| disease | Prolonged Unconsciousness |
| alias | Name Seeking Syndrome, Persistent Coma, A Syndrome in Search of A Name |
The so-called prolonged unconsciousness, as the name suggests, is a state of long-term impaired consciousness where the patient loses responsiveness to external stimuli. These patients typically suffer from severe primary or secondary brainstem injuries or prolonged cerebral ischemia and hypoxia. Due to damage to the ascending reticular activating system in the brainstem, which maintains wakefulness, external stimuli cannot effectively activate the cerebral cortex. Alternatively, widespread and irreversible degeneration and necrosis of cortical neurons may lead to the loss of cerebral cortex function. Consequently, this condition is also referred to as a decorticate state, akinetic mutism, wakeful unconsciousness, or vegetative state. Jennett and Plum (1972) even suggested calling it "A Syndrome in Search of a Name," highlighting its unique nature. According to Jennett’s observations (1976), among patients with severe traumatic brain injury and deep unconsciousness, if some eye movement remains, about 31% will eventually enter a vegetative state or die. If eye movement is reduced, this figure rises to 64%, and if eye movement is completely absent, the likelihood increases to 95%. He also found that if patients only exhibit withdrawal responses to painful stimuli, approximately 63% will die or enter a vegetative state. If the response is limited to extensor posturing or complete limb flaccidity, the rate climbs to 83%. Why are vegetative patients equated with the dead? Because those who enter a vegetative state are essentially survivors pulled back from the brink of death—or, in other words, those who narrowly escaped brain death. It goes without saying that as the diagnosis, treatment, nursing, and monitoring of severe traumatic brain injuries improve, mortality rates will continue to decline. However, when severe and irreversible damage to the central nervous system has already occurred, the number of individuals surviving in a vegetative state will not decrease.
bubble_chart Clinical ManifestationsThese patients are mostly in a persistent unconscious state after severe brain injury, either due to excessive primary brainstem injury, intracranial hemorrhage causing secondary brainstem damage from brain herniation, or severe cerebral ischemia and hypoxia resulting from sustained intracranial hypertension. In some cases, respiratory or cardiac arrest may occur, requiring resuscitation. Despite intensive treatment leading to gradual stabilization of the condition and normalization of intracranial pressure, consciousness remains in a prolonged unconscious state for at least three months or more. Clinically, most cases present with deep unconsciousness in the first 1-2 months post-injury, showing only limb extension responses to strong painful stimuli. Over the subsequent 1-2 months, eye-opening movements gradually appear in response to pain. Later, patients may exhibit instinctive spontaneous eye-opening or aimless eye movements but remain unable to follow commands or respond to speech. Concurrently, the original decerebrate rigidity disappears, and slow limb withdrawal responses to pain gradually emerge, though muscle tone remains high. Actions such as forced grasping, sucking, teeth grinding, and chewing often appear. The patient remains in a drowsy state throughout the day, with distinct wake-sleep cycles, showing indifference to the external environment—seeming unfamiliar or uncomprehending. Occasionally, the eyes may track moving people or objects, but purposeful actions are absent. They cannot adjust uncomfortable postures independently nor actively seek food. During examination, the patient stares without speaking, with increased muscle tone in all limbs. The upper limbs are often flexed and tightly held against the chest, showing painful expressions or occasional moaning when passively extended. The lower limbs are internally rotated and adducted, either extended or flexed, with the metatarsus in a flexed position. Superficial reflexes such as the abdominal reflex are absent, though the cremasteric reflex may still be present. The corneal reflex, pupillary light reflex, swallowing reflex, and cough reflex remain intact.
The diagnosis of prolonged unconsciousness primarily relies on its distinctive clinical manifestations, combined with the injury condition, duration of unconsciousness, and auxiliary examinations for confirmation. In such patients, electroencephalogram (EEG) often shows grade III abnormalities, which may manifest as diffuse high-amplitude slow-wave activity or low-amplitude 8–9 Hz alpha-like waves, predominantly in the frontal and central regions. There is no response to stimuli such as sound, light, pain, or passive eye opening, a condition also referred to as alpha-coma. Early CT and MRI scans may reveal widespread low-density or high-signal changes in the cerebral hemispheres, basal ganglia, and cerebellar white matter, with more pronounced involvement in the deep white matter extending along the gyral white matter. Hemorrhages or softening foci may sometimes be observed in the midbrain and pons, while the medulla oblongata often remains intact. Ultimately, with the progression of brain atrophy, the cerebral sulci and cisterns widen, and the ventricular system also enlarges.
bubble_chart Treatment Measures
The management of prolonged unconsciousness primarily lies in prevention, as there is currently no effective treatment once it occurs. According to individual domestic reports, there have been cases of recovery from a vegetative state after 1–2 years or even as long as 12 years, which can be considered miraculous. However, a passive attitude should not be adopted toward such patients; instead, they should receive serious treatment and meticulous care in the hope of some recovery.
