Hereditary spastic paraplegia: The disease is autosomal dominant and rarely recessive. Etiology and pathogenesis: Several mutations have been identified so far, and uncomplicated autosomal dominant variants are associated with chromosomes 2p, 8q, 14q and 15q, with the 2p variant being the most common and often combined with dementia. Autosomal recessive variants are associated with 8p, 15q and 16q, with 15q being the most common and recessive inheritance revealing uncommon corpus callosum thinning. Clinical manifestations: 1. The disease can develop at any age, but it is common in the group before 35 years of age and has a long course, manifesting as progressive spastic weakness of the legs and gradually increasing difficulty in walking, tendon reflex hyperactivity and pathological signs; in the group between 40 and 60 years of age, it often manifests as sensory loss, urinary disorder and motor tremor, etc. In simple cases, sensory and other neurological functions are completely normal. 2, the disease is mostly in childhood onset, bowed feet and foot shortening, calf muscle shortening (pseudospasticity), patients are forced to walk on their toes, need to perform orthopedic surgery. Children present with hypoplasia of the lower extremities, and lower extremity atrophy appears in children and adults. Sometimes the knee is mildly flexed, and the knee may be hyperextended and adducted. Muscle weakness is highly variable and difficult to assess, with preserved anal sphincter function. Fine sensory deficits in the feet have been reported, and the upper arms may be involved, with tendon reflexes in the upper arms present in some patients but with muscle atrophy; some cases have stiff hands with limited mobility, and there may be mild dysarthria, nystagmus, oculomotor palsy, optic nerve atrophy, pigmented punctate degeneration, ataxia (both cerebellar and sensory), sensorimotor polyneuropathy, ichthyosis, skin pigmentation, epilepsy, and dementia, respectively found in different families.