Introduction

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. 

 

History

A good history is indispensible; the following are some key points to cover.

 

  • Pain -  this is essential to ask about in order to rule out a third nerve palsy resulting from a posterior communicating artery aneurysm, which is a neurological emergency.

 

    • Binocular or Monocular - establishing the nature of the diplopia helps to narrow down the cause, this can be done simply by carrying out the cover – uncover test. If the diplopia is still present when one eye is covered, this is monocular. If the diplopia disappears when one eye is covered this is binocular and is due to misalignment of the visual axes. The differences between monocular and binocular diplopia can be seen in figure 1. 

     

    • Image alignment - is the diplopia horizontal, vertical or oblique? This can help signpost the cause of the diplopia and therefore is important to ask about.

     

    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.

     

    • Direction of gaze - this can be used to help locate the extraocular muscles involved and help to identify whether it is due to a paralytic or restrictive cause.

     

    Paralytic cause - diplopia when looking in direction of paralytic muscle

    Restrictive cause - diplopia when looking away from restrictive muscle

     

    • Constant or intermittent - the characteristic timing of the diplopia is important as intermittent diplopia which is worse at the end of the day can suggest myasthenia gravis.

     

    • Exacerbating or relieving factors - monocular diplopia can be improved by blinking if due to astigmatism or dry eyes, however there is no change if the diplopia is caused by macular disease or cataract.  

     

    • Trauma - It is important to enquire about any recent trauma. Any eye or head injury could lead to diplopia through various mechanisms.

     

    • Past medical history - This is an integral part of assessing diplopia as any childhood strabismus, past prism correction via glasses and past ocular surgeries can lead to the development of subsequent diplopia.  

     

    • Other medical conditions - It is important to remember the bigger picture and therefore other systemic diseases should be asked about such as diabetes, hypertension, temporal arteritis and thyroid disease. Neurological symptoms should also be asked about such as weakness, paraesthesia, blurred vision, loss of hearing, balance, dysphagia and headaches.

     

     

     

    Figure 1 - Difference between monocular and binocular diplopiaFigure 2 - Double vision

    Examination

    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.

     

    • Observation -  The most important aspect of examination, inspect the patient looking for clues.

     

      -       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

       

      • Visual acuity – may be reduced

       

      • Assess extraocular movements – these can be a cause of binocular diplopia. Assessment should be carried out by asking the patient to look straight ahead and follow your finger/pen as you draw a ‘H’ shape. Remember to ensure the target (finger/pen) is 50cm away from the patient to avoid convergence.

       

      -       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

       

      • Pupils – essential to assess these as ipsilateral dilatation and a painful third nerve palsy could be suggestive of a posterior communicating artery aneurysm. This can be fatal and urgent referral to a neurologist is needed. Rapid afferent pupillary defect (RAPD) can be an indication of optic nerve compression secondary to thyroid eye disease or an orbital tumour.

       

      • Fundi – these are usually normal however changes can point towards underlying diseases such as hypertension and diabetes.

       

      • Cranial nerves – a full cranial nerve exam is also necessary in binocular diplopia to exclude any other sinister causes. 

       

      Investigations

      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’. 

       

      Figure 3: Hess Chart

      Causes

      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.   

       

      Figure 4: Causes of diplopia

      Figure 5

      Important conditions

      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.

       

      Myasthenia Gravis  

      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.  

       

      Temporal Arteritis

      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. 

       

       

      Summary

      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.  

       

       

      References

      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)  

      Images

      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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