bubble_chart Overview

Acute infectious polyneuritis, also known as Guillain-Barré syndrome or acute inflammatory demyelinating polyneuropathy, is a common condition characterized by simultaneous damage to multiple spinal nerve roots and peripheral nerves (often including cranial nerves). Its clinical features include acute onset, rapidly developing symmetrical flaccid paralysis in the limbs, and cerebrospinal fluid protein-cell dissociation. It can occur at any age but is more common in males under 30 years old. Cases are reported throughout the year, with a higher incidence in summer and autumn.

bubble_chart Etiology

The etiology and pathogenesis of this disease remain incompletely understood. It is generally believed to be a delayed, hypersensitivity-related autoimmune disorder associated with infection, with the myelin sheath of peripheral nerves being the target of immune attack. The most closely implicated infectious agents include cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumoniae, Campylobacter jejuni, and hepatitis B virus. Its pathogenesis resembles experimental allergic neuritis, a cell-mediated hypersensitivity reaction. However, recent studies have detected various anti-myelin antibodies in patient sera, IgG and complement deposition on vascular walls and Schwann cell membranes within peripheral nerves, as well as monoclonal IgG antibodies in cerebrospinal fluid, indicating the involvement of humoral immunity in disease development. Therefore, the cause of this disease may be a preceding infection that triggers an immune response, while abnormal immune regulation within the body leads to damage of peripheral nerve tissue, specifically demyelination.

bubble_chart Pathological Changes

The lesions are primarily located in the spinal nerve roots, spinal nerves, and cranial nerves. The affected nerve fibers exhibit swelling, degeneration, and segmental demyelination, with perivascular infiltration of lymphocytes and macrophages in the nerve tissue. The anterior horn cells of the spinal cord, posterior root ganglion cells, spinal membranes, and brain show varying degrees of congestion, hemorrhage, degeneration, and necrosis.

bubble_chart Clinical Manifestations

Acute or subacute onset. More than two-thirds of patients experience symptoms of upper respiratory and digestive tract infections days or weeks before onset, with symptoms typically progressing rapidly after onset and peaking within days to two weeks. The main symptom is motor dysfunction. Initially, there is weakness in the lower limbs, which gradually extends distally, leading to symmetrical paralysis of all four limbs. In severe cases, paralysis can rapidly ascend, affecting the intercostal muscles and diaphragm, resulting in respiratory paralysis, manifested as dyspnea, cyanosis, weak cough, and mucus blockage. Some patients also frequently report distal limb paresthesia, numbness, or pain. Examination reveals flaccid paralysis, absent tendon reflexes, and negative pathological reflexes; sensory impairment is minimal or even absent, and when present, it often manifests as glove-and-stocking hypoesthesia.

More than half of the cases may involve cranial nerve damage, most commonly bilateral peripheral deviation of the mouth, followed by involvement of the glossopharyngeal and vagus nerves, leading to bulbar palsy symptoms such as dysarthria and dysphagia. Occasionally, there may be ophthalmoplegia, retinal hemorrhage, or optic disc edema.

Autonomic nerve damage manifests as skin flushing, profuse sweating, and edema of the hands and feet. A few cases may exhibit tachycardia, unstable blood pressure, or electrocardiogram changes. Cardiac involvement is a poor prognostic sign and may lead to sudden death. Except for a very small number of cases with transient urinary dysfunction, sphincter function is generally unaffected.

bubble_chart Auxiliary Examination

During the acute phase, peripheral white blood cells may show a grade I increase. The characteristic change is the dissociation of protein and cells in the cerebrospinal fluid, where protein levels rise while cell counts remain normal or nearly normal. Protein content typically ranges from 0.5 to 2 g/L (50–200 mg/dl) and can even reach as high as 10 g/L (1000 mg/dl). This phenomenon is most pronounced in the third week after onset, does not correlate with disease severity, and may persist for several days or up to 1–2 years. In a few cases, cerebrospinal fluid may show no changes. Nerve conduction velocity in the distal limbs is often reduced to 60–70% of normal levels.

bubble_chart Diagnosis

1. Acute or subacute onset, often with a history of infection 1-3 weeks before the illness.
2. Rapidly progressing symmetrical flaccid paralysis of the limbs.
3. Often accompanied by cranial nerve damage.
4. Cerebrospinal fluid shows protein-cell dissociation.

