The diagnosis of symmetrical lower motor neuron paresis in the extremities is based on clinical manifestations. Depending on the most severely damaged neurological site, clinical symptoms also vary according to the lesion site, and the specific subtypes are as follows: 1. Amyotrophic lateral sclerosis (ALS): the most common. The age of onset is 40-50 years old, with more men than women. The onset of the disease is insidious and progresses slowly. Clinical symptoms often begin in the distal upper limbs, manifesting as muscle atrophy and weakness in the hands, gradually developing in the forearm, upper arm and scapular girdle, with significant muscle bundle tremors in the atrophied muscles, at which time the lower limbs show upper motor neuron paresis, manifesting as increased muscle tone, hyperactive tendon reflexes, and positive pathological signs. The symptoms usually progress from one side to the other. The damage is essentially symmetric. With disease progression, symptoms of neuromotor nucleus damage in the medulla oblongata and pontine pathways, atrophy and fibrillation of the lingual muscles, dysphagia and slurred speech may gradually appear, affecting head raising and respiratory muscles in advanced stages.The main clinical features of ALS: simultaneous damage to upper and lower motor neurons. 2. Progressive medullary paralysis: The lesion is limited to the anterior horn cells of the spinal cord and does not affect the upper motor neurons. This type can be classified according to the age of onset and location of the lesion: (1) Adult type (distal type): It occurs mostly in middle-aged men, starting from the distal part of the upper limb and progressing from the hand to the proximal part, with obvious muscle atrophy and muscle weakness, reduced tendon reflexes, and muscle bundle tremors, which can progress to the lower limb or cervical muscles, causing respiratory paralysis. Very rarely, it can develop from distal to proximal. (2) Juvenile type (proximal type): Most of the disease starts in adolescence or childhood, with a family history of autosomal recessive or dominant inheritance. Clinical weakness and muscle atrophy of the pelvic girdle and proximal muscles of the lower extremities, unstable gait when walking, anterior convexity of the abdomen when standing, and then weakness and muscle atrophy of the scapular girdle and proximal muscles of the upper extremities, with manifestations of anterior horn stimulation (muscle bundle tremor), and difficulty getting up in the supine position. (3) Infantile type: It is an autosomal recessive disorder with onset in the mother or within one year after birth. Clinical manifestations include muscle weakness and atrophy of the extremities and trunk. Thus, fetuses with maternal onset are those with markedly reduced or absent fetal movements, and those with postnatal onset have a weak cry, marked cyanosis, generalized flaccid muscle weakness and muscle atrophy. The atrophy begins in the pelvic girdle and proximal lower extremities and progresses to the scapular girdle, cervical collar, and distal extremities. Muscles innervated by the cranial nerves are also highly susceptible to damage. However, muscle bundle tremors are rarely seen clinically. Intellectual, sensory and vegetative functions are relatively intact. (4) Progressive myasthenia gravis: Most of the disease develops after 40 years of age, and symptoms of damage to the medulla oblongata appear in the early stage of the lesion, and patients may have atrophy and fibrillation of the tongue muscles, difficulty in swallowing, choking on water and slurred speech. Later, due to damage to the pontine and cortical brainstem tracts, pseudo-medullary palsy can be combined, such as hyperactive tendon reflexes and positive pathological reflexes on the side of the invading corticospinal tract. (5) Primary lateral sclerosis: middle-aged males have a higher incidence of the disease, with slowly progressive upper limb motor neuron paresis, muscle weakness, increased muscle tone, hyperactive tendon reflexes and positive pathological signs. There is usually little muscle atrophy, and sensory and vegetative functions are not affected. It can invade the cortical medullary tracts of the brainstem and manifest as pseudo-medullary paralysis. Clinical manifestations are slowly progressive tonic muscle weakness, in primary lateral sclerosis in the distal parts of the limbs, and in progressive pseudomyeloparesis predominantly weakness of muscles innervated by the posterior group of cranial nerves. Muscle fasciculations and muscle atrophy may occur many years later. These disorders usually progress for several years before causing a total loss of mobility in the patient.