Guillain-Barre syndrome (GBS), also known as acute infectious polyneuritis, is an autoimmune disease characterized pathologically by demyelination of peripheral nerves and nerve roots and an inflammatory response of perivascular lymphocytes and macrophages in small vessels. The disease is a syndrome with acute onset and is characterized by nerve root and peripheral nerve damage with protein-cell separation in the cerebrospinal fluid. It is also known as Guillain-Barre syndrome. It can occur at any age and in both sexes, but is more common in young adults. The etiology and pathogenesis have not been fully elucidated yet, but it is generally believed to be a delayed allergic immune disease caused by a history of nonspecific infections and vaccinations before the onset of the disease, and the main lesion is extensive inflammatory segmental demyelination of peripheral nerves. The clinical symptoms are a history of upper respiratory or gastrointestinal tract infection or vaccination 1-4 weeks prior to the onset of the disease. The disease can develop in all seasons, with a prevalence in summer and autumn. The clinical features of the disease are the sudden onset of severe nerve root pain (mostly in the neck, shoulder, waist and lower extremities), acute progressive symmetrical limb weakness, subjective sensory impairment, and weakened or absent tendon reflexes 1 to 3 weeks after the onset of infectious disease. The specific manifestations are: 1. Movement disorders: limb and trunk muscle palsy is the main symptom of this disease. It usually starts from the lower limbs and gradually spreads to the trunk muscles, both upper limbs 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, swallowing and pronunciation difficulties. 2. Sensory impairment: generally mild, mostly starting from numbness and pins and needles sensation at the ends of the limbs. There may also be garter-like sensory loss, disappearance or hypersensitivity, as well as spontaneous pain, with pressure pain evident in the gastrocnemius and anterior wall muscle angles. Occasionally, segmental or conduction bundle sensory disorders are seen. 3, firing 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 have pathological reflex signs due to vertebral bundle involvement. 4.Phytodysfunction: Initially or during the recovery period, there is often excessive sweating and strong sweat odor, 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 ECG, 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 more common. This is followed by the motoneurotic, talipes, and abducens nerves. Occasionally, edema of the optic nerve papillae is seen, which may be due to inflammatory changes in the optic nerve itself or cerebral edema, or may be related to a significant increase in cerebrospinal fluid proteins that block the arachnoid villi and affect cerebrospinal fluid absorption. Diagnosis of the disease is based on the sudden onset of symmetric sensory, motor and nutritional deficits in the distal extremities and loss of tendon reflexes following infectious disease. Exogenous ganglioside-associated Grinbaric syndrome Italian scholar Gianluca Landi et al. reported (BMJ 1993;307: 1463-4) 24 cases of Grinbaric syndrome after the use of gangliosides, suggesting that the use of exogenous gangliosides is closely related to the development of Grinbaric syndrome. The incidence of Greenbrier syndrome in general is about 1.6/100,000, but patients using exogenous gangliosides have a 200-fold increased chance of developing Greenbrier syndrome. Germany has banned the use of exogenous gangliosides nationwide because of six deaths from their use. Three cases of Grinbaric syndrome after explicit use of gangliosides have also been reported in China, all of which were cases of monosialic acid tetrahexose ganglioside use after craniocerebral injury. Wu et al. reported six cases of Grinbarr’s syndrome after trauma and surgery, four of which had used tetrahexose monosialate ganglioside before the onset. There may also be some cases of Grinbarr’s syndrome after the use of exogenous gangliosides that were not clearly diagnosed, or if clearly diagnosed, were not reported. The clinical manifestations are mainly peripheral paralysis of the extremities, with some cases developing rapidly and may be combined with peripheral paralysis of the cranial nerves, or even respiratory muscle weakness requiring ventilator-assisted respiration, but normal urinary and fecal functions; electromyography manifests peripheral nerve damage such as slowed nerve conduction velocity, delayed or absent F reflexes, etc. The EMG shows peripheral nerve damage, mainly motor nerve axonal damage, which can be combined with peripheral damage of sensory nerves; cerebrospinal fluid tests show the typical protein-cell separation phenomenon, i.e. normal cerebrospinal fluid cell count and elevated protein. The pathogenesis may be that exogenous gangliosides induce the production of anti-ganglioside antibodies in some patients, thus causing autoimmune demyelinating lesions. In contrast, acute inflammatory demyelinating polyneuropathy is caused by the misidentification of some components of the pathogen that are similar to some components of peripheral nerve myelin, and the body’s immune system produces autoimmune T cells and autoantibodies, and an immune response occurs against peripheral nerve tissue, causing autoimmune demyelination of peripheral nerves. The differentiation of the two is mainly based on the correlation between the onset and the use of drugs. As for blood GM1-IgM (anti-ganglioside antibodies), this antibody is also present in the serum of many patients with non-ganglioside-associated Grimballi syndrome, but the subtypes of anti-ganglioside antibodies differ in patients with different types of clinical manifestations of Grimballi syndrome. In clinical practice, the possibility of adverse drug reactions should be thought of in neurological and surgical diseases when muscle weakness of the extremity muscles, respiratory machines, and eye muscles suddenly appears after the use of this exogenous ganglioside drug. The main aspects of treatment of this adverse drug reaction are discontinuation of ganglioside drugs, use of immunoglobulin antagonism (0.4g/Kg body weight per day for 5 days, if the effect is not good, a course of treatment can be continued after 1~2 weeks), high dose hormones, neurotrophic drugs, supportive symptomatic, and rehabilitation, plasma exchange therapy requires certain technical equipment conditions not suitable for popularization. The prognosis is good in most cases, and some cases may be left with varying degrees of neurological dysfunction. Therefore, the clinical use of exogenous ganglioside drugs requires extra caution.