Lateral Pontine Infarct: Expected Additional Neurologic Findings
In this patient with a lateral pontine infarct causing left facial weakness, left facial anesthesia, and left Horner syndrome, the most likely additional neurologic sign is left lateral rectus muscle weakness (CN VI palsy).
Anatomical Localization and Clinical Reasoning
The clinical presentation localizes to the lateral pons, specifically in the territory of the anterior inferior cerebellar artery (AICA). This vascular territory characteristically affects multiple cranial nerve nuclei and fascicles that are anatomically clustered in the dorsolateral pontine tegmentum 1.
Key Anatomical Relationships in the Lateral Pons
The abducens nerve (CN VI) nucleus and fascicle course through the dorsal pons in close proximity to the facial nerve nucleus, making CN VI palsy a frequent accompaniment of lateral pontine lesions 1.
The facial nerve (CN VII) wraps around the abducens nucleus before exiting the brainstem, explaining the ipsilateral facial weakness affecting both upper and lower facial muscles (peripheral pattern) 1.
The trigeminal sensory pathways (CN V) traverse the lateral pons, accounting for the ipsilateral facial anesthesia 1, 2.
Descending sympathetic fibers pass through the lateral pons, producing the ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) 3.
Why Left Lateral Rectus Weakness is Most Likely
The abducens nerve nucleus is located in the dorsal pons, and lateral pontine infarcts characteristically involve the inferolateral pontine territory, frequently extending to include CN VI structures 3, 4. Multiple case series of AICA territory infarctions document that lateral gaze palsy occurs frequently when the lesion involves the lateral pons 3.
Ruling Out Other Options
Large unreactive pupil: This would suggest CN III (oculomotor) involvement, which is located in the midbrain, not the pons 1.
Right pupil abnormality: The lesion is left-sided, so contralateral pupillary findings would not be expected from a unilateral pontine lesion 2.
Left superior oblique weakness: CN IV (trochlear nerve) originates from the dorsal midbrain, not the pons, making this anatomically inconsistent 1.
Left-sided hyperreflexia: While corticospinal tract involvement can occur with pontine lesions, the ventral pons contains these descending motor tracts. The clinical presentation (facial anesthesia, Horner syndrome) indicates a dorsolateral pontine lesion that typically spares the ventral corticospinal pathways 1, 3.
Right-sided tongue weakness: CN XII (hypoglossal nerve) originates from the medulla, not the pons, making this anatomically implausible 1.
Classic AICA Syndrome Features
The constellation of findings in this patient is consistent with AICA territory infarction, which characteristically produces 3, 4:
- Ipsilateral facial palsy (peripheral pattern affecting upper and lower face)
- Multimodal trigeminal sensory impairment (facial anesthesia)
- Horner syndrome (less common but documented)
- Lateral gaze palsy (CN VI involvement)
- Hearing loss and vestibular symptoms (when the labyrinthine artery is involved)
- Cerebellar signs (ataxia, when the middle cerebellar peduncle is affected)
Clinical Pitfall to Avoid
Do not confuse this with a cortical stroke. A cortical lesion would produce contralateral deficits only and would spare the forehead due to bilateral cortical innervation of the upper facial muscles 2, 5. The presence of ipsilateral facial involvement affecting both upper and lower face immediately localizes the lesion to the brainstem (specifically the pons) rather than the cortex 1, 2.
Diagnostic Confirmation
MRI with diffusion-weighted imaging (DWI) is essential for confirming acute pontine infarcts, which can be as small as 4mm and are easily missed on CT 2. The American Heart Association recommends urgent MRI for detecting these lesions, particularly when clinical suspicion is high despite negative initial CT imaging 2, 6.