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Emergency and Acute Medicine – Diplopia
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
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