This standard specifies the diagnostic criteria and treatment principles for occupational acute chemical poisoning neurological diseases. This standard applies to the diagnosis of toxic neurological diseases caused by chemicals in occupational activities. The diagnosis of neurological diseases caused by non-occupational acute chemical poisoning can also refer to this standard. GBZ 76-2002 Diagnostic criteria for occupational acute chemical poisoning neurological diseases GBZ76-2002 Standard download decompression password: www.bzxz.net

ICS 13.100
National Occupational Health Standard of the People's Republic of China GBZ76—2002
Diagnostic Criteria of Occupational Acute Neurotoxic Diseases Caused by Chemicals2002-04-08 Issued
Implemented on 2002-06-01
Issued by the Ministry of Health of the People's Republic of China
Article 6.1 of this standard is recommended, and the rest are mandatory. This standard is formulated in accordance with the "Law of the People's Republic of China on the Prevention and Control of Occupational Diseases". In various occupational activities, people may be exposed to some high-concentration and highly toxic chemicals in a short period of time, causing acute poisoning. Some of these chemicals are known species; some are pathogenic species that are still unclear after the poisoning has occurred; some species have been included in the list of occupational diseases, while others have not yet been included; some have independent diagnostic standards, while others have not yet developed independent diagnostic standards. However, all acute poisoning diseases have common patterns of onset. It is possible and necessary to formulate common rules to be followed when diagnosing acute poisoning. The various rules specified in this series of standards involve the diagnosis of occupational acute chemical poisoning. These rules are used to ensure the unification of the diagnostic system of occupational acute chemical poisoning. Regardless of whether the cause is known or hidden, and regardless of which target organ is damaged after poisoning, the diagnosis can be made according to the rules specified in this standard. "Diagnosis of Occupational Acute Chemical Poisoning" includes the following parts. The scope defined by each part will be explained in the preface and introduction of each part: Part 1 Diagnostic Criteria for Occupational Acute Chemical Poisoning (General Principles): Part 2
Diagnostic Rules for Occupational Acute Hidden Chemical Poisoning: Part 3
Diagnostic Criteria for Multiple Organ Dysfunction Syndrome in Occupational Acute Chemical Poisoning: Part 4
Part 5
Part 6
Part 7
Part 8 Part 9: Diagnostic criteria for occupational acute chemical-induced sudden death: Diagnostic criteria for occupational acute chemical poisoning nervous system diseases; Diagnostic criteria for occupational acute chemical poisoning respiratory system diseases; Diagnostic criteria for occupational acute toxic liver diseases; Diagnostic criteria for occupational acute toxic kidney diseases; Diagnostic criteria for occupational acute chemical poisoning heart diseases: Part 10: Diagnostic criteria for occupational acute chemical poisoning blood system diseases; Appendix A of this standard is an informative appendix, and Appendix B, C, and D are normative appendices. This standard is proposed and managed by the Ministry of Health of the People's Republic of China. This standard is drafted by the Occupational Health and Poison Control Institute of the Chinese Center for Disease Control and Prevention. The participating units include Shanghai Chemical Occupational Disease Prevention and Control Research Institute and West China Occupational Disease Hospital of Sichuan University. This standard is interpreted by the Ministry of Health of the People's Republic of China. GBZ76—2002: Diagnostic criteria for occupational acute chemical poisoning nervous system diseases Occupational acute chemical poisoning nervous system diseases refer to systemic diseases with nervous system damage as the main cause caused by workers' short-term exposure to relatively large amounts of chemicals in their occupational activities. 1 Scope
This standard specifies the diagnostic criteria and treatment principles for occupational acute chemical poisoning neurological diseases. This standard applies to the diagnosis of toxic neurological diseases caused by chemicals in occupational activities. The diagnosis of neurological diseases caused by non-occupational acute chemical poisoning can also refer to this standard. 2 Normative references
The clauses in the following documents become clauses of this standard through reference in this standard. For all dated referenced documents, all subsequent amendments (excluding errata) or revisions are not applicable to this standard. However, parties to an agreement based on this standard are encouraged to study whether the latest versions of these documents can be used. For all undated referenced documents, the latest versions shall apply to this standard.
GB/T16180
3 Diagnostic principles
Diagnostic standards for occupational acute chemical poisoning (general principles) Identification of the degree of disability caused by work-related injuries and occupational diseases of employees Based on the occupational history of short-term exposure to a large amount of chemicals, the clinical manifestations of neurological damage appear, combined with the necessary laboratory test results and on-site labor hygiene survey data, and after excluding similar diseases caused by other reasons, a diagnosis can be made.
4 Observation subjects
4.1 Observation subjects for acute toxic encephalopathy
Symptoms such as headache, dizziness, fatigue, and nausea appear, which disappear in a short time. 4.2 Observation subjects for toxic peripheral neuropathy
Have one of the following:
a) Numbness and pain in the distal extremities, heaviness and fatigue in both lower extremities, but without typical symptoms and signs of peripheral nerve damage;
b) Neuro-electromyography shows suspected neurogenic damage, but without typical symptoms and signs of peripheral nerve damage. 5 Clinical types and graded diagnosis
Occupational acute toxic nervous system damage can be caused by a variety of poisons, and the types of clinical manifestations vary. The common clinical types are as follows:
5.1 Acute toxic encephalopathy
5.1.1 Mild
Has one of the following:
a) Severe headache, dizziness, insomnia, nausea, vomiting, general fatigue, mental depression, and gait mites or mental symptoms such as easy excitability, emotional agitation, and irritability; b) Mild disturbance of consciousness, such as confusion, drowsiness or haziness. 5.1.2 Moderate
Has one of the following:
Moderate disturbance of consciousness, such as delirium and turbidity: b) Grand mal seizure-like convulsions;
The clinical manifestations of mild toxic encephalopathy are accompanied by bilateral pyramidal tract signs. c
5.1.3 Severe
Has one of the following:
a) Severe disturbance of consciousness, such as light coma, moderate coma, deep coma, vegetative state; b) Obvious mental symptoms, such as disorientation, hallucination, delusion, psychomotor excitement or aggressive behavior; c) Status epilepticus; d) Manifestations of brain herniation; e) Manifestations of focal brain damage, such as cortical blindness, cerebellar ataxia, Parkinson's syndrome, etc. Electroencephalogram examination may show moderate and severe abnormalities: the latency of the central segment of brain evoked potential may be prolonged; cranial electronic computer tomography (CT) or magnetic resonance imaging (MRI) may show brain edema. 5.2 Acute toxic myelopathy
5.2.1 Mild
Bilateral pyramidal tract signs in the lower limbs, without motor and bladder dysfunction in the lower limbs, and without the above-mentioned encephalopathy manifestations; 5.2.2 Severe
Mild spastic paraplegia, with urinary retention or incontinence, but without the above-mentioned encephalopathy manifestations. 5.3 Toxic peripheral neuropathy
5.3.1 Mild
In addition to the above symptoms, one of the following is present: a) Spontaneous burning pain in the distal extremities, with hyperalgesia; b) Symmetrical glove- and stocking-like distribution of pain, touch, and tuning fork vibration sensation in the extremities, with weakened Achilles tendon reflex;
c) Decreased pain and touch in the areas innervated by cranial nerves, and weakened corneal reflex or abnormal blink reflex; d) Neuro-EMG shows neurogenic damage. 5.3.2 Moderate
On the basis of mild poisoning, one of the following is present: a) Impairment of pain, touch, and tuning fork vibration sensation in the distal extremities reaching above the elbows and knees, accompanied by the disappearance of the Achilles tendon reflex; b) Obvious impairment of deep sensation accompanied by sensory ataxia; c) Incomplete paralysis of muscles innervated by multiple cranial nerves; d) Neuro-EMG shows obvious neurogenic damage. 5.3.3 Severe
One of the following is present:
a) Muscle strength of affected extremities decreases to level 3 or below; b) Respiratory muscle paralysis;
c) Neuro-EMG shows neurogenic damage accompanied by a significant slowing of nerve conduction velocity. Or a significant decrease in evoked potential 6 Treatment principles
6.1 Treatment principles
6.1.1 Rescue acute poisoning according to the treatment principles in GBZ71. 6.1.2 Etiological treatment: If there are corresponding indications, timely use of complexing agents, special antidotes or blood purification therapy. 6.1.3 Treatment of acute toxic encephalopathy
a) Reasonable oxygen therapy, and hyperbaric oxygen therapy if conditions permit, which is especially important for hypoxic encephalopathy; b) Actively prevent and treat cerebral edema, control fluid intake, and give hypertonic dehydrating agents, adrenal glucocorticoids, diuretics, etc.:
c) Control convulsions, use antiepileptic drugs or tranquilizers, and ultra-short-acting anesthetics when necessary: ​​d) Use drugs that promote the recovery of brain cell function; e) Other symptomatic supportive treatment.
