Andrew G. Lee, MD
Introduction
A patient presenting with a third nerve palsy is considered one of the "highest stakes" encountered by an ophthalmologist. On one hand, a patient may have an isolated, vasculopathic third nerve palsy that resolves with time. On the other hand, a patient may have a life-threatening intracranial aneurysm. Therefore, the evaluation and management of patients with a third nerve palsy is critically important.
Anatomy
The third nerve nucleus resides in the dorsal midbrain and is composed of various subnuclei. One subnucleus exists for each of the muscles innervated by the third nerve (e.g., medial rectus, superior rectus, inferior rectus, and inferior oblique muscles). The pupil has the Edinger-Westphal nucleus and the levator palpebrae muscles have a single central caudate nucleus. The nuclear innervation for the superior rectus muscle is crossed.
The third nerve fascicle travels ventrally in the midbrain past the red nucleus and corticospinal tract and exits into the subarachnoid space. In this location, the third nerve passes parallel to the posterior communicating artery and is vulnerable to compression from an intracranial aneurysm. Then, the third nerve passes anteriorly into the lateral wall of the cavernous sinus and enters the orbit through the superior orbital fissure.
The third nerve divides into a superior division (i.e., innervating the levator muscle and the superior rectus muscle) and an inferior division (i.e., innervating the pupil, the inferior oblique, medial rectus, and inferior rectus muscles). Knowledge of this anatomy is important for localization of the clinical findings in patients with third nerve palsy.
Clinical Manifestations
Patients with third nerve palsies may have binocular diplopia, ptosis, anisocoria, or a combination of these findings. If the external muscle dysfunction is complete, then ipsilateral adduction, elevation, and depression deficit may be present. The degree of external muscle dysfunction involvement may be variable (i.e., partial or complete) and some muscles may be unaffected.
When the deficit of adduction is significant, a primary position exotropia that is worse in gaze toward the paretic medial rectus muscle may occur. Depending on the pattern and severity of involvement of the extraocular muscles, an ipsilateral hypotropia or hypertropia may be present. In patients with internal muscle dysfunction, the pupil may be larger and poorly reactive or nonreactive to light and near stimuli. Other neurologic signs and symptoms may be present depending on the location of the underlying lesion.
Typically, lesions of the third nerve nucleus have other signs of mesencephalic involvement. Because of the unique anatomy of the third nerve subnuclei, the levator palpebrae superioris muscles (i.e., ptosis) and pupils are either affected bilaterally or not at all. Nuclear lesions may produce an ipsilateral third nerve palsy with a contralateral superior rectus paresis (i.e., crossed subnuclei innervation) and bilateral ptosis. Bilateral third nerve palsies with sparing of the lids (i.e., single levator subnucleus) and isolated bilateral ptosis with sparing of the extraocular muscles and pupils may also occur in nuclear lesions (Table 1).
Lesions of the third nerve fascicle may also involve other midbrain structures including:
- The red nucleus-superior cerebellar peduncle producing contralateral ataxia and cerebellar tremor (Claude syndrome)
- The cerebral peduncle causing contralateral hemiparesis (Weber syndrome)
- The red nucleus-substantia nigra producing contralateral choreiform movements or tremor (Benedikt syndrome)
In the subarachnoid space, the third nerve is susceptible to compression by an intracranial aneurysm. This usually results in a dilated and unresponsive pupil (i.e., complete internal dysfunction) because of the superficial location of the pupil fibers within the subarachnoid space. Therefore, an isolated pupil-involved third nerve palsy is an aneurysm until proven otherwise. This is known as the rule of the pupil.
Lesions of the third nerve in the cavernous sinus typically but variably involve the other ocular motor cranial nerves (e.g., fourth nerve and sixth nerve), the first (ophthalmic) branch of the trigeminal nerve, and the oculosympathetic fibers (Horner syndrome). Lesions within the superior orbital fissure or in the orbit produce other ocular motor dysfunction, optic neuropathy, and proptosis.
Evaluation
Third nerve palsies may be divided into those that are neurologically isolated and those that are not neurologically isolated.
Non-isolated Third Nerve Palsy
Non-isolated third nerve palsies should undergo neuroimaging (i.e., usually magnetic resonance imaging [MRI] with contrast) directed to the specific areas localized by the associated neurologic signs and symptoms (e.g., nucleus, fascicle, subarachnoid space, cavernous sinus, superior orbital fissure, orbit). Patients in whom a meningeal process is suspected should undergo a lumbar puncture if neuroimaging is not diagnostic.
