The Differential Diagnosis of Diplopia

Background: Diplopia is a common symptom of interdisciplinary significance that can lead to marked impairment of function. Its causes range from harmless to life-threatening conditions that must be precisely distinguished.

Methods: For this CME review article, a PubMed search was conducted in an interdisciplinary collaboration of ophthalmologists and neurologists.

Results: Systematic history-taking and a structured clinical examination are the basis for topographic-anatomical diagnosis and the differentiation of peripheral and central causes. It is important to distinguish monocular from binocular diplopia. Monocular diplopia persists when one eye is covered and is not dangerous. Binocular diplopia may arise from disturbances at a variety of anatomical levels that can result from many different causes: disturbances of fusion in strabismus, diseases of the eye muscles such as thyroid eye disease or mitochondropathies, orbital trauma, impaired neuromuscular transmission in myasthenia gravis, fascicular or nuclear lesions of the three nerves that supply the extraocular muscles (oculomotor, trochlear, and abducens), supranuclear lesions “above” the cranial nerve nuclei, and cerebellar diseases. The most common causes, together accounting for ca. 70% of cases, are decompensated latent strabismus and cranial nerve palsies, followed by orbital, brainstem, and cerebellar diseases.

Conclusion: Diplopia can be accurately diagnosed through a systematic approach that includes precise history-taking and clinical examination of eye position and eye movements. On this basis, there can be a targeted and specific search for the various underlying causes. When the patient’s leading symptom is isolated diplopia, the ophthalmologist is generally the specialist to whom the primary care physician should turn next.

Cite this as: Lagrèze WA, Lischka T, Eckstein A, Oeverhaus M, Dieterich M, Strupp M: The differential diagnosis of diplopia. Dtsch Arztebl Int 2026; 123: 367–74. DOI: 10.3238/arztebl.m2026.0006

Diplopia (double vision) is the subjective visual perception of an object as double. The task of the oculomotor system is to focus an image sharply on the macula of both eyes to enable binocular vision. Visual information from the two eyes is fused in the central nervous system, and a perception of depth is generated. This process depends on the alignment of both eyes toward a single point at a given distance. Dysfunction of the oculomotor system causes diplopia, a highly debilitating symptom that renders many everyday activities difficult or impossible. A person with diplopia is not allowed to drive a car or operate machinery. According to a study from the USA, diplopia is the chief complaint in 850,000 medical consultations per year. 16% of the patients in the study had potentially life-threatening underlying conditions (1).

The causes of diplopia range from strabismus (squint) of various types to life-threatening vascular diseases of the nervous system and mass lesions of the skull base or orbit (2, 3).

It follows that a precise understanding of the relevant anatomical structures is essential. Pathophysiologically relevant changes may lie in the optical media of the eye (cornea, lens), the soft tissue structures of the bony orbit, the extraocular muscles, the neuromuscular junction, or the nerves supplying the extraocular muscles at any point along their course: from the peripheral nerves to their central fascicular pathways, their brainstem nuclei, and higher-level (supranuclear) structures. The underlying etiologies can be congenital or acquired and are classified as inflammatory (infectious/autoimmune), ischemic, traumatic, or neoplastic.

For any patient with diplopia, history-taking should be followed by a neuro-ophthalmological examination. Decisions about further steps such as imaging, lumbar puncture, blood tests, and other studies should only be made on the basis of a working diagnosis.

Learning objectives

This article is intended to enable readers to:

• know the most common causes of diplopia,
• ask basic questions when taking the patient’s history and use the appropriate clinical tests for differential diagnosis, and
• distinguish harmless from dangerous causes of diplopia and to initiate and carry out the appropriate measures for diagnosis and treatment, based on an understanding of the pathophysiology of diplopia and the ability to recognize warning signs (red flags).

