Introduction to AIDP

Contents 1 English reference 2 Overview 3 Disease name 4 English name 5 Alias ​​of Guillain-Barré syndrome 6 Disease classification 7 ICD number 8 Epidemiological data of Guillain-Barré syndrome 9 Guillain-Barre syndrome The cause of Reye syndrome 10 The pathogenesis of Guillain-Barré syndrome 11 Clinical manifestations of Guillain-Barré syndrome 11.1 Aura symptoms 11.2 Movement disorder 11.2.1 Limb paralysis 11.2.2 Trunk muscle paralysis 11.2.3 Cranial nerve palsy 11.3 Sensation Disorders 11.4 Autonomic dysfunction 11.5 Laboratory tests 11.6 Electrophysiological tests 12 Complications of Guillain-Barré syndrome 13 Diagnosis of Guillain-Barré syndrome 13.1 The diagnosis of GBS is mainly based on clinical diagnosis 13.2 Diagnostic criteria 13.3 Laboratory tests 13.3 .1 Cerebrospinal fluid 13.3.2 Hemogram and erythrocyte sedimentation rate 13.4 Auxiliary examination 14 Diseases that need to be differentiated from Guillain-Barré syndrome 14.1 Poliomyelitis 14.2 Acute myelitis 14.3 Periodic paralysis (periodic paralysis) 15 Treatment of Guillain-Barré syndrome 15.1 Acute phase 15.1.1 Dehydration and improvement of microcirculation 15.1.2 Neurotrophic metabolic drugs 15.1.3 Hematology therapy 15.1.4 Immunosuppressants 15.1.5 Supportive and symptomatic treatment 15.2 Recovery phase 15.3 Referral 15.4 Precautions 16 Guillain-barre Prognosis of the syndrome 17 Prevention of Guillain-Barré syndrome 18 Related drugs 19 References This is a redirected entry that *shares the content of Guillain-Barré syndrome. For the convenience of reading, Guillain-Barre syndrome in the following text has been automatically replaced by AIDP. You can click here to restore the original form, or use the note method to display 1 English reference

acute inflammatory demyelinating polyneuropathy [Clinical Application of National Essential Drugs Guidelines: 2012 Edition. Chemicals and Biological Products] 2 Overview

AIDP (Guillain Barrés syndrome, GBS), also known as acute inflammatory demyelinating polyneuropathy (Guillain) Barré syndrome) [1] and acute infectious polyradiculoneuritis are an autoimmune disease caused by viral infection or infection and other reasons. It is an autoimmune disease involving peripheral nerves and nerve roots [1].

The clinical characteristics of AIDP are acute or subacute limb paralysis, varying degrees of sensory impairment, which may be accompanied by autonomic symptoms and respiratory failure [1].

The pathological characteristics of AIDP are myelin loss and infiltration of lymphocytes and macrophages around small blood vessels [1].

The cause of AIDP is unknown, and CBS is currently believed to be a post-infectious immune-mediated disease [1]. Relevant infectious pathogens may include cytomegalovirus, African lymphoma virus, Mycoplasma pneumoniae, hepatitis B virus, and Campylobacter jejuni [1].

It can occur in all age groups [1].

AIDP patients are often accompanied by facial nerve paralysis, dysphagia, vocal weakness, respiratory muscle paralysis, pulmonary infection, and a few suffer from extraocular muscle paralysis. There may be autonomic nervous system dysfunction such as tachycardia, hyperhidrosis, sudden hypertension, or bladder sphincter disorder. In severe cases, respiratory muscle paralysis can be life-threatening. Most patients have a good prognosis after active treatment. Mild cases usually get better within 1 to 3 months and fully recover within a few months to a year. Some patients may have varying degrees of sequelae, such as limb weakness, muscle atrophy, and foot drop. It is difficult to recover from limb paralysis in severe patients, and they often die due to respiratory muscle paralysis, bulbar paralysis or pulmonary complications. A few cases may recur.