6.1.4: For acute toxic myelopathy, active symptomatic supportive treatment should be given to prevent urinary tract and other site infections6.1.5 For acute toxic peripheral neuropathy, adrenocortical hormones can be applied in sufficient amounts for a short period of time as needed, and B vitamins, energy mixtures or traditional Chinese medicine with blood circulation and collateral activating effects can be used for treatment, supplemented by physical therapy and symptomatic and supportive treatment. 6.2 Other treatments
Observation subjects and patients with mild toxic central nervous system and peripheral nervous system diseases can return to their original jobs after recovery. 6.2.1
6.2.2 Patients with moderate and severe toxic central nervous system and peripheral nervous system diseases should not engage in the original toxic work. Work or rest should be arranged according to the recovery after treatment. If labor capacity assessment is required, it shall be handled in accordance with GB/T16180. Instructions for the correct use of this standard
a) Instructions for the correct use of this standard are shown in Appendix A (Informative Appendix). b) For the method of neuro-electromyography examination and the judgment criteria of neurogenic damage, see Appendix B (Normative Appendix). c) For the muscle strength classification standards, see Appendix C (Normative Appendix). d) For the classification and grading criteria of consciousness disorders, see Appendix D (Normative Appendix). Appendix A
(Informative Appendix)
Instructions for the correct use of this standard
A.1 This standard applies to the diagnosis and grading of central nervous system diseases and peripheral nervous system diseases caused by occupational acute chemical poisoning. The diagnosis of central nervous system and peripheral nervous system diseases caused by acute poisoning in daily life can be implemented as a reference.
A.2 Poisons that cause occupational acute toxic encephalopathy A.2.1 Poisons that directly affect brain tissue metabolism or inhibit enzyme activity include lead, tetraethyl lead, trialkyl tin, arsenide, borane, gasoline, benzene, toluene, carbon disulfide, trichloroethylene, methanol, ethanol, chloroethanol, methyl mercaptan, methyl chloride, methyl iodide, ethylene dichloride, tetrachloroethane, ethylene oxide, carbon tetrachloride, butyl acetate, organophosphorus, carbamates, pyrethroids, insecticides, organic mercury, phosphine, methyl bromide, nereis toxins, fluoroacetamide, tetramine, acrylamide, etc.;
A.2.2 Poisons that cause brain tissue hypoxia include carbon monoxide, hydrogen sulfide, cyanide, acetone cyanohydrin, acrylonitrile, etc.; A.3 The cause of occupational acute toxic encephalopathy is exposure to high doses of neurotoxins in a short period of time, and the onset is generally acute. However, acute poisoning by some poisons, such as tetrahexyl lead, methyl bromide, methyl iodide, trialkyl tin, and organic mercury, may develop after a latent period of several hours, days, or even 2 to 3 weeks. There may be no obvious symptoms during the incubation period, but once symptoms appear, the disease progresses rapidly. Toxic encephalopathy caused by cyanide, carbon monoxide, etc. may cause delayed encephalopathy caused by damage to the basal ganglia and subcortical white matter 2 to 3 weeks after recovery from the acute phase.
A.4 The pathological feature of acute toxic encephalopathy is cerebral edema, so it is generally manifested by whole-brain symptoms and increased intracranial pressure (such as severe headache, frequent vomiting, restlessness; or mental depression, worsening disturbance of consciousness; or repeated convulsions, bilateral pupil constriction, increased blood pressure, pulse and respiratory changes). Slow; ocular conjunctival edema or increased ocular tension; optic nerve head edema in the fundus of some patients): severe cases may show signs of brain herniation (such as when the cerebellar tentorial notch herniation is formed, the hippocampus and uncus shift downward to compress the brainstem, consciousness disorder is deep coma, eyeball fixation, bilateral pupils are small or unequal, light reaction disappears, breathing is irregular, or decerebrate rigidity occurs; when the foramen magnum herniation occurs, it can cause bilateral pupil dilation and sudden respiratory arrest); a few have focal brain damage. Its graded diagnosis is mainly based on the degree of consciousness disorder, the type of mental disorder, the occurrence of the withdrawal, the consequences of increased intracranial pressure, and whether there is focal brain damage. A.5 Asphyxia caused by excessive methane, carbon dioxide, nitrogen, etc. in the air during occupational activities can cause hypoxic encephalopathy: its pathological characteristics are also cerebral edema, and its disease classification and treatment can refer to this standard. A.6 In moderate toxic encephalopathy, pyramidal tract signs may appear when consciousness is not impaired, often manifested as decreased or absent superficial reflexes such as abdominal wall reflex and hood reflex, active or hyperactive tendon reflex, or ankle clots, or pathological reflexes such as Babinski or Chaddock signs.
