Wednesday, May 24, 2017

CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.
3 days after admission to the hospital b/c of an 8 hour history of weakness and numbness of the right side of the face and right upper extremities, a 32 y/o woman becomes comatose. On admission, she was treated with aspirin. She has fibromuscular dysplasia. Her pulse is 40/min, and BP is 160/100. She is not responsive to verbal or tactile stimuli. Exam shows an 8 mm left pupil that is nonreactive and a 3 mm right pupil that is reactive. Her left eye is deviated outward. There is occasional movement of the left hand and foot and no movement of the right side of the face or right extremities. Deep tendon reflexes are 4 + in the right upper and lower limbs. Babinski sign is present on the right. Her serum Na is 131. What’s the diagnosis?
A. Cerebellar hematoma
B. Metabolic encephalopathy
C. Midbrain hemorrhage
D. Pontine infarction
E. Uncal herniation

Uncal herniation should cause ipsilateral paresis and ipsilateral CN 3 palsy.

So I am guessing (not sure), it is midbrain hemorrhage.

Weber's syndrome (superior alternating hemiplegia) is a form of stroke characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia. It is caused by midbrain infarction as a result of occlusion of the paramedian branches of the posterior cerebral artery or of basilar bifurcation perforating arteries. This lesion is usually unilateral and affects several structures in the midbrain including: substantia nigra, corticospinal and corticobulbar tracts, and the oculomotor nerve fibers. The lesioned substantia nigra causes contralateral parkinsonism because its dopaminergic projections to the basal ganglia innervate the contralateral hemisphere motor field. The corticospinal fibers affected produce contralateral hemiparesis and typical upper motor neuron findings. Damage to the corticobulbar tract will produce difficulty with contralateral lower facial muscles and hypoglossal nerve functions. The oculomotor nerve fibers that are affected lead to ipsilateral oculomotor nerve palsy with a drooping eyelid and fixed wide pupil pointed down and out. The oculomotor damage will likely lead to diplopia.


  1. Nice post!
    Ikan I need a help- are there any posts on anatomical causes​ of palsies. I mean that I am unable to remember those,for example,in corticospinal,corticobulbar involvement,and various other parts of brain.
    Thanks a lot:)

    1. Hey! I forwarded your request to the authors team.

      Author Medha was asking you to be more specific. It'll help frame the content better.
      "So it's like the effect of lesions starting from cortex till spinal cord?" -Medha

  2. Thank you so much Ikan and Medha:)
    Yeah, it's like effect of lesions starting from cortex till spinal cord.


  3. Thank you so much 😘. I don't know how to thank you all .
    Lucky to be here.It really helped me.Thanks

    1. You are most welcome. Feel free to ask us more.,😄


This is express yourself space. Where you type create something beautiful! <3
Wondering what do I write? Well...
Tell us something you know better. You are a brilliant mind. Yes, you are! ^__^
Ask about something you don't understand @_@?
Compliment... Say something nice! =D
Be a good critic and correct us if something went wrong :|
Go ahead. Comment all you like here! (:

PS: We have moderated comments to reduce spam. ALL comments that are not spam will be published on the website.