disturbance of consciousness
Introduction
Introduction to consciousness disorder Consciousness refers to the state of perception of oneself and the surrounding environment, which can be expressed through words and actions. Consciousness disorder refers to a state in which people's perceptions of themselves and the environment are impaired, or people's mental activities that are perceived by the environment are obstacles. The disturbance of consciousness is also a manifestation of critical illness. The patient did not respond and completely lost consciousness because the advanced nerves were severely inhibited. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: pneumonia, coma
Cause
Cause of consciousness disorder
Localized lesions (35%):
(1) cerebrovascular disease: cerebral hemorrhage, cerebral infarction, transient ischemic attack, etc.; (2) intracranial space-occupying lesions: primary or metastatic intracranial tumor, brain abscess, cerebral granuloma, brain parasitism Insect cysts, etc.; (3) craniocerebral trauma: brain contusion, intracranial hematoma, etc.
Diffuse brain lesions and seizures (5%):
(1) Intracranial infectious diseases: various encephalitis, meningitis, arachnoiditis, ependymitis, intracranial sinus infection, etc.; (2) diffuse head injury; (3) subarachnoid hemorrhage (4) cerebral edema; (5) brain degeneration and demyelinating lesions.
Systemic disease (15%):
1. Acute infectious diseases: various sepsis, infection with toxic encephalopathy, etc.
2. Endocrine and metabolic diseases: such as hepatic encephalopathy, renal encephalopathy, pulmonary encephalopathy, diabetic coma, mucous edema coma, pituitary crisis, thyroid crisis, adrenal insufficiency coma, lactic acidosis.
3. Exogenous poisoning: including industrial poisons, drugs, pesticides, plant or animal poisoning.
4. Lack of normal metabolites: (1) hypoxia, (2) ischemia, (3) hypoglycemia.
5. Water and electrolyte balance are disordered.
6. Physical damage such as sunburst, heat shot, electric shock, drowning, etc.
Pathogenesis
Various intracranial and extracranial lesions can lead to varying degrees of disturbance of consciousness as long as they involve any part of the non-specific ascending reticular activation system.
The pathophysiological basis of disturbance of consciousness may be caused by mechanical damage of the brainstem or important parts of the cerebral cortex or by comprehensive damage of the brain metabolic process. Metabolic dysfunction may be caused by the transport of energy substrates (hypoxia, ischemia, Hypoglycemia) or changes in the neurophysiological response of the neuronal membrane (drug or alcoholism, epilepsy or acute head trauma).
1. Brain blood circulation and metabolism
The brain is obviously dependent on continuous blood flow and transports oxygen and glucose. The blood oxygen consumption rate per minute is 100 ml in 100 g brain tissue, and the glucose consumption rate is 5 mg. Although the loss of consciousness occurs within 8 to 10 seconds after the interruption of blood flow, the brain The amount of stored sugar can provide 2 minutes of energy after the interruption of blood flow. When hypoxia occurs in ischemia, the available glucose will be depleted more quickly. When normal, the cerebral blood flow (CBF) is 100g gray. About 75 ml in minutes, 100 g of white matter is about 30 ml per minute (an average of 100 g of brain tissue is 55 ml per minute).
Local autoregulation of cerebral blood supply can maintain an average CBF of about 50 ml per minute per 100 g of brain tissue. About 25 mmol of glucose is extracted from this 50 ml CBF, and about 150 mmol (3.5 ml) of oxygen is extracted for glucose oxidation.
The mechanism by which normal CBF matches brain metabolism is unclear. Studies have shown that substances involved in this mechanism are Ph, adenosine and nitric oxide.
Brain tissue damage is much lighter than ischemia in hypoxia, and metabolic changes in glucose oxidation can be expressed as follows:
C6H12O66CO2 6H2O
There are two steps in this reaction: glycolysis and oxidative phosphorylation. Adult brain tissue can only use glucose. Glycolysis starts from glucose phosphorylation, and then the six-carbon sugar is cleaved into two tricarbonpyruvate and dehydrogenated by lactate. The action of the enzyme converts lactic acid to pyruvate, a process that is reversible. Pyruvate enters the mitochondria where it undergoes oxidative metabolism, ie into the tricarboxylic acid cycle.
