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A 64-year-old man with a history of uncontrolled hypertension comes to the emergency department due to sudden-onset, right-sided weakness.  Blood pressure is 170/106 mm Hg.  Examination shows left facial weakness affecting the forehead and lower face.  Muscle strength is 3/5 in the right upper and lower extremities.  Deep tendon reflexes are brisk and Babinski sign is present on the right.  A midline, sagittal section of a normal brain is shown below:

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This patient's lesion is most likely located at which of the following anatomic locations?

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This patient with risk factors for stroke (eg, hypertension) has crossed signs of:

  • right arm and leg weakness consistent with an upper motor neuron pattern (ie, hyperreflexia, upgoing Babinski).

  • left facial weakness that involves the upper face (forehead) and lower face, corresponding to a lower motor neuron pattern.

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).

The facial nerve (CN VII) originates in the pons; lesions above the pons (eg, midbrain, internal capsule, or cortical strokes) lead to an upper motor neuron pattern of facial weakness (spares contralateral upper face).  Lesions at the level of the pons result in a lower motor neuron pattern of facial weakness (affects ipsilateral upper face).  Therefore, this patient's lesion is likely in the left pons, resulting in contralateral (right) arm and leg weakness with ipsilateral (left) facial nerve palsy.

(Choice A)  Lesions impacting the cortex can lead to weakness of the face and body.  However, facial weakness would have an upper motor neuron pattern (contralateral to lesion, sparing the forehead).

(Choice B)  A stroke in the midbrain can cause ipsilateral cranial nerve deficits with contralateral hemiparesis.  However, the cranial nerves involved would originate in the midbrain, most classically the oculomotor nerve (CN III), which would lead to ipsilateral ptosis and an eye in the down-and-out position.

(Choice C)  A stroke in the cerebellum often presents with vertigo, nystagmus, and ataxia.  It would not cause cranial nerve defects or hemiparesis.

(Choice E)  Medullary infarctions can cause ipsilateral cranial nerve deficits with contralateral hemiparesis.  However, the cranial nerves involved originate in the medulla: glossopharyngeal (CN IX) (diminished gag reflex, palate weakness), vagus (CN X) (dysphonia), and hypoglossal (CN XII) (tongue weakness).  In addition, medullary infarctions often result in well-known clinical stroke syndromes (eg, lateral medullary syndrome, medial medullary syndrome).

Educational objective:
A stroke in the pons can lead to contralateral weakness of the arm and leg with ipsilateral facial weakness.  Facial weakness occurs in a lower motor neuron pattern (ipsilateral, affects upper face) because the damage occurs at the level of the facial nerve (CN VII) origination.