In China, amyotrophic lateral sclerosis and motor neuron disease are generally confused and usually divided into four clinical subtypes, including amyotrophic lateral sclerosis (ALS), progressive bulbar palsy (PBP), progressive muscular atrophy (PMA) and primary lateral sclerosis (PLP). However, studies have demonstrated that some patients present with clinical diagnostic criteria for ALS that are difficult to generalize with these four subtypes. Recent studies have focused on eight clinical phenotypes of ALS according to the World Federation of Neurology El Escorial, which differ in age of onset, delay in diagnosis, rate of combined frontotemporal dementia, survival, and 3-, 5-, and 10-year survival rates. These eight phenotypes are established on the basis of the clinical presentation at the time of diagnosis, but are constantly revised during follow-up by collecting all available information from patients. 1, Classical (Charcot) ALS (C-ALS): characteristic symptoms or signs in the upper or lower extremities, with clear but not prominent cone fasciculation signs. 2. Medullary ALS (B-ALS): These patients have medullary onset with dysarthria and/or dysphagia, tongue atrophy, and tremor of the muscle bundles. There are no symptoms of peripheral spinal cord damage during the first 6 months after onset. The cone bundle signs may not be evident in the first 6 months, but should be evident thereafter. 3. Fetlock-arm syndrome (FA-ALS): Patients with this type are characterized by a gradual progression, mainly with proximal weakness and atrophy of the upper extremities. This type includes pathological deep tendon reflexes or Hoffman’s sign in the patient’s upper extremity at some point in the course of the disease, but without increased muscle tone or clonus. The affected function limited to the upper extremity is present for at least 12 months after the onset of symptoms. 4.Lench Leg Syndrome (FL-ALS): Patients are characterized by progressive, distal weakness and atrophy of the lower extremities. This type includes pathological deep tendon reflexes or Babinski’s sign in the patient’s lower extremity at some point in the course of the disease, but without increased muscle tone or clonus. Atrophy and weakness of the patient’s proximal lower extremities starting without distal involvement are classified as classic ALS. 5. Pyramidal ALS (P-ALS): The clinical manifestations of these patients are mainly pyramidal signs, which are mainly severe spastic paraplegia/quadriplegia with one or more signs: Babinski’s or Hoffmann’s sign, hyperactive tendon reflexes, paroxysmal jaw twitching, dysarthria and pseudobulbar palsy. Spastic paralysis can be present at the early onset or late in the disease. These patients may show signs of significant lower motor neuron damage such as muscle weakness and atrophy in at least two different areas at the onset, and chronic and active denervated damage on EMG. 6. Respiratory ALS (R-ALS): These patients present with diffuse respiratory impairment at onset, as resting or telangiectatic breathing or dyspnea on exertion, with only mild spinal or medullary signs after the sixth month of onset. These patients may show manifestations of upper motor neuron involvement. 7. Pure lower motor neuron syndrome (PLMND): These patients have clinical and electrophysiological evidence of progressive LMN involvement. This type excludes: (1) those with motor conduction block by standardized segmental conduction studies; (2) those with clinical signs of UMN; (3) those with a history of motor neuron-like disease syndrome; (4) those with a family history of spinal muscular atrophy; (5) those with deletion of the SMN1 gene; (6) those with inherited medullary spinal muscular atrophy extended by androgen receptor gene duplication abnormalities in CAG patients; (7) those with neuroimaging (7) Neuroimaging studies except for structural damage. 8. Pure upper motor neuron syndrome (PUMN): clinical signs of upper motor neuron damage in these patients include severe spastic paraplegia/quadriplegia, Babinski’s or Hoffmann’s signs, extremely active reflexes, clonic jaw twitching, dysarthria and pseudobulbar palsy. Excluded from this category were: (1) patients with clinical or electromyographic signs of lower motor neuron involvement according to the Escorial criteria during follow-up; (2) patients with a history of motor neuron-like disease syndrome; (3) patients with a family history of spastic paraplegia/quadriplegia; and (4) patients with genetic spastic paraplegia associated with genetic mutations.