciousness, making the examination challenging. Yet, even in the context of a suboptimal clinical examination, the findings of a pupil involving third cranial nerve palsy should be obvious. As mentioned, the eye on the involved side is deviated "down and out" from residual tone in the fourth cranial nerve (superior oblique muscle) and the sixth cranial nerve (lateral rectus muscle). Ipsilateral ptosis may also occur.[15]   

Superior and inferior division oculomotor nerve dysfunction may occur with fascicular lesions in the subarachnoid space.[1, 2, 3, 4] Here, the third cranial nerve is most likely to be affected by microvascular ischemia, albeit damage may also arise from ectatic vessels, tumors, infectious, infiltrative or inflammatory processes affecting the meninges, and trauma.[1, 2, 3, 4]  Along its sub-arachnoid course to the cavernous sinus, the third cranial nerve fascicle courses on the edge of the tentorium cerebelli.[1, 2, 3, 4, 15]  The edge of the uncus overlies the tentorium, thus in cases of increased intracranial pressure, for example, that caused by intracranial hemorrhage, brain herniation may cause displacement of the midbrain and compression of the ipsilateral oculomotor nerve, resulting in ipsilateral ophthalmoplegia and pupillary mydriasis.[1, 2, 3, 4]  Ocular motility dysfunction after anterior temporal lobectomy has been reported to occur in as many as 15% of patients. While the diplopia is most commonly attributed to fourth cranial nerve palsies in this context, the cisternal portion of the oculomotor nerve runs in close proximity to the mesial temporal lobe, thereby making it susceptible to injury from pathological processes within this area.[11]   

Microvascular Third Cranial Nerve Palsies

Older adults (older than 50 years) with vascular risk factors who present with an isolated unilateral pupil-sparing third nerve palsy are often deemed to have a microvascular ischemic process.[7]  Indeed, microvascular ischemia is believed to account for approximately 35% of all third cranial nerve palsies, 17% of all fourth cranial nerve palsies, 28% of all sixth cranial nerve palsies; and 86% of isolated third, fourth, or sixth nerve palsies.[7]  The pathobiological mechanisms believed to contribute to ischemic cranial nerve palsies include the following: alterations in the blood-nerve barrier, hypertrophy of the microvascular basement membrane, and hypoxia in endoneurial space.[7]  Cranial nerve dysfunction may arise from conduction block or demyelination, as opposed to axonal damage, thus explaining the favorable natural history for recovery from microvascular ischemic insults.[7]

Risk factors for microvascular nerve palsies include older age (93% occur in people older than 50 years), hypertension (25%), diabetes (18%), or both hypertension and diabetes (7%).[7]  In 61% of cases, third cranial nerve palsies are associated with orbital pain. Indeed, pain may precede the onset of diplopia by hours to days.[7]  This pain is believed to reflect involvement of the first division of the trigeminal nerve within the cavernous sinus, or activation of trigeminal afferent fibers in the nerve sheath of the third cranial nerve as it courses through the cavernous sinus.[7]  In the setting of microvascular ischemic third cranial nerve palsies, the extent of muscle and upper eyelid involvement may vary; pupillary involvement is less likely to occur relative to compressive lesions.[7]  Lack of pupillary involvement occurs in the setting of ischemia, because the centrally located arterial supply to the nerve is affected, sparing superficially located pupilloconstrictor fibers.[7]  Progression of third cranial nerve deficits may occur over hours to days.  The prognosis for recovery after a microvascular third nerve palsy is generally good, with resolution occurring in 8-12 weeks for most patients.[7]  Notably, however, 15-20% of patients with third cranial nerve palsies don’t experience full recovery.[7]

