Guillain-Barre syndrome (GBS) is a neurological autoimmune disease with predominant nerve root and peripheral nerve damage, accompanied by protein-cell separation in the cerebrospinal fluid, and is one of the most common demyelinating diseases of the spinal and peripheral nerves. The clinical manifestations are progressive ascending symmetrical paralysis, limb flaccidity, and varying degrees of sensory impairment, with acute or subacute clinical onset, most of which can lead to complete recovery, while a few severe cases can cause fatal respiratory paralysis and bilateral facial paralysis, mostly occurring in young and middle-aged men. The disease can occur in all seasons, but is more common in summer and autumn. The etiology of GBS is still not well understood, and autoimmune abnormalities may play a major role in the pathogenesis of GBS. It is generally believed that the precursors are the following: (1) viral infection; (2) bacterial infection; (3) vaccination, which may be related to the activation of immune function in patients after vaccination; (4) genetic factors; (5) nutritional status; (6) tumor: some tumor patients are usually accompanied by GBS disease, which may be related to the activation of the patient’s autoimmune function because the tumor antigen is an autoantigen. There are two types of GBS according to the pathological characteristics, one is demyelinating lesion type of polyneuritis and the other is neuronal axonal lesion type of polyneuritis. More than half of the patients with demyelinating lesion polyneuritis have a history of infection for several days to weeks before the onset of the disease. It begins with weakness of both lower extremities, followed by a gradual increase in paralysis and subjective sensory abnormalities, and in severe cases, life-threatening tetraplegia and respiratory paralysis. Axonal lesions are similar to and different from demyelinating lesions. The axonal lesion type of polyradiculitis has a slow and recurrent course with symptoms of muscle weakness and sensory disturbances. Weakness in the shoulders, upper arms, and thighs may be combined with weakness in the forearms, lower legs, hands, and feet, and limb weakness is often more common than trunk weakness. The clinical manifestations can be rapid progression and deterioration. Five major manifestations: (1) Motor impairment: muscle palsy of the limbs and trunk is the most important symptom of the disease. It usually starts from the lower extremities and gradually spreads to the trunk muscles, both upper extremities and cranial nerves, and can go from one side to the other. The disease usually progresses to its peak within 1 to 2 weeks. The paralysis is usually more proximal than distal, with hypotonia. If respiration, swallowing and pronunciation are involved, it can cause life-threatening paralysis of autonomic respiration, difficulty in swallowing and pronunciation. (2) Sensory impairment: generally mild, mostly starting from numbness and pins and needles sensation at the end of the limbs. There may also be garter-like sensory loss, loss of sensation or hypersensitivity, and spontaneous pain, with pressure pain evident in the gastrocnemius and anterior wall muscle angles. Occasionally, segmental or conduction bundle sensory deficits are seen. (3) Reflex disorders: tendon reflexes of the extremities are mostly symmetrically diminished or disappeared, and abdominal wall and raphe reflexes are mostly normal. A few patients may develop pathological reflex signs due to vertebral fasciculus involvement. (4) Plant nerve dysfunction: there is often excessive sweating and strong sweat odor in the initial or recovery period, which may be the result of sympathetic nerve stimulation. A few patients may have short-term urinary retention at the initial stage, which can be caused by temporary dysfunction of the vegetative nerves innervating the bladder or damage to the spinal nerves innervating the external dilator muscles; stools are often constipated; some patients may have unstable blood pressure, tachycardia and abnormal electrocardiogram, etc. (5) Cranial nerve symptoms: Half of the patients have cranial nerve damage, with peripheral paralysis of the tongue, pharynx, vagus nerve and one or both facial nerves being the most common. This is followed by motoneuria, talipes, and abducens nerves. Occasionally, edema of the optic nerve papillae may be due to inflammatory changes in the optic nerve itself or cerebral edema, or it may be related to a significant increase in cerebrospinal fluid protein, which blocks the arachnoid villi and affects cerebrospinal fluid absorption. Clinical treatment As the pathogenesis of GBS is still being studied in depth, the following treatment options are currently available for the different stages of the disease. (1) plasma exchange (2) intravenous immunoglobulin infusion: it can inhibit the immune response of leukocytes and the production of inflammatory cytokines, and studies have confirmed that intravenous immunoglobulin is an effective treatment for GBS and has therefore become the standard of care for severe GBS; (3) hormone therapy: glucocorticoids reduce the immune system by strongly suppressing the immune system. (3) Hormone therapy: Glucocorticoids reduce inflammation by strongly inhibiting the immune system, and can also act on cell membranes to promote the stability of membrane structure, reduce the degree of demyelination, and improve nerve conduction function. (4) Immunosuppressive therapy: In recent years, some scholars have adopted immunosuppressive therapy for GBS, but immunosuppression usually brings adverse effects such as bone marrow suppression and liver function impairment. Symptomatic treatment Greenbrier syndrome seriously endangers the health of patients’ lives and disturbs their families. Since respiratory muscle paralysis is the main risk of GBS, 25% of patients with Guillain-Barre syndrome require adjuvant ventilation support. Rehabilitation: Many patients with Guillain-Barre syndrome have residual symptoms. For example, weakness or muscle atrophy in both lower or upper extremities, muscle aches and pains, and foot drop. Some patients with Guillain-Barre syndrome have facial palsy, swallowing difficulties, dysarthria, choking and coughing. In some patients, vegetative dysfunction can be seen as little or excessive sweating of the hands and feet, dry skin on the extremities, or retention or incontinence of urine and stool. This has a great impact on the patient’s life. Rehabilitation training exercises the patient’s muscle tissue and maintains the mobility of the joints, which cannot rebuild the patient’s nerve pathways. Nourishing nerves and promoting nerve repair is the root of treatment Greenbrier syndrome is an acute onset disease with nerve root and peripheral nerve damage. Traditional treatment of Guillain-Barre syndrome is unable to restore the diseased nerves, so it tends to leave behind muscle weakness or paralysis, and does not lead to complete recovery. Since this disease often has an acute onset, early control to avoid the formation of chronic demyelinating neuropathy is very important. The pathological mechanism of this disease is demyelinating lesions of nerves, involving both distal and proximal nerves, upper and lower limbs; the distal end is more damaged than the proximal end, and motor nerves are more susceptible than sensory nerves, mostly manifesting as paralysis of skeletal muscles. Therefore, nourishing the nerves and promoting nerve repair is the fundamental way to treat this disease in order to achieve the recovery of motor function. Unfortunately, the current treatment for neuroprotection, nerve nutrition and nerve repair is not in place to restore the diseased nerves in a timely manner, and therefore cannot treat the root cause of Grinbarr’s syndrome. The principle of nerve repair technology for the treatment of Grinbarr’s syndrome is that through certain neurotrophic drugs, the repair of neurological damage, especially the repair of myelin sheath, is involved, so that the structure of damaged nerve tissue is reconstructed and the corresponding physiological function is restored, so the effect of nourishing nerves and promoting nerve repair in the clinical treatment of Grinbarr’s syndrome is clear and ideal. Nourishing and repairing nerves is the key to the regression of this disease.