The first step is to strengthen the management of the initial stage of traumatic brain injury, taking measures as early as possible to avoid severe cerebral ischemia and hypoxia, promptly removing intracranial hematomas, controlling cerebral edema, and reducing intracranial pressure. It is essential to prevent and treat high fever and spasms, ensure airway patency, and, under the conditions of an intensive care unit, closely monitor intracranial pressure and blood gas levels, ensuring that intracranial pressure does not exceed 4 kPa (30 mmHg) and maintaining Paa
Secondly, promptly administer neurotrophic and metabolic activators or awakening agents. Among these drugs, one category is endogenous to the human body, such as adenosine triphosphate (ATP), coenzyme A (Co-A), cytochrome C (Cytochrome C), glutamic acid (Glutamic Acid), glutamine (Glutamine), gamma-aminobutyric acid (GABA), vitamin B6 (Pyridoxine), succinic semialdehyde (SSA), and cytidine diphosphate choline (CDP-choline), all of which play significant roles in brain tissue metabolism. Administering any one of these drugs allows it to be converted into other molecules within the brain, so they can be used interchangeably with similar effects. The administration methods are as follows: ATP 20mg plus Co-A 50u plus insulin 4u/d dissolved in glucose solution for intravenous drip; Cytochrome C 15–30mg/d intravenous drip; Aceglutamide 1–3g/d intravenous drip; GABA 1–4g/d intravenous drip; Pyridoxine 50–100mg/d intravenous drip; CDP-choline 250–500mg/d intravenous drip. Additionally, nerve growth factor (NGF) has a notable effect in preventing neuronal death after brain trauma, with a common dosage of 4ml/d intramuscular injection. Another category of drugs is exogenous and promotes neuronal oxidation-reduction metabolism. Commonly used ones include: Meclofenoxate 1–2g/d dissolved in 10% glucose solution for intravenous drip; Antiradon 1g/d intravenous drip; Piracetam 8–10g/d intravenous drip; Duxil 1–2 tablets/d orally; Pyritinol 0.1–0.2g, three times daily orally; Nimodipine 20–40mg, three times daily orally; Cerebrolysin 10–30ml/d intravenous drip; Avan 30mg, three times daily orally; Calan 5mg, three times daily orally; Xanthinol Nicotinate 0.1–0.2g, three times daily orally; Cinnarizine 25mg, three times daily after meals orally; Sodium Aescinate 5–10mg/d intravenous drip. Furthermore, some have also achieved certain efficacy using the antidepressant imipramine (Imipramine) or the anti-tremor drug levodopa (L-dopa).
Thirdly, to improve cerebral blood supply and increase oxygen levels, treatments such as hyperbaric oxygen chambers, ultraviolet radiation, oxygenated blood transfusion, oxygenated or artificial fluorocarbon blood injection into the carotid artery, and carotid artery occlusion can be performed. To maintain nutritional status, in addition to oral and nasogastric feeding, intravenous nutrition, emulsified fats, amino acids, hydrolyzed proteins, vitamins, trace elements, plasma, albumin, globulin, and even periodic blood transfusions should be administered. If basic nutritional requirements still cannot be met, gastrostomy feeding may be considered. To prevent joint stiffness and muscle atrophy, a planned regimen of tuina, acupuncture, and physical therapy should be implemented. To prevent complications such as infections, epilepsy, dehydration, constipation, urinary retention, and bedsores, appropriate prophylactic medications should be administered, and meticulous nursing care must be provided. It is important to recognize that deaths in such patients are almost always caused by complications in other systems.
1. Post-traumatic hydrocephalus: Patients who develop hydrocephalus after severe brain injury often exhibit persistent unconsciousness. Although their condition stabilizes after treatment, their consciousness recovery is unsatisfactory, or even shows a worsening trend, making it easy to mistake for a vegetative state. The difference is that post-traumatic hydrocephalus is always accompanied by significant intracranial hypertension, and the condition improves rapidly after ventricular puncture and drainage. CT scans show ventricular enlargement without widening of the sulci and cisterns, along with interstitial edema around the ventricles, which can help differentiate the condition.
2. Locked-in Syndrome: This condition results from injury to the head and neck involving the brainstem or vertebrobasilar circulation, also known as pseudocoma or ventral pontine syndrome. Although not always caused by trauma, it is easily mistaken for a vegetative state in such cases. Since traumatic locked-in syndrome still holds hope for recovery, timely differentiation and active treatment are essential. The hallmark of this syndrome is mutism, quadriplegia, preserved consciousness, and the ability to communicate through eye movements, such as opening and closing the eyes to convey meaning. In contrast, patients in a vegetative state lack consciousness and cannot communicate, let alone follow commands to open or close their eyes. Sometimes, during the acute phase after trauma, if the patient remains unconscious due to brainstem injury, distinguishing the two can be challenging. However, as the condition gradually improves, recovery always begins with consciousness—meaning the patient regains awareness but remains unable to move, losing the ability to open the mouth, swallow, or exhibit emotional expressions like crying or laughing, presenting as mutism and flaccid quadriplegia.
3. Brain Death: In cases of severe brain injury leading to central failure, the patient’s breathing ceases, but with the aid of a ventilator, the heartbeat can be maintained for hours or even days, with some reports lasting up to 74 days. In such situations, the patient shows no response to any external stimuli, lacks spontaneous breathing, exhibits muscle relaxation, experiences a drop in body temperature, and loses brainstem reflexes, followed by signs of circulatory failure. Occasionally, the spinal cord, no longer under brain control, may still display limb extension reflexes, but this does not indicate preserved central nervous function—the brain is already dead, and the heartbeat persists independently of central regulation. Some patients, despite extremely severe injuries, may survive if aggressive resuscitation prevents complete brain death, but they often end up in a vegetative state due to extensive brain damage. Typically, the determination of brain death must include the following four criteria: no response to any stimuli for at least six consecutive hours of observation; absence of spontaneous breathing and movement for over one hour; bilateral dilated and fixed pupils with loss of light and corneal reflexes; and a flat-line EEG recorded for at least four minutes with a gain of 5μV/mm or higher. In special cases, additional methods such as cerebral angiography, isotope cerebral angiography, contrast-enhanced CT, or transcranial Doppler vascular scanning may be used to confirm the cessation of cerebral blood flow. There is no unified standard for the minimum observation period to confirm brain death, but testing usually begins after maintaining artificial respiration for over 12 hours post-respiratory arrest. Confirmation requires two separate clinical examinations, spaced six or twelve hours apart.
