Locked-In Syndrome

Locked-in syndrome (LIS) results from bilateral destruction of the ventral pons, most commonly caused by basilar artery thrombosis or embolism occluding the paramedian branches that supply the basis pontis. The ventral pons contains the corticospinal tracts (voluntary motor control of the body), corticobulbar tracts (voluntary motor control of cranial nerve-innervated muscles including face, pharynx, and tongue), and the abducens nuclei (cranial nerve VI for lateral eye movement). Destruction of these structures produces complete quadriplegia, bilateral facial paralysis, anarthria (inability to speak), and loss of horizontal eye movements. Critically, the dorsal pons -- containing the reticular activating system (responsible for consciousness and arousal), the tegmentum (sensory pathways), and the vertical gaze centers -- is spared. This means the patient is fully conscious, cognitively intact, able to see and hear, and retains full sensation, but is unable to produce any voluntary movement except vertical eye movements and blinking, which are controlled by the intact midbrain (oculomotor nuclei, CN III). The clinician must differentiate LIS from coma (no consciousness), persistent vegetative state (arousal without awareness), akinetic mutism (reduced drive to move or speak...