Methods

For this review, we searched in PubMed for articles containing the terms “diplopia,” “differential diagnosis,” “ocular motility disorder,” “cranial nerve palsy,” “strabismus,” “orbit*,” and “supranuclear,” with the Boolean operators AND/OR. Relevant articles for review were selected from the list retrieved publications by a manual search.

Diagnostic evaluation

History-taking begins with the determination whether diplopia is monocular or binocular. Binocular diplopia, which is much more common, disappears when one eye is covered. Misaligned visual axes do not always cause diplopia; some patients complain of blurry or unfocused vision.

A patient with binocular diplopia should be asked whether the distance between the two images depends on the direction of gaze; this is characteristic of orbital diseases and cranial nerve palsies. The precise temporal course of the symptom is key, as acute diplopia can be due to ischemia and other vascular events (4).

The patient should always be asked about headache. There follows a review of the patient’s ocular and general medical history, and of the family history.

The physical examination (Table) further narrows down the possible causes. The initial examination, which can also be performed by physicians who are not ophthalmologists, begins with inspection of the patient’s head posture and of the orbital soft tissues. Next, the position of the eyes is assessed. Finally, ocular motility, various types of eye movements, and binocular function are tested (5).

Table

Clinical testing of eye movements in the diagnostic evaluation of diplopia

Further specialized examination can only be performed by an ophthalmologist. It includes the measurement of strabismus angles, slit-lamp examination, and evaluation of the fundus, with the aid of optical coherence tomography (OCT) if necessary.

There is only one acutely life-threatening constellation of symptoms and signs to be mentioned in this context. Diplopia in a patient with unilateral ptosis and (sometimes) a mydriatic pupil generally reflects oculomotor nerve palsy. If this situation arises acutely in combination with a severe headache, the cause is likely to be an enlarging or ruptured aneurysm at the base of the brain, and the patient should be taken to a hospital emergency room at once for further neurological and neuroradiological evaluation.

During the examination, particular attention should be paid to visible changes such as cutaneous abnormalities of the eyelid, ptosis or lid retraction, exophthalmos, horizontal or vertical misalignment of the eyes, nystagmus, and abnormal head posture. It is helpful to compare the light reflexes—e.g., from a distant light source on the two corneas—which should be at the same distance from the corneal margin or the pupil. The eyes are then examined with a slit lamp, with special attention to changes in the tear film, cornea, and lens (monocular diplopia). Direct or indirect ophthalmoscopy is used to assess the optic disc (sharp vs. blurred edges) and the central retina (macula). Optical coherence tomography (OCT) yields a high-resolution view of structural changes in the macula, such as the retinal deformation caused by epiretinal gliosis. OCT of the peripapillary nerve fiber layer also plays a role in the assessment of intracranial hypertension, which can cause swelling of the nerve fiber layer—a finding that should always be evaluated in the context of the macular ganglion cell complex.

The cover test is used to distinguish manifest from latent strabismus. In this simple test, patients are asked to fixate on an object. First, the examiner covers and uncovers the right eye repeatedly with either a cover disc or a hand, then does the same with the left eye (unilateral cover test). Next, the cover is shifted back and forth from one eye to the other (alternating cover test). In the unilateral cover test, if uncovering of an eye is immediately followed by an adjusting movement of the other eye, this indicates heterotropia (manifest strabismus)—esotropia if it moves laterally, exotropia if it moves medially. In the alternating cover test, an adjusting movement of the eye that has just been uncovered indicates heterophoria (latent strabismus). If heterophoria is found, the uncover test can be performed afterward to assess fusion: a covered eye is uncovered and observed for any fusion movement.

Ocular motility is examined in nine positions of gaze with attention to eye alignment and to the amplitude of the movements. The patient is asked to fixate on a moving object (e.g., a fingertip or the tip of a pen).

Aspects of ocular motility that are mediated by supranuclear structures include fixation, pursuit, saccades (rapid shifts of gaze to a target), gaze holding, the convergence reflex in near vision, optokinetic nystagmus (OKN), and the vestibulo-ocular reflex (VOR) (Table) (6, 7).