Cerebral angiography may be necessary for patients suspected of harboring an underlying aneurysm. Patients with signs of subarachnoid hemorrhage (e.g., severe headache, change in mental status, other neurologic deficit) often require a non-contrast computed tomography scan, may require a lumbar puncture, and further imaging to rule out aneurysm. Myasthenia gravis mimics any pupil-spared ophthalmoplegia, including a third nerve palsy, and should be considered in the differential diagnosis.
Aberrant Regeneration of the Third Nerve
Patients recovering from a third nerve palsy may have aberrant regeneration. Aberrant regeneration involves any of the external somatic branches of the third nerve or the pupil (e.g., lid retraction in downgaze or adduction, pupil constriction in adduction, or depression).
Patients with primary (i.e., no prior third nerve palsy) or secondary (i.e., after a third nerve palsy) aberrant regeneration should undergo a neuroimaging study to exclude a compressive lesion including cavernous sinus lesion (e.g., carotid artery or other aneurysm).
Ischemic third nerve palsies do not produce aberrancy and the development of aberrant regeneration in a presumed ischemic palsy should prompt neuroimaging.
Isolated Third Nerve Palsy
Patients with isolated third nerve palsies are defined as those without other neurologic findings. These neurologically isolated palsies may be classified by the amount of external muscle dysfunction into complete and incomplete external dysfunction third nerve palsies.
A complete external dysfunction third nerve palsy involves all of the somatic branches of the third nerve (e.g., the extraocular muscles innervated by the third nerve) and an incomplete third nerve palsy either does not involve all of the branches of the third nerve (e.g., superior divisional palsy) or does not involve all of the muscles to a significant degree (e.g., no ptosis or no adduction deficit).
Third nerve palsies with complete external dysfunction may be further subdivided by the degree of internal dysfunction into pupil-sparing (normal internal muscle function) and pupil-involved (abnormal internal muscle function) third nerve palsies. The degree of pupil involvement may be partial (i.e., relative pupil sparing) or complete (i.e., fixed and dilated pupil). The evaluation is different for each type of isolated third nerve palsy depending upon the completeness of the external and internal dysfunction.
Isolated Complete External Dysfunction Third Nerve Palsy Without Internal Dysfunction
An isolated third nerve palsy with a normal pupillary sphincter and completely palsied extraocular muscles is rarely caused by an aneurysm. Although a single case has been reported due to a basilar artery aneurysm, this is a rare clinical exception to the general rule. The neurologically isolated, complete external dysfunction, pupil-spared third nerve palsy is usually due to ischemia and is often caused by diabetes mellitus.
Lack of internal muscle dysfunction (pupil-sparing) in diabetic third nerve palsies is presumably due to the lack of vascular damage to the periphery of the nerve where the majority of pupillomotor fibers are thought to pass. This is in distinction to the pupil involved third nerve palsy due to aneurysm compressing the superficially located pupil fibers. Therefore, neuroimaging may be deferred in adult patients with known vasculopathic risk factors (e.g., diabetes, hypertension) who develop an acute isolated, but complete external dysfunction, pupil-sparing third cranial nerve palsy.
As with any pupil-spared ophthalmoplegia, myasthenia gravis should also be considered. In patients without vasculopathic risk factors or in patients with progressive or unresolved third nerve palsies, neuroimaging should be performed, preferably cranial contrast-enhanced MRI with magnetic resonance angiography (MRA) or computed tomographic (CT) angiography (CTA).
Patients with pupil sparing should be observed within the first 24 hour to 48 hours of onset for delayed pupil involvement. If pupil involvement occurs, then further evaluation is warranted. Patients should be evaluated and treated for underlying vasculopathic risk factors (e.g., diabetes mellitus, hypertension, increased cholesterol, and smoking).
Elderly patients should be questioned regarding symptoms of giant cell arteritis (e.g., headache, jaw or tongue claudication, polymyalgia rheumatica) and should have further evaluation as indicated (e.g., erythrocyte sedimentation rate and temporal artery biopsy).
An isolated third nerve palsy would be an unusual presentation for giant cell arteritis. As with other non-isolated third nerve palsies, a lumbar puncture may be indicated to rule out infectious, inflammatory, or neoplastic meningitis.
Incomplete External Dysfunction with Normal Internal Function Third Nerve Palsy
Patients with neurologically isolated but incomplete external dysfunction third nerve palsy (e.g., divisional palsy) require more careful assessment. Patients with an incomplete external dysfunction but no internal dysfunction usually require a cranial MRI with contrast to rule out a mass lesion.
An MRA or computed tomography angiography (CTA) should also be considered to evaluate for intracranial aneurysm. If the MRI with an MRA or CTA are normal, then cerebral angiography may still be considered to rule out an aneurysm or a carotid cavernous sinus fistula depending on the pre-test likelihood of aneurysm. This pre-test likelihood for aneurysm is in part dependent on the patient's age (e.g., young adult), the presence or absence of pain or other findings, the temporal course of the palsy, and other risk factors for aneurysm.
