Correct Answer: D. Lateral pons
This is a classic crossed syndrome (alternating hemianesthesia) that localizes to the lateral pons. The key discriminator is the combination of ipsilateral facial sensory loss (CN V) with contralateral body pain/temperature loss (spinothalamic tract). In the lateral pons, the trigeminal nerve nucleus (CN V) receives pain and temperature fibers that are organized somatotopically—the face is represented in the rostral pons. Simultaneously, the spinothalamic tract carrying pain and temperature from the body crosses at spinal levels and ascends contralaterally in the brainstem. A lateral pontine lesion damages the ipsilateral trigeminal nucleus (causing right facial sensory loss) while sparing the already-crossed spinothalamic tract on the left side, which still carries sensation from the left leg. This dissociation—facial loss on the lesion side, body loss on the opposite side—is pathognomonic for lateral pontine pathology. The medial pons and medulla would produce different patterns (medial lesions spare CN V and affect motor tracts; lateral medulla causes Wallenberg syndrome with different CN involvement).
Why the other options are wrong
A. Medial pons — Medial pontine lesions (e.g., superior alternating hemiplegia) damage the corticospinal tract and CN VI/VII nuclei, causing ipsilateral facial weakness and contralateral body weakness—not sensory loss. Pain and temperature sensation are preserved because the spinothalamic tract runs laterally. This option confuses motor syndromes with sensory crossed syndromes. B. Medial medulla — Medial medullary lesions (Medial Medullary Syndrome) damage the pyramidal tract and CN XII, causing ipsilateral tongue weakness and contralateral hemiparesis. The spinothalamic tract is spared. This does not produce the facial sensory loss described, making it anatomically incompatible with the clinical presentation. C. Lateral medulla — Lateral medullary lesions (Wallenberg syndrome) damage CN V, VIII, IX, X, and the spinocerebellar tracts, but the trigeminal nucleus in the medulla represents the face differently than in the pons. Wallenberg typically presents with ipsilateral facial pain loss but also includes vertigo, nystagmus, and ipsilateral vocal cord paralysis—features absent in this case. The crossed sensory pattern is less prominent.
High-Yield Facts
- Lateral pons lesion → ipsilateral CN V sensory loss (face) + contralateral spinothalamic loss (body) = crossed syndrome.
- Trigeminal nucleus in rostral pons receives facial pain/temperature; organized somatotopically with face rostral, neck caudal.
- Spinothalamic tract crosses at spinal cord level and ascends contralaterally; lateral pontine lesion spares it but damages ipsilateral CN V.
- Wallenberg syndrome (lateral medulla) includes CN V loss but also vertigo, nystagmus, and ipsilateral vocal cord paralysis—distinguishes it from lateral pons.
- Medial pons/medulla lesions produce motor syndromes (weakness), not sensory crossed syndromes—key differential in brainstem localization.
Mnemonics
LATERAL BRAINSTEM = SENSORY CROSSED SYNDROME Lateral lesions damage CN nuclei (ipsilateral) + spare spinothalamic (contralateral already crossed) → sensory dissociation. Medial lesions damage motor tracts → weakness, not sensory loss. PONS vs MEDULLA CN V Pons: CN V nucleus rostral → facial sensory loss only. Medulla (Wallenberg): CN V + VIII + IX + X → facial loss + vertigo + hoarseness. Use to rule out medulla.
NBE Trap
NBE pairs facial sensory loss with medullary lesions (Wallenberg syndrome) to lure students who memorize syndromes without understanding somatotopy. The key trap: Wallenberg includes multiple CN deficits and vertigo; this case has isolated facial sensory loss with contralateral body sensory loss—only lateral pons fits.
Clinical Pearl
In Indian clinical practice, lateral pontine infarcts (often from vertebral artery disease or small-vessel disease in hypertensive patients) present with this crossed sensory pattern. Recognition of the dissociation—facial loss on one side, leg loss on the other—immediately narrows localization to lateral pons and guides urgent neuroimaging (MRI DWI) and vascular assessment.
_Reference: Robbins & Cotran Pathologic Basis of Disease, Ch. 28 (Central Nervous System); Harrison's Principles of Internal Medicine, Ch. 379 (Stroke and Transient Ischemic Attacks); Clinically Oriented Anatomy by Moore (Brainstem vascular syndromes)_