Guillain-Barre syndrome, also known as acute inflammatory demyelinating polyneuropathy, is considered to be related to autoimmune mechanisms. For the precursors of Guillain-Barre syndrome, the patient may have symptoms of gastrointestinal or respiratory infection 1-4 weeks before the onset of the disease, and some patients are clinically vaccinated, and after 1-4 weeks the patient may develop Guillain-Barre syndrome. Patients may first develop symmetrical paralysis of the limbs, mostly starting in the lower extremities, gradually progressing proximally as the disease progresses, reaching a peak in about two weeks. If the disease is critical, the patient may develop quadriplegia or respiratory muscle paralysis. Clinically, some patients with Guillain-Barre syndrome have sensory disturbances as a precursor, complaining of abnormal sensations in the limbs such as burning, numbness, tingling, etc. There is also the phenomenon of glove and garter-like distribution. In some patients, the precursor of Grin-Barre syndrome is the development of bilateral facial palsy, which requires a neurological consultation for treatment such as propecia.