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The cover and uncover tests help to further classify concomitant squints. These tests are not for patients with incomitant squints. Comitant squints that are present at all times of the day are called tropias (manifest squints), while those are only present when the binocular fusion is broken are called phorias (latent squints).
Technique
An object to focus on is held in front of the patient who is instructed to focus on it.
Cover test
One eye is completely occluded for several seconds and the uncovered eye is observed for movement as it focuses on the object. This eye is then covered and the other eye is observed for movement. Movement of the eye outwards confirms that there is an esotropia (the eye was turned inwards initially) and vice versa for exotropia. If a tropia is identified then the uncover test is not done.
Uncover test
One eye is completely occluded for several seconds and then uncovered. Observe for movement upon uncovering the eye. Movement of the eye outwards on uncovering confirms an esophoria (the eye was turned inwards when binocular fusion was broken), and vice versa for exophoria.
Clinical importance
Tropias are clinically important conditions as their presence indicate that the eyes are constantly misaligned. As they usually occur during early childhood, the brain may compensate for confusion by suppressing the vision of the misaligned eye. This causes poor development of vision in the affected eye and is termed amblyopia. Phorias are not clinically important because misalignment is only present occasionally. The eye tends to drift inwards or outwards when binocular fusion is weak. This is common during major illness or when tired at the end of the day. With age, binocular fusion weakens and patients may have increasing episodes of phoria.
Common mistakes in examinations
Performing the cover and uncover test at the same time. It is best to perform the cover test for each eye first and then perform the uncover test for each eye afterwards to avoid confusion.
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Stereopsis (three dimensional vision) is important in our every day lives. This ability is dependent on aligning both foveae on the same object with slightly dissimilar perspectives to give a perception of depth. The loss of ability to align and co-ordinate our eyes result in the loss of stereopsis, and can lead to diplopia (double vision), especially when loss of co-ordination is acute in onset.
Technique
Ocular alignment
Hold a torch an arm’s length away from the patient and shine it equally on both eyes. Look at the position of the corneal light reflection (not the red light reflex). This is usually at the centre of each pupil. If one side or the other is towards the outer edge, this indicates an inward deviation of the globe (esotropia) and if there is a reflex more towards the inner edge of the pupil, there is an outward deviation of the globe (exotropia).
Ocular motility
Sit the patient directly opposite you at one arm’s length distance
Advise the patient you will help keep his/her head still during the examination
Advise the patient to fixate on a target (red pin or finger) and follow the object with their eyes only
Gently but firmly place a hand on their forehead and with the other, test all the positions of gaze in that hemifield. Swap hands and do the same in the other hemifield. Look for limitation of globe movement, presence of nystagmus and ask for diplopia, blurring or loss of the image. By the end you will have drawn a union jack with your hand movements
Clinical importance
An abnormality in ocular alignment in the primary position is called a squint. After identification of a squint, they can further classified as concomitant or incomitant on testing the extraocular movement. A concomitant squint is one where the angle of deviation between the two eyes remains the same at all directions of gaze. The underlying cause is usually a co-ordination problem between the two eyes and is the most common form of squint. These patients usually do not have diplopia as the brain has been given time to suppress one of the two images. An incomitant squint is one where the angle of deviation between the two eyes changes according to the direction of gaze. The underlying cause is usually a muscle paralysis (ophthalmopegia) or restriction. Paralytic conditions include cranial nerve palsies (mono-neuritis), neuromuscular junction disease (myasthenia gravis), muscle weakness (mitochondrial diseases – Kearns-Sayre syndrome). Restrictive conditions include orbital fractures with herniation/entrapment of extra-ocular muscles, or inflammatory diseases of the extraocular muscles (thyroid eye disease).
Approach to a patient with diplopia
When coming across a patient reporting diplopia, the most important question to ask is whether the double vision is still present when either eye is closed.
