Diplopia Flashcards

1
Q

What is diplopia?

A

Double vision.

Diplopia is a common complaint in medical practice. It may be monocular or binocular. An understanding of the anatomy of the eye, external ocular muscles and their innervation is essential to approach diagnosis of the cause.

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2
Q

What is binocular diplopia?

A

This occurs when the images produced by the two eyes do not absolutely match, so that the images produced are misaligned relative to one another. The diplopia disappears when one eye is covered.

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3
Q

What is monocular diplopia?

A

This is much less common. It affects one eye only and continues when the unaffected eye is covered. It can be caused by abnormalities of the lens, cornea or retina, which result in splitting of the image.

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4
Q

What are the causes of diplopia?

A

Cornea and lens problems
Eye muscle disorders
Nerve problems
Brain problems

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5
Q

What are examples of cornea and lens problems resulting in diplopia?

A

This leads to production of unequal images.
These include refractive errors, keratoconus, cataracts, corneal scarring, subluxation and herpes zoster. Dryness of the cornea can occasionally cause double vision.

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6
Q

What are examples of eye muscle disorders resulting in diplopia?

A

Myasthenia gravis
Grave’s disease
Myotonic dystrophy
Muscles such as inferior rectus may be trapped during basal orbital fracture.
Convergence insufficiency (treated with glasses, eye exercises or prisms)

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7
Q

What are examples of nerve problems resulting in diplopia?

A

Problems affecting the nerve that control the eye muscles.
MS, GBS and DM.
Temporary palsy from Lyme disease, GCA, DM and HTN.
Nerves trapped in traumatic fracture of the orbital bones.

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8
Q

What are examples of brain problems resulting in diplopia?

A
Strokes 
Aneurysms 
Space occupying lesions
Migraine
Causes of raised ICP
-Raised ICP affects CNVI more as it has the longest intracranial course. 
Alcohol intoxication 
Concussion
Side effects of phenytoin, lamotrigine, opioids, zolpidem and ketamine.
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9
Q

How does diplopia present?

A

Diplopia presents either with a complaint of double vision or the observation of squint.

Paralysis of a muscle means that the eye will not move fully in the direction in which it pulls. At rest, when the other muscles are unopposed, the eye may therefore deviate in the opposite direction from the pull of the affected muscle.

Diplopia may occur alone or in conjunction with other symptoms such as pain on eye movement, pain around the eyes, ptosis, headache or nausea.

The patient will often complain of double vision. Images may overlap or be adjacent. It is helpful to ask about image alignment, whether they appear (or worsen) on a particular direction of gaze, and whether they are intermittent or constant.

It is also helpful to find out if the double vision disappears on closing one eye, and whether both images are in focus.

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10
Q

What are the signs associated with diplopia?

A

Check for ptosis which is often the first sign of weakness and eyelid elevation is partly controlled by CN III

Check the light reflex

Fundoscopy to rule out papilledema

Attempt to identify which eye is affected and which direction of gaze is limited. This will allow determination of which structures are likely to be involved. Examine the alignment of the eyes in various head positions and on looking in every direction.

Note whether one eye seems to be deviated. Isolated palsy of only one of the muscles supplied by the oculomotor nerve is unusual.

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11
Q

What are the causes of diplopia?

A
Abducens nerve palsy as seen in space-occupying lesion and DM. 
Psychosomatic- inconsistency of hx and unusual elements such as monocular double vision in both eyes.
Tiredness can cause transient diplopia. 
Myasthenia gravis
Parkinson's disease
Encephalopathy 
Progressive supranuclear palsy 
Sepsis 
Ophthalmoplegic migraine is a rare cause. 
GCA is another rare cause.
Sarcoidosis 
CJD
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12
Q

What are the red flags of diplopia?

A

Pupil involvement with third nerve palsy: large poorly reactive pupil with diplopia is the most common presentation of an aneurysm of the posterior communicating artery.

Diplopia affecting two or more of lip, pupil and eye movement. This may suggest isolated third nerve palsy (as above), Horner’s syndrome (small pupil and ptosis) due to carotid dissection, or inflammatory neuropathy (Guillain-Barré syndrome).

