Editors' Note: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

Abstract

Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive. Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive.