Blown pupil causes1/5/2024 With the darkness stimulating the dilation of both pupils, and the light stimulating nothing (owing to the optic nerve pathology on the tested side), the pupil exposed to light will dilate abnormally, until it is the same diameter as the unlit pupil. During the swinging light test, there is a moment when the contralateral (healthy) pupil is again submerged in darkness, while the ipsilateral (affected) pupil has light shining upon it. It means that the tested optic nerve is damaged in the pre-chiasmal portion. This is an afferent pupilalry defect, or a Marcus Gunn pupil. With rapid sequential light stimulus, the affected pupil will paradoxically dilate in response to light. This demonstrates normal optic nerve, 3rd nerve and midbrain function. Normally, with swinging light, the pupils of both eyes will constrict whenever light is directed at either pupil. The pupils consensually constrict in the presence of light, and rapidly re-dilate when the light source is removed. Massive midbrain damage can be ruled out.Įither the tested optic nerve is damaged and light is not registering in the midbrain, or the midbrain is massively damaged. The optic nerve on the tested side, the midbrain and both the third nerves are probably intact. Normal consensual reaction of both pupils Uncal herneation - stretch of the 3rd nerve across the petroclinoid ligament Midbrain lesion- ipsilateral damage to the Edinger-Westphal nucleus of the 3rd nerve (thus resulting in loss of parasympathetic input to the ipsilateral eye) due to hypoxia)Ī much more extensive list of causes of bilateral myriasis can be seen in the discussion section for Question 27 from the first paper of 2019. basilar artery infarctīilateral 3rd nerve damage, eg. That is what the end of brainstem herniation looks likeīilateral midbrain lesion- eg. Late Holmes-Adie pupils (initially, they are dilated).Neurosyphilis (bilateral Argyll-Robertson pupils).Organophosphate poisoning (thus, a pharmacological excess of parasympathetic stimulation) A Summary of Pupil Examination Findings Unaided observations of the pupillary diameterīilateral pontine lesion, with damage to the descending sympathetic fibersīilateral thalamic lesion, also with damage to descending sympathetic fibers Question 21.1 from the second paper of 2015 (and the identical Question 30.2 from the second paper of 2018) instead asked for three causes of coma with bilateral miosis, each cause being worth 5% of the marks. This important topic has come up in Question 5 from the first paper of 2007, which asked about pupil reactivity and diameter in the context of coma. Unlike the crisp and clean interior of Talley and O'Connor, this hoary incunabula is overgrown with trailing fronds of references, featuring obscure and apocryphal authors, and discussing rare and extinct physical findings. Rather than escaping into comforting familiarity of well-known examination medicine textbooks, I will instead refer to a more ancient and venerable "Clinical Methods: The History, Physical, and Laboratory Examinations (3rd edition)" - specifically Chapter 58, by Rober H Spector. To the unpoetic intensivist, they are more like keyholes into the dressing room of the upper brainstem, and barometers of intracranial pressure. This is where the money is, as far as the ICU cranial nerve examination is concerned. The eyes, the poets say, are the windows to the soul.
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