A.7 In most patients with acute toxic encephalopathy, EEG shows abnormalities, and the main manifestations of abnormalities are widespread α rhythm disorder and α wave reduction. When consciousness disorder or convulsion occurs, the e wave and 8 wave amplitude activities increase, and in severe cases, they are highly arrhythmic or spike waves and wave-like waves appear. However, the degree of EEG abnormality is not necessarily completely parallel to the severity of the clinical condition. A.8 At present, the commonly used brain evoked potentials are somatosensory evoked potentials (SEP), visual evoked potentials (VEP), and brainstem auditory evoked potentials (BAEP). In toxic encephalopathy, these brain evoked potentials often show abnormalities in the central segment and are related to the degree of consciousness disorder. They can be used to assist in monitoring brain function and judging prognosis, and are also helpful in predicting the occurrence of delayed encephalopathy. A.9Computed tomography (CT) and cranial magnetic resonance imaging (MRI) have auxiliary diagnostic value for cerebral edema, encephalomalacia, subcortical white matter demyelinating lesions, etc. In acute toxic encephalopathy, magnetic resonance or CT examinations can show smaller lateral ventricles, diffuse low-density changes in subcortical white matter, or decreased density of the globus pallidus and putamen. MRI often shows cerebral edema lesions earlier than CT, but the above changes may not be detected in the early clinical onset. Other functional brain imaging techniques include positron emission tomography (PET), regional cerebral blood flow (RCBF), single photon emission computed tomography (SPECT), and FLAIR. Due to their high prices and lack of mature experience in their application in toxic encephalopathy, they are not included in this standard. A.10 The focus of treatment for acute toxic encephalopathy is to improve brain oxygen supply and prevent and treat cerebral edema. Reasonable oxygen therapy (hyperbaric oxygen can be used when conditions permit), hypertonic dehydration agents: diuretics and short-term adequate adrenal cortical hormones, anti-epileptic drugs or tranquilizers to control convulsions, and drugs that promote brain cell function recovery should be used for symptomatic and supportive treatment. For patients with status epilepticus or psychomotor excitement that is not well controlled by anti-epileptic drugs or tranquilizers, or with central high fever without obvious liver or kidney dysfunction, ultra-short-acting anesthetics such as sodium thiopentane can be used. If there is toxic liver and kidney dysfunction at the same time, the choice of sedatives and control agents should be cautious. Generally, for patients with liver dysfunction, chloral hydrate, acetylpromazine, and haloperidol are suitable, and for patients with renal impairment, paraformaldehyde, perphenazine, haloperidol, amobarbital, or secobarbital (sucamine) are suitable. A.11 Simple toxic myelopathy is relatively rare and may occur in patients with delayed neuropathy caused by moderate acute or subacute organic mercury poisoning or certain acute organic phosphorus poisoning. Due to damage to the lateral cord of the spinal cord, the main clinical manifestations are pyramidal tract signs in the bilateral lower limbs, and in severe cases, spastic mild paraplegia, urinary retention or incontinence. A,12 The poisons that cause occupational acute toxic peripheral neuropathy include thallium, arsenic, and certain organophosphate compounds, such as trichlorfon, dichlorvos, methamidophos, dimethoate, omethoate, parathion, malathion, propylamine fluoride, tri-o-cresyl phosphate (TOCP), n-hexane, ethylene oxide, etc. Mononeuropathy may occur in acute carbon monoxide poisoning. A.13 Symptoms of acute toxic peripheral neuropathy may appear within 1 to 2 days of exposure to the poison, but in acute poisoning of arsenic and some organic phosphorus, degenerative peripheral neuropathy may appear after a latent period of 2 to 3 weeks. Some cases of organophosphorus poisoning develop neuromuscular junction disease 1 to 5 days after the acute cholinergic crisis is eliminated, and the "intermediate myasthenia syndrome" appears, which is manifested as weakness of the flexor muscles of the neck and proximal muscles of the limbs or respiratory muscles innervated by the cranial nerves. A.14 Neuro-electromyography examination is of great significance for the early diagnosis of toxic peripheral neuropathy. The examination method and result judgment criteria are shown in Appendix B of this standard. Disposable concentric needle electrodes should be used as much as possible. When measuring nerve conduction velocity in occupational groups, surface electrodes are generally used, and a few people use the proximal nerve method [see Chinese Journal of Neuropsychiatry 1988, 2 (2): 87]. The limb muscle strength classification standard is shown in Appendix C of this standard. A.15 Differential diagnosis is very important. When diagnosing occupational acute chemical toxic encephalopathy, it is necessary to differentiate it from central nervous system infection, cerebrovascular accident, craniocerebral trauma, metabolic disorders, epilepsy, acute drug poisoning, psychogenic mental disorders, etc. Peripheral neuropathy can be caused by other causes, such as acute infectious polyneuropathy (Guillain-Barre Syndrome), diabetes, hereditary diseases, drug poisoning, etc. Therefore, these diseases should be excluded when diagnosing toxic peripheral neuropathy. Appendix B
(Normative Appendix)
Neuro-electromyography examination method and judgment criteria for neurogenic damage B.1 Electromyography examination method
B.1.1 Preparation before examination
B.1.1.1 First, explain the examination requirements and precautions to the examinee clearly to avoid mental tension and strive for the cooperation of the examinee.
B.1.1.2 The examinee takes a suitable posture so that the muscles are supported and stable, and can relax naturally and do various exercises as required.
B.1.1.3 Place the ground electrode on the same limb as the muscle being examined. B.1.1.4 Disinfect the local skin with 2.5% iodine and 75% alcohol. B.1.2 Inspection procedures
B.1.2.1 Myoelectric activity during insertion: insert the concentric needle electrode (needle core area is 0.45mm2) into the muscle belly quickly, with a scanning speed of 50~100ms/cm and a sensitivity of 100uv/cm, and observe the characteristics of the electrical activity during the insertion of the needle electrode and whether there is myotonia, myotonia-like discharge or prolonged insertion electrical activity. B.1.2.2 Electrical activity during muscle relaxation: scan at a speed of 5~10ms/cm and a sensitivity of 100μv/cm, and observe whether there are spontaneous potentials, such as fibrillation potentials, positive phase potentials and fasciculation potentials. B.1.2.3 Myoelectric activity during small force contraction (mild contraction): the conditions are the same as B.1.2.2. When the muscle contracts slightly, measure the average time limit and average voltage of the 20 motor unit potentials, and the percentage of multi-phase potentials. (To determine the average duration of the motor unit, 2 to 3 different positions should be selected for examination in the same muscle if necessary). To avoid errors, each wave must appear 2 to 3 times at the same time before it can be counted. The duration is from the initial deflection of the baseline to the final deflection back to the baseline. The phase of the motor unit is based on the peak crossing the baseline.
B.1.2.4 Myoelectric activity during strong contraction: scanning speed 50~100ms/cm, sensitivity 500μv/cm~1mv/cm. When the subject contracts the tested muscle with maximum force, observe whether it is an interference phase, mixed phase or simple phase, and measure its peak-to-peak amplitude B.2 Nerve conduction velocity
The subject's skin temperature is kept above 30℃, and the tested area should be cleaned with alcohol to remove oil stains; the surface electrode is correctly placed on the nerve, and the skin should not be pushed: when giving electrical stimulation, attention should be paid to safety, and the ground electrode is placed between the stimulating electrode and the recording electrode.
B.2.1 Motor nerve conduction velocity
B.2.1.1 Electrode placement
Surface electrodes are used as stimulating electrodes. Except for the use of surface electrodes when examining the common nerve, concentric axis electrodes are used as recording electrodes. The electrode placement sites of the main examined nerves are as follows: Ulnar nerve: The proximal stimulation point is placed between the medial superior humerus and the olecranon fossa of the ulna, and the distal stimulation point is at the ulnar edge of the wrist crease: the recording electrode is placed on the hand's little finger extension.