2. Pathophysiology of white matter ischemia and hypoxia
(1) Differences in white matter gray matter ischemic damage: gray matter hypoxia depolarization promotes the release of excitatory glutamate, further opening up all glutamate-gated ion channels, the latter somewhat Ca2 permeability, Ca2 permeability channels The opening causes Ca2 to flow into the cells in a large amount, and activates destructive enzymes such as intracellular esterase and protease to cause permanent damage to the cells.
There is no glutamate synapse in the white matter, so the ischemic membrane depolarization of the white matter does not cause glutamate-mediated damage, but causes Na to continuously flow into the cell via a Na channel that is not inactivated by persistence. The normal transmembrane Na gradient collapses, the Na gradient disappears and the membrane depolarization causes the Ca2 to be taken out of the cell under normal conditions in exchange for the Na-Ca2 exchange protein of Na to form a Ca2 influx, and the intracellular Ca2 overload causes permanent damage. And loss of function.
(2) The role of -aminobutyric acid and adenosine: -aminobutyric acid (GABA) and adenosine are present in the white matter of the central nervous system, and there are no synaptic terminals in the white matter, so these neuroactive substances are not Synaptic release, and more likely due to the reverse action of Na and membrane potential-dependent uptake proteins.
(3) Discussion of the mechanism of action: In general, GABA and adenosine act on completely different specific receptors to exert intracellular effects, but in hypoxic white matter, GABA and adenosine appear to act on the same intracellular components. This protective effect is necessary because of the limited potency of GABA and adenosine produced by white matter.
Extracellular extracellular GABA and adenosine molecules stimulate the intracellular sequential response of the receptor, thereby increasing the tolerance of cells to hypoxia. GABA acts on GABA- receptor, which is coupled to intracellular protein kinase C (protein kinase). C, PKC), activated PKC transfers phosphate to a variety of intracellular proteins, resulting in altered function of the latter.
K outflow and Na influx caused by hypoxic damage of white matter, leading to the reverse opening of Na-Ca2 translocation protein, promote Ca2 into cells, hypoxia is also associated with endogenous GABA, adenosine release, activated GABA- Receptors and adenosine receptors activate intracellular PKC via G-protein coupling. Protein kinase C activation is often associated with downregulation of membrane-operating proteins. PKC may also down-regulate hypoxic white Na channels and affect Na influx.
Prevention
Prevention of consciousness
Try to prevent early, early detection, and early treatment. Maintain environmental sanitation, pay attention to personal hygiene and public health, and be in a good environment. If you are uncomfortable or have other diseases, don't blindly treat yourself. You should go to a regular hospital for professional treatment to avoid delaying your illness. Pay attention to supplement nutrition, and work and rest. Pay attention to your health.
Complication
Consciousness of consciousness disorder Complications pneumonia coma
It can be accompanied by changes in vital signs such as aspiration pneumonia, respiratory heartbeat, and traumatic injuries caused by coma.
Symptom
Symptoms of consciousness disorder Common symptoms Recent events Forgetting phenomenon Inactive silent pattern Orientation disorder Drowsiness Thinking incoherent response Slow breathing Irregular coma dementia
The change in consciousness is conceptually divided into two categories.
A class of arousal, the "switching" system of consciousness, presents a series of continuous unified behavioral states from awareness to coma. The clinical differences are: 1 awareness; 2 lethargy ; 3 confusion; (confusion); 4 slumber and coma (coma), these states are dynamic, can change with time, there is no clear boundary between the two, except for the coma and stun, It also belongs to the category of consciousness change and affects the level of awakening.
Another type of "consciousness" refers to the "content" of mental (psychological) activities, that is, the advanced functions of the brain, involving cognition and affective activities. Examples of such changes in consciousness include dementia, forgetting, delusion and Inattention, etc., in addition to deep dementia, such changes in consciousness do not involve the level of arousal.
The only normal form of consciousness change is sleep.
Awareness or consciousness is a complete and normal state of awakening.
1. Drowsiness: The early manifestation of disturbance of consciousness, the patient often falls asleep, can be awakened, wakes up after the consciousness is basically normal, or has mild disorientation and unresponsiveness.
2. Consciousness of confusion: The patient's time, space and character orientation are obviously obstacles, the thinking is inconsistent, often answering questions, the illusion can be outstanding performance, illusion is rare, and emotion is indifferent.
