Persistent vegetative state

Introduction to persistent plant status The persistent vegetative state (PVS) was first proposed by Jennett and Plum in 1972. It means that after a period of time, people with severe brain damage still lack consciousness activities, lose language, and only retain the state of unconscious posture adjustment and motor function. . Vegetative state refers to the state of existence in which the body can survive and develop, but is unconscious and thinking, lacking the ability to perceive itself and its surroundings. The patient has a sleep-wake cycle, partially or completely preserves the function of the hypothalamus and brainstem, but lacks any adaptive response, lacks any functional thinking to receive and reflect information, and the plant state can be temporary or persistent. (PVS). Some people think that the state of the plant is more than one month, or one year is called PVS, but it is generally considered that it is necessary to diagnose PVS for >1 year. Persistent plant status (PVS) behaves like a coma, which is easily confused with coma, and, at first, a comatose patient, which gradually develops into these states after varying lengths of time. Once the patient has a sleep-wake cycle, the real coma no longer exists. The identification of persistent vegetative state (PVS) and true coma is important for proper treatment and prognosis. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific people Mode of infection: non-infectious Complications: Epilepsy Atrial fibrillation

Persistent phytopathology

Acute injury (25%):

This is the most common cause of PVS, the most common trauma, including traffic accidents, gunshot wounds and birth injuries, non-traumatic injuries including hypoxic ischemic encephalopathy caused by various causes, such as cardiac arrest, suffocation, hanged , drowning, etc.; severe persistent hypotension, cerebrovascular accidents, such as cerebral hemorrhage, cerebral infarction, subarachnoid hemorrhage, etc.; in addition, central nervous system infections, tumors, poisoning and so on.

Degenerative and metabolic diseases (20%):

Alzheimer's disease, multiple cerebral infarction, dementia, Pick disease, Creutzfeldt-Jakob disease, Parkinson disease, Huntington disease is a common cause in adults, common in children with ganglion lipid deposition, adrenal white matter dystrophy, mitochondrial encephalopathy, gray matter Degenerative diseases.

Developmental malformation (25%):

Including no brain malformations, congenital hydrocephalus, microcephaly, brain swelling and so on.

Pathogenesis

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

In 1994, Kinney reported brain pathological examination of patients with persistent vegetative state and found that the thalamus is the most important lesion. It is believed that the thalamus is very important for consciousness and perception, while the significance for arousal is secondary.

In 1997, Reinder reported that plant status may be associated with damage to the gray matter of the caudate nucleus, and that some focal ischemic changes are also important in addition to diffuse damage.

However, there are roughly two pathological changes in PVS caused by trauma or non-traumatic brain injury.

1. Chronic cortical layer necrosis is mainly seen in hypoxic ischemic encephalopathy. Dougherty reported 10 autopsy data. There were 7 cases of neocortical necrosis, 2 cases of multifocal infarction, and embolic infarction. For example, neuronal loss and gliosis in 1 case, the new cortical damage is most obvious in the occipital lobe, in addition, hippocampus, striatum, thalamus, cerebellum mostly have neuronal loss and gliosis, in 10 cases, 9 cases of brain stem All were normal, and only one case had a quadrant infarction.

2. Diffuse axonal damage This 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. Sometimes diffuse axonal damage can be accompanied by primary or secondary For the brain stem injury, the hypothalamus can also be seriously damaged.

Persistent plant state prevention

Maintain proper temperature and humidity in the ward and strengthen warmth in winter; oral care is the basis for prevention and control of infection. Through oral care, keep the mouth clean and moist, and improve the antibacterial ability of oral mucosa.

Persistent phytopathic complications Complications epilepsy atrial fibrillation

Frequent complications of various complications occurred: 2241.51% of pulmonary infection; 1018.87% of epilepsy; 59.43% of deep venous thrombosis of lower extremity; 23.77% of multiple organ failure; 23.77% of cerebral infarction; 11.89% of hypoproteinemia; 11.89% of hypokalemia %; hiccup 11.89%; atrial fibrillation 11.89%; hepatomegaly 11.89%; filamentous keratitis 11.89%; stupor state 11.89%; cerebrospinal fluid leakage 11.89%; diabetes insipidus 11.89%; anemia 11.89%; renal failure 11.89 %; gastrointestinal bleeding 11.89%.

Persistent vegetative symptoms Common symptoms Pharyngeal reflex coma cognitive neurological loss sensory disturbance

Persistent vegetative state patients lose cognitive function, but retain autonomic function, which occurs after coma, characterized by unconscious or cognitive deficiencies in the surrounding things, but maintains a sleep-wake cycle, spontaneous movements can occur, to the outside world The stimulus will blink, but it will not speak and will not obey the order.