3 Disease name

AIDP 4 English name

GuillainBarre syndrome 5 Alias ​​of AIDP

Acute infectious polyradiculoneuritis; Guillain-Barre syndrome; Guillain-Barre syndrome Symptoms; acute infectious polyradiculoneuritis; Guillain-Barre syndrome; acute inflammatory demyelinating polyradiculopathy; acute inflammatory demyelinating polyradiculoneuropathy 6 Disease Classification

< p> Neurology> Spinal nerve diseases

Nervous system diseases> Peripheral nerve diseases> Polyperipheral neuropathy

Nervous system diseases> Peripheral nerve diseases> Immune-mediated peripheral neuropathy 7 ICD number

G61.9 8 Epidemiological data of AIDP

AIDP can occur at any age, but is more common in young and middle-aged men. It can also occur in the elderly. The disease occurs in all seasons, and is more common in summer and autumn. It shows acute or subacute onset, and a few have slow onset. Nearly 50% of patients first have prodromal symptoms of viral infection. Death often occurs due to respiratory muscle paralysis, bulbar paralysis or pulmonary complications, with a case fatality rate of 5.7% to 23.2%. A few cases may recur. 9 The cause of AIDP

The cause of AIDP is not yet completely clear. In the past, it was thought to be related to viral infection, such as upper respiratory tract infection, diarrhea, etc. It is now clear that GBS is a disease mediated by cellular and humoral immunity, and is a disease in which antibodies triggered by specific antigens in peripheral nerves lead to demyelination.

The infection rate of campylobacter jejuni (CJ) before GBS is high, which is an important factor in promoting the disease. 10 Pathogenesis of AIDP

Early serological studies found that 48% of patients had positive complement fixation tests for various viruses, such as cold and paracold viruses, monovirus, adenovirus, etc. In recent years, it has been found both at home and abroad that patients with GBS have a higher rate of Campylobacter jejuni infection before the disease occurs, but this does not directly infect peripheral nerves, but is only an important factor in promoting the disease.

A***ury et al. compared the clinical pathology of patients who died from this disease with the manifestations of experimental allergic neuritis (EAN) and believed that the two were very similar. Domestic scholars tested the cerebrospinal fluid and peripheral blood lymphocyte subpopulations of patients with GBS in the acute phase and found that T cells in the cerebrospinal fluid increased and T cells in the peripheral blood decreased (Zhou Shanren et al., 1983). Recently, it was found that the plasma concentrations of tumor necrosis factor α (TNFα) and interleukin 2 (IL2) in patients with tumor necrosis were significantly increased, and during the recovery period when the condition improved after receiving glucocorticoid treatment, both concentrations decreased and were close to normal. It is suggested that TNFα and IL2 secreted by macrophages and antigen-activated T cells may directly and indirectly participate in the pathological damage of peripheral nerve demyelination (Xiong Ying et al., 2000).

Other studies have detected complement-binding anti-myelin IgM antibodies as well as a variety of high-titer anti-glycosphingolipid antibodies and anti-GM1 antibodies in patient serum. In addition, IgG and IgA increased in cerebrospinal fluid, and oligoclonal IgG appeared. Recent studies believe that autoimmune reactive T cells and activated monocytes and macrophages enter peripheral nerves from the blood and participate in the process of damaging peripheral nerves, and intercellular adhesion molecule (ICAM1) plays a certain role.

Although the results of some experimental studies are not entirely consistent, it is clear that GBS is a disease mediated by cellular and humoral immunity, and that antibodies triggered by specific antigens in peripheral nerves lead to myelin degeneration.

Neuropathological changes are mainly in the peripheral nervous system. It is an extensive segmental demyelination and inflammatory cell infiltration in the spinal nerve root system. The axonal changes are relatively mild, with only swelling and distortion.

The anterior roots of the spinal nerves are damaged first and are more severe than the posterior roots. The proximal end of the peripheral nerves is more severe and the distal end is relatively lighter. In the early stage of the disease, nerve edema and lymphocytes and macrophages form perivascular cuffs. Mononuclear cells infiltrate and increase in spinal nerve roots and peripheral nerves. Mononuclear cells and macrophages destroy the Schwann cell basement membrane, resulting in extensive segmental disease. Sexual demyelination, occasionally involving the spinal cord. Significant proliferation of endoneurial fibroblasts can be seen in the middle stage of the disease, and Schwann cell proliferation can be seen in the late stage of the disease.

In some fulminant cases, axons may be damaged, broken or even granulated due to the extremely strong immune response in the acute phase. A few also have severe axonal degeneration during the recovery period of the disease (6 to 7 weeks).