MRI and MRA (or CTA) usually have sufficient sensitivity to detect an aneurysm causing a third nerve palsy (>5 mm in size), but cerebral angiography remains the gold standard for the diagnosis of cerebral aneurysms.
The combination of an adequately performed and interpreted MRI and MRA or CTA may be up to 98% sensitive in the detection of an aneurysm that will bleed. Spiral CTA may be superior to MRA in the evaluation of third nerve palsies but for practical purposes, the MRI is superior for evaluating patients for compressive non-aneurysmal causes and thus most clinicians would perform an MRI with MRA rather than an MRI with CTA combination. Individual clinicians must decide on the techniques that are best at their institution.
The decision to rely on the MRI and MRA (or CTA) depends on three factors:
- The reliability of the technique and interpretation of the MRA or CTA at the individual medical institution
- The pre-test likelihood of aneurysm based on clinical findings and risk factors
- The risk of catheter angiography in the individual patient
The risk of catheter angiography must be weighed against the risk of missing an aneurysm in the individual patient despite a negative MRI with MRA (or CTA). As opposed to the complete external dysfunction with normal internal function third nerve palsy, lack of internal dysfunction in the setting of partial external dysfunction is not true "pupil-sparing".
Patients may have an aneurysm that produces a divisional third nerve palsy or does not involve the pupil because of a lesser degree of compression of the third nerve. Although improvement over time suggests a non-aneurysmal etiology, improvement may occur in aneurysmal third nerve palsy as well.
Incomplete or Complete External Dysfunction with Partial Internal Dysfunction Third Nerve Palsy
Isolated incomplete or complete external dysfunction third nerve palsy with partial internal dysfunction has been termed a relative pupil-sparing third nerve palsy. Patients with a partial or relative internal dysfunction (relative pupil-sparing) third nerve palsy should probably undergo MRI and MRA (or CTA) to exclude a compressive lesion including aneurysm. Jacobson described 24 isolated relative pupil-sparing third nerve palsies, and 10 of these patients had a tumor or aneurysm.
The presence or absence of pain and the degree of internal or external dysfunction in this study did not differ between the two groups. Therefore, catheter angiography may still be required if the MRI and MRA (or CTA) are negative because of the possibility of a cerebral aneurysm. There is insufficient evidence in the literature to recommend that an MRI with MRA (or CTA) alone can be relied upon to exclude aneurysm in this setting.
The pre-test likelihood for aneurysm in any one patient should include determination of other risk factors for aneurysm (e.g., headache, acute onset of symptoms, family history of aneurysm, risk factor for aneurysm, and young adult to middle-age adult). The pre-test likelihood of aneurysm is the major determinant of whether to perform catheter angiography in patients. Cullom and colleagues reported a prospective study of 10 patients with relative pupillary-sparing third nerve palsies and none had an aneurysm. However, other authors have reported internal carotid artery, posterior communicating artery, and basilar artery aneurysms with relative pupillary sparing. Therefore, cerebral angiography may be required if the MRI and MRA (or CTA) are negative.
Between 10% and 20% of patients with ischemic third nerve palsies have pupilloparesis (internal dysfunction). Therefore, some of these patients may need to undergo a negative catheter angiogram to exclude aneurysm. Jacobson reviewed 26 patients with diabetes-associated presumed ischemic third nerve palsy. In these patients, the degree of anisocoria is usually less than 1 mm (partial internal dysfunction) and no patients have a fully dilated unreactive pupil (complete internal dysfunction). An MRI with MRA (or CTA) combination may be sufficient in patients with a low pre-test likelihood for aneurysm.
Isolated Complete or Incomplete External Dysfunction with Complete Internal Dysfunction
The pupil-involved third nerve palsy is the highest risk scenario for aneurysm. Typically, aneurysms produce complete internal dysfunction and the rule of the pupil states that "an isolated pupil-involved third nerve palsy is due to an aneurysm until proven otherwise."
These patients should undergo MRI and MRA (or CTA) to exclude a non-aneurysmal cause but even if the neuroimaging studies are negative, a cerebral angiogram should be strongly considered to exclude aneurysm. Patients with complete internal dysfunction third nerve palsy may have partial or complete external dysfunction. Spinal fluid evaluation may be needed if the neuroimaging studies are negative and the patient has persistent or progressive deficit.
Summary of Evaluation for Isolated Third Nerve Palsy
The evaluation of the isolated third nerve palsy remains problematic. The evidence is summarized and graded in Table 2 and recommendations are made based upon the degree of completeness of external dysfunction and internal dysfunction.
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