Hereditary spastic paraplegia is a degenerative lesion of the nervous system and is divided into simple and complex types. The simple form is characterized by progressive spastic muscle weakness of the lower extremities, knee and ankle clonus, increased muscle tone and hyperactive tendon reflexes; the complex form may have abnormalities of the cerebral cortex, medulla, corpus callosum, nucleus basalis and cerebellum, resulting in abnormal intellectual development or dementia, extrapyramidal symptoms and optic nerve atrophy, and in some patients, bowed foot deformity. HSP has three modes of inheritance: autosomal dominant, recessive, and X-linked recessive, and some cases are disseminated. At least 19 autosomal dominant (AD-HSP) subtypes, 27 autosomal recessive (AR-HSP) subtypes, 5 X-linked subtypes and 1 maternally inherited subtype have been identified in HSP. About 20% of patients with AR-HSP carry the mutated KIAA1840SPG11 gene. Point mutations, small deletion mutations, splice site mutations and small insertion mutations in these genes cause genetic defects that result in clinical symptoms. Although there is no specific therapy to prevent, delay, or reverse HSP, symptomatic supportive therapy with cytidylcholine, coenzyme A, coenzyme Q10, ATP, baclofen, butylphthalide, and drugs such as levodopa, benzhexol (Antan), buspirone, and diazepam can lead to partial reduction of symptoms.