Approach to diplopia: Clinical sciences

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Introduction 0:00–0:28

Diplopia, or double vision, is the visualization of two images of a single object. Diplopia might be the result of impaired function of the structures within the eye itself, or due to impaired ocular motility that causes misalignment of the eyes.
Diplopia can be classified as monocular, if it’s present when one eye remains closed, or binocular if it’s present only when both eyes are open.
Now, if your patient presents with double vision, start with a focused history and physical exam. They might describe double vision like seeing two images of the same object side by side or one above the other.

History and physical/Monocular diplopia 0:28–1:14

If on physical exam, these symptoms persist with one eye closed, that’s monocular diplopia. This means that there’s pathology in the eye that perceives the visual abnormality, the open eye.
Next, perform a pinhole exam, in which you ask the patient to read an eye chart through a pinhole. If their vision does not improve, the likely diagnosis is macular disease.
Some common causes include macular edema from diabetic retinopathy, age-related macular degeneration, and uveitis. On the flip side, if the patient’s vision does improve with the pinhole exam, your next step is to assess for lens opacity on the fundoscopic exam.

Cataract/Refractive error 1:14–1:53

If lens opacity is present, you should diagnose a cataract. Risk factors for cataract development include advanced age, sunlight exposure, tobacco use, diabetes, and corticosteroid use.
However, if lens opacity is absent, you can diagnose refractive error. The different types of refractive error are hyperopia, otherwise known as farsightedness; myopia, known as nearsightedness; and astigmatism, which is an irregular curvature of the cornea.
Okay, let’s go back to the history and physical exam and look at some different findings. As before, patients report double vision.

Binocular diplopia 1:53–2:18

However, their symptoms improve with either eye closed on a physical exam, meaning that the double vision is due to misalignment of the eyes.
In this case, we are talking about binocular diplopia. To find the cause you should assess the orientation of diplopia.
If your patient sees one object on top of the other, they are experiencing vertical diplopia, which is suggestive of cranial nerve IV, or trochlear nerve, palsy.

Cranial nerve 4 palsy 2:18–3:05

The trochlear nerve innervates the superior oblique muscle, which intorts, depresses, and abducts the eye. Here’s a clinical pearl!
In trochlear nerve palsy, the patient will likely have a head tilt away from the affected eye. If there is a history of a chronic head tilt, which might be present in photos or by report, they have decompensated congenital cranial nerve IV palsy.
In this case, they were born with trochlear nerve palsy, but experience symptoms later in life. On the flip side, if history reveals a recent head trauma, you are dealing with traumatic cranial nerve IV palsy.
Next, let’s consider a patient with horizontal diplopia, meaning they see the same object side by side. Here, you’ll need to assess for pupillary dilatation.

Cranial nerve 3 palsy 3:05–5:04

Parasympathetic innervation of the pupil comes from cranial nerve III, or oculomotor nerve, of the same side, and allows for pupillary constriction.
If you see a dilated pupil that doesn’t react to light, consider cranial nerve III palsy. The oculomotor nerve also innervates the inferior oblique muscle, and the superior, medial, and inferior recti muscles, as well as the levator palpebrae superioris, which elevates the upper eyelid.
So, if the exam shows impaired adduction, elevation, and depression of the eye; the eye position is “down and out” at rest; and there is ptosis, diagnose a cranial nerve III, or oculomotor nerve, palsy.
Time for a couple of clinical pearls! Patients with oculomotor nerve palsy might also report an oblique or diagonal orientation of their diplopia, as the muscles that control both horizontal and vertical movements are affected.
Also, because adduction is impaired, patients might report worsening double vision when looking at near objects. Now, in some cases of oculomotor nerve palsy, the pupil size and reflex will appear normal.
This happens with ischemic mononeuropathy, which is caused by decreased blood supply due to microvascular damage that can occur with diabetes or hypertension.
Parasympathetic fibers of cranial nerve III that innervate the pupillary sphincter and constrict the pupils run along the outer surface of the nerve, so they are less susceptible to ischemia.
On the other hand, if there is compression of the nerve causing pressure on the parasympathetic fibers, the pupil will become dilated and the pupillary reflex will be sluggish or absent.
A common cause of compression is an aneurysm on the posterior communicating artery, which you can confirm with angiography.
Okay, let’s talk about cases where the pupil is not dilated, which should make you consider cranial nerve VI palsy or internuclear ophthalmoplegia.

