GBS is an acute, usually rapidly progressive form of inflammatory polyneuropathy of unknown etiology, but may be due to autoantibodies attacking the peripheral nerve myelin sheaths, resulting in acute episodic paralysis and disturbance of neurological conduction. Although it is possible for affected patients to recover on their own, about 75% of patients will suffer from persistent neurological disorders and about 5% will die from the corresponding complications. Signs and symptoms: It usually starts with a fairly symmetrical muscle weakness with sensory abnormalities in both lower extremities and then extends to the upper extremities. 90% of cases reach their peak within 3 weeks. Muscle weakness is always more pronounced than sensory symptoms or signs, and may be most severe in the proximal extremities. Tendon reflexes are absent. Sphincter function is usually preserved. In more severe cases, more than 50% of patients have weakness of the facial and oropharyngeal muscles, and in 5-10% of cases, tracheal intubation is required due to respiratory failure. In severe cases, autonomic dysfunction (including fluctuations in blood pressure), inappropriate secretion of antidiuretic hormone, cardiac arrhythmias, and pupillary changes may occur. Respiratory paralysis and autonomic dysfunction can be life-threatening. Death occurs in about 5% of cases. Diagnostic criteria: 1. Progressive limb weakness, basically symmetrical, or rarely asymmetrical. In mild cases, the lower limbs are weak, and in severe cases, the limbs are paralyzed, including trunk paralysis, ball palsy, facial muscle and even extraocular muscle paralysis, and the most serious one is respiratory muscle paralysis. 2.Tendon reflexes are weakened or disappeared, especially the distal end often disappears. 3, the onset of the disease is rapid, the disease is progressive aggravation, often in a few days to 1-2 weeks to peak, to 4 weeks to stop the development, stable into the recovery period. 4, more complaints of sensory impairment, objective examination is relatively light, may present glove, sock-like sensory abnormalities or no obvious sensory impairment, a few have sensory hypersensitivity, nerve trunk pressure pain. 5, cranial nerve to the linguopharynx, vagus, sublingual nerve involvement is common, other cranial nerves can also be damaged, but the optic and auditory nerves are almost not involved. 6.It may be combined with vegetative nerve dysfunction, such as tachycardia, hypertension, hypotension, vasomotor disorders, sweating, and momentary difficulty in urination. 7.About half of them have respiratory tract, intestinal infection, unexplained fever, chickenpox, herpes zoster, mumps, mycoplasma, malaria, rain, cold, fatigue, trauma, surgery, etc. 1-6 weeks before the disease. 8, 2-4 weeks after the disease into the recovery period, but can also be delayed to several months to start recovery. 9, cerebrospinal fluid examination: WBL <10×106/L, 1-2 weeks, protein may be elevated, showing protein-cell separation (if the cells exceed 10×106/L, predominantly multinucleated, other diseases need to be excluded), cytological classification is mainly lymphomonocytes, but also a large number of phagocytes may appear. 10, electrophysiological examination: after the disease may appear significantly slowed nerve conduction velocity, F wave reflects the proximal nerve trunk conduction slowed. Clinical typing: 1. Light: muscle strength of the extremities is grade III or higher, and the patient can walk independently. 2.Medium: the muscle strength of the limbs is below grade III and cannot walk. 3.Heavy: IX, X and other cranial nerve paralysis, inability to swallow, along with weakness to paralysis of the limbs, mild respiratory distress with activity, but no tracheotomy and artificial respiration are required. 4.Extremely heavy: In a few hours to 2 days, it develops into quadriplegia, swallowing inability, respiratory muscle paralysis, must be immediately tracheotomy, artificial respiration, with severe cardiovascular dysfunction or explosive type also merged into this type. 5, re-occurrence: several months (4-6 months) to more than 10 years can have multiple re-occurrence, light and heavy as the above symptoms, should pay extra attention. Often heavier than the first, can be from light to very heavy symptoms. 6, chronic type or chronic inflammatory demyelinating polyneuropathy: from 2 months to months or even years of slow onset, persistent, with little cranial nerve damage, significant muscle atrophy of the extremities, and persistent increase in cerebrospinal fluid protein. 7. Variants: pure motor GBS; sensory GBS; multicranial nerve GBS; pure total vegetative neurological insufficiency GBS, and Fisher syndrome, a few GBS with transient pyramidal fasciculations and GBS with cerebellar ataxia, etc.