Congenital polyarticular contracture is a syndrome characterized by stiffness of multiple joints throughout the body due to fibrosis of muscles, joint capsules and ligaments. A review of the literature has found that congenital polyarticular contracture can be associated with cerebral white matter hypoplasia, anencephaly, intellectual deficits, pituitary ectopia, peripheral neuropathy, congenital ophthalmoplegia, congenital glaucoma, temporomandibular joint stiffness, small chin, cervical fusion, atlantoaxial subluxation, scoliosis, syndactyly, short finger, and tuberous sclerosis. The treatment of this disease faces many difficulties, as the affected joints require multiple surgeries, and the recurrence rate is high after surgery, requiring repeated surgeries. However, the IQ of the affected children is higher than that of ordinary children, and after effective treatment, they can achieve amazing self-care ability. Therefore, physicians and parents should have confidence. The goal of treatment is to increase the range of motion of the affected joints so that the child can walk independently or with assistance, and to improve the ability to manipulate the upper extremities and hands as much as possible. The natural history of congenital polyarticular contracture is relatively optimistic, with the most severe joint contracture at birth, and most children are treated satisfactorily with manipulative therapy in early infancy. Physical therapy should be started shortly after birth and parents should be properly instructed in home rehabilitation, including manual massage, joint stretching and passive activities, etc., and in the process, emotional communication between the child and parents should be improved, and treatment should be gentle to avoid injury. Treatment during the first 4 months of life is essential to improve joint mobility, maintain and enhance muscle growth, and reduce the chance and magnitude of surgery. The pathology can be divided into two completely different pathological changes: neurological and muscular. Among the pathological changes of the neurological type, the most important feature is the disappearance, degeneration or reduction in cell volume of the anterior horn cells of the bone marrow. There are also pathological changes such as thinning of the cervical and lumbar segments of the spinal cord and reduction in the number of anterior spinal nerve roots. In contrast, there are no abnormalities in the posterior or lateral horn of the spinal cord, or in the dorsal root ganglion cells. Brain damage includes cerebral hypoplasia, incomplete sulcus formation, enlarged lateral ventricles, and reduced cortical Betz cells. The severity of these neurological lesions determines the pathological changes in the innervated limb muscles. The limb muscles may be completely normal in volume, color and texture, or they may be reduced in size or even completely absent. Microscopically, the number of muscle fibers is low and the diameter of muscle fibers is reduced, but the transverse lines are mostly preserved. The articular cartilage may be completely normal initially, but in older children, articular cartilage destruction and degenerative changes occur. The joint capsule of the affected joint is also thickened by fibrosis. In the muscular form, there is no primary anterior horn lesion of the spinal cord and no abnormalities of the brain or neuromotor branches. The affected muscles are grayish in color and have a stiff, fibrous tissue-like texture. Microscopically, the affected muscles show fibrous and fatty degeneration, a disorganized distribution of coarse and fine muscle fibers, and an increase in the fibrous component of the endomysium. The pathological changes of the articular cartilage and joint capsule were similar to those of the neurological type.