Radicular Pain

Radicular pain has been discerned as the pain perceived of as arising in a limb or
trunk which is caused by ectopic activation of nociceptive afferent fibers in a spinal
nerve or its roots or other neuropathic mecha- nisms . Radiculitis, rather incorrectly,
suggests the inflamma- tory process as being solely responsible for the causation of
radicular signs and symptoms. Thus, more accurately, radicular pain is a term
applied to describe pain that results from the stimulation of, or a disorder of, a nerve
root. The extension of the terms radicular pain and radiculitis is radiculopathy,
which implies that damage to the root has produced a clinically appli- cable motor
or sensory neurological deficit in the distribution of the nerve root. Consequently,
radiculopathy is a disorder in which conduction along a nerve root is blocked,
resulting in objective neurologic signs such as numbness or weakness, or in which
the blood supply to a nerve root is compromised, result- ing in paresthesia. Thus,
the term radicular syndrome may be the most accurate in that it correctly suggests
a constellation of clinical signs and symptoms of variable etiologies secondary to
pathology or dysfunction of the nerve root or dorsal root gan- glia (DRG).
Furthermore, radicular pain, radiculitis, radiculop- athy, radicular syndrome and
sciatic have been applied often erroneously to any or all forms of pain of spinal
origin per- ceived in an extremity. While radicular pain in the lumbar spine is
commonly followed by pain in the cervical spine, its occurrence in the thoracic
spine appears to be rare.

In contrast to the common occurrence of spinal axial pain, the prevalence of

radicular pain is uncommon with prevalence estimates ranging between 1.2 and
43% of lumbar radiculitis in the general population, an annual age-adjusted
incidence of radiculopathy of 0.83% in the cervical spine, and radiculopathy in the
thoracic spine being uncommon.

Lumbar radicular pain is secondary to disc herniation in >90% of the cases, whereas
cervical radicular pain is secondary to spon-dylosis resulting in foraminal
encroachment in 70% of cases. Disc herniation is defined as a localized
displacement of disc material, either nucleus pulposus and/or annulus fibrosis,
beyond the normal margins of the intervertebral disc space, resulting in pain,
weakness or numbness in a myotomal or der- matomal distribution. In contrast,
spinal stenosis is defined as a narrowing of the spinal canal secondary to degenera-
tive changes in the spinal canal, resulting in lower extremity pain and fatigue with
or without back pain seen in the elderly . Lumbar disc herniations occur in about
95% of the patients at L4/5 and L5/S1 levels in individuals aged 25–55, whereas
disc herniation above this level is more common in people aged over 55 years.
Similarly, cervical disc herniations and cervical spondylosis encroaching on the
foramen occur most commonly between C5/6 and C6/7 vertebral bodies. While
cervical disc herniation occurs in the younger population with traumatic ori- gin
and compresses the nerve roots, spondylosis is a chronic degenerative condition in
the elderly with formation of osteo- phytes. Thoracic disc herniation occurs least
commonly .

Even though the exact pathophysiology of radicular pain continues to be unclear,

local mechanical effects of direct contact of the herniated disc with the nerve root
play a major role, in conjunction with inflammatory components. The proposed
etiologies in radiculitis include neural compres-sion with dysfunction, vascular
compromise, inflammation and biochemical influences. Nerve injury initiates
multiple events that lead to changes in the nerve function and result in sponta- neous
firing at the DRG. Risbud and Shapiro. described the pathophysiology of disc
degeneration and pain showing that in the inflammatory milieu, neurogenic factors,
in particular nerve growth factor (NGF) and brain-derived neurotropic factor
(BDNF) generated by the disc and immune cells, induce an expression of pain
associated with cation channels in the DRG. Risbud and Shapiro also showed that
disc degeneration is characterized by three distinct but overlapping phases in which
cytokines play a central role with an initiating event resulting in phenotypic changes
and production of cytokines and chemo- kine by the both nucleus pulposus and
annulus fibrosis cells in the first phase, followed by further amplification of the
inflam- matory response by infiltrating immunocytes, as well as neovas-
cularization and nerve ingrowth into the structurally deficient disc tissues in the
second phase. In the final phase, nerve end- ings are sensitized and the modulation
of DRG pain channel activity is altered by inflammatory mediators and
neurotrophins resulting in pain. In addition, Olmarker et al. Showed that spinal
nerve roots, when compressed, exhibited intraneural edema, deprived nutritional
supply and loss of amplitude of nerve conduction . In fact, these experimental
findings were confirmed by Kuslich et al. Who reported that noncom- pressed nerve
roots did not reproduce the patient’s pain when stimulated intraoperatively in awake
surgical patients.