An early sign of third cranial nerve disease may be simply mydriasis. However, careful evaluation may show that other functions of the third cranial nerve are also affected, Look for a small vertical muscle imbalance that may be seen only on up-gaze, for a slight ptosis, or for an ipsilateral decrease in accommodation. Repeated testing of the pupil with light may show pupillary fatigue in the abnormal eye, whereas the fellow eye continues to constrict normally, even when repeatedly tested.
Partial internal ophthalmoplegia has the same differential diagnosis and serious implications as described for total third cranial nerve paralysis. The most serious and urgent implication is an aneurysm. Pupil-sparing ocular motor palsy secondary to internal carotid-posterior communicating aneurysms was once considered rare. Now this sign is seen in about 8% of such cases.
Kerr and Hollowell confirmed Sunderland's work on the location of the pupil fibers in the third nerve. They are located dorsomedially and medially in the nerve. This has particular significance in predicting the ability to produce mydriasis with pressure on the third nerve. It takes less pressure on the medial aspect of the nerve than on the dorsal or lateral aspect to cause mydriasis. For instance, displacement of the brain with compression of the third nerve against the tentorial edge readily causes myclriasis, whereas increased intracranial pressure with pseudotumor cerebri does not.
It is important, therefore, to identify other causes that can produce internal ophthalmoplegla. Infections, such as varicella and botulism, on occasion have been reported to cause internal ophthalmoplegia. Internal ophthalmoplegia has also been reported after panretinal photocoagulation. The probable mechanism created by the photocoagula lion is damage to the short ciliary nerves traveling anteriorly in the sclera.
Accommodation problems have been reported to occur during the regulation of diabetes. This is besides the usual refractive error so commonly encountered. These findings are not associated with pupillary or Motility signs. The accommodative changes are usually mild and often missed. However, they can be severe on occasion, and their possible association with diabetes should be remembered. The cause is unknown, but it is suggested that a similar mechanism that affects the resiliency of the lens during changes in blood sugar also accounts for changes in accommodation.
Aberrant regeneration of the third cranial nerve can also affect only pupillary fibers. The aberrant association of pupillary contraction with innervation of the medial rectum has been well described by Ford, Walsh, and King.
Czarnecki and Thompson described three other pupillary signs of misdirection: (a) contraction of the iris sphincter to eye movements similar to that described by Ford, Walsh, and King but only in certain sectors of the iris, suggesting not only aberrant but partial regeneration of the third cranial nerve; (b) also similar sector contractions to light stimulation; and (c) in the dark and in the absence of light stimulation and with pupils that had no light reaction, there was hippus but asynchronous with the normal eye. Since there is no efferent arc to stimulate the pupil, one explanation is that fibers intended for the third cranial nerve muscle group now innervate the pupil.
Recent studies suggest that pupil-sparing ihird nerve palsy may not be as sparing as once thought. The pupil cycle times were found to be abnormal in cases of diabetic ophthalmoplegia. However, pupil abnormalities in diabetics are well known. There is not uncommonly some autonomic denervation of the iris as well.