Median nerve: The proximal stimulation point is placed above the medial superior humerus, the distal stimulation point is at the midpoint of the wrist crease, and the recording electrode is placed on the hand's extensor pollicis brevis.
Tibial nerve: The proximal stimulation point is placed in the center of the brain fossa (Weizhong acupoint), the distal stimulation point is at the back of the medial malleolus, and the recording electrode is placed on the abductor hallucis muscle:
Posterior tibial nerve: The positive and negative needle poles of the stimulation electrode are inserted into the subcutaneous tissue at the midpoint of the line connecting the medial malleolus and the heel, 1 cm apart, and the negative needle tip is moved forward and upward to approach the posterior tibial nerve until the stimulation amount is less than 1 mA to elicit the evoked potential. The irrelevant electrode is inserted into the subcutaneous tissue nearby, 2 cm apart. The recording electrode is placed on the abductor hallucis muscle. Common peroneal nerve: The proximal stimulation point is placed at the outer and lower part of the fibular head, the distal stimulation point is at the transverse line of the ankle bone, and the recording electrode is placed on the extensor hallucis brevis.
B.2.1.2 Give single pulse square wave stimulation, 1~1.5 times/second, square wave duration 0.1~0.2ms, the stimulation intensity must reach super-strong stimulation (that is, after increasing the stimulation, the evoked potential no longer increases), and then increase the intensity by 30%. B.2.1.3 Measure the time (ms) from the stimulation artifact to the beginning of the evoked potential waveform, called the latency. Measure the latency of the proximal and distal stimulation points respectively. The difference between the two is the conduction time (ms) between the two points of the nerve segment. B.2.1.4 Use a steel ruler or pelvic ruler to accurately measure the distance between the proximal and distal stimulation points, which is the length (cm) between the two points of the nerve segment.
According to the following formula, the conduction velocity between the two points of the nerve segment can be calculated. Conduction velocity (m/s) =
Distance (cm)
Conduction time (ms)
The distal nerve conduction is expressed by the distal motor latency. B.2.2 Sensory nerve conduction velocity
B.2.2.1 Stimulation electrodes, except for the surface electrodes used for the examination of the enteric nerve, are all ring electrodes, which are wrapped around the fingers or toes, with the negative electrode placed on the proximal knuckle and the positive electrode placed on the distal knuckle. The distance between the two electrodes is at least 1 cm. The electrode placement sites are as follows: Median nerve: index finger.
Ulnar nerve: little finger
Sural nerve: posterior and inferior to the lateral malleolus.
Posterior tibial nerve: big toe.
Except for the needle electrode used for the examination of the posterior tibial nerve, all recording electrodes are surface electrodes. The placement sites, whether distal or proximal, should be placed at the site where the maximum evoked potential is elicited when measuring the motor nerve conduction velocity. When examining the sural nerve, the recording electrode is placed 14 cm behind the calf from the stimulating electrode.
B.2.2.2 Use single pulse square wave electrical stimulation, 1~1.5 times/s, 0.1~0.2ms each time, and increase the stimulation intensity until the subject feels obvious numbness in the fingers or toes (the stimulation amount of the constant current stimulator is generally 30~40mA, and the maximum does not exceed 50mA). B.2.2.3 A superposition device is required, and the number of superpositions can be determined according to the clarity of the graphics. B.2.2.4 The peak-to-peak height of the evoked potential is the potential amplitude (voltage). B.2.2.5 The method for determining the latency, the distance between the stimulating electrode and the recording electrode, and the calculation formula for the nerve conduction velocity are the same as those in B.2.1.4.
B.3 Normal values ​​of neuro-electromyography
Strictly speaking, each laboratory should have its own normal values: since no unit with its own normal values ​​has been established yet, the normal values ​​listed in Tables 1 to 3 can be referred to, but the examination methods should be consistent. B.3.1 Normal values ​​of electromyography
B.3.1.1 Insertion activity: The discharge lasts no more than 2 seconds after the needle electrode is inserted. B.3.1.2 Spontaneous potentials (fibrillation waves, positive sharp waves) generally do not appear at rest. (About 4.3% to 10% of normal muscles can have spontaneous potentials at one site.)
Average duration of motor units: The normal value of the average duration of 20 motor units is shown in Table B1. B.3.1.3
20 motor units average duration normal
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11.8 11.6
finger product companion
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early stage
[2.3 12.3
[2.5 12.7
12.7 13.1
13.0 13.4
13.4 13.8
13.7 14.0
13.9 14.3
J4.2 14.7
Short myoelectric period
Note: The normal values ​​in each column of the table are from [1J LudinHP (translated by Tang Xiaofu et al.): Practical Electromyography, Tianjin Science and Technology Press, 1984; [2] Tang Xiaofu et al.: Electromyographic findings of 310 normal people. Chinese Medical Journal 1984, 64 (2): 91
B.3.1.4 Percentage of polyphasic potential: The phase of the motor unit is 5 or more phases. The polyphasic potential of general muscles does not exceed 20%, deltoid muscle does not exceed 25%, and tibialis anterior muscle does not exceed 35%. B.3.1.5 Interference phase is present during strong contraction.
B.3.1.6 There are many factors that affect the voltage of the motor unit, which can be judged based on the normal values ​​of each laboratory. B.3.2 Normal values ​​of motor nerve conduction velocity are shown in Table B2B3.3
Normal values ​​of sensory nerve conduction velocity are shown in Table B3Criteria for judging neurogenic damage
B.4.1 Electromyography
Spontaneous potentials (fibrillation waves, positive sharp waves) appear at three locations in a muscle. B.4.1.2 The average duration of 20 motor units during small-force contraction is extended by more than 20% compared with the normal value of the corresponding age group. B.4.1.3 The percentage of multiphasic potential increases during small-force contraction, exceeding 20% ​​of the 20 motor units of general muscles, exceeding 25% of deltoid muscles, and exceeding 35% of tibialis anterior muscles.
B.4.1.4: Mixed phase or simple phase during strong contraction. One of the first two of the above four items must be present, and the other two items must be referred to before it can be determined as neurogenic damage. B.4.2 Nerve conduction velocity
If any of the following is present, it can be defined as neurogenic damage: B.4.2.1 Slowed sensory nerve conduction velocity (more than the normal mean - 2 standard deviations), B4.2.2 Slowed motor nerve conduction velocity (more than the normal mean - 2 standard deviations) or prolonged distal motor latency (more than the normal mean + 2 standard deviations).
