Spina bifida is associated with varying degrees of neurologic and musculoskeletal impairment and ranges from complete paralysis and/or paresthesia to minimal or no impairment. The anatomic level of the lesion generally correlates with the motor and sensory deficit. Although the occult dysraphic state may go undetected in early childhood, as the spinal cord ascends to its normal position in life (L1-L2), patients may later present with foot deformities, gait disturbances, scoliosis, and sphincter dysfunction. The failure of the spinal cord to ascend secondary either to primary malformation or to secondary tumor is known as tethering of the cord. Foot deformities make the foot more vulnerable to ulceration via bony deformities and altered foot biomechanics.
Bony deformities alter the natural protective fat pads located on the plantar surface of the foot, which normally protect the foot by distributing weight-bearing forces evenly over a large area. Excessive focal pressure developed during the midstance and heel-rise parts of the gait cycle may cause skin loss or hypertrophy of the stratum corneum (callus) over bony prominences. These changes in the foot increase the possibility of ulceration by two orders of magnitude. Shearing, pressure, and frictional forces also all play a role in the breakdown of the cutaneous barrier, since they are concentrated over the abnormal bony prominences. The risk of ulceration is proportional to the number of risk factors and is increased by 1.7 in persons with peripheral neuropathy, by 12 in patients with peripheral neuropathy and foot deformity, and by 36 in those who have peripheral neuropathy, foot deformity, and previous amputation, as compared with those without risk factors.