Together, these enclose the vertebral foramen, which contains the spinal cord. Because the spinal cord ends in the lumbar spine, and the sacrum and coccyx are fused, they do not contain a central foramen. The vertebral arch is formed by a pair of pedicles and a pair of laminae, and supports seven processes, four articular, two transverse, and one spinous, the latter also being known as the neural spine. Two transverse processes and one spinous process are posterior to (behind) the vertebral body. The spinous process comes out the back, one transverse process comes out the left, and one on the right. The spinous processes of the cervical and lumbar regions can be felt through the skin. Above and below each vertebra are joints called facet joints. These restrict the range of movement possible, and are joined by a thin portion of the neural arch called the pars interarticularis. In between each pair of vertebrae are two small holes called intervertebral foramina. The spinal nerves leave the spinal cord through these holes. Individual vertebrae are named according to their region and position. From top to bottom, the vertebrae are:

Cervical spine: 7 vertebrae (C1–C7)
Thoracic spine: 12 vertebrae (T1–T12)
Lumbar spine: 5 vertebrae (L1–L5)
Sacrum: 5 (fused) vertebrae (S1–S5)
Coccyx: 4 (3–5) (fused) vertebrae (Tailbone)The combined region of the thoracic and lumbar vertebrae is known as the thoracolumbar division, or region. Shape
The vertebral column is curved in several places, a result of human bipedal evolution.
Although it is unknown how changes in this enzymes function lead to the signs and symptoms of infantile neuroaxonal dystrophy, phospholipid metabolism problems have been seen in both this disorder and a related disorder called pantothenate kinase-associated neurodegeneration. These disorders, as well as the more common Alzheimer disease and Parkinson disease, also are associated with changes in brain iron metabolism. Researchers are studying the links between phospholipid defects, brain iron, and damage to nerve cells, but have not determined how the iron accumulation that occurs in some individuals with infantile neuroaxonal dystrophy may contribute to the features of this disorder.A few individuals with infantile neuroaxonal dystrophy have not been found to have mutations in the PLA2G6 gene. The genetic cause of the condition in these cases is unknown; there is evidence that at least one other gene may be involved.Mutations in the NAGA gene, resulting in alpha-N-acetylgalactosaminidase deficiency, cause an infantile neuroaxonal dystrophy known as Schindler disease. Diagnosis
In some cases, signs and symptoms of infantile neuroaxonal dystrophy first appear later in childhood or during the teenage years and progress more slowly. Children with infantile neuroaxonal dystrophy experience progressive difficulties with movement. Generally they have muscles that are at first weak and "floppy" (hypotonic), and then gradually become very stiff (spastic). Eventually, affected children lose the ability to move independently. Lack of muscle strength causes difficulty with feeding and breathing problems that can lead to frequent infections, such as pneumonia.