3. Drowsiness: The patient is in deep sleep, can not be awakened, can not answer, and will avoid or wake up to noxious stimuli such as acupuncture, pressure, etc., but immediately fall asleep.
4. Coma: loss of consciousness activity, can not be perceived by various external stimuli or internal needs, may have unconscious activities, any stimuli can not be awakened, according to stimulation response and reflex activity can be divided into three degrees:
Light coma: random activity disappears, responds to painful stimuli, various physiological reflexes (swallowing, coughing, corneal reflex, pupillary response to light, etc.) exist, body temperature, pulse, and breathing are not significantly changed, and may be accompanied by convulsions or agitation.
Deep coma: random activities completely disappeared, no response to various stimuli, various physiological reflexes disappeared, there may be irregular breathing, blood pressure drop, incontinence, muscle relaxation, and brain rigidity.
Extremely coma: also known as brain death, the patient is in a state of sudden death, no spontaneous breathing, various reflexes disappear, EEG is pathological electrical rest, brain function loss lasts for more than 24 hours, eliminating the influence of drug factors.
5. Class coma: Many different behavioral states can behave like coma or confused with coma, and patients who are initially comatose can gradually develop into one of these states after varying lengths of time. These behavioral states mainly include: locked-in syndrome, also known as the difference state, persistent vegetative state, non-kinetic mutism, volition (abulia), catatonia, pseudo coma, once the patient has a sleep-wake cycle, the real coma no longer exists. The identification of these states with true coma is the use of appropriate treatment and prognosis. important.
6. Delirium state: more serious than consciousness, disorientation and self-knowledge are obstacles, can not normally contact with the outside world, often have rich illusions and hallucinations, vivid and realistic illusion can cause fear, escape or injury Behavior, the clinical features of sputum, with attention deficits, low levels of consciousness, disturbances in perception, and disturbances in the sleep-wake cycle are the main symptoms.
Consciousness disorder is often volatility and transitional. In order to determine the severity of disturbance of consciousness, to assess its progress, to observe treatment response and to judge prognosis, foreign countries have developed various scales since 1949. These scales can be roughly divided into two categories. One is a coma scale, which combines various symptoms independently to obtain the severity of coma; the other is a scoring system, which is different from the coma scale, which scores and analyzes each symptom independently, and finally According to the score to determine the degree of disturbance of consciousness, the Glasgow Coma Scale developed by Teasdale and Jennett (1974) is the most widely used in China. It has been widely used in clinical practice in China.
The Glasgow Coma Scale has a maximum score of 15 points and a minimum score of 3 points. The higher the score, the clearer the consciousness. The scale is less, simple and practical, but the children under 3 years old, the elderly, speechless, Dumb people, mental patients, etc. are limited in application due to difficulty in cooperation. In addition, the scale cannot judge the conscious pre-consciousness disorder, and the emotional response and behavioral disorder of the patient cannot be described.
Examine
Examination of disturbance of consciousness
(1) Determine whether there is a disturbance of consciousness.
(2) Determine the degree or type of disturbance of consciousness. Common methods are:
1. Clinical classification, mainly to give speech and various stimuli, to observe the patient's reaction to judge, such as breathing their name, pushing their shoulders and arms, pressing on the sacral incision, acupuncture the skin, talking to it and performing it. Purposeful action, etc.
2. Glasgow Coma Scale Assessment Method: This method is based on the method of assessing the degree of disturbance of consciousness in response to blinking, verbal stimuli and command actions.
(3) Identify the cause of the disturbance of consciousness.
(4) Diagnostic procedures for disturbance of consciousness.
1. Focus on the examination of neurological signs and meningeal irritation, pay attention to body temperature, breathing, pulse, blood pressure, pupil, sclera, face, lip color, oral and ear conditions, exhaled smell.
2. Laboratory tests: such as blood, venous blood, urine, anal finger, stomach content, chest, electrocardiogram, ultrasound, cerebrospinal fluid, cranial radiography, CT and MRI.
Diagnosis
Diagnosis of consciousness disorder
diagnosis
Brain stem reflex is the key to determining the site of damage in patients with disturbance of consciousness.
1. In general, the patient is in a coma and the brainstem reflex is normal, suggesting extensive damage or dysfunction in the bilateral cerebral hemisphere.