The GBS variant discovered in northern my country in the early 1990s is acute motor axonal neuropathy (AMAN). Its pathological changes are mainly in axons. Wallerian-like degeneration of varying degrees in the anterior roots and peripheral nerves, mild demyelination, and rare inflammatory lesions. Although there is no lymphocyte infiltration in the diseased fibers, macrophages can be found in the degenerated areas. It is also believed that this type is particularly closely related to CJ infection (Li Chunyan et al., 1993).

11 Clinical manifestations of AIDP 11.1 Premonitory symptoms

AIDP often has prodromal symptoms of upper respiratory tract or digestive tract infection such as fever, diarrhea, etc. before the onset of AIDP. 11.2 Movement disorders 11.2.1 Limb paralysis

Symmetrical lower motor neuron paralysis of the limbs often starts from the lower limbs and gradually spreads to both upper limbs, or from one side to the other. A very small number of patients are first limited to both lower limbs. The condition usually reaches its peak within 1 to 2 weeks and then stabilizes. Paralysis is generally more severe in the proximal end, with low muscle tone in the limbs, weakened or disappeared tendon reflexes, most abdominal wall and cremaster reflexes are normal, and a few may have pathological reflex signs due to pyramidal tract involvement. Muscle atrophy gradually occurs 2 to 3 weeks after the onset of symptoms. 11.2.2 Trunk muscle paralysis

People with cervical muscle paralysis cannot raise their heads. People with paralysis of the intercostal muscles and diaphragm may develop respiratory muscle paralysis (20% to 30%), manifesting as chest tightness, shortness of breath, muffled voice (like a cat meowing), weak cough, inability to lie down, and difficulty in chest or abdominal breathing movements. The intercostal muscles are usually paralyzed earlier than the diaphragm and the breath sounds are weakened. In severe cases, coma and death may occur due to hypoxia or respiratory complications. 11.2.3 Cranial nerve palsy

About half of the patients may have cranial nerve damage. Peripheral paralysis of the glossopharyngeal, vagal and one or both facial nerves is the most common, followed by oculomotor, trochlear, and abduction. nerve. Occasionally, optic disc edema may be caused by inflammatory changes in the optic nerve itself or cerebral edema; it may also be related to a significant increase in cerebrospinal fluid protein, which blocks the arachnoid villi and affects the absorption of cerebrospinal fluid. 11.3 Sensory impairment

The first symptom is often subjective sensory impairment, which usually starts with numbness and pins and needles at the end of the limbs. During the examination, stretching the nerve roots can often aggravate the pain (such as a positive Kernig sign), and there may be obvious tenderness in the muscles (especially the bilateral gastrocnemius muscles). Objective examination may show glove, sock-like and/or hypoesthesia in the trigeminal nerve innervation area, or there may be no sensory impairment. Sensory impairment is much lighter than motor impairment, which is one of the characteristics of this disease. 11.4 Autonomic nervous system dysfunction

In the early or recovery period, there is often excessive sweating and a strong odor, which may be the result of sympathetic nerve stimulation. A small number of patients may have short-term urinary retention in the early stage, which may be caused by temporary imbalance of the autonomic nerve function that controls the bladder or damage to the spinal nerve that controls the external sphincter. Some patients may develop cardiovascular dysfunction such as unstable blood pressure, tachycardia, and abnormal electrocardiogram. 11.5 Laboratory examination

The phenomenon of protein cell separation in the cerebrospinal fluid occurs 1 to 2 weeks after the onset of the disease, and is most significant in the 2 to 8 weeks, and then gradually recovers. The number of white blood cells does not exceed 10×106/L. The cytological classification is mainly lymphocytes and monocytes, and macrophages can be seen. The protein content increased significantly. Sugar and chloride are normal. 11.6 Electrophysiological examination

Motor nerve conduction velocity is significantly slowed down, and F wave latency is prolonged or disappeared, which is seen in demyelinating GBS. If it is AMAN, the motor nerve conduction velocity is normal or slightly slowed down. The F-wave latency of sensory fibers is normal or slightly prolonged.