These clinical tests enable the formulation of a working diagnosis that provides a basis for further diagnostic evaluation, ranging from neurocranial and orbital magnetic resonance imaging (MRI) to laboratory tests and lumbar puncture for CSF examination. A computerized tomographic (CT) scan of the head is indicated in cases of orbital fracture or when, e.g., a bleed or mass is suspected.

Red flags, i.e., clues to dangerous conditions that can be checked even in the primary care setting, include the following:

• acute onset of diplopia
• severe headache
• pupillary changes (anisocoria)
• further neurological abnormalities
• acute nystagmus

Causes and diagnoses

In this section, we systematically discuss the underlying conditions that cause diplopia in peripheral-to-central order, i.e., from the eye to the brain. This order bears no particular relation to the relative frequencies of the various conditions. No population-based studies are available on this topic, but the most common causes of diplopia are decompensated latent strabismus (phoria) in ca. 40% of cases, cranial nerve palsies (ca. 30%), and orbital diseases, mainly thyroid eye disease (ca. 15%). Brainstem and cerebellar disorders account for ca. 10% of cases of diplopia.

Causes of monocular diplopia

Monocular diplopia can be due to abnormalities in the eye’s refractive media. Possible causes include pressure from the eyelids in ptosis; astigmatism and other corneal irregularities, such as keratoconus; corneal dystrophies; or a decentered ablation zone after refractive laser surgery on the cornea. Other typical causes include an elevated tear meniscus due to impaired tear drainage, or a cataract. Monocular diplopia always involves images that are very close together. Patients often report perceiving a second, blurred image superimposed on the first—similar to a double contour—rather than two distinct images.

Myogenic and orbital causes

Eye movements can be affected by changes in the eyelid suspension and eye muscles, and by orbital processes. Rapidly progressive processes impair ocular motility more commonly than slowly progressive ones.

Fractures of the bony orbit can cause diplopia directly by entrapment of orbital tissues in the fracture gap, indirectly via orbital emphysema, or neurologically via cranial nerve palsies (which usually arise when the fracture involves the floor or medial wall of the orbit). Entrapment (the “trap-door” mechanism) is common in younger patients and must be treated within 24 hours to prevent permanent oculomotor dysfunction. Fractures that do not cause entrapment can be treated with a delay of up to one week.

Metastatic tumors in the orbit usually restrict eye movements mechanically, possibly also causing enophthalmos and ptosis. Such findings are typical of orbital metastases of breast cancer.

Various other conditions can alter the anatomy of the eye muscles and cause an oculomotor disturbance that is either restrictive (due to volume increase or fibrosis) or paretic (due to weakness). In restrictive disturbances, the two visual images are farthest apart when the patient looks away from the normal direction of pull of the affected muscle; in paretic disturbances, they are farthest apart when the patient looks toward the direction of pull of the affected muscle. Depending on the cause, a single extraocular muscle, multiple muscles, or all of them may be affected. The various conditions causing myogenic diplopia each have their own pathophysiology.

In myasthenia gravis, autoantibodies against certain antigens at the motor end-plate (acetylcholine receptor, muscle-specific kinase, low-density lipoprotein receptor-related protein 4) are usually, but not always, detectable. These block neuromuscular transmission and cause diplopia of the paretic type; fatigue on continuing muscle activation is typical (8). The distance between the two images is not constant. It increases with exertion and is often accompanied by exertion-induced ptosis.

Mitochondrial disorders such as chronic progressive external ophthalmoplegia (CPEO) cause slowly progressive, paretic dysfunction of the eye muscles, usually accompanied by ptosis, but often without diplopia. Progressive impairment of convergence may lead to exotropia on near vision (9).

Autoimmune diseases of the orbit restrict ocular motility. In thyroid eye disease (TED), autoantibodies stimulate TSH and IGF-1 receptors, causing muscle thickening and fibrosis. The medial and inferior recti are most commonly affected; the result is an inability to look upward, combined with esotropia and hypotropia (10).