2. The size, shape and response of the pupil are normal, suggesting that the parasympathetic efferent fibers of the oculomotor nerve that shrink from the upper cerebral sinus are complete (the afferent fibers of this reflex arc are the optic nerve).
When the pupil is less than 2 mm, it is difficult to evaluate the reaction to light. If the indoor light is too strong, it is not easy to check the pupil response to light. The circular pupils (2.5 to 5 mm in diameter) with large photoreactions on both sides can often eliminate midbrain damage.
Pupil dilated (greater than 5mm), no response to light or poor, may be damage to the midbrain (on the same side); or apocalypse oppression of the midbrain and / or oculomotor nerve, unilateral pupil dilated The ipsilateral space-occupying lesion is suggested, but occasionally occurs on the opposite side, which is caused by the midbrain being pushed to the opposite side of the canopy.
Oval and slightly off-center pupils (pupil ectopic) are often accompanied by early midbrain and oculomotor nerve compression, bilateral pupil dilation and loss of light response suggest severe damage to the midbrain, and most likely due to the oppression of the apocalypse Therefore, it may also be anticholinergic drug poisoning.
Bilateral small pupils respond to light, but not pinpoint-like pupils (1 to 2.5 mm in diameter), suggesting metabolic encephalopathy or deep bilateral hemisphere lesions (such as hydrocephalus or thalamic hemorrhage), which are due to the thalamus Sympathetic nerve fibers are damaged, and deep coma caused by barbiturate poisoning can also produce similar small pupils. The bilaterally small (less than 1mm) but photoreactive pupils suggest an overdose of anesthesia, but may also be seen in acute extensive Bilateral pons bleeding.
3. Check eye movements to assess the function of a large area of the brainstem.
The eyelid should be observed first, pay attention to the position of the eyeball at rest and the spontaneous movement of the eyeball. The horizontal separation of the eyes in the static state is the position of the eyeball that normally sleeps, and the eye is closed at rest, suggesting that the nerve is damaged. Caused by external rectus tendon, which means that the pons is damaged. When the intracranial pressure is increased, bilateral nerve palsy often occurs. This is a pseudo-localization sign. At the time of rest, the eye abduction is often accompanied by dilated pupils on the same side. Ocular nerve paralysis causes internal rectus spasm, almost all vertical axis separation or eyeball deflection is caused by cerebral bridge or cerebellar damage, accompanied by enlarged cerebral ventricle, hydrocephalus, the position of the double eye is often lower than the horizontal line This is called "sun set sign".
Spontaneous eye movements in coma are mostly horizontal floating of the eyes. This exercise indicates that the cerebellum and pons are damaged, which is the same as normal reflex eye movement. "Ocular bobbing" refers to the rapid downward movement of both eyes and A state of slow upward movement indicates that the horizontal movement mechanism of both eyes is damaged and is characteristic of bilateral pons lesions.
"Ocular dipping" refers to a slow downward movement that occurs in a patient with normal reflex levels of gaze, and subsequent rapid upward movement of both eyes, which is especially common in diffuse hypoxic injury. Patients with cerebral cortex may have persistent upward or downward gaze. When the thalamus and upper midbrain are injured, the eyes may turn downwards and inward.
The "doll eye" or the movement of the eye movement is to firstly rotate the head from the side to the other side or to rotate the head vertically, and to induce a reflective eye movement opposite to the direction of the head movement. These reactions are originated from getting lost. The brainstem reflex movement of the vestibular nucleus and the neck proprioceptor, the visual gaze controlled by the cerebral hemisphere in the awake person, normally suppresses these reflexes, and the neuronal channels of the reflex horizontal movement require the integrity of the paranuclear region And through the medial longitudinal bundle (MLF) and the contralateral ocular nerves.
Two kinds of information can be obtained by examining the reflex eye movement. First, the disturbance of consciousness caused by bilateral hemisphere lesions or early metabolism or drug inhibition, the eyes are prone to the movement from one side to the other side opposite to the direction of the head. The inhibition of the brainstem reflex on the opposite side of the damaged cerebral hemisphere is relieved. In patients with lethargy, the head rotation starts 2 to 3 times, causing the movement of the eyes in the opposite direction. After the movement of the eyeball, this technique itself can cause The patient's arousal and reflex movement stopped, and secondly, the full head-eye joint movement proved that the brain stem nerve passage from the high cervical spinal cord, the medulla to the midbrain is intact (the high cervical spinal cord and the medulla are the vestibular and caused by the rotor itself). The proprioceptive input is the starting part of the impulse; the midbrain is the part of the oculomotor nerve). Therefore, the cephalic reflex examination method is to prove that the brain stem nerve channel is functionally intact.