GBS can happen again. Recurrent GBS usually occurs months to years apart. Symptoms are often more severe when a recurrence occurs than during the first attack. Fisher syndrome is another variant of GBS. The onset of this type shows an acute progression, mainly characterized by the triad of extraocular muscle paralysis, ataxia, and loss of tendon reflexes. Occasionally, it may be accompanied by quadriparesis and CSF protein cell separation. The pathogenesis of these GBS variants is different from those in which demyelination is the main cause. 12 Complications of AIDP

AIDP is often accompanied by facial nerve paralysis, dysphagia, vocal weakness, respiratory muscle paralysis, pulmonary infection, and rarely, extraocular muscle paralysis. There may be autonomic nervous system dysfunction such as tachycardia, hyperhidrosis, sudden hypertension, or bladder sphincter disorder. In severe cases, respiratory muscle paralysis can be life-threatening. 13 Diagnosis of AIDP 13.1 The diagnosis of GBS is mainly based on clinical diagnosis

(1) Based on the history of respiratory or gastrointestinal infection or vaccination history within 1 to 4 weeks before the disease [1].

(2) Acute or subacute onset [1].

(3) Symptoms of bilaterally symmetrical motor and sensory polyneuropathy: flaccid paralysis of the limbs. In severe cases, intercostal muscles and respiratory muscles may be involved, leading to respiratory paralysis. There is abnormal sensation in the distal limbs and glove-like and sock-like sensory disturbances. Cranial nerve damage may occur, with bilateral facial nerve palsy being the most common, followed by glossopharyngeal and vagal nerve palsy [1].

(4) The phenomenon of protein cell separation in cerebrospinal fluid: increased protein content but normal or slightly higher white blood cell count [1].

(5) Neuroelectrophysiological abnormality: nerve conduction velocity is slowed or blocked, usually lower than 60% of normal, distal latency is extended up to 3 times normal, F wave or H reflex is delayed Or disappear etc.[1]. 13.2 Diagnostic criteria

In 1993, the editorial board of the Chinese Journal of Neuropsychiatry formulated my country's diagnostic criteria for GBS based on international data.

Generally, this disease should be considered based on the presence of precursor symptoms of upper respiratory tract or gastrointestinal tract infection before the disease, rapid development of lower motor neuron paralysis of the limbs 1 to 2 weeks later, and bulbar paralysis and respiratory muscle paralysis in severe cases.

If the CSF shows protein-cell separation, electrophysiological testing of the paralyzed limbs may indicate proximal or distal damage to the peripheral nerve trunk, which is more helpful for diagnosis. 13.3 Laboratory examinations 13.3.1 Cerebrospinal fluid

There is often a phenomenon of increased protein and normal or close to normal cell number, which is another characteristic of this disease. Cerebrospinal fluid protein often begins to increase 7 to 10 days after onset (with varying degrees of increase), reaches a peak after 4 to 5 weeks, and gradually decreases after 6 to 8 weeks. There is no parallel relationship between the increase in cerebrospinal fluid protein content and the disease. After a few patients recover from limb paralysis, the cerebrospinal fluid protein content is still high, and in some patients, the protein content is always normal. Immunological tests of cerebrospinal fluid and blood are often abnormal. 13.3.2 Blood picture and erythrocyte sedimentation rate

An increase in the total number of white blood cells and a rapid increase in erythrocyte sedimentation rate often indicates a serious condition or pulmonary complications. 13.4 Auxiliary examination

The changes in electromyography examination are related to the severity and course of the disease. In the acute phase (within 2 weeks after the disease), motor unit potentials often decrease, amplitude decreases, motor nerve conduction velocity may be normal, and some may have prolonged terminal latency, but F waves (proximal motor fiber conduction) often have prolonged latency or waveforms. disappear. Motor evoked potential (MEP) can also be measured to understand the degree of damage to the nerve roots and proximal peripheral nerves, and the abnormality rate can reach 74.1%. After 2 weeks, denervation potentials [such as fibrillation and/or positive sharp waves] gradually appeared. When the disease enters the recovery period or later, polyphasic potentials increase and small motor unit potentials (new potentials) appear. Motor nerve conduction velocity is often significantly slowed down, and terminal latency is prolonged. Sensory nerve conduction velocity may also be slowed. 14 Diseases that need to be differentiated from AIDP

