Spastic diplegia is one of the main types of cerebral palsy, manifested by spasticity of both lower extremities with slight involvement or incoordination of both upper extremities, and is commonly seen in premature infants with cerebral white matter injury. Sometimes it needs to be differentiated from hereditary spastic paraplegia. Hereditary Spastic Paraplegia (HSP) was first described by Strumpell in 1883 and further elaborated by Lorrain. The disease may be X-linked, autosomal dominant or recessive. The main lesion is terminal degeneration of the corticospinal tracts in the spinal cord, with fibers innervating the lower extremities being much more heavily involved than those innervating the upper body, although patients often have varying degrees of upper extremity fiber involvement, but are usually asymptomatic. Common features: progressive, severe bilateral lower limb spasticity. Clinical features: HSP, also known as familial spastic paraplegia or Strumpell-Lorrain syndrome, is not a single disorder but a group of disorders with different clinical and genetic mechanisms, with the common feature of progressive, usually severe lower limb weakness and spasticity. Autosomal dominant simplex HSP, normal gestational weeks, delivery and early development are followed by progressive lower limb stiffness and gait abnormalities (waddling, stumbling), caused by weak hip flexion and difficulty with dorsal foot flexion. Classification: HSP is usually divided into simple and complex types. The onset of simple HSP is seen at any age, from infancy to old age, with most onset in the late teens to early thirties. It often presents with progressive lower extremity weakness, bladder sphincter dysfunction, and sometimes abnormal sensation in the feet. Complex HSP has other symptoms: peripheral neuropathy, epilepsy, ataxia, optic neuropathy, retinopathy, dementia, ichthyosis, mental retardation, deafness, speech, swallowing and breathing problems, and other clinical rarities. Some symptoms may be caused by other independent disorders not directly related to HSP. Patients are simplex with one or more other disorders. Examples include peripheral neuropathy caused by diabetes mellitus or unrelated epilepsy. HSP can also be classified by clinical type, (X-linked, often dominant, often recessive) and each type is subdivided into different subtypes by genetic loci, with widely varying clinical symptoms and genetic type not predictive of severity. In the past, HSP was classified as type I or type II based on age of onset and spasticity specific weakness value, and this classification is no longer used because both types can occur within a family. To date, only a few genes have been localized, and at least seven simplex types are known to be dominantly inherited. There are at least 3 recessive inheritors and 2-3 X-linked inheritors. Classical symptoms: progressive walking difficulties, with some patients eventually requiring a wheelchair and some patients not requiring any assistive device. Patients have difficulty lifting their toes, resulting in toe dragging, especially when walking up stairs and on uneven surfaces; later, weakness in flexion of the femoral muscles, inability to lift the leg when walking, there may be decreased balance perception, increased muscle tone, some patients have decreased sensation in the distal lower extremities, urinary problems, (e.g., incontinence, urinary urgency), and hyperreflexia, many of which are due to muscle spasm, weakness, and hyperreflexia, rather than direct symptoms of HSP. Other defects, such as visual impairment, muscle wasting, muscle tremors, dementia, epilepsy, and peripheral neuropathy are not clinical symptoms of simplex patients, but should be thoroughly examined for comorbidities. Some families with often inherited simplex HSP present with progressive spastic paraplegia in childhood (before 6 years of age), with little or no progression of symptoms after adolescence. These patients usually do not have bladder dysfunction and can usually maintain the ability to walk but require assistance. Treatment: Currently, no specific treatment is available to prevent, delay, or reverse progressive functional disability in patients with HSP. The goal of pharmacologic treatment is to reduce disability and prevent complications. Regular PT therapy is extremely important to maintain and improve ROM and muscle strength and maintain aerobic fitness conditions of the cardiovascular system, but does not stop progression. Patients must undergo exercise therapy several times a week under the guidance of a PT instructor to reduce muscle wasting atrophy, improve endurance, reduce fatigue, prevent spasticity and cramping, improve and maintain ROM and muscle strength, and reduce tension and have a psychotherapeutic effect. The following PT programs are available: plyometric training, which improves the strength of undamaged muscles and compensates for the muscle strength of weak muscles, and at the same time, slows down muscle atrophy especially in the calf muscles and relieves back pain; stretching training to maintain or improve ROM and reduce complications such as tendonitis, bursitis and cramps; aerobic training to improve cardiovascular adaptations, reduce fatigue and improve endurance. Walking, cycling, swimming and water aerobics are the best choices.