BACKGROUND: The mechanism of reflex pupillary dilation was investigated in eight 
patients who were declared brain dead after rupture of intracranial vascular 
malformations and in eight awake volunteers. The authors hypothesized that the 
reflex was primarily a spinal sympathetic reflex that would be blocked by 
topical application of the alpha1-adrenergic blocking agent dapiprazole and that 
it would be present in organ donors with intact spinal reflexes and no history 
of hypoxia.
METHODS: In volunteers, pupil size was measured with an infrared pupillometer 
while brief painful electric stimuli were delivered to the finger. Pain was 
assessed with a visual analog scale and adjusted with each volunteer to equal 3 
on a visual analog scale of 0-10. Subjects were studied before and after topical 
application of the alpha1-adrenergic antagonist dapiprazole. In organ donors, 
the authors measured pupil size after high-intensity tetanic electric 
stimulation and in dapiprazole-blocked and -unblocked pupils after surgically 
induced nociception.
RESULTS: In volunteers, the pupil dilated 0.43 +/- 0.23 mm after nociceptive 
stimuli. Dapiprazole eyedrops blocked this dilation, confirming that the reflex 
in awake humans is primarily a sympathetic reflex. Baseline diameters were 5.7 
+/- 0.5 mm before dapiprazole and 4.1 +/- 0.9 mm after dapiprazole. In organ 
donors, a tetanic electric current failed to dilate the pupil, whereas the skin 
incision dilated the pupil 0.4 +/- 0.4 mm, but this dilation was not blocked by 
dapiprazole.
CONCLUSION: The authors conclude that pupillary reflex dilation, as it is 
clinically performed in awake subjects by stimulating somatic nociceptors, is a 
sympathetic reflex. Because it is not present in organ donors, the neural 
pathway must require a supraspinal component for completion.