Etiology and pathogenesis of open-eye coma

  Open-eyed coma is the common name for a persistent vegetative state. It is a specific form of impaired state of consciousness, also known as waking coma. It is manifested by the patient’s clear consciousness but inability to move except for eye movements, and the ability to follow instructions to open and close the eyes or make eye movements in all directions. The patient completely loses perception of himself and his surroundings, has a sleep-wake cycle, and maintains or partially protects the autonomic functions of the hypothalamus and brainstem.  Etiology: Open-eye coma can be caused by a variety of reasons: among them are drug intoxication, CO intoxication, alcohol intoxication, severe craniocerebral trauma, cerebrovascular disease, encephalitis, cerebral fat embolism, severe ischemic-hypoxic encephalopathy such as self-hanging and drowning.  The pathogenesis is divided into two types: decerebrate cortical state and inactive mutism: decerebrate cortical state: due to extensive damage to the cerebral cortex, the patient loses consciousness, but the upstream activation system is preserved and the sleep-wake cycle exists.  Inactive mutism lesions: mainly in the superior reticular activating system of the brainstem, mostly in the gray matter around the posterior aqueduct of the third ventricle or in the cingulate gyrus on both sides. Patients are drowsy and may also have some sleep-wake cycles, silent and limbless, and may have clinical signs of midbrain or mesencephalic injury.