What is the locked in syndrome?
Locked in syndrome occurs in patients with bilateral ventral pontine lesions. Its most common cause is pontine infarction.
Other common causes include pontine hemorrhage, trauma, central pontine myelinolysis, tumor, and encephalitis.
The patient is quadriplegic because of bilateral damage to the corticospinal tracts in the ventral pons. He or she is unable to speak and incapable of facial movement because of involvement of the corticobulbar tracts.
Horizontal eye movements are also limited by the bilateral involvement of the nuclei and fibers of cranial nerve VI. Consciousness is preserved because the reticular formation is not damaged.
The patient has intact vertical eye movements and blinking because the supranuclear ocular motor pathways that run dorsally are spared.
The patient is able to communicate by movement of the eyelids, but otherwise is completely immobile. Sometimes an incomplete state of this syndrome may occur when the patient retains some horizontal gaze and facial movement.
The locked-in syndrome must be distinguished from the persistent neurovegetative state (such as coma vigil or akinetic mutism), in which the patient appears awake but does not react to environmental stimuli and is unable to communicate in any form (thought to be due to a lesion in the rostral midbrain, basal–medial frontal region, or limbic lobes).