Myositis may have no identifiable cause (idiopathic myositis). In acute cases, the affected muscles are painful and paretic; as the condition progresses, restriction may develop as well. For the vast majority of myopathic disorders, the treatment is focused on the underlying disease. Systematic therapeutic approaches for certain conditions (e.g., myasthenia gravis (8) or TED (10)) have been formulated in the relevant guidelines. Myositis in the posterior portion of the orbit poses the danger of compressive optic neuropathy and should therefore be treated promptly and with maximal escalation. As no drug-approval trials have been performed for idiopathic myositis, and steroids may not bring sufficient improvement, off-label treatment (e.g., with rituximab) should be applied for without delay (11).

In an elderly patient, fusion can be impaired by laxity of the orbital ligamentous structures, resulting in strabismus and diplopia. This condition, called sagging eye syndrome, is becoming more common as the population ages.

Local anesthetic injection for retrobulbar anesthesia (e.g., in cataract surgery) may lead to scarring of the inferior rectus muscle, vertical strabismus, and diplopia.

Heterophoria

A very common cause of diplopia is heterophoria, which is defined as latent strabismus that becomes evident only when fusion is disrupted, with a deviation of the visual axis of one eye (12). It is classified as esophoria or exophoria depending on the direction of the deviation. Heterophoria is not primarily a disease, but rather a common, mostly asymptomatic phenomenon (approximately 80% of the population has some degree of heterophoria) (13, 14). Symptoms arise only when compensation is impaired, e.g., by fatigue or low visual acuity. Aside from diplopia, the patient may have other (“asthenopic”) symptoms such as burning eyes or headache. The diagnostic evaluation includes a targeted medical history (e.g., symptoms after a change in eyeglass prescription, symptoms all day long), objective and subjective refraction testing, and quantification with the alternating prism cover test. The differential diagnosis includes strabismus of other types (e.g., intermittent divergent strabismus), accommodation disorders, uncorrected refractive errors, and neurological causes.

Strabismus

Diplopia is suppressed by central mechanisms in the early-infancy strabismus syndrome (15), which is the most common disease that causes strabismus, as well as in primary or intermittent exotropia. Acute diplopia or closure of one eye in a child aged 3 to 8 is often due to normosensory late-onset strabismus, accommodative strabismus, or decompensated microstrabismus. All these conditions are characterized by an esotropia that is independent of the direction of gaze (concomitant strabismus). Concomitant esotropia in older children can also be due to a cerebellar disorder. From puberty onward, acquired types of strabismus become more common, including acute esotropia and vertical strabismus associated with high myopia, as well as strabismus due to dysfunction of the oblique eye muscles (e.g., strabismus sursoadductorius). In such cases, the superimposed double images may be perceived as tilted, particularly on lateral gaze. Examiners without special training may have difficulty distinguishing these conditions from trochlear nerve palsy (16).

Disorders involving cranial nerves III, IV, and VI

Palsies affecting the nerves to the extraocular muscles impair ocular motility and manifest themselves with diplopia, compensatory head posture, and marked distress. A typical feature is that the angle of deviation depends on the direction of gaze (incomitant strabismus). The causes are diverse, including microangiopathy, inflammatory disorders, trauma, and cancer. Meticulous differential diagnosis is the key to a good outcome, as the underlying disease may be life-threatening. In persons aged 60 and above, vascular causes are the most common. The courses of the nerves supplying the extraocular muscles are shown in Figure 1 .

Figure 1

Anatomy of the orbit, skull base, and brainstem including the course of the oculomotor (pink), trochlear (light blue), and abducens (green) nerves from their brainstem nuclei to the extraocular muscles that they supply. *Muscle shown only in part; n., nerve; nn., nerves, m., muscle.

