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. To the unpoetic intensivist, they are more like keyholes into the dressing room of the upper brainstem, and barometers of intracranial pressure. 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. 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.
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. 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.
|Unaided observations of the pupillary diameter|
|Miosis||Bilateral miosis||Bilateral pontine lesion, with damage to the descending sympathetic fibers|
|Bilateral thalamic lesion, also with damage to descending sympathetic fibers|
|Organophosphate poisoning (thus, a pharmacological excess of parasympathetic stimulation)|
|Unilateral miosis||Horner's syndrome|
|Sympathetic damage at any level:
Ipsilateral thalamic lesion
Ipsilateral pontine lesion
Ipsilateral sympathetic chain lesion
|Mydriasis||Bilateral mydriasis||That is what the end of brainstem herniation looks like|
|Bilateral midbrain lesion- eg. basilar artery infarct|
|Bilateral 3rd nerve damage, eg. due to severe base of skull fracture|
|Severe global brain injury (eg. due to hypoxia)|
|A 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.|
|Unilateral mydriasis||Midbrain lesion- ipsilateral damage to the Edinger-Westphal nucleus of the 3rd nerve (thus resulting in loss of parasympathetic input to the ipsilateral eye)|
|Uncal herneation - stretch of the 3rd nerve across the petroclinoid ligament|
|Direct trauma to the eyeball|
The reaction to light
|Normal consensual reaction of both pupils||The optic nerve on the tested side, the midbrain and both the third nerves are probably intact. Massive midbrain damage can be ruled out.|
|Failure of either pupil to constrict||Either the tested optic nerve is damaged and light is not registering in the midbrain, or the midbrain is massively damaged.|
The reaction to swinging light
|The pupils consensually constrict in the presence of light, and rapidly re-dilate when the light source is removed.||Normally, with swinging light, the pupils of both eyes will constrict whenever light is directed at either pupil. This demonstrates normal optic nerve, 3rd nerve and midbrain function.|
|With rapid sequential light stimulus, the affected pupil will paradoxically dilate in response to light.||This is an afferent pupilalry defect, or a Marcus Gunn pupil. It means that the tested optic nerve is damaged in the pre-chiasmal portion. 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. 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.|
Test of accomodation
|The pupil dilates to observe distant objects, and constricts to regard near objects.||This is a normal accomodation reflex.|
|The pupil accomodates to near and far objects, but fails to react to light||This is an Argyle-Robertson pupil, and it is seen in various conditons:
Alcoholic midbrain degerenation
The "blown pupil"
Uncal herneation causes a third nerve palsy by streching the oculomotor nerve over the petroclinoid ligament, a delicate band of dura stretching between the clinoid process and petrous portion of the temporal bone (purists may remark that it is an extention of the tentorium cerebelli). As the brainstem is pushed down through the foramen magnum, so the oculomotor nerve is dragged down with it, and the ligament becomes the fulcrum point where it is compressed. The parasympathetic fibres in the nerve no longer supply the iris in such circumstances, and there is unopposed sympathetic input into the pupil's diameter.
This pattern occurs early in uncal herneation because the third nerve is stretched before any major structures are being crushed. In contrast, when the hernation is central, the pupils are usually small - their parasympathetic supply remains un disturbed while the sympathetic fibers in the braisntem are being squashed. Late in the game, Cheyne-Stokes respiration and fixed mid-dilated pupils develop.
As far as the eye movements go, there are several pearls one should recall:
- Presence of spontaneous eye movements excludes brainstem pathology as the cause of coma. The 3rd, 4th and 6th nerves are all engaged, and the medial longitudinal fasciculus coordinates conjugate eye movements.
- Horisontal movements of the eyes are coordinated by the contralateral hemisphere, via the ipislateral pons. The right hemisphere commands the left pons to look right. Thus, in hemisphric cortical pathology, the eyes will look towards the lesion, whereas in pontine pathology they will deviate away from it.
- Vertical movements of the eyes are coordinated by both hemispheres.