Sensory Deficit

Partial or complete absence of different sensory modalities predisposes individuals with spina bifida

SEGMENTAL INNERVATION

Figure 9.1 Musculoskeletal, sensory, and sphincter dysfunction by segmental level.

to skin injuries because of decreased ability to per­ceive pressure, pain, trauma, or heat (23,24,25,27). Skin breakdown tends to occur over areas of prom­inence and weight bearing. The lower back, inter- gluteal, perineum, feet, heels, and toes are the sites of predilection, but any area with sensory loss may be affected. Scoliotic and kyphotic prominences are areas prone to breakdown (26). Pressure ulcers often heal slowly, tend to get infected, and often recur. A pressure ulcer may be a symptom of a tethered cord. Long-standing ulceration with deep tissue necro­sis may spread to bone and lead to acute or chronic osteomyelitis.

Other complications of denervation include vaso­motor instability, neuropathic Charcot joints, and oste­oporosis in individuals with extensive lower extremity weakness (25,26,27,28).

The spinal cord defect usually results in a lower motor neuron process. Spasticity is present in most individuals with spina bifida across their lifetime (29). The presence or gradual development of spasticity above the level of the spinal cord lesion may be related to teth­ering of the spinal cord, Chiari type II malformation exerting pressure on the cervical spinal cord, decompen­sating hydrocephalus, ventriculitis, syringohydromyelia, or coexistent encephalopathy sustained at birth (30-33).