Oculomotor nerve palsy (cranial nerve [CN] III) can be classified as external, internal, or combined. External palsy presents with ptosis, inability to elevate, depress, or adduct the eye, and exo- and hyotropia; internal palsy presents with mydriasis, anisocoria, and accommodation paralysis owing to the involvement of parasympathetic fibers. Internal oculomotor nerve palsy suggests a compressive lesion at the skull base (e.g., an aneurysm); sparing of the pupil does not rule out such a lesion (17). It follows that any patient with an oculomotor nerve palsy should undergo an imaging study of the brain, and an acute oculomotor nerve palsy accompanied by headache is a medical emergency calling for immediate imaging and often lumbar puncture. An overview of the causes is found in (18).

Trochlear nerve palsy (CN IV) presents as oblique-vertical diplopia with compensatory head tilt toward the opposite side. It affects the superior oblique muscle alone, is a common sequela of traumatic brain injury, and is particularly evident when the patient looks down (e.g., when going downstairs or reading). Congenital and phenotypically similar forms (known as strabismus sursoadductorius) may become symptomatic through decompensation in adulthood. An overview of the causes is found in (19). An important differential diagnosis is vestibular skew deviation as a component of the ocular tilt reaction.

Abducens palsy (CN VI) impairs abduction, causing horizontal diplopia (esotropia). Total inability of the eye to cross the midline is called abducens paralysis. There is compensatory turning of the head toward the affected side to eliminate the need for abduction. The abducens nerve has a long intracranial course and is thus susceptible to skull base diseases, high intracranial pressure, and vascular processes. An overview of the causes of abducens palsy is found in (20).

On history-taking, attention should be paid to the precise temporal course, vascular risk factors, and trauma. It is important to recognize warning signs such as pain or rapid progression. An abducens palsy that develops within a day, if not of traumatic origin, will usually have a vascular cause. Treatment options include prisms, occlusion, or, if symptoms persist, eye muscle surgery—though this should be performed no sooner than six months after symptom onset, as spontaneous remission may occur.

Nuclear lesions

Nuclear lesions of cranial nerves III, IV, and VI are characterized by mixed findings, i.e., a combination of apparently “peripheral and central” neurological signs—especially central oculomotor disturbances (21)—because the centers controlling various types of eye movements are also located in the brainstem. For instance, the abducens nucleus controls ipsilateral horizontal eye movements. A nuclear lesion therefore impairs all ipsilateral horizontal eye movements, while convergence-related movements are preserved. A unilateral lesion of the oculomotor (CN III) nucleus causes ipsilateral third nerve palsy as well as contralateral upward gaze palsy and ptosis because of the crossing of the corresponding motor neurons at the level of the oculomotor nuclei.

Supranuclear lesions

While diplopia is usually the main symptom of peripheral and infranuclear eye movement disorders, supranuclear disorders—i.e., those due to lesions at higher levels of neural control than the cranial nerve nuclei—present with different, characteristic clinical manifestations (22). In such cases, the disturbance of ocular motility is often combined with vertigo (23), gait unsteadiness, and oscillopsia (image wobble). The causes are varied: an acute onset is usually ischemic in nature, while a chronic, progressive course often reflects a neurodegenerative disease. The nuclei that coordinate various eye movements are illustrated in Figure 2.

Figure 2

Sagittal section through the brainstem, from the midbrain (top) to the medulla (bottom). The supranuclear centers subserving specific types of eye movement are shown: NPH, nucleus prepositus hypoglossi; PPRF, paramedian pontine reticular formation; riMLF, rostral interstitial nucleus of the medial longitudinal fasciculus.

The ocular tilt reaction (OTR) is a typical example of an acute vertical eye deviation, known as vestibular skew deviation (SD). It consists of a constellation of findings including head tilt, vertical eye misalignment, and torsion of both eyes in the same direction toward the lower-lying eye. It is accompanied by a perceptual disturbance of the subjective visual vertical in the form of a tilt, also toward the side of the lower-lying eye (24). Patients mainly notice vertically displaced diplopia that is caused by the skew deviation, as well as instability of stance and gait, with a tendency to fall to one side. Lower brainstem lesions cause ipsilateral OTR, while higher brainstem lesions cause contralateral OTR.

