Nerve Root Block

The spinal cord gives rise to 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal. Spinal nerves exit the spinal cord and course outward to the peripheral body through intervertebral foramina, which begin at C2/3. The first intervertebral neural foramen is formed at C2/3 and transmits the C3 nerve root. There are no neural foramina above C2/3 and the spinal nerve roots of C1 and C2 lie posterior to the atlanto-occipital and atlanto-axial joints respectively. Spinal nerve roots from C3 to L5 exit anterior to the facet joints through the neural foramina.

Each spinal nerve consists of a dorsal and a ventral root, which come together to create a short, unified segment within the intervertebral neural foramen. This short, intraforaminal segment is the spinal nerve proper although it is sometimes imprecisely referred to as the spinal nerve root. Once the spinal nerve is formed, it quickly bifurcates into a dorsal and ventral ramus as it exits the spinal column.

Pain from disc herniation can arise from nerve root compression and stimulation of nociceptors in the annulus or posterior longitudinal ligament. Nerve root edema can result from microvascular injury inside the nerve roots, and has also been noted to produce pain in nerve roots. In patients with stenotic nerve root canals there can also be mechanical compression of an exiting nerve root. The nerve roots, as they exit the intervertebral foramina, have a poorly developed epineurium, rendering them particularly vulnerable to mechanical and chemical injury. Painful spinal stenosis may result from disc bulging, protrusion, and herniation combined with osteophytes and arthritic changes of facet joints that cause narrowing of the spinal canal or neural foramina. Thus, various proposed mechanisms for radicular pain include partial axonal damage, neuroma formation, focal demyelination, intraneural edema and impaired microcirculation.

The other explanation surrounds the theory of chemical irritation and inflammation around the discs and nerve roots, which is considered a pain generator in conjunction with or without mechanical factors

Various terms have been used to describe what a number of practitioners consider to be the same procedure- transforaminal, paraforaminal, nerve root block, SNRB and periradicular injections. The basic difference between a transforaminal injection and a selective nerve root block is probably just semantic and may be technically limited to only a few millimeters of the final needle tip position (in the medial to lateral plane). In a transforaminal injection, considered by some to be more of a therapeutic procedure, the injectate is delivered more medially and therefore more proximally to the anterior epidural space. It is spread on to adjacent nerves inside the spinal canal and is considered to limit the validity due to the lack of control of the spread of the injectate. By contrast, SNRBs could possibly permit greater specificity. The fact that this injection is extraforaminal and that the delivery of drugs would be distal to the convergence of the ventral and dorsal rami, a more confined spread could be achieved and therefore have improved legitimacy as a diagnostic tool.

MRI scan of the spine is considered the gold standard for investigating radicular pain or sciatica. CT Scan can be considered if MRI scan is contraindicated due to presence of pace maker, metal clips in the brain or other neural implants. Scans can accurately show the nerve root compression but it is important to note that the clinical presentation may not always match the pathology evident on the scan. Radiographic changes are equally common in non- symptomatic individuals. In addition, compression of the nerve roots in some patients may only be evident in standing position and standing MRIs are not widely available as yet. Good history taking and examination, in conjunction with imaging can improve the accuracy of diagnosis and interpretation of pathology seen on the scans.

Selective nerve root blocks are used to clarify challenging clinical situations, in order to determine the pathophysiology of clinical pain, the site of nociception and the pathway of afferent neural signals. This may provide valuable information to the surgeons in determining the exact level of pathology and thereby the surgical procedure offered to the patient.

Injections are generally avoided in patients with systemic infection or skin infection over puncture site, bleeding disorders or coagulopathy, allergy to local anaesthetics or any of the medications to be administered.

The procedure is usually done on an outpatient basis. The procedure is performed under fluoroscopic guidance to ensure accuracy of needle placement. Patients need to be aware that the outcome of the procedure is variable and they may not receive the desired benefits. Similarly, they must be aware of the transient nature of the therapeutic benefits and that there may need repeated injections.

Generally a mixture of local anaesthetic and steroid is injected. The local anaesthetic agent within the injectate may act on the nerve root to prevent abnormal firing , whereas corticosteroids may reduce inflammation of around the nerve root. The anaesthetic is probably responsible for immediate pain relief, whereas steroids are believed to be responsible for pain relief 2–6 days after their administration. For a diagnostic block, a short-acting anaesthetic alone is sufficient.

Complications are rare, particularly if injections are performed using a precise needle-positioning technique. Severe allergic reactions to local anaesthetics are uncommon. Steroid injections may produce local reactions, occurring most often immediately after injection. These local reactions last for 24 to 48 hours, and are relieved by application of ice packs. Post-procedural pain flare-up may occasionally occur, and may be treated with painkillers. Neurological complications including paraesthesias, numbness and paralysis have been described but are rare. Infections including epidural abscess and chemical meningitis can occur but the incidence is very low as the procedure is performed under strict aseptic conditions.

In recent years, embolic events have been reported after transforaminal epidural steroid injections with particulate steroids. These embolic phenomena can result in serious complications including spinal cord injury, stroke and death. Undetected vascular injections of the vertebral artery or spinal radicular arteries with particulate steroids are postulated to have caused embolic infarctions. Complications can be minimized with meticulous technique, injecting contrast under live fluoroscopy and using non-particulate steroids.