In Optician 15.02.2019, we published an article looking at anomalies of the pupil and how to assess them (click here to view the article as a pdf). Here is a brief reminder of some of the key points raised in the article. 

  • Though there is a large variability both between the average pupil diameters of one individual’s eyes and also between the diameters of different individuals. A typical resting diameter of a pupil in a healthy young adult in daylight conditions is 4mm.
  • It is possible to categorise pupil function as having the following roles:
    • Social signal
    • Light regulation
    • Optical aperture stop
    • Clinical tool
  • Differences in pupil diameters is termed anisocoria. In most cases, therefore, this is a physiological anomaly and usually of no concern. Most authorities suggest that clinicians need only be concerned when presented with anisocoria of greater than 2mm difference, in the absence of other determining factors of course.
  • Anisocoria may be have a number of aetiologies. These can be categorised into three types:
    • Physiological – this describes pupils that are unequal simply due to variation in anatomy. As such they are not assumed to be related to any disease process or tissue damage and the patient may simply need reassurance.
    • Efferent defects – these are due to damage to the efferent innervation of the pupils resulting in anisocoria.
    • Secondary – this blanket term is here used to describe unequal pupils due to previous damage, either pathological (for example after recurrent anterior uveitis), iatrogenic (for example as a complication of intraocular surgery), pharmacological (for example as a result of asymmetric influence of a systemic drug), or age-related (as due to asymmetric atrophy of the iris muscle fibres with age).
  • Note that afferent defects, where there is disruption of the reflex pathways, may present with apparent isocoria (equal pupil size) and will only be elicited by testing of the reflexes.
  • Physiological anisocoria – to confirm that any pupil diameter difference is physiological, it is simply a matter of confirming that each pupil responds in a normal manner and both behave symmetrically. This is best done by simply dimming the room lights and bringing them back up again. As this is done, the pupils should first dilate with decreasing light levels and then constrict as brightness is restored. Physiological anisocoria can be confirmed (and a patient reassured) if the difference between the two diameters remains constant throughout.
  • Pathological anisocoria – the pupils respond differently as ambient light levels are changed. One may remain large or small and fixed or each might respond at differing rates.
  • Where a disease is suspected, there are some further pharmacological tests that may help with a final diagnosis. Figure 1 summarises a diagnostic systematic approach.

Efferent defects worth remembering are:

  • Adie’s tonic pupil – part of what is termed Holmes-Adie syndrome. This presents as a dilated tonic round or vermiform pupil (but can be bilateral), typically in 30 to 50-year-old women. Like Bell’s palsy (transient facial, 7th cranial, nerve palsy), it is thought to result from an autoimmune response to residual infective material from an old viral infection. It is usually transient and recovery is hope for after months. Mydriasis and cycloplegia present as blurring and photophobia and may be managed as required.
  • Oculomotor (3rd cranial) nerve palsy – the expected triad of signs would be a full ptosis (loss of levator palpebrae innervation), hypo and exotropia, and a dilated pupil. Where the nerve damage is vascular in origin, as with for example diabetes, the pupil dilation might not be present (so-called pupil sparing).
  • Horner’s syndrome – the triad of signs is a miosed pupil, a partial ptosis (the paralysis of Muller’s muscle may be subtle and hard to see), and dryness (anhidrosis) on the cheek of the affected side. The sympathetic innervation of the iris follows a long and tortuous path from the spinal ganglion in the lower cervical region (where there is input from the hypothalamus), over the apex of the lung (where a Pancoast neoplasm may damage the nerve, and adjacent to many important vascular structures). The trauma of birth can damage the nerve pathway, and congenital Horner’s is often differentiated by a heterochromia, with the affected eye being pale and depigmented. Recently acquired Horner’s may be due to an aneurysm so ophthalmological advice should be immediately sought.

Anisocoria due to secondary influences includes a wide range of possible causes and careful history is necessary to elicit the cause. This may be:

  • Iris atrophy – it is not unheard of for the irises to atrophy in asymmetric fashion.
  • Previous history of eye disease – for example, unilateral chronic anterior uveitis, iris neoplasm and so on.
  • Iatrogenic – iris damage subsequent to surgery.
  • Pharmacological – there are many legal and licensed drugs that can influence pupil state.

Interactive Exercise

The interactive exercise is related to the management of a worried woman who has noticed a change in the appearance of her eyes. A brief case scenario for your discussion has been designed to focus on practice procedure regarding such a walk-in, how to ascertain the nature of anisocoria, and what to do with your likely diagnosis.

This exercise is designed to encourage discussion by both optometrists and dispensing opticians as either group might be expected to deal with the challenges either within or outside the consulting room. Obviously, each would be expected to answer according to their particular professional responsibility.

Before you attempt the exercise, complete six multiple choice questions which assess an overall understanding of paediatric assessment.