Still present on covering either eye – Monocular diplopia
Reversed with pinhole, indicates local ocular diseases such as refractive errors, cataracts, eccentric intraocular lens implants, misaligned spectacles, non-organic causes
There is one main image and one ghost image (less clear), they are always touching
Absent when covering either eye – Binocular diplopia
Indicates the likely presence of an incomitant squint
There is no ghost image. Both images are as sharp as each other
Examine extraocular movement, pupils and eyelid (for mass)
Always remember to rule out a dangerous orbital condition when multiple cranial nerves are involved: orbital cellulitis, local invasion of the orbital apex by a tumor (most commonly nasopharyngeal carcinoma in Hong Kong), cavernous sinus thrombosis. If the superior orbital fissure or cavernous sinus are suspected to be involved, always check ipsilateral corneal sensation (V1) and cheek sensation (V2)
Four orbital conditions you must not miss: orbital lymphoma, lacrimal gland epithelial tumors, mucormycosis, giant cell arteritis
To investigate for orbital involvement consider neuroimaging:
o Computed tomography scan of the orbit with contrast: better for pre-operative planning as the extent of bone erosion can be assessed
o Magnetic resonance imaging of the orbit with contrast: better for determining the extent of soft tissue lesions
Diagnostic considerations for isolated cranial nerve palsies affecting extraocular movement
Whilst most acquired isolated oculomotor and abducent nerve palsies are due to mononeuritis, it is important to note than 16-19% of oculomotor nerve palsies are caused by aneurysms. This is a potentially life-threatening condition and an oculomotor nerve palsy may be the only prodrome to a ruptured aneurysm. For a ruptured aneurysm 45% of patients die before reaching the hospital. Of the remaining 55%, only 20% are alive at 10 years. Furthermore 65% of survivors suffer permanent cognitive impairment. The most common location of the aneurysm is at the junction of the internal carotid artery and the posterior communicating artery. If an aneurysm is suspected, an angiogram is indicated.
The most common cause of acquired trochlear nerve palsy is head trauma.
Magnetic resonance angiogram
Detects 98% of all aneurysms
High sensitivity for lesions 3 mm or larger
However a magnetic resonance angiogram is difficult to obtain on an emergency basis
Computed tomography angiogram
100% sensitive for large aneurysms
65% sensitive for small aneurysms
However, no patient with a negative computed tomography angiogram scan has ever had ruptured aneurysms in reported literature
Important differential diagnosis of isolated cranial nerve palsies affecting extraocular movement – Myasthenia gravis
Always consider myasthenia gravis as a differential diagnosis for a patient presenting with ophthalmoplegia. Signs to look for include ptosis and ophthalmoplegia, especially with associated fatigability. Ocular myasthenia gravis is common in Asia and there may be no other systemic signs. This condition is able to mimic any disorder causing binocular diplopia except for pupil involving oculomotor nerve palsy. The type of ophthalmoplegia may vary at different times of day and different clinic visits. Myasthenia gravis can occasionally mimic inter-nuclear ophthalmoplegia, however saccadic movement is not reduced.
Specific tests for ocular myasthenia gravis
Cogan’s lid twitch: Advise the patient to look down for 5-15 seconds. This frees up as many acetylcholine receptors as possible. Then ask the patient to look straight ahead. Patients with myasthenia gravis may show a twitch on looking straight ahead due to hypersensitivity of the neuromuscular junction.
Enhancement of ptosis: This is based on Hering’s law of equal innervation of both eyelids. If you manually elevate one eyelid, there is decreased muscle tone on the ipsilateral and contralateral eyelids, causing the contralateral side to come down. This is exacerbated in patients with myasthenia gravis.
Osher’s peek sign: Ask the patient to close their eyes tightly. Myasthenic patients have weak orbicularis oculi and thus one or both eyes may appear to be peeking.
Sleep test: Asking the patient to sleep in a quiet room for 30-45 minutes may show marked enhancement of eyelid and extraocular muscle function.
Ice pack test: Reduction of temperature reduces anti-AChR antibody activity. Place an icepack on both closed eyes for 2 minutes and then reassess eyelid and extraocular muscle function. Myasthenic patients will show improvement.
For generalized myasthenia gravis, cholinesterase inhibitors are the mainstay for treatment. However this has been shown to be of limited effectiveness in ocular myasthenia gravis. Instead systemic steroids or other immunosuppressant agents are 2-3 times more likely to improve ocular systems than cholinesterase inhibitors. There is also a role for systemic steroids in preventing secondary development of generalized myasthenia gravis.
Common mistakes in examinations
Performed too quickly, preventing patients from properly reaching the limits of their extra-ocular movement
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Direct ophthalmoscopy is a troublesome skill for medical students and practitioners, but when practiced frequently, this is a technique that can be very useful in clinical practice. It is advisable that each medical student should purchase their own direct ophthalmoscopes as this technique is assessed in junior clerkship, senior clerkship and specialty clerkship. It is an essential skill for every medical practitioner.
Technique
Sit the patient comfortably in a dimly lit room. Explain to the patient that you are going to get very close to his/her face and shine a bright light into his/her eye. Advise the patient not to look directly into the light. Dilating the pupils greatly improves fundal view.