The patient looks awake, blinks freely, stares at the eye or turns the eyeball without purpose, but has no consciousness activities, lack of consciousness, thinking, emotion, will and other activities, without any spontaneous language and purposeful limb activities, speech, surroundings And lack of conscious reactions, no words, subconscious activity under the cortex, such as chewing, swallowing reflex, pupillary light reflection, corneal reflex, eyelash reflex, cough reflex, exist, painful expression or painful or harmful stimulation Escape the response, but usually there is no localization reaction, there may be unconscious crying, there is an irregular sleep-wake cycle, visual reflex can be preserved to a certain extent, and primitive reflexes such as sucking and strong grip can occur, and bilateral pathological reflexes are positive. The patient's heartbeat, breathing, blood pressure and body temperature are normal, but the incontinence is incontinent.

Continuous phyto state examination

Including whole blood routine, blood sugar, liver function, kidney function, blood ammonia, blood gas analysis, urine analysis, urine drug screening.

1. EEG changes in EEG and their diagnostic value are different. Early Jennett et al. believe that the initial stage of PVS should be equipotential EEG, and obvious electrical activity occurs after several days. A rhythm appears, and some scholars later believe that the EEG change of PVS is resting potential or equipotential EEG, but most scholars believe that the electroencephalogram of most PVS patients shows extensive diffuse polymorphic and waves, and When waking into sleep is often accompanied by de-synchronization of background activities, 10% of patients have normal EEG in the late stage, and there is rarely typical epileptiform activity in PVS. With the improvement of clinical symptoms, in EEG Corresponding to the wave, the a rhythm reappears.

2. Evoked potential somatosensory evoked potential (SEP) is the most sensitive and reliable method for PVS. Hanosita pointed out that the main manifestation of SEP is the extension of central conduction time (CCT) and the decrease of N20 amplitude of N13-N20. Zegerl et al also believe that after onset One week, the disappearance of bilateral somatosensory evoked potentials is an important indicator that consciousness can not be restored. Tsao et al reported that 1 case of SPE in children with PVS caused by drowning was normal, and finally the consciousness recovered completely, indicating that the prognosis of patients with normal SEP may be good.

3. Imaging examination CT and magnetic resonance imaging (MRI) can only prove diffuse multifocal lesions in the gray matter and white matter of the brain. Chu reported the early and late stages of PVS (4 months to 3 years) in 6 cases of hypoxic encephalopathy. CT changes, early CT showed no special changes except general cerebral edema, late manifestations of cerebral cortex or border zone infarction (5 cases), basal ganglia low density lesions (4 cases), posterior cerebral artery infarction (3 cases), when surviving After more than 8 months, there is obvious ventricular enlargement, and it is not commensurate with cortical atrophy. As time goes on, the ventricle enlargement tends to be larger and larger, and the brain tissue is progressively atrophied. De Jong reports in 1997, PET examines the mother to tell the story. The patient found that the cerebral blood flow in the head of the cingulate gyrus, the right middle iliac crest and the premotor cortex increased, which was higher than the control group (non-verbal acoustic stimuli), suggesting that even if the vegetative state is diagnosed accurately, It indicates that the cortex is resting. There is a report indicating that patients with plant status may have some "implicit" recognition ability, but whether the sensory cortical response suggests a recovery from plant status remains to be further studied.

Other auxiliary examinations include chest radiographs, electrocardiograms, etc.

Persistent plant state diagnosis

Diagnostic criteria

Many syndromes that are not exactly defined are used as synonyms for persistent vegetative states, including alpha coma, neocortical death, and permanent unconsciousness. These names lack precision and are avoided as much as possible. The diagnosis of the disease should be cautious and can only be made after a long period of observation.

There are many different opinions about the diagnostic criteria of PVS, and there are no fewer than 10 kinds of reports in the world.

(1) The diagnostic criteria of the American Association of Ethics and Neurology (1993) are:

1 Loss of perception of yourself or the environment, can be reflective or spontaneous blinking.

2 The patient cannot talk or write communication with the doctor. The patient has no emotional reaction to the speech, and may have accidental gaze tracking, usually not moving with the stimulation target.

3 can't speak words or speak.

4 can smile, frown or yell, but has nothing to do with external stimuli.

5 There is a sleep-wake cycle.

6 There are primitive reflections such as sucking, chewing, swallowing, pupils reflecting light, heart-reflecting, holding and tendon reflections may exist.

7 can not learn or imitate any movement, but there may be flexion activities for harmful stimuli.

8 blood pressure regulation, heartbeat and respiratory function still exist, but there is incontinence.

(2) China established the clinical diagnostic criteria (tentative) for PVS in Nanjing in 1996. These standards are:

1 Loss of cognitive function, unconscious activity, unable to execute instructions.

2 Maintain spontaneous breathing and blood pressure.

3 has a sleep-wake cycle.

4 can not understand or express language.

5 Automatic blinking or irritating under the eyes.

6 can have no purpose eye tracking movement.

7 The hypothalamus and brainstem function are basically preserved.

If the above symptoms persist for more than one month after brain injury, it can be designated as PVS.