Internuclear ophthalmoplegia (INO) is a further cause of intermittent horizontal diplopia (25). One eye fails to be adducted during attempted conjugate gaze to the opposite side, but convergence (adduction of both eyes for near vision) remains intact. INO is typically found in younger patients with multiple sclerosis and in older patients who have had a lacunar stroke.

The disturbances revealed by examining skew deviation, eye torsion, the subjective visual vertical in both binocular and monocular vision, and the eye movements mentioned above (see Table) fall into characteristic patterns that are caused by lesions at specific anatomical sites. This enables the precise topographical localization of the disturbance. An etiological classification (e.g., ischemia, hemorrhage, multiple sclerosis, mass lesions) is usually possible by history-taking, imaging studies, laboratory tests, and cerebrospinal fluid analysis.

Cerebellar disorders can also cause diplopia, as the cerebellum plays an important role in binocular vision. This is especially true of horizontal diplopia on distant gaze in a middle-aged or elderly patient, which is often due to cerebellar divergence insufficiency or esophoria/esotropia (26).

In diplopia of neurological origin, an important question is whether the responsible lesion lies in the central or the peripheral nervous system. The authors of one study concluded as follows (27):

• Dizziness more commonly accompanies diplopia of central origin (44%) than diplopia of peripheral origin (10%).
• Oculomotor disorders of a central type (saccadic smooth pursuit, INO, SD) are more common in patients with central lesions (87% versus 33%).
• A pathological deviation from the subjective vertical, as determined by monocular testing of the unaffected eye, is more common in central (77%) than in peripheral (39%) disorders.
• The presence of all three factors has a positive predictive value of almost 100% (95% confidence interval: [50; 100]) for the presence of a central lesion.

Conflict of interest statement
WAL is co-editor of the journals Die Ophthalmologie, Klinische Monatsblätter für Augenheilkunde, and Neuroretina. He has received lecture honoraria from Thea, Infectopharm, and MedUpdate. He serves as a consultant for Santen, Amgen, and Boehringer Ingelheim. He has received grants for clinical trials from the DFG and the BMBF.

AE has received lecture honoraria from Amgen, Argenx, Viridian, Sling, and Sanofi. She has served on advisory boards for Amgen, Viridian, Roche, and Argenx and has received research support from Sling, Argenx, Sanofi, and Ethyreal. She has participated in clinical trials for Amgen, Viridian, Argenx, Roche, Immunovant, and Novartis.

MO has received lecture honoraria from Santhera and Chiesi and funding for clinical trials from Chiesi and the DFG.

MD has received study funding from the DFG and the German Neurology Foundation.

MSt is co-editor of the Journal of Neurology, editor-in-chief of Frontiers of Neurootology, and co-editor of Sektion F1000. He has received lecture honoraria from Abbott, Auris Medical, Biogen, Eisai, Grünenthal, GSK, Henning Pharma, Interacoustics, J&J, MSD, NeuroUpdate, Otometrics, Pierre-Fabre, TEVA, UCB, and Viatris and funding for clinical studies from Decibel (USA), Cure within Reach (USA), and Heel (Germany). He markets the “M-Glasses” and the free “Positional Vertigo App.” He serves as a consultant for Abbott, AurisMedical, Bulbitec, Heel, Sensorion, Vifor, and Vertify. He is a scientific co-founder, investor, and shareholder of IntraBio.

TL is a board member of the German Society for Strabology, Neuro-Ophthalmology, and Pediatric Ophthalmology (GSNK).

Manuscript received on 18 September 2025, revised version accepted on 20 January 2026.

Translated from the original German by Ethan Taub, M.D.

Corresponding authors
Prof. Dr. med. Wolf Alexander Lagrèze

Prof. Dr. med. Dr. h.c. Michael Strupp

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