B.4.2.3 Decreased sensory potential amplitude (more than the normal mean - 2 standard deviations). B.4.2.4 The evoked motor potential amplitude is significantly decreased (less than 1mV) or the waveform is significantly complex (more than 4 phases).45mm2) Rapidly insert the needle into the muscle belly, with a scanning speed of 50~100ms/cm and a sensitivity of 100uv/cm, and observe the characteristics of the electrical activity when the needle is inserted and whether there is myotonia, myotonia-like discharge or prolonged electrical activity when the needle is inserted. B.1.2.2 Electrical activity during muscle relaxation: The scanning speed is 5~10ms/cm, and the sensitivity is 100μv/cm. Observe whether there are spontaneous potentials, such as fibrillation potentials, positive phase potentials and fasciculation potentials. B.1.2.3 Myoelectric activity during small force contraction (light contraction): The conditions are the same as B.1.2.2. When the muscle contracts slightly, measure the average time limit and average voltage of 20 motor unit potentials, and the percentage of multi-phase potentials. (To determine the average time limit of the motor unit, if necessary, 2~3 different positions should be selected in the same muscle for inspection). To avoid errors, each wave must appear 2~3 times at the same time before it can be counted. The time limit is from the initial deflection of the baseline to the final deflection back to the baseline. The phase of the motor unit is based on the peak crossing the baseline. bzxz.net
B.1.2.4 Myoelectric activity during strong contraction: scanning speed 50~100ms/cm, sensitivity 500μv/cm~1mv/cm. When the subject contracts the tested muscle with maximum force, observe whether it is an interference phase, mixed phase or simple phase, and measure its peak-to-peak amplitude B.2 Nerve conduction velocity
The subject's skin temperature is kept above 30℃, and the tested area should be cleaned with alcohol to remove oil stains; the surface electrode is correctly placed on the nerve and the skin should not be pushed: when giving electrical stimulation, safety should be paid attention to, and the ground electrode is placed between the stimulating electrode and the recording electrode.
B.2.1 Motor nerve conduction velocity
B.2.1.1 Electrode placement
Use surface electrodes as stimulating electrodes. Except for the use of surface electrodes when examining the common nerve, concentric axis electrodes are used as recording electrodes. The electrode placement sites of the main nerves to be examined are as follows: Ulnar nerve: The proximal stimulation point is placed between the medial superior humerus and the olecranon fossa of the ulna, and the distal stimulation point is at the ulnar edge of the wrist crease: The recording electrode is placed on the hand little finger extension.
Median nerve: The proximal stimulation point is placed above the medial superior humerus, the distal stimulation point is at the midpoint of the wrist crease, and the recording electrode is placed on the hand abductor pollicis brevis.
Tibial nerve: The proximal stimulation point is placed in the center of the brain fossa (Weizhong point), the distal stimulation point is at the back of the medial malleolus, and the recording electrode is placed on the abductor pollicis:
Posterior tibial nerve: The positive and negative needle poles of the stimulating electrode are inserted into the subcutaneous part of the midpoint of the line connecting the medial malleolus and the heel, 1 cm apart, and the negative needle tip is moved forward and upward to approach the posterior tibial nerve until the stimulation amount is less than 1 mA to elicit the evoked potential. The irrelevant electrode is inserted into the subcutaneous part nearby, 2 cm apart. The recording electrode is placed on the abductor pollicis. Common peroneal nerve: The proximal stimulation point is placed at the outer and lower part of the fibular head, the distal stimulation point is at the transverse line of the ankle bone, and the recording electrode is placed on the extensor hallucis brevis.
B.2.1.2 Give single pulse square wave stimulation, 1~1.5 times/second, square wave duration 0.1~0.2ms, the stimulation intensity must reach super-strong stimulation (that is, after increasing the stimulation, the evoked potential no longer increases), and then increase the intensity by 30%. B.2.1.3 Measure the time (ms) from the stimulation artifact to the beginning of the evoked potential waveform, called the latent period, and measure the latent period of the proximal stimulation point and the distal stimulation point respectively. The difference between the two is the conduction time (ms) between the two points of this nerve segment. B.2.1.4 Use a steel ruler or pelvic ruler to accurately measure the distance between the proximal stimulation point and the distal stimulation point, which is the length between the two points of this nerve segment (cm).
The conduction velocity between the two points of this nerve segment can be calculated according to the following formula. Conduction velocity (m/s) =
Distance (cm)
Conduction time (ms)
Distal nerve conduction is expressed by distal motor latency. B.2.2 Sensory nerve conduction velocity
B.2.2.1 Except for the surface electrode used for the examination of the enteric nerve, the stimulation electrode is a ring electrode wrapped around the finger or toe, with the negative electrode placed on the proximal knuckle and the positive electrode placed on the distal knuckle. The distance between the two electrodes is at least 1 cm. The electrode placement sites are as follows: Median nerve: index finger.
Ulnar nerve: little finger
Sural nerve: below the posterior lateral malleolus.
Posterior tibial nerve: big toe.
Except for the needle electrode used for the examination of the posterior tibial nerve, the recording electrode is a surface electrode. The placement site, whether distal or proximal, should be placed at the site where the maximum evoked potential is elicited when measuring the motor nerve conduction velocity. When examining the sural nerve, the recording electrode is placed 14 cm behind the calf from the stimulating electrode.
B.2.2.2 Use single pulse square wave electrical stimulation, 1~1.5 times/s, 0.1~0.2ms each time, and increase the stimulation intensity until the subject feels obvious numbness in the fingers or toes (the stimulation amount of the constant current stimulator is generally 30~40mA, and the maximum does not exceed 50mA). B.2.2.3 A superposition device is required, and the number of superpositions can be determined according to the clarity of the graph. B.2.2.4 The peak-to-peak height of the evoked potential is measured as the potential amplitude (voltage). B.2.2.5 The method for determining the latency, the distance between the stimulating electrode and the recording electrode, and the calculation formula for the nerve conduction velocity are the same as B.2.1.4.
B.3 Normal values ​​of neuro-electromyography
Strictly speaking, each laboratory should have its own normal values: since no unit with its own normal values ​​has been established yet, the normal values ​​listed in Tables 1 to 3 can be referred to, but the inspection methods should be consistent. B.3.1 Normal value of electromyogram
B.3.1.1 Insertion activity: The discharge lasts no more than 2 seconds after the needle is inserted. B.3.1.2 Spontaneous potentials (fibrillation waves, positive sharp waves) generally do not appear at rest. (About 4.3-10% of normal muscles can have spontaneous potentials in one part.)
Average duration of motor units: The normal value of the average duration of 20 motor units is shown in Table B1. B.3.1.3
20 motor units average duration normal
three-headed stage medical blue
11.8 11.6
finger product companion
one bone secretion
small sample is muscle
early stage
[2.3 12.3
[2.5 12.7
12.7 13.1
13.0 13.4
13.4 13.8
13.7 14.0
13.9 14.3
J4.2 14.7
Short myoelectric period
Note: The normal values ​​in each column of the table are from [1J LudinHP (translated by Tang Xiaofu et al.): Practical Electromyography, Tianjin Science and Technology Press, 1984; [2] Tang Xiaofu et al.: Electromyographic findings of 310 normal people. Chinese Medical Journal 1984, 64 (2): 91
B.3.1.4 Percentage of polyphasic potential: The phase of the motor unit is 5 or more phases. The polyphasic potential of general muscles does not exceed 20%, deltoid muscle does not exceed 25%, and tibialis anterior muscle does not exceed 35%. B.3.1.5 Interference phase is present during strong contraction.