Multiple cranial nerve palsies: this suggests intracranial or meningeal tumour, polyneuropathy or cavernous sinus lesion.

Diplopia with weakness or fatigue: suggests myasthenia gravis.

Diplopia with new-onset headache and scalp tenderness: suggests giant cell arteritis.

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13
Q

What are the investigations done for diplopia?

A

Before referral, check for diabetes (if it is not already diagnosed) and check blood pressure in case of hypertension.

MRI scan may show a tumour, an area of infarction or even an arterial aneurysm pressing on a nerve. It can also show demyelination.

CXR may reveal malignancy or sarcoidosis.

Other specialist investigations may be offered depending on the suspected cause.

Isolated cranial nerve palsies in patients with diabetes and hypertension do not usually need investigation unless they progress or fail to resolve over time.

Multiple nerve palsies are usually imaged, as are isolated nerve palsies in patients aged under 50 years without a long history of vasculopathy.

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14
Q

What is the management of diplopia?

A

People with diplopia must not drive. They may resume driving on confirmation to the licensing authority that the diplopia is controlled by glasses or by a patch which the licence holder undertakes to wear whilst driving. There will probably be permanent revocation of an LGV or PCV licence.

Exceptionally, a stable uncorrected diplopia of six months’ duration or more may be compatible with driving if there is consultant support indicating satisfactory functional adaptation.

Diplopia (seeing double) can be very distressing.

All patients should be referred to an orthoptist (an orthoptist is an allied health professional who can investigate, diagnose and treat defects of binocular vision and abnormalities of eye movement)

In the first instance a patient may just simply choose to patch their eye – this will allow the brain to receive only one image.

If the patient wears spectacles, a temporary prism – fresnel prism, can be fitted and the power adjusted as the palsy resolves.

If a patient is left with residual diplopia, permanent prisms in their glasses can be considered or surgical intervention to realign the eyes.

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15
Q

What is oculomotor nerve palsy?

A

Oculomotor nerve palsy is a condition resulting from damage to the oculomotor nerve. The most common structural causes include:

  • Raised intracranial pressure (compresses the nerve against the temporal bone).
  • Posterior communicating artery aneurysm
  • Cavernous sinus infection or trauma.
  • Note: there are other pathological causes of oculomotor nerve palsy such as diabetes, multiple sclerosis, myasthenia gravis and giant cell arteritis.
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16
Q

How does oculomotor nerve palsy present?

A

The oculomotor nerve provides motor and parasympathetic innervation to some of the structures within the bony orbit. Therefore, the clinical features of CN III injury are associated with the eye:

  • Ptosis (drooping upper eyelid) – due to paralysis of the levator palpabrae superioris and unopposed activity of the orbicularis oculi muscle.
  • ‘Down and out‘ position of the eye at rest – due to paralysis of the superior, inferior and medial rectus, and the inferior oblique (and therefore the unopposed activity of the lateral rectus and superior oblique).
  • The patient is unable to elevate, depress or adduct the eye.
  • Dilated pupil – due to the unopposed action of the dilator pupillae muscle.
17
Q

What is the urgent consideration with oculomotor nerve palsy?

A

Urgently referred to the neurosurgeons as a posterior communicating artery/internal carotid artery aneurysm is found with neuroimaging- CT angiogram

18
Q

How does trochlear nerve palsy present?

A

Trochlear nerve palsy commonly presents with vertical diplopia, exacerbated when looking downwards and inwards (such as when reading or walking down the stairs). Patients can also develop a head tilt away from the affected side.

19
Q

What are the causes of trochlear nerve palsy?

A

They are commonly caused by microvascular damage from diabetes mellitus or hypertensive disease. Other causes include congenital malformation, thrombophlebitis of the cavernous sinus, and raised intracranial pressure.
Most commonly due to trauma

20
Q

What causes abducens nerve palsy?

A

Abducens nerve palsy can be caused by any structural pathology which leads to downwards pressure on the brainstem (e.g. space-occupying lesion). This can stretch the nerve from its origin at the junction of the pons and medulla.