Lesions of the Cavernous Sinus

The cavernous sinus is a unique anatomical site that contains many critical structures. The oculomotor nerve is housed in the dural fold of the lateral wall and bifurcates into the superior and inferior division of the oculomotor nerve in the anterior cavernous sinus.[1, 2, 3, 4, 16]  The fourth nerve as well as the first and second division of the trigeminal nerve also travel within the lateral wall of the cavernous sinus.[1, 2, 3, 4, 16]  The sixth nerve lies freely within the sinus medially to the lateral wall and inferotemporally to the internal carotid artery. The internal carotid artery travels within the cavernous sinus and brings with it the third-order sympathetic fibers before they “jump” to the sixth nerve and finally travel with the first division of the trigeminal nerve.[1, 2, 3, 4, 16]  The anatomy of the cavernous sinus is critical to understand two classic syndromes that localise to this anatomical region. Parkinson’s sign denotes a sixth nerve palsy accompanied by an ipsilateral Horner syndrome.[17]  The so-called “cavernous sinus syndrome” presents with a combination of ipsilateral ophthalmoplegia (involving the oculomotor nerve, trochlear nerve, abducens nerve), dysautonomia (Horner Syndrome), and sensory paresthesia (V1, V2).[16]  When a patient presents with any combination of these deficits, the clinician must have a strong suspicion of a cavernous sinus lesion. It can be challenging to elucidate a subtle trochlear nerve deficit in the context of a complete oculomotor palsy. The trochlear nerve supplies innervation to the superior oblique muscle, which has its strongest action on the globe in infra-adduction; a position that is unachievable in patients with an oculomotor palsy. In these scenarios, the clinician must carefully assess for intorsion of the globe (primary action of the superior oblique muscle) in attempted downgaze.[18] This can be observed by landmarking conjunctival vessels to help appreciate the torsional movement of the globe. The absence of intorsion signifies a concomitant fourth nerve palsy.[18]

In theory, the main feature that differentiates cavernous sinus lesions from orbital apex lesions is the presence of afferent dysfunction in the latter. This is because the optic nerve does not travel through the cavernous sinus. In reality, many lesions are large enough to affect both anatomical locations. The third cranial nerve is particularly susceptible to compression, as compared with other cranial nerves, as it lies adjacent to the inter-clinoid ligaments above and the petroclinoid ligament below. As such, pituitary adenomas or other lesions of the sellar space can lead to an isolated third cranial nerve palsy. Furthermore, these cases can be challenging clinically, as they are accompanied with a chiasmal pattern of vision loss. This clinical constellation should prompt clinicians to investigate for a sellar lesion with neuroimaging.

There are many causes of cavernous sinus syndrome. A retrospective study of 151 cases of cavernous sinus syndrome found that 30% of cases were caused by tumors, 24% by trauma, and 23% by inflammation (10% of which were characterized as questionable inflammation).[19] Of the tumors causing a cavernous sinus syndrome, nasopharyngeal cancer and pituitary adenoma were the most common.[19]

Orbital Apex Syndrome

The orbital apex is the most posterior part of the orbit and is located at the junction of the four orbital walls.[20]  Within the orbital apex, the optic canal lies medially to the superior orbital fissure.[20]  The superior orbital fissure is divided into the extraconal space and the intraconal space by the annulus of Zinn. The contents of the extraconal superior orbital fissure include the lacrimal nerve, the frontal nerve that originate from the first division of the trigeminal nerve as well as the trochlear nerve and the superior ophthalmic vein.[20]  The acronym LOFT (Lacrimal, Ophthalmic Vein, Frontal Nerve, Trochlear Nerve) can be helpful in remembering the contents of this compartment. The contents of the intraconal space include the superior and inferior divisions of the oculomotor nerve, the nasociliary nerve, the ocular sympathetic supply, and the abducens nerve. It can be helpful to recall the anatomical structures in this anatomical location with th mnemonic “3n3=6” (superior division of the third cranial nerve, the nasociliary nerve, the inferior division of the third cranial nerve, and the abducens nerve). 

