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Interesting Neuro Case Requires ER Doc To Recall Forgotten Med School Knowledge

Yesterday, I presented the case of a woman with double vision and ptosis and challenged you all to a game of “spot the lesion.” To be honest, I found this stuff impenetrable as a medical student and it was only by sheer force of will that I was able to commit it to memory for exactly long enough to pass a test on it before immediately purging it from my memory. I did this several times for various board exams and such, but it never really “stuck.” Hated neuro beyond words, I did.

As mind-numbing as I found it all in the abstract, I get excited about these cases in application. I may not remember where exactly the internal capsule is or what it does, but when I see someone with an interesting neuro deficit due to a lesion there, all of a sudden it makes so much more sense, and is, dare I say it, cool. I know, kinda sad.

This case is as classic (and cool) as you will ever see. It’s a complete palsy of the Oculomotor Nerve (CN 3 for those keeping score at home).

So how do you approach figuring that out?

First of all, it’s unilateral. Note the movements of the left eye are all normal. Some other things, systemic diseases, can cause ptosis (the droopy eyelid) or diplopia (double vision) — think neuromuscular stuff like myasthenia gravis, botulism, etc. But those are usually bilateral. As an isolated right-sided finding, however, that should prompt you to think about either a central cause or a direct neuropathy. But central causes of this sort of thing are not likely, because the oculomotor nuclei are located deep in the midbrain, and are crossed, so a stroke or something bad there is not likely to give unilateral or isolated neurological findings. Therefore, we know it’s a peripheral neuropathy. Yay! But which one?

The ptosis — especially a complete paralysis of the levator palpebrae — should be a huge red flag that the third nerve is involved. Even I remember this mnemonic from medical school:

The III is the pillar that holds the eye open; the 7 is the hook that closes it. Then you look at the pattern of movements that the eye has lost and note that it matches the oculomotor muscles which are innervated by the third nerve:

extraocular muscles
She can abduct it, so CN6 is intact, but up, down and adduction are shot, which are all CN3. The fact that with straight gaze and lateral gaze the right eye is a bit down compared to the left is due to the preserved function of CN4. Thus, the classic pattern of CN3 palsy — “down and out.”

Then you look at the pupil. It’s big — so you know this isn’t a Horner’s syndrome, though that wouldn’t cause ophthalmoparesis either. And it’s not reactive, either. The most common cause of acquired CN3 palsies is diabetic microvascular ischemia — one of the many peripheral neuropathies that the sugar causes. But those are usually pupil-sparing. This involves the pupil, so something is compressing or otherwise pissing off the nerve directly.

The solution (as for just about everything in neurology, it seems) is to order your MRI, but in this case, you definitely want an MRA as well. Because the next most common cause of CN3 palsy is compression by an aneurysm (notoriously the PCA – posterior communicating artery). The deficit can apparently be intermittent with an aneurysm. But all sorts of things can do it, and the treatment will depend on the cause. It could be direct compression from a pituitary tumor, or a cavernous sinus thrombosis. If the patient presents with stiff neck and meningismus, either subarachnoid hemorrhage or meningitis should be considered, as they can do this. Demyelinating diseases can also do this, so if all else fails and if the demographic makes sense, consider MS. In older patients, consider arteritis, too. Herpes zoster can also rarely do this, though it’s more classically the seventh nerve. These can occur post-traumatic, but be sure that the pattern of the deficit matches the nerve and that you’re not going to miss an orbital wall fracture! I recently saw a patient with a port-traumatic transient internuclear ophthalmoplegia, which was also pretty cool. Sadly, I didn’t have the presence of mind to get pics of that one.

In the incident case, the MR showed a suprasellar mass invading the cavernous sinus, most likely a pituitary macroadenoma:


Not something you can see commonly, but very classic, and a nice opportunity to review and relearn all the neuroanatomy we learned in medical school, but in the context of a real case.

*This blog post was originally published at Movin' Meat*

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