What Is a Persistent Vegetative State?

Persistent vegetative state (PVS), also known as plant survival, has similar symptoms such as decortical syndrome, blinking coma, coma, neocortical death, awake coma, long-term coma, persistent loss of consciousness, and persistent coma. In 1993, the American Academy of Neurology recommended that only three names be retained in clinical consciousness naming, namely, coma, atresia, and persistent vegetative state. Other names should be abolished. ^[1]

Persistent vegetative state

Persistent plant state concept

Causes of persistent vegetative state

The causes of persistent vegetative states can be roughly divided into three categories:

Acute injury: This is the most common cause of PVS. Traumas are the most common, including traffic accidents, gunshot wounds, and birth injuries. Non-traumatic injuries include hypoxic-ischemic encephalopathy caused by various reasons, such as cardiac arrest, asphyxia, hanging, drowning, etc .; severe persistent hypotension, cerebrovascular accidents, such as cerebral hemorrhage, cerebral infarction, cobwebs Hembrane hemorrhage, etc .; In addition, there are infections, tumors, and poisoning of the central nervous system.

Degeneration and metabolic diseases: Alzheimer disease, multiple cerebral infarction, dementia, Pick disease, Creutzfeldt-Jakob disease, Parkinson disease, and Huntington disease are common causes in adults. It is common in children with ganglion lipid deposition disease, adrenal white matter malnutrition, mitochondrial encephalopathy, gray matter degeneration and other diseases.

Development malformations: including anencephaly, congenital hydrocephalus, microcephaly, and brain bulge. ^[2]

Pathogenesis of persistent vegetative state

The pathological changes in patients with PVS often vary from person to person, and the time between brain damage and death varies, which can affect the nature and severity of the pathological changes, and the patient's primary disease can also affect the test results.

In 1994, Kinney reported that the pathological examination of the brain in patients with persistent vegetative states found that the thalamus was the most important lesion. He believed that the thalamus was very important to consciousness and perception, and the significance of awakening was secondary.

In 1997, Hunter (Reinder) reported that the plant state may be related to the damage to the gray matter of the caudate nucleus, and believed that in addition to diffuse damage, some focal ischemic changes are also very important.

However, whether it is PVS caused by trauma or non-traumatic brain injury, there are roughly two pathological changes:

chronic cortical necrosis. This type of change is mainly seen in ischemic hypoxic encephalopathy. Dougherty reported autopsy data of 10 cases, 7 cases of neocortical layer necrosis, 2 cases of multifocal infarction, 1 case of embolic infarction, 1 case of neuron loss and glial hyperplasia. Neocortical damage is most obvious in the occipital lobe. In addition, most of the hippocampus, striatum, thalamus, and cerebellum have neuronal loss and glial hyperplasia. Nine of the 10 cases had normal brainstems, and only 1 had a quadruple infarction.

diffuse axonal damage. This kind of abnormality is seen in acute craniocerebral injury, because extensive subcortical axonal damage interrupts the connection between the cerebral cortex and other parts of the brain, and sometimes diffuse axonal damage can be accompanied by primary or secondary brain stem damage. Individual reports of hypothalamus may also have severe damage. ^[2]

Persistent vegetative status

Sacral atresia syndrome

Locked-in syndrome is also known as the deaf transferred state. Atresia syndrome was reported by Nordgren in 1971. Due to the lesions at the base of the bilateral pontine, the cortical nucleus and corticospinal tract on the ventral side of the brainstem are damaged, resulting in silence and quadriplegia, which looks like a coma, but in fact, the consciousness is completely clear, and the patient can close the eyes with Answer the question.

The patient remains alert and aware of his situation, but quadriplegia and cerebral palsy below the ocular motor nerve can only be signaled by vertical movement of the eye and blinking.

Atresia syndrome is common in pontine infarction caused by basal artery thrombosis. Other causes include brain stem tumors and central pontine myelinolysis. Severe polyneuropathy, especially Guillain-Barre syndrome and myasthenia Weakness, as well as the use of neuromuscular blockers, can also produce paralysis similar to atresia syndrome.

Coma

Coma is a persistent, deep pathological disorder of consciousness, characterized by closed eyes that cannot be awakened. It differs from PVS in that the latter can wake up without cognition, while the comatose can neither wake up nor have cognition.

Brain death

Brain death is a permanent and irreversible loss of all brain (especially brainstem) functions, characterized by deep coma and involuntary breathing, which must be maintained with a ventilator, and all brainstem reflexes are lost.

Akinetic mutism

Non-kinetic mutism patients do not speak, have no spontaneous activity, do not move under stimulation, can open their eyes and look around, have no or only local response to painful stimuli, incontinence, and sleep-wake cycle. Multiple lesions can be caused, including subacute traffic hydrocephalus, tumors in the posterior third ventricle and aqueduct, bilateral frontal lobe lesions involving the cingulate cortex (bilateral anterior cerebral artery thrombosis), and bilateral brain stem ascending reticular Structure and local lesions of the median nucleus of the thalamus. The common feature of this type of lesion is that it impairs the dynamic network activation system that receives internal and external environmental information. ^[3]

Continuous vegetative state treatment

At present, there is no effective treatment for PVS, mainly for the treatment of the cause. In order to maintain a stable condition and promote the recovery of brain function, at the same time do some non-specific treatments, such as maintaining respiratory circulation function; ensuring water and electrolyte balance; ensuring adequate nutrition; using brain metabolism promoting drugs (such as cerebrolysin, citicoline, ATP, cytochrome C, etc.); sound, light, electrical stimulation; hyperbaric oxygen chamber and ventricular shunt.

Haig et al. Reported an exceptional traumatic PVS with a course of 6 months, and consciousness recovered after treatment with Sinemet. Tsubokawa of Japan and others used electrical stimulation of the midbrain reticular structure and non-specific nuclei for more than 6 consecutive months. As a result, consciousness recovered in 3 of 8 cases. The life of patients with PVS has been stable. As long as the care is appropriate, most patients will continue to survive, and there are no shortage of clinical cases that survive for 10-20 years.

But after more than 12 months of observation and the condition does not improve, the chance of sobering is slim. The cost per patient is quite staggering. According to US statistics, the cost of each hospitalized PVS patient in the first three months is approximately $ 149,200, and in general clinics, it costs $ 302 to 500 per day ($ 126,000 to 180,000 per year). PVS treated in the family child. The first year costs approximately $ 97,000. Based on this situation, the Institute of Ethical Issues in Medical Biology and Behavior Research (1983), the American Academy of Neurology (1989), and the American Medical Association (1990) announced that as long as the family members of the patient and the patient's life require it, Stop all forms of treatment, including infusions and nutrition. ^[4]