What is the likely location of a stroke in a patient who suddenly lost the ability to speak and move, but can still hear, breathe normally, and communicate through eye movements?

Stroke Location: Pontine Lesion

The clinical presentation described—sudden loss of speech and movement with preserved hearing, normal respiration, and ability to communicate through eye movements—is most consistent with a pontine stroke (Option B), specifically representing "locked-in syndrome." 1

Clinical Reasoning

Classic Locked-In Syndrome Features

The patient's presentation demonstrates the pathognomonic features of locked-in syndrome, which localizes to the ventral pons:

• Quadriplegia and anarthria (inability to speak or move limbs) due to disruption of the corticospinal and corticobulbar tracts in the ventral pons 1
• Preserved consciousness and hearing because the reticular activating system and auditory pathways remain intact 1
• Preserved vertical eye movements and blinking as these functions are controlled by midbrain structures (rostral interstitial nucleus of the MLF) and facial nerve nuclei, which are not affected by ventral pontine lesions 2, 3
• Normal respiration as the respiratory centers in the medulla remain functional 1

Why Other Options Are Incorrect

Left anterior cerebellum (Option A):

• Cerebellar strokes typically present with ataxia, nausea, vomiting, and dizziness—not paralysis 2
• Would not cause the profound motor paralysis or speech loss seen in this patient 2

Basal ganglia (Option C):

• Basal ganglia strokes cause contralateral hemiparesis and sensory deficits, not complete quadriplegia 4
• Would not preserve vertical eye movements and consciousness in this pattern 4

Midbrain (Option D):

• Midbrain lesions characteristically impair vertical gaze and cause pupillary abnormalities 3
• The preservation of vertical eye movements in this patient effectively excludes midbrain pathology 5, 3
• Midbrain strokes affecting the oculomotor nuclei would produce vertical gaze paresis, not the locked-in pattern 5

Anatomical Correlation

Pontine vascular territories are well-defined, and the clinical syndrome localizes to the ventral (anteromedial) territory 6:

• The basilar artery supplies the pons, and mid-basilar occlusions specifically produce locked-in syndrome 1
• Ventral pontine infarction disrupts descending motor pathways while sparing dorsal tegmental structures that control consciousness and vertical gaze 6
• The preservation of blinking (facial nerve nuclei in pons) and vertical eye movements (midbrain control) helps distinguish this from more extensive brainstem involvement 2

Clinical Pitfalls to Avoid

Recognition challenges:

• Locked-in syndrome can be mistaken for coma or unresponsiveness if vertical eye movements are not specifically tested 1
• The NIHSS may underestimate posterior circulation strokes, as patients can have devastating deficits with relatively low scores 1
• Posterior circulation strokes often have non-specific prodromal symptoms and can be missed initially 1

Diagnostic approach:

• Always test for vertical eye movements and blinking in patients with apparent unresponsiveness 1
• Maintain high clinical suspicion for brainstem stroke even with subtle initial symptoms 7
• Urgent vascular imaging (CTA or MRA) is essential for posterior circulation evaluation 1