Cranial nerve 6 palsy 5:04–6:59

To distinguish between the two, assess ocular motility. Remember that cranial nerve VI, also known as the abducens nerve, innervates the lateral rectus muscle.
So, if the physical exam reveals impaired abduction of one or both eyes, think cranial nerve VI palsy. Remember, since abduction is affected, patients might report worsening of double vision with far vision.
Here’s a clinical pearl! Unilateral abducens nerve palsy is often due to ischemic mononeuropathy of the cranial nerve VI.
However, if you see bilateral abducens nerve palsies, consider increased intracranial pressure as the cause, and make sure to obtain head imaging.
A fundoscopic exam in this case may also show papilledema. Alright, if the physical exam shows impaired adduction in one eye and nystagmus of the contralateral abducting eye during lateral gaze, consider internuclear ophthalmoplegia.
This is due to a lesion in the medial longitudinal fasciculus which is in the dorsomedial brainstem and connects cranial nerves III and VI on opposite sides to coordinate gaze.
The most common cause of internuclear ophthalmoplegia in younger patients is demyelinating disease, such as multiple sclerosis, while the most common cause in older patients is stroke.
A brain MRI will help with your diagnosis. Here’s a high-yield fact!
Cranial neuropathies can result from injury of the nerve axon or the nuclei. Any lesion in the brainstem, such as a stroke, demyelination, or tumor, can affect cranial nerve nuclei, cause cranial nerve palsy, and affect eye movements.
Okay, let’s go back to the orientation of diplopia and discuss patients with both vertical and horizontal diplopia. Your next step here is to assess for external ocular findings, such as proptosis, chemosis, conjunctival injection, or periorbital edema.

Cavernous sinus syndrome 6:59–7:51

If these symptoms are present, assess for ipsilateral trigeminal neuropathy, or dysfunction of cranial nerve V, which would manifest as facial numbness.
If facial numbness is present, cavernous sinus syndrome is the likely cause of double vision. The cavernous sinus contains cranial nerves III, IV, the ophthalmic and maxillary branches of cranial nerve V, as well as cranial nerve VI.
In other words, lesions in the cavernous sinus, such as a thrombus or infection, could cause dysfunction of any of these nerves.
On the flip side, if your patient has external ocular findings, in particular proptosis, lid retraction, and conjunctival injection, but no facial numbness, consider thyroid-associated ophthalmopathy.

Thyroid-associated ophthalmopathy 7:51–8:37

Other exam findings you may see in this condition include goiter and pretibial myxedema, which is discoloration and thickening of the skin on the shin, along with edema.
In this case, send labs for TSH receptor antibodies and thyroid function tests, and get a CT or MRI of the orbits. If TSH receptor antibodies are elevated, with or without abnormal thyroid function tests, and imaging shows edema and hypertrophy of the extraocular muscles, you should diagnose thyroid-associated ophthalmopathy.
Finally, let’s talk about patients with both vertical and horizontal diplopia but no external ocular findings. Your next step here is to assess the time course of diplopia.

GBS: Miller-Fisher variant 8:37–9:22

If your patient’s initial symptoms have been progressively worsening over days to weeks, and they’ve noticed new symptoms since onset, consider the Miller-Fisher variant of Guillain-Barré syndrome.
These patients typically have a triad of ocular muscle weakness, ataxia, and absent reflexes. To make the diagnosis, perform a lumbar puncture and analyze the CSF.
If the CSF shows albuminocytologic dissociation, in other words, elevated protein in the setting of a normal white blood cell count, diagnose the Miller-Fisher variant of Guillain-Barré syndrome.
Lastly, if the patient reports intermittent double vision that gets worse with sustained gaze or at the end of the day, consider myasthenia gravis.

Myasthenia gravis 9:22–9:58

This condition is due to an autoimmune attack of the postsynaptic receptors at the neuromuscular junction and can cause weakness of the extraocular muscles, along with muscles of the head, neck, limbs, and those used in respiration.
In this case, order serum antibodies against acetylcholine receptor, muscle-specific kinase, and lipoprotein receptor-related protein 4.
If any of these are positive, you can diagnose myasthenia gravis. Alright, as a quick recap… Monocular diplopia suggests macular disease, cataract, or refractive error.

Review 9:58–10:46

On the other hand, binocular diplopia suggests impaired ocular motility. If the diplopia is vertical, consider cranial nerve IV palsy.
If the diplopia is horizontal and the pupil is dilated with poor reactivity, think cranial nerve III palsy. However, if there is no pupil involvement, consider cranial nerve VI palsy or internuclear ophthalmoplegia.
Lastly, if there is both vertical and horizontal diplopia, assess for external ocular findings. If you see any, consider cavernous sinus syndrome or thyroid-associated ophthalmopathy.
However, if there are no external ocular findings, consider Miller-Fisher variant of Guillain-Barré syndrome or myasthenia gravis.