B.3.1.6 There are many factors that affect the voltage of the motor unit, which can be judged based on the normal values ​​of each laboratory. B.3.2 Normal values ​​of motor nerve conduction velocity are shown in Table B2B3.3
Normal values ​​of sensory nerve conduction velocity are shown in Table B3Criteria for judging neurogenic damage
B.4.1 Electromyography
Spontaneous potentials (fibrillation waves, positive sharp waves) appear at three locations in a muscle. B.4.1.2 The average duration of 20 motor units during small-force contraction is extended by more than 20% compared with the normal value of the corresponding age group. B.4.1.3 The percentage of multiphasic potential increases during small-force contraction, exceeding 20% ​​of the 20 motor units of general muscles, exceeding 25% of deltoid muscles, and exceeding 35% of tibialis anterior muscles.
B.4.1.4: Mixed phase or simple phase during strong contraction. One of the first two of the above four items must be present, and the other two items must be referred to before it can be determined as neurogenic damage. B.4.2 Nerve conduction velocity
If any of the following is present, it can be defined as neurogenic damage: B.4.2.1 Slowed sensory nerve conduction velocity (more than the normal mean - 2 standard deviations), B4.2.2 Slowed motor nerve conduction velocity (more than the normal mean - 2 standard deviations) or prolonged distal motor latency (more than the normal mean + 2 standard deviations).
B.4.2.3 Decreased sensory potential amplitude (more than the normal mean - 2 standard deviations). B.4.2.4 The evoked motor potential amplitude is significantly decreased (less than 1mV) or the waveform is significantly complex (more than 4 phases).45mm2) Rapidly insert the needle into the muscle belly, with a scanning speed of 50~100ms/cm and a sensitivity of 100uv/cm, and observe the characteristics of the electrical activity when the needle is inserted and whether there is myotonia, myotonia-like discharge or prolonged electrical activity when the needle is inserted. B.1.2.2 Electrical activity during muscle relaxation: The scanning speed is 5~10ms/cm, and the sensitivity is 100μv/cm. Observe whether there are spontaneous potentials, such as fibrillation potentials, positive phase potentials and fasciculation potentials. B.1.2.3 Myoelectric activity during small force contraction (light contraction): The conditions are the same as B.1.2.2. When the muscle contracts slightly, measure the average time limit and average voltage of 20 motor unit potentials, and the percentage of multi-phase potentials. (To determine the average time limit of the motor unit, if necessary, 2~3 different positions should be selected in the same muscle for inspection). To avoid errors, each wave must appear 2~3 times at the same time before it can be counted. The time limit is from the initial deflection of the baseline to the final deflection back to the baseline. The phase of the motor unit is based on the peak crossing the baseline.
B.1.2.4 Myoelectric activity during strong contraction: scanning speed 50~100ms/cm, sensitivity 500μv/cm~1mv/cm. When the subject contracts the tested muscle with maximum force, observe whether it is an interference phase, mixed phase or simple phase, and measure its peak-to-peak amplitude B.2 Nerve conduction velocity
The subject's skin temperature is kept above 30℃, and the tested area should be cleaned with alcohol to remove oil stains; the surface electrode is correctly placed on the nerve and the skin should not be pushed: when giving electrical stimulation, safety should be paid attention to, and the ground electrode is placed between the stimulating electrode and the recording electrode.
B.2.1 Motor nerve conduction velocity
B.2.1.1 Electrode placement
Use surface electrodes as stimulating electrodes. Except for the use of surface electrodes when examining the common nerve, concentric axis electrodes are used as recording electrodes. The electrode placement sites of the main nerves to be examined are as follows: Ulnar nerve: The proximal stimulation point is placed between the medial superior humerus and the olecranon fossa of the ulna, and the distal stimulation point is at the ulnar edge of the wrist crease: The recording electrode is placed on the hand little finger extension.
Median nerve: The proximal stimulation point is placed above the medial superior humerus, the distal stimulation point is at the midpoint of the wrist crease, and the recording electrode is placed on the hand abductor pollicis brevis.
Tibial nerve: The proximal stimulation point is placed in the center of the brain fossa (Weizhong point), the distal stimulation point is at the back of the medial malleolus, and the recording electrode is placed on the abductor pollicis:
Posterior tibial nerve: The positive and negative needle poles of the stimulating electrode are inserted into the subcutaneous part of the midpoint of the line connecting the medial malleolus and the heel, 1 cm apart, and the negative needle tip is moved forward and upward to approach the posterior tibial nerve until the stimulation amount is less than 1 mA to elicit the evoked potential. The irrelevant electrode is inserted into the subcutaneous part nearby, 2 cm apart. The recording electrode is placed on the abductor pollicis. Common peroneal nerve: The proximal stimulation point is placed at the outer and lower part of the fibular head, the distal stimulation point is at the transverse line of the ankle bone, and the recording electrode is placed on the extensor hallucis brevis.
B.2.1.2 Give single pulse square wave stimulation, 1~1.5 times/second, square wave duration 0.1~0.2ms, the stimulation intensity must reach super-strong stimulation (that is, after increasing the stimulation, the evoked potential no longer increases), and then increase the intensity by 30%. B.2.1.3 Measure the time (ms) from the stimulation artifact to the beginning of the evoked potential waveform, called the latent period, and measure the latent period of the proximal stimulation point and the distal stimulation point respectively. The difference between the two is the conduction time (ms) between the two points of this nerve segment. B.2.1.4 Use a steel ruler or pelvic ruler to accurately measure the distance between the proximal stimulation point and the distal stimulation point, which is the length between the two points of this nerve segment (cm).
The conduction velocity between the two points of this nerve segment can be calculated according to the following formula. Conduction velocity (m/s) =
Distance (cm)
Conduction time (ms)
Distal nerve conduction is expressed by distal motor latency. B.2.2 Sensory nerve conduction velocity
B.2.2.1 Except for the surface electrode used for the examination of the enteric nerve, the stimulation electrode is a ring electrode wrapped around the finger or toe, with the negative electrode placed on the proximal knuckle and the positive electrode placed on the distal knuckle. The distance between the two electrodes is at least 1 cm. The electrode placement sites are as follows: Median nerve: index finger.
Ulnar nerve: little finger
Sural nerve: below the posterior lateral malleolus.
Posterior tibial nerve: big toe.
Except for the needle electrode used for the examination of the posterior tibial nerve, the recording electrode is a surface electrode. The placement site, whether distal or proximal, should be placed at the site where the maximum evoked potential is elicited when measuring the motor nerve conduction velocity. When examining the sural nerve, the recording electrode is placed 14 cm behind the calf from the stimulating electrode.
B.2.2.2 Use single pulse square wave electrical stimulation, 1~1.5 times/s, 0.1~0.2ms each time, and increase the stimulation intensity until the subject feels obvious numbness in the fingers or toes (the stimulation amount of the constant current stimulator is generally 30~40mA, and the maximum does not exceed 50mA). B.2.2.3 A superposition device is required, and the number of superpositions can be determined according to the clarity of the graph. B.2.2.4 The peak-to-peak height of the evoked potential is measured as the potential amplitude (voltage). B.2.2.5 The method for determining the latency, the distance between the stimulating electrode and the recording electrode, and the calculation formula for the nerve conduction velocity are the same as B.2.1.4.
