Diplopia or ‘seeing double’, can have many causes ranging from the severity of an intracranial tumour to more benign causes such as dry eye. It can be a common presenting complaint in ophthalmology therefore it is important to have a good approach to this. There are two types of diplopia; monocular diplopia is usually the result of a refractive error, whilst binocular diplopia is commonly due to impaired extraocular muscle function.
A good history is indispensible; the following are some key points to cover.
Horizontal diplopia with no vertical separation, as can be seen in figure 2, is due to impaired function of lateral rectus and/or medial rectus. This can also commonly occur due to a sixth nerve palsy.
Vertical or tilted diplopia can be indicative of a fourth nerve palsy.
Paralytic cause - diplopia when looking in direction of paralytic muscle
Restrictive cause - diplopia when looking away from restrictive muscle
The assessment of diplopia varies slightly depending on the presence of monocular or binocular diplopia, however regardless of the cause a good basic examination of the eye is essential.
- Head posture – a turned face points towards a sixth nerve palsy, whilst a downward facing chin indicates a fourth nerve palsy.
- Strabismus – is there an obvious squint?
- Proptosis, lid lag, lid retraction – all suggest underlying thyroid disease
- Ptosis – could be due to a complete or partial third nerve palsy or myasthenia gravis
- Limited abduction - sixth nerve palsy
- All movements limited except abduction – third nerve palsy or restrictive thyroid eye disease
- Nystagmus in extreme abduction and adduction – multiple sclerosis
These investigations are mainly conducted for binocular diplopia. The main investigation is the Hess Chart; this is used to assess patient eye position and movement. This produces a pictorial representation of eye movements, as seen in figure 3.
Other investigations in the case of diplopia relate to the suspected pathology. The main modes of imaging are CT and MRI, again, these should be requested when relevant and should not be carried out ‘blindly’.
The causes of diplopia vary greatly and therefore a broad outlook is needed when approaching this. The various conditions are summarised in figure 4, as well as a general clinical approach to diplopia.
There are some important conditions to consider when dealing with a patient presenting with diplopia; these are summarised with the key presenting features in figure 5 and are covered in more detail below.
Complete third verve palsy – Oculomotor
This involves the oculomotor nerve which supplies the majority of the extraocular muscles of the eye. The eye deviates down and out as there is intact functioning of the abducens and superior oblique muscles. There is also ptosis due to the paralysis of levator palpebrae superioris, which is the main lid retractor. A dilated pupil is also seen as the parasympathetic pupil-constrictor fibres originate from the Edinger-Westphal nucleus and travel within the third nerve.
The majority of these are due to ischaemic events at the nerve secondary to hypertension or diabetes. The most important diagnosis to rule out is a posterior communicating artery aneurysm that may be pushing on the nerve. An MRI and angiography may be necessary to identify the underlying cause.
Sixth nerve palsy - Abducens
This supplies the lateral rectus and a palsy of this nerve leads to the loss of the ability to abduct the eye (turn out). Patients often turn their head to compensate for the diplopia.
Fourth nerve palsy - Trochlear
This innervates the superior oblique muscle. This is one the most difficult palsies to diagnose and often gets missed. Patients present with an upward deviation of the affected eye and ‘cyclotorsion’ may be present where there is twisting of the eye that makes the patient tilt their head away from the lesion.
A fourth nerve palsy can be due to trauma, an ischemic event, or be a late presentation of a congenital abnormality. This nerve is the most susceptible to injury as it runs the longest course within the cranial vault.
This is a rare autoimmune disease where antibodies are produced to the nicotinic acetylcholine receptors at the neuromuscular junction of striated muscle. Patients present with muscle fatigue which can often involve the eye, leading to diplopia and ptosis. These are usually worse on upward gaze.
Diagnosis is made by conducting a tensilon test where edrophonium chloride (an anticholinesterase) is given and the patient is observed for any improvement in symptoms as their ACh levels build up. Treatment depends on the stage of the disease progression; initially acetylcholinesterase inhibitors are of some benefit, later on steroids are found to be useful.
This is also known as giant cell arteritis. It can lead to blindness and therefore it is important to be mindful of this in the context of diplopia.
Temporal arteritis is a vasculitis of the medium-sized blood vessels. It predominantly affects the arteries supplying the head, face, and eyes. If blood supply to the eye is affected this can lead to visual loss. The typical patient is usually older than 60, presenting with sudden, painless loss of vision. Other symptoms to be aware of include scalp tenderness, headache, jaw claudication, myalgia, fever and weight loss.
Investigations such as ESR are important but diagnosis is made by temporal artery biopsy. High dose steroids should be started promptly; the main reason for treatment is to protect the vision in the unaffected eye.
Diplopia can relate to many different pathologies varying in severity. This can be challenging to deal with and a systemic approach starting with a good history and examination forms the basis of establishing a diagnosis, leading to good patient management.
Danchaivijitr C, Kennard C. Diplopia and eye movement disorders. J Neurol Neurosurg Psychiatry. 2004;75:24-28
Karmel M. Deciphering Diplopia. Eyenet Nov/Dec 2009. p31-34. http://www.aao.org/publications/eyenet/200911/feature.cfm [accessed 2012 July 25]
OphthoBook. Introduction to Neuro-ophthalmology. http://www.ophthobook.com/chapters/neuroophthalmology [accessed 2012 July 26)
Figure 3 & 4 – Adapted from Danchaivijitr C, Kennard C. Diplopia and eye movement disorders. J Neurol Neurosurg Psychiatry. 2004;75:24-28
Figure 5 – Adapted from Karmel M. Deciphering Diplopia. Eyenet Nov/Dec 2009. p31-34. http://www.aao.org/publications/eyenet/200911/feature.cfm [accessed 2012 July 25]
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