The orbital apex syndrome shares many of the features seen in the cavernous sinus syndrome. This includes involvement of the oculomotor, trochlear and abducens nerves along with dysfunction of the first division of the trigeminal nerve. What defines the orbital apex syndrome is the afferent visual function impairment that results from optic nerve compression due to the anatomical positioning of the superior orbital fissure and the optic canal at the tip of the orbital apex.[20]

Superior Orbital Fissure Syndrome

Differentiating between a cavernous sinus syndrome, orbital apex syndrome, and superior orbital fissure syndrome can be challenging.[21] Similar to the cavernous sinus syndrome, the optic nerve is not involved in the superior orbital fissure syndrome. The main differentiator between a cavernous sinus syndrome and a superior orbital fissure syndrome lies in the involvement of the second division of the trigeminal nerve. The second division of the trigeminal nerve penetrates the orbit through the inferior orbital fissure and is uninvolved in a superior orbital fissure syndrome. It is important for the clinician to check sensation over the V2 distribution to differentiate between these two entities.[21]  Compared with the cavernous sinus, the orbit is more prone to inflammatory and infectious pathologies. Localization of lesions to the orbital apex or superior orbital fissure warrants investigations for vasculitic (IgG4 disease) and infectious entities such as mucormycosis and aspergillosis. 

Table 3: Localization and Differentiation Between the Cavernous Sinus Syndrome, Orbital Apex Syndrome and the Superior Orbital Fissure Syndrome.

Table. (Open Table in a new window)


Cranial Nerve Involved

Clinical Pearl

Cavernous Sinus Syndrome

CNIII, CNIV, CNV1, CNV1, CNV2 (posterior), sympathetic innervation

CNII spared

Orbital Apex Syndrome



Superior Orbital Fissure Syndrome


CNII spared, CNV2 spared

Orbital Lesions

Orbital causes of an oculomotor palsy are often associated with orbital signs of dysfunction, inflammation, or congestion. The clinician should assess the patient for the following signs: 

  • Proptosis should be measured qualitatively (worms eye view) or quantitatively (Hertel or Naugle Exophthalmometer). 
  • Retropulsion should be measured by pressing on the globe and noting the resistance to posterior displacement. 
  • Chemosis and injection of the conjunctiva
  • Lid Swelling

Lesions in the orbit commonly cause afferent dysfunction accompanied by oculomotor, trochlear and/or abducens nerve palsies. Localizing an oculomotor palsy to the orbit is aided by the fact that the oculomotor nerve is divided into a superior and inferior branch within the orbit. This division can lead to partial oculomotor nerve palsies that may only affect the superior division (levator palpebrae superioris and superior rectus) or the inferior division (inferior rectus, inferior oblique, medial rectus, ciliary ganglion) of the oculomotor nerve. The most common etiologies of orbital oculomotor palsies include trauma, masses, inflammation, infection and infiltrative processes.[12, 20]



There are many causes of an acquired third nerve palsy. In the nuclear location and fascicular midbrain segments, etiologies include the following: infarction, hemorrhage, neoplasm, and abscess.[4]  The subarachnoid fascicular segment of the third cranial nerve may be damaged by aneurysm, infectious meningitis, infiltrative processes [carcinomatous/lymphomatous/leukemic infiltration, granulomatous inflammation (sarcoidosis, lymphomatoid granulomatosis, granulomatosis with polyangiitis], and the formerly known ophthalmoplegic migraine.[4]  Within the cavernous sinus, the third cranial nerve may be compressed by pituitary adenomas (with or without apoplexy), meningiomas, craniopharyngiomas, metastatic carcinomas, and intra-cavernous carotid artery aneurysms. Other cavernous sinus lesions that may present with oculomotor nerve dysfunction include the following: carotid artery-cavernous sinus fistulas (CCFs), carotid dural branch-cavernous sinus fistulas, cavernous sinus thrombosis, microvascular ischemic lesions, and inflammatory conditions such as Tolosa-Hunt syndrome (idiopathic or granulomatous inflammation). The third cranial nerve may be involved in orbital syndromes of an inflammatory nature [idiopathic orbital inflammatory syndrome (orbital pseudotumor, orbital myositis)], tumors, lymphangiomas, infiltrative lesions, and meningiomas.[4]