B.3 Normal values ​​of neuro-electromyography
Strictly speaking, each laboratory should have its own normal values: since no unit with its own normal values ​​has been established yet, the normal values ​​listed in Tables 1 to 3 can be referred to, but the inspection methods should be consistent. B.3.1 Normal value of electromyogram
B.3.1.1 Insertion activity: The discharge lasts no more than 2 seconds after the needle is inserted. B.3.1.2 Spontaneous potentials (fibrillation waves, positive sharp waves) generally do not appear at rest. (About 4.3-10% of normal muscles can have spontaneous potentials in one part.)
Average duration of motor units: The normal value of the average duration of 20 motor units is shown in Table B1. B.3.1.3
20 motor units average duration normal
three-headed stage medical blue
11.8 11.6
finger product companion
one bone secretion
small sample is muscle
early stage
[2.3 12.3
[2.5 12.7
12.7 13.1
13.0 13.4
13.4 13.8
13.7 14.0
13.9 14.3
J4.2 14.7
Short myoelectric period
Note: The normal values ​​in each column of the table are from [1J LudinHP (translated by Tang Xiaofu et al.): Practical Electromyography, Tianjin Science and Technology Press, 1984; [2] Tang Xiaofu et al.: Electromyographic findings of 310 normal people. Chinese Medical Journal 1984, 64 (2): 91
B.3.1.4 Percentage of polyphasic potential: The phase of the motor unit is 5 or more phases. The polyphasic potential of general muscles does not exceed 20%, deltoid muscle does not exceed 25%, and tibialis anterior muscle does not exceed 35%. B.3.1.5 Interference phase is present during strong contraction.
B.3.1.6 There are many factors that affect the voltage of the motor unit, which can be judged based on the normal values ​​of each laboratory. B.3.2 Normal values ​​of motor nerve conduction velocity are shown in Table B2B3.3
Normal values ​​of sensory nerve conduction velocity are shown in Table B3Criteria for judging neurogenic damage
B.4.1 Electromyography
Spontaneous potentials (fibrillation waves, positive sharp waves) appear at three locations in a muscle. B.4.1.2 The average duration of 20 motor units during small-force contraction is extended by more than 20% compared with the normal value of the corresponding age group. B.4.1.3 The percentage of multiphasic potential increases during small-force contraction, exceeding 20% ​​of the 20 motor units of general muscles, exceeding 25% of deltoid muscles, and exceeding 35% of tibialis anterior muscles.
B.4.1.4: Mixed phase or simple phase during strong contraction. One of the first two of the above four items must be present, and the other two items must be referred to before it can be determined as neurogenic damage. B.4.2 Nerve conduction velocity
If any of the following is present, it can be defined as neurogenic damage: B.4.2.1 Slowed sensory nerve conduction velocity (more than the normal mean - 2 standard deviations), B4.2.2 Slowed motor nerve conduction velocity (more than the normal mean - 2 standard deviations) or prolonged distal motor latency (more than the normal mean + 2 standard deviations).
B.4.2.3 Decreased sensory potential amplitude (more than the normal mean - 2 standard deviations). B.4.2.4 The evoked motor potential amplitude is significantly decreased (less than 1mV) or the waveform is significantly complex (more than 4 phases).3. Myoelectric activity during small force contraction (light contraction): The conditions are the same as those in B.1.2.2. When the muscle contracts slightly, measure the average duration and average voltage of 20 motor unit potentials, and the percentage of multiphase potentials. (To determine the average duration of the motor unit, if necessary, 2 to 3 different positions should be selected in the same muscle for inspection). To avoid errors, each wave must appear 2 to 3 times at the same time before it can be counted. The duration is from the initial deflection of the baseline to the final deflection back to the baseline. The phase of the motor unit is based on the peak crossing the baseline.
B.1.2.4 Myoelectric activity during strong contraction: scanning speed 50~100ms/cm, sensitivity 500μv/cm~1mv/cm. When the subject contracts the examined muscle with the maximum force, observe whether it is an interference phase, a mixed phase or a simple phase, and measure its peak-to-peak amplitude. B.2 Nerve conduction velocity
The subject's skin temperature should be kept above 30℃, and the examined area should be cleaned with alcohol to remove oil stains; the surface electrode should be correctly placed on the nerve, and the skin should not be pushed: when giving electrical stimulation, attention should be paid to safety, and the ground electrode should be placed between the stimulating electrode and the recording electrode.
B.2.1 Motor nerve conduction velocity
B.2.1.1 Electrode placement
Surface electrodes are used as stimulating electrodes. Except for the use of surface electrodes when examining the common nerve, concentric axis electrodes are used as recording electrodes. The electrode placement sites of the main examined nerves are as follows: Ulnar nerve: The proximal stimulation point is placed between the medial superior humerus and the olecranon fossa of the ulna, and the distal stimulation point is at the ulnar edge of the wrist crease: The recording electrode is placed on the little finger of the hand.
Median nerve: The proximal stimulation point is placed above the medial humerus, the distal stimulation point is at the midpoint of the wrist crease, and the recording electrode is placed on the abductor pollicis brevis.
Tibial nerve: The proximal stimulation point is placed in the center of the brain fossa (Weizhong point), the distal stimulation point is at the back of the medial malleolus, and the recording electrode is placed on the abductor pollicis brevis:
Posterior tibial nerve: The positive and negative needle poles of the stimulation electrode are inserted into the subcutaneous part of the midpoint of the line connecting the medial malleolus and the heel, 1 cm apart, and the negative needle tip is moved forward and upward to approach the posterior tibial nerve until the stimulation amount is less than 1 mA to elicit the evoked potential. The irrelevant electrode is inserted into the subcutaneous part nearby, 2 cm apart. The recording electrode is placed on the abductor pollicis brevis. Common peroneal nerve: The proximal stimulation point is placed below the outside of the fibular head, the distal stimulation point is at the transverse crease of the ankle bone, and the recording electrode is placed on the extensor pollicis brevis.
B.2.1.2 Give single pulse square wave stimulation, 1~1.5 times/second, square wave duration 0.1~0.2ms, the stimulation intensity must reach super-strong stimulation (that is, after increasing the stimulation, the evoked potential no longer increases), and then increase the intensity by 30%. B.2.1.3 Measure the time (ms) from the stimulation artifact to the beginning of the evoked potential waveform, called the latency, and measure the latency of the proximal stimulation point and the distal stimulation point respectively. The difference between the two is the conduction time (ms) between the two points of the nerve segment. B.2.1.4 Use a steel ruler or pelvic ruler to accurately measure the distance between the proximal stimulation point and the distal stimulation point, which is the length between the two points of the nerve segment (cm).
The conduction velocity between the two points of the nerve segment can be calculated according to the following formula. Conduction velocity (m/s) =
Distance (cm)
Conduction time (ms)
The distal nerve conduction is expressed by the distal motor latency. B.2.2 Sensory nerve conduction velocity
B.2.2.1 Stimulating electrodes, except for the surface electrodes used for the examination of the enteric nerve, all use ring electrodes, which are wrapped around the fingers or toes, with the negative electrode placed on the proximal knuckle and the positive electrode placed on the distal knuckle, with the two electrodes at least 1 cm apart. The electrode placement sites are as follows: Median nerve: index finger.
