VA AM Report (in Japan) Cool Cases from the LT bureau

Hey squad,

Good morning from Japan and LT on his travels. Wanted to share a cool case. We’ll try something new, I’ll give you a brief case presentation, you guys leave your hypotheses/questions comments (a la think like a doctor in the NYT), and then I’ll give you a little more and then the answer.

Case: 78F seen in urgent care for a mech fall with a head lac, sown up sent out. PMH isn’t really contributory. She comes back the next day w/ ptosis and what looks like bell’s palsy, rest of neuro exam normal. No other complaints, labs look normal. What else do you want?


Thanks to Kresh, Rabih, and KD for contributing. I’ll add some answers to questions and give you more data. CT w/ contrast head negative for any abnormality, ESR 33, to Kresh’s question there is NO Horner’s, just ptosis and then some facial droop looks like Bell’s. On HD 3 she begins to complain of bilateral jaw pain worse with chewing, when asked it localizes to the masseter muscles. Otherwise no clinical changes.


Thanks for the great comments all! Yes, confusing combination of exam findings. Last little nugget, on HD 4 she develops trismus, a re-examination of the scalp wound shows poor healing. As guessed, this is a case of cephalic tetanus. teaching points here: four kinds of tetanus: cephalic, generalized (most common), localized (around the wound), and neonatal. The textbook (Victor and Adam’s Neurology) presentation of cephalic tetanus is basically this patient. It carries a high case mortality rate (up to 50% untreated) and often can progress to generalized tetanus. Treatment is anti-toxin or IVIG if not immediately available, this patient got IVIG and did well, able to leave the hospital. Awesome, LT has sent some others so will do this again soon! Thanks for participating!


9 thoughts on “VA AM Report (in Japan) Cool Cases from the LT bureau”

  1. Such a cool case. Acute neurologic issues make me think of vascular causes. While ptosis can definitely be from a NMJ issue (m.gravis, botulism) the concomitant bell’s makes me think of the peripheral nerve as the most likely culprit. The rest of the eye exam (pupils, EOM) can be helpful in teasing out CN III versus horners. I’d:
    1) Look closely in her ear to look for reactivation on VZV (in setting of trauma) –> Ramsay Hunt
    2) Think hard about CTA/MRA for dissection/aneurysm.


  2. Interesting case CVG. I would think that the history of the fall is somehow related but hard to tease the chicken from the egg. I also think it is hard to know if this is true CNIII palsy vs Horner’s based on the stem. Exam of pupils and EOMI will be helpful in distinguishing the two. If it is CNIII AND CNVII, a single lesion affecting these two cranial nerves while sparing the other cranial nerves in-between is hard to imagine being done by any mass, vascular cause, herniation etc. I suppose TB, sarcoid and leoptomeningeal disease pick things while sparring other. If it is Horner AND CNVII that may be done by a single lesion affecting the lateral medulla at the origin of CNVII nucleus, and stroke would be possible but would expect other findings on neuro exam (weakness, sensory changes). I vote on getting imaging, I suspect we may need an MRI if CT angio neg for stroke.


  3. This is awesome. I miss you guys!

    Love what’s been said thus far. The new jaw pain on HD #3 is an interesting wrinkle to what seems to be a peripheral nerve problem. I am going to assume it’s related to the neuro findings (though this is always harder to do when seeing cases in real-time).

    Whenever I think about jaw pain I think claudication, and temporal arteritis comes to mind, but the low ESR makes that less likely. Like Rabih, I was thinking about zoster without a rash (“sine herpete”) but the bilateral pain decreases my suspicion.

    I think the key for me is the combination of multiple cranial nerve involvement (facial nerve palsy + probable CN III) along with bilateral jaw pain. And then, could the jaw pain be early trismus?

    Cephalic tetanus can present with focal cranial nerve involvement following head/neck injuries (which this patient had), as well as trismus. Interestingly, of all cranial nerves, the facial nerve is most commonly involved, but you can see others too.

    I think further imaging is warranted in this case (and with leptomeningeal disease on the DDx, perhaps an LP), but I would also inquire about the patient’s immunization status.


    1. I like this case idea. Long time reader, first-time commentator from the EM side of UCSF.

      When I see cranial nerve findings in someone with head/neck trauma, I think of dissection amongst other things as other readers have mentioned. You can also have jaw claudication symptoms if a dissection takes out the maxillary branch – sometimes even bilateral symptoms resulting from a unilateral injury, which can also present with partial Horner’s from damage to the nerve running along the artery, e.g. an isolated ptsosis +/- the other elements. We simple-minded folks in EM tend to think of findings in trauma patients as being secondary to injury, with other etiologies as a diagnosis of exclusion, but I am loving the vast differential generated above.

      I have a harder time fitting the facial droop that “looks like a Bell’s” into this diagnosis, but I would vote for a CTA or MRA as a next step.


      1. I’ll also add that I like the idea of tetanus, which could occur even if the patient got their life-saving pertussis vaccination in the ED since it takes like 2 weeks for it to kick in and thereby doesn’t really prevent infection from the index wound. The progression of symptoms is weird, but ~ 3 days could fit. If the cranial nerve findings were bilateral, I would also consider wound botulism! (Though it doesn’t explain the claudication symptoms as well.)


  4. Hm agree with Dan. Interesting twist. Still having trouble putting together the initial presentation too. Seems like something related to her actual fall is less likely with the CT imaging that we now have. What’s odd to me is that she has ptosis on the ipsilateral side of the facial paralysis (that appears to be peripheral based on your description as Bell’s-like). Usually that causes an INability to close the eye on the side affected by facial paralysis. But with normal EOM and no evidence of Horner’s, it becomes harder to explain the ptosis with what we know so far. I like Dan’s commentary about the new addition of jaw pain.


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