Differential Diagnoses 

Aside from causes of an acquired third nerve dysfunction outlined in this section there are clinical syndromes which can cause diagnostic confusion, because they have a similar clinical presentation not involving the oculomotor nerve, but instead involving extraocular muscles and the neuromuscular junction. Common causes for diagnostic uncertainty include the following: acquired exotropia, apex orbital fracture, CCFs, chronic progressive external ophthalmoplegia (CPEO), congenital exotropia, congenital ptosis (drooping eyelid), contact lens complications, giant cell arteritis, migraine, internuclear ophthalmoplegia (caused by multiple sclerosis or brainstem stroke), myasthenia gravis, thyroid ophthalmopathy, and other orbital inflammatory syndromes.[4] . It is therefore important to determine if the clinical findings are due to the oculomotor nerve itself, or a muscle/neuromuscular junction-based process mimicking third cranial nerve dysfunction.

Recurrent Painful Ophthalmoplegic Neuropathy (RPON)

Recurrent painful ophthalmoplegic neuropathy (RPON) was previously known as “ophthalmoplegic migraine’. This condition has an estimated annual incidence of 0.7 per million, ergo it is rare.[22, 23]  RPON is characterized by headache and ophthalmoplegia, most often affecting children and young adults.[22, 23]  Typically, patients present with repeated attacks of paralysis affecting one or more ocular motor nerves, with the third cranial nerve most frequently involved.[22, 23]  The head pain tends to be ipsilateral to the eye with ophthalmoplegia, and pain symptoms can precede deficits by up to 2 weeks.[22, 23]  The International Classification of Headache Disorders defined RPON has having the following diagnostic criteria: (1) at least two attacks; (2) unilateral headache accompanied by ipsilateral paresis of the ocular motor nerves; (3) the exclusion of orbital, parasellar, or posterior fossa lesions; and (4) the absence of another diagnosis that could better account for the patient's condition.[24]  Hence RPON is considered a diagnosis of exclusion. Standard investigations often include a cranial and orbital MRI scan with gadolinium, which often shows enhancement and thickening of the affected third cranial nerve. Serological tests tend to be normal. The natural history of RPON is favorable, and recovery typically manifests within days to weeks. A minority of patients have persistent neurological deficits.[22, 23]

Primary and Secondary Aberrant Regeneration of the Third Cranial Nerve

Aberrant regeneration of the oculomotor nerve (also known as oculomotor synkinesis) is a paradoxical firing of nerve fibers leading to co-contraction of muscles.[25]  During the regeneration of the nerve, the fibers grow to erroneously supply muscles other than their original muscles. Primary aberrant regeneration occurs with no previous inciting event.[25] Secondary aberrant regeneration occurs after injury to the oculomotor nerve and most commonly occurs weeks to months following injury.[25]  Approximately 15% of patients will develop aberrant regeneration after acute oculomotor nerve injury.[26] Importantly, microvascular oculomotor palsies should not develop aberrant regeneration and the presence of this sign should prompt further investigations for alternate causes.

The signs of aberrant regeneration of the oculomotor are as follows[27] :

  • Pseudo Von-Graefe sign: Aberrant regeneration of muscle to the eyelid causing retraction and elevation of the eyelid in attempted downard gaze.
  • Pseudo-Argyll Robertson pupil: Aberrant regeneration of muscle to the pupil leading to greater constriction of the pupil to convergence than to light. 
  • Adduction of the eye on attempted upward or downward gaze .
  • Co-contraction of the superior and inferior rectus leading to limitation of elevation and depression of the eye with retraction of the globe on attempted vertical movement.

Carotid-Cavernous Sinus Fistula (CCF)

A CCF is an abnormal vascular communication between the internal or external carotid artery and the cavernous sinus. There are two main types of fistulas seen in practice: direct and indirect types.[28]  The more common carotid-cavernous fistula encountered is the direct fistula, which is generally a result of trauma.[29]  These fistulas tend to be more acute and severe in presentation. Often times, they present with the classic triad of pulsatile exophthalmos, orbital bruit, and chemosis.[28] Patients may report conjunctival swelling and injection, retro-orbital pain, headache, diplopia and vision loss.[29]  Diplopia in the setting of CCFs may be caused by involvement of the extraocular nerves but also arise from congestion of the orbital affecting muscle function, due to impaired venous outflow.

