1, the onset of disease around the age of 50, before the age of 20 years after the age of 70 years is rare, more men than women. 2.Subconscious onset, most of them progress slowly, very few progress sharply. The first symptom is muscle weakness and muscle atrophy in the distal upper limb, followed by bulbar palsy, muscle bundle tremor, cone bundle sign, and a few sensory abnormalities such as numbness/pain/chill in the limb. The distal upper extremity is the preferred site of onset, followed by the medullary innervated muscles. The main clinical symptoms are limb weakness, limb and lingual muscle atrophy, pyramidal fasciculus signs, and limb and lingual muscle fasciculus tremors. The motor nucleus of the linguopharyngeal/vagus nerve is most frequently involved, and damage to the motor nucleus of the hypoglossal, paramedian, and facial nerves is also seen, with rare damage to the remaining cranial nerves. The form of onset is: one upper limb → contralateral upper limb → lower limb → ball palsy symptoms, ball palsy symptoms (ball palsy type) → extremity or lower limb → upper limb. 4, EMG shows neurogenic changes. ALS patients with simultaneous loss of upper and lower motor neuron involvement may show progressive muscle atrophy and weakness in different areas, which may be accompanied by muscle jumping. patients with ball involvement have dysphagia and dysarthria, and often die clinically due to respiratory muscle involvement or intrapulmonary infection leading to respiratory failure. In the past, it was thought that ALS only damaged motor neurons and did not affect other neurological functions such as sensory functions, but in recent years, it has been found that very few ALS patients also have abnormal sensory functions, and many clinical observations have revealed that ALS patients may also have symptoms of autonomic nervous system, extrapyramidal system and cognitive-behavioral dysfunction, which suggests that ALS may be a neurodegenerative disease with multi-system involvement. Even in early ALS, there may be many subclinical autonomic nervous system impairments, including cardiovascular, gastrointestinal, and glandular secretion dysfunctions. And in ventilator-dependent patients, autonomic abnormalities may lead to circulatory collapse or sudden death.