Intervertebral disc herniation: Pathophysiology and emerging therapies

Approximately 2.6 % of the US population visits a physician for treatment of spinal disorders annually (Fraser 2009) with costs of $7.1 billion from lost work days alone (Ricci et al. 2006). Herniation of the intervertebral disc is one of the several spinal disorders that contribute to this very high incidence, with potential to cause significant pain, neurological deficit, and functional disability in affected individuals. Herniation presents as a protrusion or extrusion of discal tissue into the epidural cavity, resulting in nerve root impingement and disc tissue exposure (Fig. 19.1). Both mechanical compression and tissue exposure contribute to pain and disability associated with intervertebral disc herniation (Goupille et al. 1998; Mixter et al. 1934; Olmarker and Rydevik 1991). In areas innervated by the affected nerves, it is commonly seen as low back pain, radiating leg pain (i.e., radiculopathy or sciatica), muscle weakness, gait abnormality, muscle atrophy, asymmetric reflexes, or loss of function (Atlas et al. 2005; Frymoyer 1988; Hart et al. 1995). The incidence of sciatica related to intervertebral disc herniation peaks between the fourth and fifth decades of life and is most frequently associated with herniations between the L3 and S1 vertebral levels (Atlas et al. 2005; Awad and Moskovich 2006). The severity of herniation symptoms in the cervical or lumbar regions has been shown to relate to the size or nature of the herniated fragment, whether it is simply protruding into the neural cavity, extruded, or completely sequestered from the parent structure.