Always use your right eye to examine the patient’s right eye and your left eye for the patient’s left eye. Stand on the same side of the eye you are examining.
Stand at one arm’s length away from the patient and shine the ophthalmoscope on the patient’s pupil to look for a red-light reflex (while you are looking through the ophthalmoscope). The presence of a strong red-light reflex indicates a lack of media opacity (cataracts, vitreous haemorrhage, intraocular tumors).
Continue to fixate on the red-light reflex while you move closer to the patient’s eye. The first structure to look for is the optic disc (on the nasal side of the retina). Once you have found this, adjust the focus of your ophthalmoscope till the structures are at its sharpest. Look for optic disc pallor or swelling.
Then work your way along each of the four main retinal vascular branches to look for exudates and haemorrhage.
Finally ask the patient to look directly at the light to see the patient’s macula.
Clinical importance
The most important situation where a medical practitioner will have to perform a direct ophthalmoscope examination is in a patient with severe headache, where an intracranial space-occupying lesion is suspected. The presence of bilateral optic disc swelling (papilloedema) should point the examiner to raised intracranial pressure. Urgent referral to the Accident and Emergency Department is warranted. Direct ophthalmoscopy is also useful in the assessment of disorders of the optic nerve.
Approach to optic neuropathies
Disorders of the optic nerve may present with optic disc swelling during the acute phase and optic atrophy during the chronic phase. In both phases, signs of optic nerve dysfunction will be present and should be looked for.
Important signs to check
Visual acuity
Red-green colour desaturation
Visual field
Relative afferent pupillary defect
The diagnosis of an optic neuropathy and the determination of its cause usually cannot be made based on disc appearance alone.
Most common causes in children (usually bilateral)
Tumors compressing on the visual pathway
Trauma to the optic nerve
Hereditary optic neuropathies
Most common causes in adults
Ischaemic optic neuropathies
Optic neuritis
Tumors compressing on the visual pathway
Scenario 1: Acute unilateral visual loss with normal fundus exam
Young adult with sudden onset visual loss with pain around and behind eye as well as pain on eye movement
The most important differential diagnosis is optic neuritis
In this condition women are affected more than men
There is decreased central vision and more important red-green desaturation (often out of proportion to the drop in visual acuity). Relative afferent pupillary defect is positive
In 2/3 of patients with optic neuritis, the disc appearance is normal, as it is a retrobulbar neuritis
The most common cause in Western countries is demyelination
In Asia, although demyelination is still the most likely diagnosis, systemic inflammatory and infectious diseases should be considered (syphilis, Cat-scratch disease)
If an infective cause has been ruled out, patients are usually treated with a course of systemic steroids to hasten recovery
Patients should then be investigated with investigations such as cranial +/- spinal magnetic resonance imaging (to determine whether there are other demyelinating lesions), lumbar puncture for oligoclonal bands and blood for anti-aquaporin-4 antibody (in patients with neuromyelitis optica – also known as anti-NMO antibody)
Scenario 2: Subacute unilateral visual loss with a normal fundus
The most common diagnosis is non-arteritic ischaemic optic neuropathy
There is usually no eye pain or pain on movement
Red-green desaturation usually mirrors the drop in visual acuity
Visual field examination usually gives an altitudinal or arcuate field defect
Relative afferent pupillary defect is usually present
Patients are usually over 55 years of age, men and women are equally affected
Look for underlying systemic vasculopathy (hypertension, hyperlipidaemia, diabetes mellitus, migraine, obstructive sleep apnea). Other risk factors include use of erectile dysfunction drugs (vasodilators) and amiodarone use
One important differential diagnosis is arteritic ischaemic optic neuropathy secondary to underlying giant cell arteritis (also known as temporal arteritis)
Clinical features of this condition include profound cupping of the disc with a pale neuro-retinal rim (chalky white appearance)
Associated local symptoms include jaw claudication, tongue claudication, scalp tenderness and ear pain
Associated systemic include recent weight loss, flu-like illness, polymyalgia rheumatica
Scenario 3: Acute bilateral simultaneous visual loss
Differential diagnoses include: intracranial mass, optic neuritis (especially that associated with neuromyelitis optica) and ischaemic optic neuropathy
The most common area of compression by an intracranial mass is at the optic chiasm by a pituitary lesion. If the patient develops acute visual loss with bitemporal hemianopia, pituitary apoplexy should be suspected
Common mistakes in examinations
Claiming to see the red light reflex without looking through the ophthalmoscope
Injuring the patient with the ophthalmoscope
Accidentally kissing the patient during examination
Failure to get close enough to properly focus on the patient’s retina
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