Complete lack of eye-adduction movement, indicating that the ipsilateral midbrain (occal nerve damage) or MLF-mediated reflex eye movements are damaged (such as internuclear ophthalmoplegia), oculomotor damage is often accompanied by dilated pupils and At the time of rest, the eyeball is horizontally skewed; when the MLF is involved, these two kinds of performances do not exist. It is difficult to make the endoscopic retraction when the head is turned, which is a mild symmetry abnormality when checking the doll's eye. Explain carefully.
A variable temperature test (vestibular eye reflex) for vestibular function testing is a useful auxiliary test for the head-eye test.
The joint movement of the eyeball at rest is incomplete or the coordinated movement of the eyes when the head is turned, indicating that the pons damage on the paralyzed side or the contralateral frontal lobe damage can be summarized as "both eyes gaze the hemisphere damage side and deviate from the brain stem." The side of the lesion, the eye deflection associated with frontal lobe lesions can usually be overcome by a quick turn. Epilepsy can also cause the opposite eyeball skew with rhythm, the movement of the sacral eye to the gaze side, and occasionally The eyes are contradictoryly offset from the side of the hemisphere lesion, which is "wrong-way-eyes".
When the drug inhibits the reflex movement of the eye, the result of using the manual examination should be interpreted very carefully. Usually, the eyes often rotate with the head, but in the case of drug poisoning, when the head is rotated and the eyeball seems to be fixed in place, it is easy to be Misdiagnosed as brain stem damage, these drugs such as phenytoin, tricyclic antidepressants, barbiturate poisoning, occasional alcohol, phenothiazine, neuromuscular blocker poisoning also inhibit binocular reflex movement, pupil size Normal and presence of light reflexes distinguishes most drug-induced disturbances from brain stem damage.
4. Although the use of corneal reflex alone is not large, it can confirm the abnormality of eye movement, because corneal reflex also depends on the integrity of the pons.
5. Observing the breathing pattern of patients with disturbance of consciousness, it is helpful for diagnosis. The shallow and slow breathing with time rhythm suggests metabolic diseases or drug poisoning. Fast and deep breathing often indicates metabolic acidosis, but it may also be seen in the pons. And lesions in the midbrain plane, Chen-Shi breathing has a typical cycle, with a short apnea during termination, suggesting diffuse or metabolic inhibition of bilateral hemispheres.
Differential diagnosis
When a patient becomes comatose, he or she needs to be identified with the following special disturbances of consciousness:
1. Decoricate syndrome: due to massive destruction or deterioration of cerebral cortical nerve cells, loss of function, subcortical function is relatively intact or restored, at this time the patient is unconscious, but has a wake-up cycle and no language. Can blink, the eyeball can rotate, the muscles of the limbs are high, there are retracting movements and defensive movements, there are sucking, chewing, holding the reflex, appearing in the cortical posture, common in the recovery period of coma, do not mistake the patient is still in a coma .
2. Akinetic mutism: also known as awakening coma, caused by partial destruction of the brain stem rise activation system, the patient's awakening state is reduced, silence, no movement, incontinence, but directed reaction exists, autonomic nerve The reaction is normal, the pain partially disappears, the swallow is still preserved, the chewing is reflected, and the brain is often straightened.
3. Locked-in syndrome: ventral injury of the pons, damage to the bilateral corticospinal tract and cortical medullary bundle, so that the function of the movement below the lesion is lost. At this time, the patient can blink and close the eye, not horizontal. Exercise, able to move vertically, can answer "yes" or "no" by closing or vertical movement of the eye. Because the system is not damaged and the activation is activated, the patient is unconscious and has no spontaneous language, so it is also called pseudo coma.
4. Persistent vegetative disturbance: cerebral cortex, subcortical damage, patient disturbance, no language, no activity, and autonomic dysfunction (vegetative).