bubble_chart Treatment Measures

(1) Acute Phase Treatment

1. Hormone Therapy: Early use of adrenal corticosteroids. Commonly used dexamethasone 10-15mg/d or hydrocortisone 200-300mg/d, added to 5-10% glucose solution for intravenous drip, continued for 10-14 days. For critically ill patients, high-dose shock therapy can be used, with dexamethasone 30-60mg/d or hydrocortisone 300-600mg/d, continued for 3-5 days. Afterwards, oral prednisone is maintained at 20-40mg/d, gradually tapering the dose. Generally used for about 1 month. During this period, attention should be paid to supplementing potassium salts and monitoring for gastrointestinal bleeding and secondary infections.
2. Treatment of Respiratory Paralysis: Respiratory paralysis is the greatest danger of this disease. Maintaining respiratory function and keeping the airways clear are key to increasing the cure rate and reducing mortality. If grade I cyanosis, dysphoria, or mucus blockage occurs, a tracheotomy or tracheal intubation should be performed promptly to clear secretions from the trachea, and a ventilator should be used if necessary to assist in improving ventilation. Strengthen nursing care to prevent complications.
3. Infection Control: Appropriate antibiotics can be selected.
4. Plasma Exchange Therapy: Many reports suggest that this method can remove myelinotoxic antibodies, inflammatory chemical mediators, fibrinogen, etc., from the plasma, thereby avoiding toxic damage to nerve myelin, promoting myelin repair and regeneration, and alleviating clinical symptoms. It is generally believed that early use in young, critically ill cases yields better results.
5. Autologous Blood Photon Therapy (autologous blood transfusion therapy after ultraviolet irradiation and oxygenation): Considered to have definite efficacy in the acute progressive phase, its mechanism may be related to increasing the number of peripheral blood T cells and improving immune function disorders. However, some believe that ultraviolet light can damage chromosomes, increase micronucleus rates, and be harmful to the body.
6. Other Therapies: High-dose B vitamins, vitamin C, as well as adenosine triphosphate, cytidine diphosphate choline, coenzyme Q10, etc., can be used as appropriate. If arrhythmia or hypertension occurs, corresponding medications should be selected.

(2) Convalescence Stage Treatment

Acupuncture, tuina, physiotherapy, and other active or passive functional exercises can be used to facilitate paralysis recovery.

bubble_chart Prognosis

The prognosis of this disease is favorable. More than two-thirds of cases begin to recover within 1 to 4 weeks, with most achieving full recovery within six months to a year. Some cases may experience varying degrees of sequelae, and a few may relapse. The prognosis is poor for those with respiratory paralysis, pulmonary infections, or heart failure.

bubble_chart Complications

1. Acute respiratory failure: Caused by respiratory paralysis, it is the primary cause of death in this disease.
2. Pulmonary infection: Due to weakened cough reflex and impaired clearance of respiratory secretions, bacteria proliferate in the respiratory tract. Some cases may be related to tracheotomy. Pulmonary infection is often one of the causes of death in this disease, making its prevention and treatment critically important.
3. Arrhythmia: Mostly caused by mechanical ventilation impairment, metabolic, acid-base, and electrolyte imbalances, it is also one of the life-threatening risk factors of this disease. Immediate treatment is required once it occurs.

bubble_chart Differentiation

1. Acute Poliomyelitis: This disease is more common in children, with muscle paralysis often being segmental, asymmetrical, and without sensory impairment. Muscle atrophy is pronounced, and both cerebrospinal fluid protein and common bletilla tuber cells are increased.
2. Acute Myelitis: This disease presents with significant pyramidal tract signs below the level of the lesion, conduction tract-type sensory impairment, and sphincter dysfunction. There is no cranial nerve damage, and the cerebrospinal fluid is normal or shows minor changes.
3. Periodic Paralysis: This disease has a history of recurrent episodes, with reduced blood potassium, hypokalemic ECG changes, no cranial nerve damage, no sensory impairment, and normal cerebrospinal fluid. Potassium supplementation therapy can lead to rapid recovery.
4. Generalized Myasthenia Gravis: This disease has a slow onset, fluctuating symptoms, no sensory impairment, and normal cerebrospinal fluid. The neostigmine test results in rapid improvement in muscle strength.