The earliest description of cerebral palsy (CP) was made by William J. Little in the mid-1800s. In a series of lectures, entitled 'Deformities of the human frame' , Little included a description of cerebral paralysis. Although his main focus emphasised musculoskeletal complications, such as joint contractures and deformities as a result of chronic spasticity and paralysis, he specifically noted that the spasticity and paralysis was as a result of brain damage during infancy which resulted from preterm birth or perinatal asphyxia. [1] CP was therefore initially referred to as Little's disease. [2] William Osler (1889) and Sigmund Freud (1893) both further contributed to the field of CP. [3,4] In his article 'Cerebral Palsies of Children' Osler documented 151 cases which he classified as 'cerebral palsies' based on neuroanatomical pathology distribution into three main groups: infantile hemiplegia, bilateral spastic hemiplegia (i.e. spastic diplegia) and spastic paraplegia. [3] Freud had contrasting ideas to both Little's and Osler's work, and suggested classifying CP using clinical findings only. He recognised that the pathological findings resulted from both the initial lesion as well as the repair process and, in addition, he noted differences in clinical manifestations in patients with similar neuropathology. Freud further suggested that rather than perinatal asphyxia being the cause of CP, the aetiology of the brain damage present in CP could be multifactorial. He identified three major groups of causal factors: (i) maternal and idiopathic congenital; (ii) perinatal; and (iii) postnatal factors. [4] It is worth noting that Freud's ideas and work still form part of our modern-day definition of CP. [2] The primary condition of CP is non-progressive over time in the neurological sense. [2] However, secondary conditions of CP develop over time as a result of the primary conditions. [5] Manifestations can be grouped into primary and secondary manifestations. Primary manifestations include abnormal tone, loss of motor control, impaired balance, spasticity, hypotonia and dyskinesia. Secondary manifestations are growth and spasticity related and include contractures (initially dynamic and progress to static over time), upper extremity deformities, hip subluxations and dislocations, foot deformities, gait disorders and fractures, and spinal deformities. [6] Spinal deformities are more commonly seen in people with CP and range from a scoliosis to increased thoracic kyphosis, increased lumbar lordosis, spondylolysis and spondylolisthesis. [7] The preferred method of measuring a spinal curvature, is with an X-ray in standing position (if possible). The curvature is described in relation to the body's anatomical planes: coronal (frontal), sagittal (lateral) and horizontal (axial or transverse). [8] The most common spinal abnormalities are a scoliosis, a hyperkyphosis, a hyperlordosis and a spondylolysis and/or spondylolisthesis. Objectives To provide a scientific overview of how spinal curvatures should be measured, what t...