Despite these criteria, accurate diagnosis of PVS patients is difficult because coma and plant status can be converted in the same patient. Clinically, cases often show vegetative state when coma is improved, and have short-term vegetative state. The patient developed a deep coma as the condition progressed to worsening.

Therefore, some clinicians suggest distinguishing the permanent vegetative state from PVS. In addition, Ota Toshio et al. proposed transient vegetative syndrome and incomplete vegetative syndrome. And other concepts, to distinguish from PVS, the former refers to those who have some reaction to external language stimuli (such as nodding) or have some ability to execute language instructions and can issue monosyllabic; the latter includes Those who can show some emotional reactions and have eye tracking intentions, it is clear that although these two types of patients also have some symptoms of PVS, but strictly speaking they are not typical PVS, some of their symptoms may be the condition Temporary performance during the conversion process.

Therefore, in the tentative standard for the diagnosis of PVS in China, it is proposed that the plant state must be diagnosed as PVS for more than one month. This consideration is comprehensive and necessary. It is helpful to clarify the common confusion in the current domestic clinical diagnosis, especially It should be pointed out that some patients who are conscious but severely injured by sight and hearing are also easily misdiagnosed as PVS patients. According to Andrew et al. (1996), the rate of misdiagnosis is as high as 37% to 40%.

2. The concept and clinical manifestations of persistent vegetative state are clear, but there are widespread misdiagnosis cases, even experienced neurologists will occur. Tresch et al. examined 62 patients diagnosed with PVS by other medical institutions, and 11 cases existed. Regarding the environment and its own perception, Childs et al reported 49 cases of PVS diagnosed in hospitals. 37% of patients were found to have sensory ability after admission, and did not meet the state of continuous vegetative state. Andrews et al reported 40 patients diagnosed with PVS in other hospitals. Of the 16 patients (40%) who had sensory ability, 11 patients were able to restore their localization, orientation and cognitive function after treatment.

The diagnosis of plant state can affect the treatment and care of patients, and it has a huge impact on society and families. It has important significance in law and morality. It is directly related to the evaluation of clinical treatment effects and scientific and effective treatment methods. It has a key role, so doctors must be highly aware of the seriousness of misdiagnosis and the factors that cause misdiagnosis.

Analysis of the reasons for misdiagnosis may have the following aspects:

(1) The concept of the definition of plant state is unclear, and it is mainly confused with coma.

(2) The observation conditions are not ideal, and the observation of the condition is not detailed, especially the opinions of people who are in close contact with the patient, such as family members.

(3) Observing the difficulty of patients with motor and sensory disturbances.

Many authors have put forward important recommendations for diagnosing vegetative conditions: in the evaluation of patients with brain injuries with severe limb disability, the need for examination skills, time and repeated observation; many of the misdiagnosed patients are blind or severely impaired, so lack of blinking and Sight tracing is an unreliable manifestation; early observation can be used by patients for any activity of communication and regular follow-up; determining the perceived ability of patients with severe and complex neurological dysfunction requires an experienced treatment team.

Differential diagnosis

1. Locked-in syndrome is also known as the deaf transferred state. The atresia syndrome was reported by Nordgren in 1971. The ventral cortex nucleus of the brain stem is due to bilateral basal lesions. The bundle and the cortical spinal cord are damaged, and the resulting silence and quadriplegia look a lot like a coma, but in fact the consciousness is completely clear, and the patient can answer the question with a closed eye.

The patient remains alert and aware of his or her situation, but the quadriplegia and cranial nerve palsy below the eye movement can only be indicated by the vertical movement of the eye and the blink of an eye.

This disease is common in cerebral infarction caused by basilar artery thrombosis. Other causes include brain stem tumor and central pontine myelinolysis. Severe polyneuropathy, especially Guillain-Barré syndrome, myasthenia gravis And the use of neuromuscular junction blockers can also occur in a state of paralysis similar to the atresia syndrome.

2. Coma is a persistent, deep pathological disturbance of consciousness characterized by closed eyes that cannot be aroused. It differs from PVS in that the latter can be awakened without cognition, while a coma can neither awaken nor No cognition.

3. Brain Death Brain death is a permanent and irreversible loss of the brain's function (especially the brainstem). It is characterized by deep coma and no spontaneous breathing. It must be maintained by a ventilator and all brain stem reflexes are lost.

4. Non-kinetic mutism patients do not speak, no spontaneous activity, do not move under the incentive, can blink around, no response to pain stimuli or only local reactions, size Incontinence, there is a sleep-wake cycle, multiple lesions can be caused, including subacute transitive hydrocephalus, third ventricle posterior and aqueduct tumors, bilateral frontal lobe lesions involving the cingulate cortex (bilateral anterior cerebral artery thrombosis) ), the bilateral brainstem reticular structure and the localized lesions of the midbrain nucleus, the common feature of such lesions is the damage to the dynamic reticular activation system that accepts internal and external environmental information.

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