Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease where the immune system mistakenly attacks the body’s healthy tissues. Diplopia, or double vision, is a visual symptom where a single object appears as two images. SLE can definitively cause diplopia, though it is a less frequent but serious manifestation. Diplopia signals that the systemic inflammatory process of lupus has affected the structures responsible for coordinating eye movement.
Systemic Inflammation and Neurological Impact
The underlying mechanism connecting SLE to visual disturbance is the widespread inflammation characteristic of the disease. This systemic inflammation can target the central nervous system, a condition referred to as Neuropsychiatric SLE (NPSLE). An overactive immune system generates autoantibodies and immune complexes that deposit in tissues, triggering an inflammatory cascade.
A primary pathway for neurological damage is vasculitis, the inflammation of blood vessel walls. This inflammation can narrow or block the small blood vessels supplying the nerves and brain structures that control eye movement. The resulting lack of blood flow, or ischemia, starves the neural tissue of oxygen and nutrients, leading to damage. When this microvascular injury affects the brainstem, it directly compromises the relay centers for visual coordination.
Chronic inflammation can disrupt the blood-brain barrier, allowing immune cells and inflammatory molecules to enter the central nervous system. This causes localized damage that results in the physical symptom of double vision. The resulting injury often manifests as an acute neurologic event, correlating with periods of high systemic disease activity.
Direct Causes of Double Vision in Lupus
One common cause of diplopia is cranial nerve palsy, which involves damage to the nerves controlling the six muscles surrounding the eye. The Oculomotor (III), Trochlear (IV), and Abducens (VI) nerves are most frequently implicated in eye movement disorders.
Damage to these nerves, often due to microvascular ischemia from vasculitis, prevents the coordinated movement of the eyes. Abducens nerve (VI) palsy, which controls the muscle that turns the eye outward, is a common abnormality. Oculomotor nerve (III) involvement can cause the eye to deviate downward and outward, often accompanied by a drooping eyelid.
Another mechanism is orbital myositis, the inflammation of the extraocular muscles themselves. Immune-mediated inflammation causes the muscles to swell, restricting movement and coordination. This condition presents with eye pain, swelling, and restricted eye movement, leading directly to double vision.
The third source of diplopia is involvement of the brainstem, which houses the nuclei for the eye movement nerves. Lesions here, caused by cerebral vasculitis or small strokes, can result in conditions like internuclear ophthalmoplegia, where the eyes fail to coordinate horizontal gaze.
Clinical Evaluation and Therapeutic Approaches
When a person with known or suspected SLE develops double vision, a prompt clinical evaluation is necessary to confirm the underlying cause. This requires collaboration between a rheumatologist, neurologist, and ophthalmologist. The first step is determining if the diplopia is monocular or binocular, as binocular double vision strongly suggests a neurological or muscular coordination problem.
Diagnostic imaging, such as a magnetic resonance imaging (MRI) scan of the brain and orbits, is routinely performed. Imaging identifies inflammatory lesions, brainstem involvement, or muscle enlargement consistent with orbital myositis. It also helps rule out other causes of diplopia, such as tumors or large vessel strokes. Blood tests assess lupus activity, looking for elevated inflammatory markers and specific autoantibodies like anti-double-stranded DNA and low complement levels.
The primary goal of treatment is to rapidly suppress the underlying autoimmune activity causing the inflammation. High-dose systemic corticosteroids, such as intravenous methylprednisolone, are typically the first line of therapy to quickly reduce inflammation.
Following the acute phase, treatment transitions to long-term immunosuppressive medications to maintain disease remission. These drugs include cyclophosphamide, azathioprine, or mycophenolate mofetil. Early intervention offers the best chance for the resolution of cranial nerve palsy or myositis and the recovery of normal vision.