Ulnar nerve: little finger
Sural nerve: below the posterior lateral malleolus.
Posterior tibial nerve: big toe.
Recording electrodes, except for the needle electrodes used for the examination of the posterior tibial nerve, all use surface electrodes. The placement site, whether distal or proximal, should be placed at the site where the maximum evoked potential is elicited when measuring the motor nerve conduction velocity. When examining the sural nerve, the recording electrode is placed 14 cm behind the calf from the stimulating electrode.
B.2.2.2 Use single pulse square wave electrical stimulation, 1~1.5 times/s, 0.1~0.2ms each time, and increase the stimulation intensity until the subject feels obvious numbness in the fingers or toes (the stimulation amount of the constant current stimulator is generally 30~40mA, and the maximum does not exceed 50mA). B.2.2.3 A superposition device is required, and the number of superpositions can be determined according to the clarity of the graph. B.2.2.4 The peak-to-peak height of the evoked potential is measured as the potential amplitude (voltage). B.2.2.5 The method for determining the latency, the distance between the stimulating electrode and the recording electrode, and the calculation formula for the nerve conduction velocity are the same as B.2.1.4.
B.3 Normal values ​​of neuro-electromyography
Strictly speaking, each laboratory should have its own normal values: since no unit with its own normal values ​​has been established yet, the normal values ​​listed in Tables 1 to 3 can be referred to, but the inspection methods should be consistent. B.3.1 Normal value of electromyogram
B.3.1.1 Insertion activity: The discharge lasts no more than 2 seconds after the needle is inserted. B.3.1.2 Spontaneous potentials (fibrillation waves, positive sharp waves) generally do not appear at rest. (About 4.3-10% of normal muscles can have spontaneous potentials in one part.)
Average duration of motor units: The normal value of the average duration of 20 motor units is shown in Table B1. B.3.1.3
20 motor units average duration normal
three-headed stage medical blue
11.8 11.6
finger product companion
one bone secretion
small sample is muscle
early stage
[2.3 12.3
[2.5 12.7
12.7 13.1
13.0 13.4
13.4 13.8
13.7 14.0
13.9 14.3
J4.2 14.7
Short myoelectric period
Note: The normal values ​​in each column of the table are from [1J LudinHP (translated by Tang Xiaofu et al.): Practical Electromyography, Tianjin Science and Technology Press, 1984; [2] Tang Xiaofu et al.: Electromyographic findings of 310 normal people. Chinese Medical Journal 1984, 64 (2): 91
B.3.1.4 Percentage of polyphasic potential: The phase of the motor unit is 5 or more phases. The polyphasic potential of general muscles does not exceed 20%, deltoid muscle does not exceed 25%, and tibialis anterior muscle does not exceed 35%. B.3.1.5 Interference phase is present during strong contraction.
B.3.1.6 There are many factors that affect the voltage of the motor unit, which can be judged based on the normal values ​​of each laboratory. B.3.2 Normal values ​​of motor nerve conduction velocity are shown in Table B2B3.3
Normal values ​​of sensory nerve conduction velocity are shown in Table B3Criteria for judging neurogenic damage
B.4.1 Electromyography
Spontaneous potentials (fibrillation waves, positive sharp waves) appear at three locations in a muscle. B.4.1.2 The average duration of 20 motor units during small-force contraction is extended by more than 20% compared with the normal value of the corresponding age group. B.4.1.3 The percentage of multiphasic potential increases during small-force contraction, exceeding 20% ​​of the 20 motor units of general muscles, exceeding 25% of deltoid muscles, and exceeding 35% of tibialis anterior muscles.
B.4.1.4: Mixed phase or simple phase during strong contraction. One of the first two of the above four items must be present, and the other two items must be referred to before it can be determined as neurogenic damage. B.4.2 Nerve conduction velocity
If any of the following is present, it can be defined as neurogenic damage: B.4.2.1 Slowed sensory nerve conduction velocity (more than the normal mean - 2 standard deviations), B4.2.2 Slowed motor nerve conduction velocity (more than the normal mean - 2 standard deviations) or prolonged distal motor latency (more than the normal mean + 2 standard deviations).
B.4.2.3 Decreased sensory potential amplitude (more than the normal mean - 2 standard deviations). B.4.2.4 The evoked motor potential amplitude is significantly decreased (less than 1mV) or the waveform is significantly complex (more than 4 phases).3. Myoelectric activity during small force contraction (light contraction): The conditions are the same as those in B.1.2.2. When the muscle contracts slightly, measure the average duration and average voltage of 20 motor unit potentials, and the percentage of multiphase potentials. (To determine the average duration of the motor unit, if necessary, 2 to 3 different positions should be selected in the same muscle for inspection). To avoid errors, each wave must appear 2 to 3 times at the same time before it can be counted. The duration is from the initial deflection of the baseline to the final deflection back to the baseline. The phase of the motor unit is based on the peak crossing the baseline.
B.1.2.4 Myoelectric activity during strong contraction: scanning speed 50~100ms/cm, sensitivity 500μv/cm~1mv/cm. When the subject contracts the examined muscle with the maximum force, observe whether it is an interference phase, a mixed phase or a simple phase, and measure its peak-to-peak amplitude. B.2 Nerve conduction velocity
The subject's skin temperature should be kept above 30℃, and the examined area should be cleaned with alcohol to remove oil stains; the surface electrode should be correctly placed on the nerve, and the skin should not be pushed: when giving electrical stimulation, attention should be paid to safety, and the ground electrode should be placed between the stimulating electrode and the recording electrode.
B.2.1 Motor nerve conduction velocity
B.2.1.1 Electrode placement
Surface electrodes are used as stimulating electrodes. Except for the use of surface electrodes when examining the common nerve, concentric axis electrodes are used as recording electrodes. The electrode placement sites of the main examined nerves are as follows: Ulnar nerve: The proximal stimulation point is placed between the medial superior humerus and the olecranon fossa of the ulna, and the distal stimulation point is at the ulnar edge of the wrist crease: The recording electrode is placed on the little finger of the hand.
Median nerve: The proximal stimulation point is placed above the medial humerus, the distal stimulation point is at the midpoint of the wrist crease, and the recording electrode is placed on the abductor pollicis brevis.
Tibial nerve: The proximal stimulation point is placed in the center of the brain fossa (Weizhong point), the distal stimulation point is at the back of the medial malleolus, and the recording electrode is placed on the abductor pollicis brevis:
Posterior tibial nerve: The positive and negative needle poles of the stimulation electrode are inserted into the subcutaneous part of the midpoint of the line connecting the medial malleolus and the heel, 1 cm apart, and the negative needle tip is moved forward and upward to approach the posterior tibial nerve until the stimulation amount is less than 1 mA to elicit the evoked potential. The irrelevant electrode is inserted into the subcutaneous part nearby, 2 cm apart. The recording electrode is placed on
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