Third nerve palsy, also known as oculomotor nerve palsy, results from damage or dysfunction of the third cranial nerve (CN III). This nerve controls most of the muscles that move the eye and the muscle that raises the eyelid. When this nerve is compromised, it leads to a specific set of symptoms affecting both the appearance and function of the eye. The sudden onset of these symptoms is a serious medical concern because it can signal a potentially life-threatening issue, such as a brain aneurysm. Prompt medical evaluation is required to identify the cause and initiate appropriate treatment.
The Role of the Oculomotor Nerve
The oculomotor nerve (CN III) carries signals from the brain that regulate eye movement and certain involuntary functions. This nerve controls four of the six external muscles that move the eyeball, making it the primary driver of eye motion. The muscles innervated by the oculomotor nerve are the superior rectus, medial rectus, inferior rectus, and inferior oblique. These muscles rotate the eye upward, downward, and inward toward the nose.
The oculomotor nerve also innervates the levator palpebrae superioris muscle, which lifts the upper eyelid. The nerve also carries parasympathetic fibers that control the internal muscles of the eye. These fibers regulate the sphincter pupillae muscle, which constricts the pupil, and the ciliary muscle, which adjusts the shape of the lens for focusing.
Failure of the nerve results in a predictable pattern of symptoms. The nerve’s control over both voluntary eye movement and involuntary functions means that a palsy affects multiple aspects of vision.
Recognizing the Clinical Signs
The failure of the oculomotor nerve produces a constellation of distinct and observable physical signs. One of the most common signs is ptosis, or a drooping of the upper eyelid, which can be severe enough to completely cover the pupil. This occurs because the levator palpebrae superioris muscle is paralyzed.
Paralysis of the four major eye-moving muscles leads to a characteristic misalignment of the affected eye. With the medial, superior, and inferior rectus muscles non-functional, the unopposed action of the remaining muscles pulls the eye into a resting position. This position is deviated outward and slightly downward, often described as “down and out.”
This misalignment causes diplopia, or double vision, because the images from the two eyes can no longer be fused into a single clear picture by the brain. However, the severe ptosis accompanying the palsy often blocks light, preventing the perception of double vision. The pupil on the affected side may also be dilated and unresponsive to light, depending on which nerve fibers are damaged.
Identifying Underlying Causes
The causes of third nerve palsy are categorized based on the mechanism of injury, primarily distinguishing between ischemic and compressive lesions. Ischemic or microvascular causes are the most common in older adults, occurring when the blood supply to the nerve is compromised. This is frequently associated with systemic conditions like long-standing diabetes mellitus and hypertension.
Ischemic palsies often present as “pupil-sparing,” meaning the eye muscles are affected but the pupil reacts normally to light. This is because the parasympathetic fibers that control pupil constriction are located on the surface of the oculomotor nerve and have a more robust collateral blood supply. The deeper somatic fibers, which control the eye-moving muscles, are more susceptible to damage from small vessel disease.
Compressive lesions are a major concern because they can indicate a life-threatening condition. These lesions, such as an aneurysm of the posterior communicating artery or a brain tumor, press on the nerve from the outside. Because the pupil-controlling fibers lie on the exterior of the nerve, they are the first to be affected by external pressure. A third nerve palsy that involves a fixed and dilated pupil is a critical red flag, strongly suggesting the presence of an aneurysm and demanding immediate medical intervention.
Other causes include trauma, inflammation, and conditions like giant cell arteritis or pituitary apoplexy. Any new-onset third nerve palsy requires a thorough, urgent evaluation to determine the precise etiology.
Management and Treatment Options
The initial management focuses on immediate diagnostic workup to rule out a compressive cause. If the pupil is involved, urgent neuroimaging, typically a computed tomography (CT) scan or magnetic resonance imaging (MRI), is performed to identify potential aneurysms or other space-occupying lesions. Magnetic resonance angiography (MRA) or computed tomography angiography (CTA) may also be used to visualize the blood vessels around the nerve.
Treatment is dependent on the underlying cause. If a compressive lesion like an aneurysm is found, surgical intervention is often required immediately to relieve pressure on the nerve. For ischemic palsies, treatment involves managing the underlying systemic risk factors, such as optimizing blood sugar control for diabetes and regulating blood pressure for hypertension. Ischemic cases often show improvement spontaneously within a few months.
For patients with chronic or residual deficits, long-term management strategies are employed to improve vision and function. Double vision can be managed with prism lenses, which bend light to help the brain fuse the two images, or with temporary eye patching. If the eye misalignment is permanent after observation, eye muscle surgery may be performed to realign the eyes. Ptosis can also be corrected later with eyelid surgery.