AIDP needs to be differentiated from poliomyelitis, acute myelitis, hypokalemic periodic paralysis, myasthenia gravis, etc. [1]. 14.1 Poliomyelitis

Poliomyelitis often presents with fever, muscle paralysis is often segmental and asymmetrical, and there is no sensory impairment. The white blood cell count in the cerebrospinal fluid is often increased. 14.2 Acute myelitis

Although acute myelitis also presents with flaccid paralysis in the acute phase, pyramidal tract signs and transverse sensory impairment are often present, and sphincter dysfunction is more obvious. Cerebrospinal fluid proteins and cells were slightly increased or normal. 14.3 Periodic paralysis (periodic paralysis)

Periodic paralysis has an acute onset and may present as symmetrical flaccid paralysis of the limbs. In a few cases, respiratory muscle paralysis may also occur, but serum potassium content is often reduced and hypokalemia is present. The electrocardiogram changes and the course of the disease is short. It can recover quickly after potassium supplementation, and usually heals itself within a few hours to 3 to 4 days.

Attention should be paid to distinguishing acute toxic polyneuropathy and cancerous polyneuropathy caused by lead and arsenic. 15 Treatment of AIDP 15.1 Acute phase

Intravenous immunoglobulin therapy is the first choice and should be implemented as early as possible before respiratory muscle paralysis occurs [1]. 15.1.1 Dehydration and improvement of microcirculation

①20% mannitol or 10% glycerol glucose solution (except for diabetic patients): 250 or 500ml intravenous infusion once/d, 7 to 10 times as a course of treatment . If the condition is severe and there are cardiopulmonary complications, diuretics (such as furosemide) can be appropriately combined.

②Hydroxyethyl starch (706 generation plasma): 250~500ml intravenous infusion, once/d, 7~10 times as a course of treatment.

③ Hormone treatment: For severe cases, high-dose methylprednisolone can be used for short-term pulse treatment. In the first 1 to 2 days, add 1000 mg to 250 ml of normal saline for intravenous infusion. On days 3 to 7, use 500 mg for intravenous infusion. After 1 week, use oral administration. Stop taking it after half a month.

The efficacy of hormone therapy is uncertain[1]. Regular doses of hormones cannot prevent the progression of the disease and shorten its course [1]. 15.1.2 Neurotrophic metabolic drugs

For example, large doses of B vitamins, 0.25 to 0.5g of citicoline by intramuscular injection or intravenous infusion. You can also choose nerve growth factor, methylcobalamin (Mecobalamin, 500 μg), and recombinant bovine (human) fibroblast growth factor (bFGF1 600U) for intramuscular injection 1 to 2 times/ d. Ganglioside (GM1) 20 to 40 mg, intramuscular injection once/d.

In the acute phase, adequate amounts of B vitamins, vitamin C, coenzyme Q10 and high-calorie easily digestible diet are given [1]. 15.1.3 Blood therapy

For those who are seriously ill or have respiratory muscle paralysis or pulmonary complications, the following treatments can be used early.

① High-dose human immunoglobulin: daily dose of 0.3-0.4g/kg, used 3-5 times. The therapeutic mechanism is related to regulating immune function.

Intravenous immune globulin therapy should be implemented as soon as possible before respiratory muscle paralysis occurs, at 0.4g/kg per day for 5 days [1]. Contraindications are patients with immunoglobulin allergy or congenital IgA deficiency [1].

②Plasma exchange therapy: It can remove harmful substances such as antibodies and immune complexes in the plasma to reduce the toxic damage of myelin and promote the repair and regeneration of myelin. About 1000-1500ml of plasma is exchanged at one time, 2-3 times a week, 3-5 times is a course of treatment. Since this therapy still has certain shortcomings, it has a tendency to be replaced by plasma adsorption therapy, which is safer.

Plasma exchange therapy can shorten the course of treatment and reduce the severity of the disease. A common side effect is post-plasma transfusion hepatitis. It can be performed in qualified tertiary general hospitals or specialized hospitals [1].