Indirect low-flow CCF fistulas can be asymptomatic and gradual in onset. Often times, these patients seek medical attention for a persistent red eye and are treated as a conjunctivitis delaying treatment. With progressive worsening of the fistula, the patient can develop elevated intraocular pressure, proptosis, corkscrew vessels (secondary to conjunctival arterialization), cranial nerve palsies, eyelid edema, blood in Schlemm’s canal, pulsatile exophthalmos, disc swelling, dilated retinal veins, optic neuropathies, central retinal vein occlusion and choroidal detachment.[28] A study by Lewis et al [30]  found that 48% of patients admitted with a CCF had an abducens nerve palsy, 11% had an oculomotor nerve palsy, and 6% had a trigeminal nerve deficit. In total, 65% of patients had an incomintant strabismus on admission to hospital for their CCF.

Patients suspected of having a CCF should undergo emergent cranial orbital imaging with contrast-enhanced computed tomography (with angiography) or magnetic resonance imaging with angiography to assess for dilation of the superior ophthalmic vein that would signify impaired venous outflow (causing engorgement of the orbit) and arterialized blood flow.[28] If a CCF is evident on non-invasive imaging, the patient should undergo formal catheter angiography which, in many cases, is both diagnostic and curative.

Myasthenia Gravis

Myasthenia gravis is an autoimmune disease characterized by antibodies directed against acetylcholine receptors at the post-synaptic neuromuscular junction.[31] Myasthenia gravis does not cause a third cranial nerve palsy but can mimic dysfunction thereof. Patients with myasthenia gravis have muscle fatigability and weakness that fluctuate and worsen with exertion. Ocular manifestations of myasthenia gravis usually precede systemic manifestations.[31] The most common ocular sign is ptosis but myasthenia can also cause an incomitant strabismus mimicking motor cranial nerve palsies such as a oculomotor palsy.[32] Importantly, the pupils are not involved in myasthenia gravis, which is one important clinical clue that can help distinguish true third cranial nerve involvement from this disorder of the neuromuscular junction.[31, 32] The clinician should consider myasthenia in patients with fluctuating symptoms and orthoptics measurements. Systemic signs may also be present including fatigability of the muscles of mastication and proximal limb muscles.

In patients with suspected myasthenia gravis, office-based techniques such as the sleep test and ice test can be helpful to assess reversal of ptosis. However, serum anti-acetylcholine receptor antibody and anti-muscle specific kinase (MuSK) antibody assay should be considered for patients suspected of having myasthenia gravis.[31] Single-fiber electromyography remains the gold standard in diagnosing this condition. Consideration should also be acquire chest imaging to evaluate the thymus gland for hypertrophy or a thymoma. Medical management of myasthenia gravis includes pyridostigmine, steroids, and immunomodulators.[31]

Duane’s Retraction Syndrome

Duane’s retraction syndrome is a congenital strabismus that presents with horizontal duction deficits, globe retraction, and narrowing of the palpebral fissure.[33] It is caused by anomalous innervation of the lateral rectus muscle by a branch of the oculomotor nerve. The simultaneous activation of the medial rectus and lateral rectus muscles in adduction causes globe retraction and narrowing of the palpebral fissure.

There are three main types of Duane Retraction which are characterised by the following deficits[33] :

  • Type 1 comprises 75-80% of patients and presents with an abduction deficit. These patients are often esotropic in primary position.
  • Type 2 comprises 5-10% of patients and presents and adduction deficit. These patients are often exotropic in primary position. 
  • Type 3 comprises 10-20% of patients and presents with an abduction and adduction deficit and are generally orthophoric in primary position. 

Type 2 Duane’s in particular, can be mistaken for an oculomotor palsy. Careful examination of the eyelid and globe positioning should allow the clinician to differentiate these two entities.