Other causes include diabetic neuropathy and thrombophlebitis of the cavernous sinus (in these cases, it is rare for the abducens nerve to be affected in isolation).

21
Q

How does abducens nerve palsy present?

A

Clinical features of abducens nerve palsy include diplopia, the affected eye resting in adduction (due to unopposed activity of the medial rectus), and inability to abduct the eye.

The patient may attempt to compensate by rotating their head to allow the eye to look sideways.

Worse to affected side and at distance fixation

22
Q

What is thyroid eye disease?

A

Thyroid eye disease (TED) is the most common extra-thyroidal manifestation of Graves’ disease. It may also be associated with other forms of thyroid dysfunction and it may also occur in the absence of any biochemical thyroid dysfunction at all.

23
Q

What is the pathophysiology of TED?

A

TED is an organ-specific idiopathic autoimmune disease.

Infiltration of lymphocytes into orbital tissue stimulates the release of cytokines (eg, tumour necrosis factor and interleukin-1) which promote the release of mucopolysaccharides from fibroblasts.

The resulting hyperosmotic shift leads to oedema of the orbital fat and extraocular muscles, forcing the eyeball forward and leading to the typical appearance of exophthalmos.

It usually begins with an active inflammatory orbital phase lasting 6-24 months, during which expansion of extraocular muscles and orbital fat occurs.

There is progressive deterioration initially, followed by a peak before spontaneously improving.
The inflammatory phase is followed by an ‘inactive’ fibrotic phase.

The inactive phase is a chronic ‘burn-out’ phase where further changes are unlikely.

Sight loss can occur, usually when there has been delay in starting treatment.

The onset of hyperthyroidism and TED are usually within 18 months of one another. However, TED may also develop years before or after the onset of hyperthyroidism.

24
Q

What is the presentation of TED?

A

Initially, they relate to an increasingly ‘crowded’ orbit:
-Ocular irritation and ache (worse in the mornings) behind the eye, especially when looking up, down or sideways.
-Red eyes, cosmetic changes and diplopia (restricted ocular mobility, initially involving the inferior rectus muscles).
-Change in the appearance of the eyes (usually the patient or family notices staring or bulging eyes), dry or watery eye and mild photophobia.
-Swelling of the upper and lower lids, redness of the lids and eyes and difficulty moving the eyes.
-Proptosis (exophthalmos) may develop gradually, accompanied by:
Lid retraction and lid lag.
Conjunctival injection and chemosis (oedema).
Orbital fat prolapse.
Exposure keratopathy (photophobia, tearing, grittiness, pain) due to incomplete lid closure.

25
Q

What are the differentials for TED?

A
Allergic conjunctivitis 
Dry eye 
Orbital myositis 
Chronic progressive external ophthalmoplegia 
Myasthenia gravis 
Cushing’s syndrome
26
Q

What are the investigations for TED?

A

TFTs
CT or MRI of the orbit
Orthoptist review

27
Q

What are the associated diseases of TED?

A

Grave’s disease

Hashimoto’s disease

28
Q

What is the management of TED?

A

Ideally TED should be managed in a joint endocrinology and ophthalmology clinic where there is experience and expertise in the condition.

Treatment options include:
-Prisms to control diplopia.
-Botulinum toxin to reduce upper lid swelling.
-Medical treatments:
Oral or systemic steroids
Octreotide and lanreotide
Ciclosporin
Intravenous immunoglobulin
-Emerging treatments:
Selenium
Rituximab
Anti-tumour necrosis factor
Orbital radiotherapy.
-Surgical interventions:
Orbital decompression
Strabismus surgery
Lid-lengthening surgery
Blepharoplasty
29
Q

What is the prognosis of TED?

A

In thyrotoxic patients, 90% of proptosis improves and 30% of restrictive myopathy improves but proptosis rarely improves without further treatment. Poor prognostic factors include:

  • Older age at onset.
  • Rapid progression at onset.
  • Longer duration of active disease.
  • Drop in visual acuity during the active phase.
  • Male gender.
  • Smoker.
  • Diabetes.