Formally, this is an interrogation of the third, fourth and sixth nerves, However, examination of the eye movements tends to also reveal cerebellar pathology (as nystagmus). The gaze palsies are a difficult bunch of disorders, and for the purposes of the CICM fellowship exam one should become familiar with the main ones, but one should not feel compelled to become a master of this area. One should be able to recognise a third nerve palsy, a fourth nerve palsy and a sixth nerve palsy. If one is able to recognise internuclear ophthalmoplegia, one is ahead of the herd. If one is able to discourse intelligently about the disorders of conjugate gaze, then one has probably wasted their time with neurology, because the large swaths of cognitive real estate occupied by these complex topics could be better used on issues which are worth more marks. One's performance in the written paper or in the hot case is unlikely to hinge on the ability to discriminate between causes of pendular nystagmus.
Past paper SAQs on this topic include the following:
The ideal reference for this is "Cranial Nerves III, IV, and VI: The Oculomotor, Trochlear, and Abducens Nerves" - Chapter 60 from "Clinical methods." (1990)- by J. Donald Fite and H. Kenneth Walker.
This one is easy.
Ask the patient to track a convenient object. The physician's exam candidate will have a brightly coloured hat pin. The hat pin, of course, is anachronistic wankery. Some of you might have a briefcase full of such detritus, and you might even be proud of it. The ICU fellowship candidate has no time for such nonsense.
Get the patient to follow your finger. The finger should ideally be held at least 1m away from the eye, otherwise non-pathological nystagmus might be elicited.
Using your finger, trace an imaginary H. The idea is to test all six movements of the eyes, as depicted above.
The specific lesions are discussed in following chapters, dedicated to each nerve individually:
One cannot get the comatose patient to track one's finger, but one can still test eye movements by testing the Oculocephalic and cold caloric reflexes. This is discussed elsewhere, as it has specific meaning associated with testing the 8th nerve (CN VII, the vestibulocochlear nerve).
Before you grab the head and start rotating it violently, it is also possible to derive meaning from simply looking at the unconscious patient's eyes, and watching their spontaneous position and movement.
Peel back the lids. You will see one of three things.
These things have meaning, as discussed below.
First, in brief:
Now, in detail:
Fixed midline gaze
Fixed midline eyes which do not appear to be doing anything is a meaningless finding. The patient could be dead, or in a deep coma, or paralysed with curare darts. Until you try a doll's eye reflex, you won't know.
If one watches for long enough, one might see weak roving eye movements. A sufficiently deep metabolic coma can be associated with a loss of conjugate roving eye movements; as the coma resolves, so the eye movements gradually return.
Strabismus and roving eye movements
Strabismus exists in most people to some degree, and for some reason it worsens with coma. Plum and Posner recommend you politely ignore this finding.
Roving eye movements are typical of metabolic encephalopathy. The important feature is conjugate gaze: are the eyes roving in the same direction, or are they pointing in random directions, like a chameleon? If the roving movements are conjugate, the ocular motor system in its entirety is intact.
Plum and Posner go on to discuss the vast territory of spontaneous unconscious eye movements. In someoene who is studying for the CICM fellowship exam, terms like "ping-pong gaze" and "ocular bobbing" may arouse a mixture of suspicion and despair. However, the pragmatic exam candidate may safely ignore this exotica. One's pass or fail in the hot cases will not depend on one's ability to discriminate between reverse ocular dipping and converse bobbing. In case somebody is actually interested, one may explore Table 2.3 in Plum and Posner (page 69).
Conjugate lateral gaze deviation
Plum and Posner say that one wont typically see this assymetrical pattern with metabolic encephalopathy.
Classically, the eyes look towards the destructive cortical lesion, and away from the side of hemiparesis which is inevitably associated therewith. In some situations, there may be tonic deviation of the eyes in epilepsy (called Todd's paralysis) and in this case the eyes deviate away from the focus of epilepsy (the "irritative" lesion").
In order to remember this binary factoid, one should think of an irritative lesion as a bright light. The eyes will tend to look away from it.
If there has been a destruitive lesion, the tonic deviation will go away over the period of days. Unfortunately, there is no convenient way to remember the various lesions which are associated with a lateral gaze deviation. One needs to get good at memorising lists if one is ever to understand neurology.
To discriminate between causes of lateral gaze palsy, one should go on to test the oculocephalic and cold caloric (oculovestibular) reflexes. Lateral gaze palsy due to thalamic or cortical (hemispheric) lesions can be overcome by cold caloric testing, i.e. the deviated eyes will "un-deviate" to look towards the ice water syringe in the ear. Damage to the pons, however, usually cannot be overcome by cold caloric testing. Specifically, any pontine lesion involving the abducens nerve nucleus will not respond to caloric testing.
Conjugate vertical gaze deviation
Conjugate upward deviation occurs as a part of an "oculogyric crisis" in the context of dystonia, eg. following the administration of an excess of metaclopromide, or with large quantities of neuroleptic drugs. Plum and Posner also report bilateral damage to the basal ganglia as one of the causes.
Conjugate downward deviation apparently occurs with pressure on the tectal plate. Causes include pineal mass and thalamic haemorrhage.
Non-conjugate lateral gaze deviation
This refers to a situation where an unconscious patient, at rest, has some sort of fixed gaze devition of both eyes in different directions.
This usually means that one eye is "healthy", while the other is affected by some sort of craial nerve palsy which has resulted in a weakness of one of the ocular muscles, with the resulting "pull" of the eye in the oppsite direction. I suppose you could also have two different cranal nerve palsies (eg. a CN III on one side and an isolated CN VI on the other, or something equally ridiculous) but it would be a rare finding indeed, and probably buried in other pathology (eg. among many other cranial nerve palsies in a base of skull fracture).
Generally speaking, this sort of thing will be discovered only on active oculomotor testing, i.e. when you test the oculocephalic and cold caloric (oculovestibular) reflexes.
Non-conjugate vertical gaze deviation
Whatever the findings, one should go on to test the oculocephalic and cold caloric (oculovestibular) reflexes.
Walker, H. Kenneth, W. Dallas Hall, and J. Willis Hurst. "Clinical methods." 3rd edition.(1990).Chapter 60 Cranial Nerves III, IV, and VI: The Oculomotor, Trochlear, and Abducens Nerves - by J. Donald Fite and H. Kenneth Walker.
Twenty five years out of date, but still relevant.
These authors, in turn, reference even more ancient vellum:
Leigh RJ, Zee DS. The neurology of eye movements. Philadelphia: FA Davis, 1983.
Miller NR. Walsh and Hoyt's clinical neuro-ophthalmology. Vol 2. 4th ed. Baltimore: Williams and Wilkins, 1985.
Broadway, David C. "How to test for a relative afferent pupillary defect (RAPD)."Community Eye Health 25.79-80 (2012): 58.
Fincham, Edgar F. "The accommodation reflex and its stimulus." The British journal of ophthalmology 35.7 (1951): 381.
Maramattom, Boby Varkey, and Eelco FM Wijdicks. "Uncal herniation."Archives of neurology 62.12 (2005): 1932-1935.
Karatas, Mehmet. "Internuclear and supranuclear disorders of eye movements: clinical features and causes." European Journal of Neurology 16.12 (2009): 1265-1277.