The pupillary response to light is controlled by the autonomic nervous system. The direct pupillary light reflex refers to miosis that occurs in the stimulated eye; the consensual pupillary light reflex refers to miosis that occurs in the other eye. The reflex has a latent period with length of the period, amplitude of the response, and the speed of the pupillary constriction dependent on the intensity of the stimulus employed.1 For the reflex to be truly tested, an intense stimulus and close observation are required. The reflex has afferent, efferent and central connections; therefore non-response to light (i.e. reflex iridoplegia) indicates a disturbance in one or all of these connections.
As areas in the brainstem controlling consciousness are anatomically adjacent to the autonomic fibres controlling the pupillary responses, the pupillary light reflex is a valuable guide to the presence and location of brainstem diseases causing coma. Moreover, because the pupillary response is relatively resistant to metabolic insult, the presence or absence of the light reflex is often used as the single and most important physical sign to distinguish a structural (i.e. potentially irreversible) from a metabolic (i.e. reversible) cause of coma. With brainstem destruction the pupillary reflex is lost whereas the size of the pupil may change (albeit slowly),2 thus the ‘fixed’ element is more important than the ‘dilated’ element in the clinical sign of ‘fixed dilated pupils’
Although interobserver agreement on the presence or absence of the light reflex is one of the most consistent measures of brain-stem function, approximately 30% disagreement exists regarding the status of this reflex in comatose patients.3,4,5 The interobserver disagreement arises partially from the lack of a standard method to elicit the reflex. Traditionally the pupillary light reflex is determined using a penlight (i.e. pencil torch) and factors such as the amount of ambient light in the room, the observer’s visual acuity, the distance of the penlight bulb from the patient’s pupil and strength of the penlight batteries can alter the validity of the visual assessment of the reflex. The reflex is also more difficult to detect with a wide pupil (e.g. a 0.2 mm reflex in a 5 mm diameter pupil is only a 4% reflex, whereas the same reflex in a 2 mm diameter pupil is a 10% reflex) and in a dark iris (as the ambient light must be high for the iris to be seen, which reduces the step increase induced by the penlight).6
If the pupillary light reflex amplitude is less than 0.3 mm and the maximum constriction velocity is less than 1 mm/s, the reflex is unable to be detected using a penlight.6 In conscious patients with Holmes-Adie and Argyll-Robertson pupils with ‘absent’ pupillary light reflexes, small light reflexes have been detected using infrared pupillometry.7 Also in post-resuscitation non-brain dead critically ill patients with ‘absent’ pupillary reflexes, the reflex has been demonstrated using a portable infrared pupillometer.6
Thomas8 describes a case of Guillain Barré syndrome presenting with weakness and fixed dilated pupils who subsequently became ‘locked in’ with absence of any clinical response to external stimuli. A positive brain stem auditory evoked response was used to indicate normal brain stem function. In another recent report, a case of ‘reversible fixed dilated pupils’ was associated with carbamazepine and venlafaxine overdosage.9 Both reports highlight the importance of the reflex and together probably give the reader a complete list of the common and rare causes of ‘fixed dilated pupils’. However, from recent reports it would appear that some of these conditions might be associated with ‘clinically undetectable’ rather than ‘absent’ pupillary light reflexes.
–Author: Nina Jaitly, MD, LivingHealthyWorldWide.com
REFERENCES
1. Ellis CJ. The pupillary light reflex in normal subjects. Br J Ophthalmol 1981;65:754-759.
2. Ishiguro T, Tamagawa S, Ogawa H. Changes of pupil size in brain death patients. Seishin Shinkeigaku Zasshi 1992;94:864-873.
3. Teasdale G, Knill-Jones R, van der Sande J. Observer variability in assessing impaired consciousness and coma. J Neurol Neurosurg Psychiatry 1978;41:603-610.
4. van den Berge JH, Schouten HJ, Boomstra S, et al. Interobserver agreement in assessment of ocular signs in coma. J Neurol Neurosurg Psychiatry 1979;42:1163-1168.
5. Wilson SF, Amling JK, Floyd SD, et al. Determining interrater reliability of nurses’ assessments of pupillary size and reaction. J Neurosci Nurs 1988;20:189-192.
6. Larson MD, Muhiudeen I. Pupillometric analysis of the ‘absent light reflex’. Arch Neurol 1995;52:369-372.
7. Loewenfeld IE. Midbrain syndromes. In: The Pupil: Anatomy, Physiology, and Clinical Applications. Detroit, Michigan: Wayne State University Press. 19931:956-1001.
8. Thomas PD. The differential diagnosis of fixed dilated pupils: a case report and review. Critical Care and Resuscitation 2000;2:34-37.
9. Cordova S, Lee R. Fixed, dilated pupils in the ICU: another recoverable cause. Anaesth Intensive Care 2000;28:91-93.