A 70-year-old man is brought to the emergency department an hour after sudden-onset, right-sided weakness and double vision. Medical history is significant for type 2 diabetes mellitus, hypertension, and hyperlipidemia. Blood pressure is 160/102 mm Hg and pulse is 82/min. The patient is alert, oriented, and able to follow commands. Speech is normal. On examination, the left eye has ptosis and is fixed in the outer position, and the pupil is dilated. The right eye, the right pupil, and right eye movements are normal. Muscle strength is normal in the left upper and lower extremities and is 3/5 in the right. Deep tendon reflexes are 3+ on the right and 2+ on the left. Babinski sign is present on the right and absent on the left. There is no ataxia. Sensation is intact. Which of the following is the most likely location of this patient's lesion?
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This patient with risk factors for stroke (eg, hypertension, diabetes mellitus) has crossed signs of:
left oculomotor nerve (CN III) dysfunction (eg, ptosis, impaired pupil constriction, down-and-out eye, diplopia).
right (ie, contralateral) arm and leg weakness with upper motor neuron signs (eg, hyperreflexia, upgoing Babinski).
Because most cranial nerves (other than CN II & IV) do not decussate while most of the body's motor and sensory fibers cross the midline in the medulla, brainstem strokes are characterized by ipsilateral cranial nerve deficits accompanied by contralateral hemiparesis or hemisensory loss (ie, crossed signs).
CN III originates in the midbrain of the brainstem, further localizing the lesion. Left CN III palsy with contralateral arm and leg weakness (corticospinal tract) is most likely caused by a left midbrain infarction due to occlusion of the mesencephalic branches of the posterior cerebral artery (ie, Weber syndrome). This can develop from obstruction of perforating arteries of the basilar bifurcation.
(Choice A) A stroke in the cerebral cortex can lead to weakness with upper motor neuron (UMN) signs. However, it is often accompanied by cortical signs (ie, deficits localizing to the cortex) that may include Visual disturbances (eg, hemianopia, gaze preference), Aphasia (ie, typically expressive Broca), Neglect, and cortical Sensory deficits (eg, inability to recognize movement drawn on the palm) (ie, VANS stroke scale). Cranial nerve deficits would not be expected.
(Choice B) A stroke in the internal capsule leads to contralateral hemiparesis. Because it is such a small anatomic area, in addition to the arm and leg, there is also usually facial weakness sparing the upper face (UMN-type weakness). Cranial nerve deficits are more consistent with a brainstem stroke.
(Choice D) Pontine infarctions can cause ipsilateral cranial nerve deficits with contralateral hemiparesis. However, the involved cranial nerves originate in the pons: Trigeminal (CN V) (facial paresthesia), abducent (CN VI) (abducens palsy), facial (CN VII) (facial palsy), and vestibulocochlear (CN VIII) (vertigo). A pontine infarction would not likely cause CN III deficits.
(Choice E) Medullary infarctions can cause ipsilateral cranial nerve deficits with contralateral hemiparesis. However, the involved cranial nerves originate in the medulla: Glossopharyngeal (CN IX) (diminished gag, palate weakness), vagus (CN X) (dysphonia), and hypoglossal (CN XII) (tongue weakness). Medullary infarctions often result in well-known clinical stroke syndromes (eg, lateral medullary syndrome, medial medullary syndrome).
Educational objective:
Crossed signs (ie, cranial nerve dysfunction with contralateral limb weakness) raise suspicion for brainstem stroke. Midbrain infarction due to occlusion of the posterior cerebral artery results in Weber syndrome characterized by ipsilateral oculomotor nerve (CN III) dysfunction accompanied by contralateral hemiparesis.