Approach Considerations


Table 4:  Investigations to Consider in Evaluating Patients with Third Cranial Nerve Palsies (Open Table in a new window)



Serological Testing

Cell count with differential, hemoglobin AIC, serum sedimentation rate, c-reactive protein, free T3, free T4, TSH, prolactin, FSH, LH, free testosterone, lipid profile, IGF-1, morning cortisol, anti-acetylcholine receptor antibodies, anti-MuSK antibodies, serum lactate, connective tissue screen, genetic testing for mitochondrial disorders and oculopharyngeal muscular dystrophy.

Serological tests are indicated for suspected cases of diabetic microvascular ischemic cranial nerve palsy, pituitary macroadenomas, giant cell arteritis, myasthenia mimics, and thyroid related eye disease. Chronic progressive external ophthalmoplegia and oculopharyngeal muscular dystrophy can be evaluated with specific genetic testing.

Cerebrospinal Fluid Analysis

CSF cell count with differential, glucose, protein, cytopathology, gram stain, viral cultures, fungal cultures, and opening pressure as indicated

CSF analysis can help determine infectious (meningitis), inflammatory (cyto-albuminemic dissociation), malignant, and raised intracranial pressure mechanisms of third cranial nerve palsies.


CT head, cranial and orbital MRI with gadolinium and gadolinium enhanced views, cranial MRI or CT angiography/venography, catheter angiography, CT scan of the chest, whole body PET imaging, orbital ultrasound

CT imaging is needed acutely in the setting of ICH or hydrocephalus with raised intracranial pressure. CT or MRI with detailed vascular imaging can be used to localize lesions along the fascicle, in the cavernous sinus, in the region of the superior orbital fissure and orbital apices, and orbit. Orbital ultrasound can detect arterialized flow through the superior ophthalmic vein, and help localize cases of CCFs. CT imaging of the chest is needed to check for hilar lymphadenopathy in the case of sarcoid, and thymic hyperplasia/thymoma in suspected MG. Whole body PET CT is useful in detecting inflammatory conditions such as sarcoid and systemic diseases/neoplasms.


Nerve conduction studies (NCS), electromyography (EMG), repetitive nerve stimulation (RNS) studies and single fiber EMG.

EMG/NCS/SF-EMG and RNS studies can be used to identify cases of neuromuscular junction abnormalities (myasthenia gravis) versus mitochondrial disorders and OPMD.

Tissue Analysis

Temporal artery biopsy, muscle biopsy, lesion biopsy (pituitary tumors, lesions of the parasellar space and cavernous sinus)

TAB is needed to confirm a diagnosis of GCA, whereas characteristic findings on muscle biopsy will characterize underlying myopathies.

CSF: cerebrospinal fluid

TSH: thyroid stimulating hormoneFSH: follicule-stimuating hormoneLH: lutenizing hormone

CT: computer tomographyMRI: magnetic resonance imagingPET: positrion emission tomography

ICH: intracranial hypertension

MG: myasthenia gravis

EMG: electromyography

NCS: nerve conduction study

SF-EMG: single fibre electromyography

RNS : repetitive nerve stimulation

OPMD: oculopharyngeal muscular dystrophy

TAB: temporal artery biopsy

GCA: giant cell arteritis

The localization and management of acquired third cranial nerve palsies depend upon the patient’s clinical presentation (symptom onset, progression, age, pain, and associated findings) and related comorbidities (vascular risk factors, underlying cancers, etc).  For example, sudden onset headache, altered level of consciousness, and ophthalmoplegia should raise immediate concern for a vascular event such as pituitary apoplexy or subarachnoid hemorrhage. In this setting, patients need urgent cranial computed tomography (CT) imaging, which is the “go to” imaging modality in the setting of trauma, suspected intracranial hemorrhage, and quickly evolving hydrocephalus.[12]  For patients aged greater than 50 years, concern for giant cell arteritis should be paramount, prompting serological evaluation for acute phase reactants including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), with or without a temporal artery biopsy. Traditionally, older individuals (age>50 years) with vascular risk factors presenting with acute isolated ocular motor cranial mononeuropathy were sometimes  followed without neuro-imaging as spontaneous resolution of the palsy is expected in about 8–10 weeks.[34]  Yet, most physicians in the current era image patients with third cranial nerve palsies. Studies examining the role of MR imaging among patients with isolated ocular motor palsies have shown that this imaging modality detects neoplasms, infarcts, aneurysms, demyelination, and pituitary apoplexy in 43 cases (16.5%).[1, 35]



Approach Considerations

Specific medical and surgical treatments for third cranial nerve palsies will depend on whether the underlying etiology has a favorable natural history (microvascular ischemic third nerve palsy or RPON) or is amenable to treatment. Non-steroidal anti-inflammatory agents often are used to manage pain in these clinical situations. From a practical standpoint, diplopia can be treated with patching (acutely) or Fresnel prisms after formal orthoptic consultation. For more refractory cases, ground in prism can be modified with spectacles or patients may be candidates for strabismus surgery is to provide alignment in primary and reading position.


Questions & Answers


What is third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the pathophysiology of third cranial nerve palsy (oculomotor cranial nerve palsy)?

How common is third cranial nerve palsy (oculomotor cranial nerve palsy) in the US?

What is the mortality/morbidity of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the prognosis of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What should patients with third cranial nerve palsy (oculomotor cranial nerve palsy) be educated about?


What are the symptoms of third cranial nerve palsy (oculomotor cranial nerve palsy) associated with lesions?

What neurologic symptoms of third cranial nerve palsy (oculomotor cranial nerve palsy) are associated with lesions?

What are the symptoms of oculomotor nerve palsy due to lesions in the nuclear portion of the third cranial nerve?

What are the symptoms of oculomotor nerve palsy due to lesions in the fascicular midbrain portion of the third cranial nerve?

What are the symptoms of oculomotor nerve palsy due to lesions in the fascicular subarachnoid portion of the third cranial nerve?

What are the symptoms of oculomotor nerve palsy due to lesions in the fascicular cavernous sinus portion of the third cranial nerve?

What are the symptoms of third cranial nerve palsy (oculomotor cranial nerve palsy) due to lesions in the orbit?

What are the physical findings in third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are physical exam findings in unilateral third cranial nerve palsy (oculomotor cranial nerve palsy)?

How are the margin reflex distances (MRD) measured in unilateral third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the pupillary findings in unilateral third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the physical findings in nuclear third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the physical findings in fascicular midbrain third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the physical findings in fascicular subarachnoid third cranial nerve palsy (oculomotor cranial nerve palsy)?

How is fourth cranial nerve palsy diagnosed in the setting of third cranial nerve palsy (oculomotor cranial nerve palsy)?

How is trigeminal nerve sensory function tested in third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the physical findings in orbital third cranial nerve palsy (oculomotor cranial nerve palsy)?

What causes third cranial nerve palsy (oculomotor cranial nerve palsy)?

What causes nuclear third cranial nerve palsy (oculomotor cranial nerve palsy)?

What causes fascicular third cranial nerve palsy (oculomotor cranial nerve palsy)?


Which condition is associated with pupil-sparing third cranial nerve palsy (oculomotor cranial nerve palsy)?

What are the differential diagnoses for Third Nerve Palsy (Oculomotor Nerve Palsy)?


What are the approach considerations in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

Which imaging studies are indicated in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the role of MRI/MRA in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the role of CT scanning in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the role of lumbar puncture in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What is the role of cerebral angiography in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What histologic findings are associated with third cranial nerve palsy (oculomotor cranial nerve palsy)?

Which lab studies are indicated in the workup of third cranial nerve palsy (oculomotor cranial nerve palsy)?


What medical care is indicated in the treatment of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What surgical care is indicated in the treatment of third cranial nerve palsy (oculomotor cranial nerve palsy)?

Which specialist consultations are indicated in the treatment of third cranial nerve palsy (oculomotor cranial nerve palsy)?

What activity restrictions are indicated in patients with third cranial nerve palsy (oculomotor cranial nerve palsy)?