Author: Boqing Chen, MD, PhD Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey-New Jersey Medical School
Epidural steroid injections (ESIs) have been endorsed by the North American Spine Society and the Agency for Healthcare Research and Quality (formerly, the Agency for Health Care Policy and Research) of the Department of Health and Human Services as an integral part of nonsurgical management of radicular pain from lumbar spine disorders.
Radicular pain is frequently described as a sharp, lancinating, radiating pain, often shooting from the low back down into the lower limb(s) in a radicular distribution. Radicular pain is the result of a nerve root lesion and/or inflammation. Clinical manifestations of nerve root inflammation include some or all of the following: radicular pain, dermatomal hypesthesia, weakness of muscle groups innervated by the involved nerve root(s), diminished deep tendon reflexes, and positive straight or reverse leg–raising tests. In contrast to oral steroids, ESIs offer the advantage of a more localized medication delivery to the area of affected nerve roots, thereby decreasing the likelihood of potential systemic side effects. Studies have indicated that ESIs are most effective in the presence of acute nerve root inflammation.
The first documented epidural medication injection, which was performed using the caudal approach (see Approaches for Epidural Injections), was performed in 1901, when cocaine was injected to treat lumbago and sciatica (presumably pain referred from lumbar nerve roots). According to reports, epidurals from the 1920s-1940s involved using high volumes of normal saline and local anesthetics. Injection of corticosteroids into the epidural space for the management of lumbar radicular pain was first recorded in 1952.
ESIs can provide diagnostic and therapeutic benefits. Diagnostically, ESIs may help to identify the epidural space as the potential pain generator, through pain relief after local anesthetic injection to the site of presumed anatomic pathology. In addition, if the patient receives several weeks or more of pain relief, then it may be reasonable to assume that an element of inflammation was involved in his or her pathophysiology. Since prolonged pain relief is presumed to result from a reduction in an inflammatory process, it is also reasonable to assume that during the period of this analgesia, the afflicted nerve roots were relatively protected from the deleterious effects of inflammation. Chronic inflammation can result in edema, wallerian degeneration, and fibrotic changes to the neural tissues.
In these authors’ opinion, ESIs are best performed in combination with a well-designed spinal rehabilitation program. In most cases, epidural injections should be considered as a treatment option after other treatment attempts (eg, physical therapy, including therapeutic exercise, manual therapy, and medications) have failed to improve the patient’s symptoms. However, ESIs may be indicated earlier in the treatment algorithm in some selected patients. Examples might include patients with medical contraindications to certain oral analgesics and patients whose pain severity substantially limits their ability to appropriately engage in therapeutic exercise.
A variety of approaches can be used to inject corticosteroids into the epidural space (see Approaches for Epidural Injections). For purposes of this article, the authors generally refer to all epidural steroid injections as ESIs, only specifying the specific type of approach if needed for a point of distinction or clarification.
As mentioned above, radicular pain often is the result of nerve root inflammation +/- mechanical irritation. Clinical practice and research demonstrate that mechanical compression alone to the nerves causes only motor deficits and altered sensation but does not necessarily cause pain. Inflammation within the epidural space and nerve roots, as can be provoked by a herniated disk, is a significant factor in causing radicular pain.
Historical evidence of nerve root inflammation has been demonstrated during surgery in patients with radicular low back pain (LBP) from lumbar disk herniation. Animal research in dogs and rats also has revealed severe inflammation locally within the epidural space and nerve root after injection of autologous nuclear material into the epidural space. A high level of phospholipase A2 (PLA2), an enzyme that helps to regulate the initial inflammatory cascade, has been demonstrated in herniated disk material from surgical samples in humans. Leukotriene B4, thromboxane B2, and inflammatory products also have been discovered within herniated human disks after surgery. Animal models have demonstrated that injection of PLA2 into the epidural space induces local demyelination of nerve roots, with resultant ectopic discharges (which is considered to be the primary pathophysiologic mechanism for sciatica [radicular pain]).
The radicular LBP caused by spinal stenosis is probably related to the inhibition of normal nerve root vascular flow with resultant nerve root nutrition, nerve root edema, and nerve root dysfunction. Chronic nerve root compression can induce axon ischemia, impede venous return, promote plasma protein extravasation, and cause local inflammation. If dorsal root ganglia are chronically compressed and irritated, this theoretically can lead to their sensitization and resultant radicular pain. Similar mechanisms of radicular pain are postulated to occur in the thoracic and cervical spine as well.
In summary, clinical practice and animal research suggest that radicular pain is the result of inflammation of the nerve root in the epidural space provoked by leakage of disk material, compression of the nerve root vasculature, and/or irritation of dorsal root ganglia from spinal stenosis.