③ Ultraviolet radiation oxygenation and autoblood transfusion therapy: once a day or every other day, 5 to 10 times as a course of treatment. It can enhance oxygen metabolism and regulate immune function. 15.1.4 Immunosuppressants

In the acute phase of AIDP, azathioprine can be used when other drugs are ineffective or contraindicated, or in chronic AIDP, and attention should be paid to its cytotoxicity [1]. 15.1.5 Supportive and symptomatic treatment

Supportive and symptomatic treatment includes maintaining water, electrolyte and acid balance; preventing complications of long-term bed rest; such as preventing accumulation or aspiration pneumonia; preventing deep veins in the lower limbs Thrombosis and resulting pulmonary embolism [1].

① Strengthen the maintenance of respiratory function and keep the respiratory tract unobstructed: For those who may develop respiratory muscle paralysis, if the patient has shallow breathing, increased frequency, weak coughing, and poor phlegm discharge, it is advisable to start early A tracheotomy and mechanical ventilation were performed.

② Prevention and treatment of pulmonary complications: Turn over regularly, pat the back, suction sputum regularly, pay attention to aseptic operation, prevent lung infection, and use appropriate antibiotics in the early stage.

③ To prevent electrolyte imbalance, in hospitals with conditions, cardiac and pulmonary function monitoring of severe patients should be carried out.

④ Ensure adequate nutrition, water and rest: Adequate rest is very important for preserving physical strength and enhancing disease resistance. Therefore, benzodiazepines can be appropriately used for those who are irritable and have poor rest. Sedatives. Fresh whole blood or plasma can be transfused regularly. Nasal feeding can be used early for patients with dysphagia to ensure adequate nutrition, water and medication, and to reduce the occurrence of aspiration pneumonia. 15.2 Recovery period

During the recovery period, you can continue to use B vitamins and drugs to promote the recovery of neurological function, and use physiotherapy, physical therapy, acupuncture, massage and other rehabilitation measures as appropriate. 15.3 Transfer

Severely ill patients need to be transferred to a tertiary general hospital or a specialized hospital for treatment [1]. 15.4 Precautions

1. Respiratory muscle paralysis is the main risk of this disease. If there is no improvement in a short period of time after giving oxygen through the nasal cannula and clearing the respiratory tract, the arterial oxygen partial pressure is lower than 70mmHg and the trachea should be Intubation or tracheotomy, early mechanical ventilation [1].

2. If the patient is complicated by cranial nerve palsy of IX and X, endotracheal intubation or tracheostomy should be considered earlier [1].

3. Pay attention to rehabilitation treatment and carry out passive limb activities early to prevent contracture [1]. 16 Prognosis of AIDP

Most AIDP patients have a good prognosis after active treatment. Mild cases usually get better in 1 to 3 months and fully recover within a few months to a year. Some patients may have varying degrees of sequelae. Such as limb weakness, muscle atrophy and foot drop. It is difficult to recover from limb paralysis in severe patients, and they often die due to respiratory muscle paralysis, bulbar paralysis or pulmonary complications. A few cases may recur.

Li Danian reported 231 cases treated between 1963 and 1973. The main drug relied on at that time was hydrocortisone intravenous drip. The main treatment for respiratory muscle paralysis is early tracheotomy and oxygen administration. The case fatality rate is 23.2%. Almost all those who died had respiratory muscle paralysis. Later, 111 survivors were followed up for a long time, with an average follow-up time of 3 years and 2 months (6 months to 10 years). 64.4% of them fully recovered, 32.2% had sequelae, and the fatality rate was 3.4%. This is close to reports from other hospitals during the same period (Department of Neurology, Affiliated Hospital of Henan Medical College, 1975).

In recent years, with the development of therapeutic drugs and the improvement of technical equipment such as ventilators, reasonable treatment can be obtained at an early stage, so the mortality rate has been greatly reduced. Li Danian reported 176 cases treated between 1994 and 2000, with a fatality rate of 5.7%. In addition, due to the improvement of neurological rehabilitation equipment and standardized training, the degree of disability has also been significantly improved. 17 Prevention of AIDP

There is no good way to prevent autoimmune diseases. Pay attention to the following points to prevent relapse in clinically cured patients:

1. Strengthen nutrition, enhance physical fitness, and prevent colds.

2. Practice correct methods of coughing and expectoration to prevent secondary lung infection.

3. Vaccination, pregnancy, and surgery can induce this disease.

4. Severely ill patients who suddenly lose their ability to move are prone to anxiety, tension and other emotions and should receive appropriate psychological counseling.

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