Radiculopathy

Point/Counterpoint

Guest Discussants: Sayed E Wahezi, MD, Andrew Lederman, MD, Eric H Elowitz, MD Feature Editor: Jaspal Ricky Singh, MD

Conservative Treatment Versus Surgery for Lumbosacral Radiculopathy with Muscle Weakness and Loss of Reflexes

What is radiculopathy?

A compressed or irritated nerve in the spine can cause pain, numbness, tingling, or weakness along the path of the nerve. This condition is called radiculopathy. It can occur in any part of the spine, but it is most common in the low back (lumbosacral radiculopathy, sometimes called sciatica) and neck (cervical radiculopathy). Patients involved in heavy labor or contact sports are more prone to develop radiculopathy than those with a more sedentary lifestyle.

What causes radiculopathy?

Spinal disks are located between each vertebra of the spine, acting as shock absorbers when the body moves. A disk is made up of a tough fibrous outer surface with a soft, gel-like inner substance. A forceful movement can injure the lumbar spinal disks, or repetitive straining can gradually damage them over time.

With a mild injury, the disk can be stretched or pinched. With a more severe injury, the outer surface can be weakened, allowing the substance inside to push towards the outside. This is known as a bulging or herniated disk. Disk herniation reduces the amount of space in the spinal canal and compresses the exiting nerve. This is called “mechanical radiculopathy.”

With further damage, the outer surface can tear, and the disk fluid inside might leak out. This is known as a complete herniation or extrusion. The disk material may then irritate nearby nerves as they exit the spinal cord. This is called “chemical radiculopathy.”

How is radiculopathy diagnosed?

A physician will begin by asking the patient his or her medical history and performing a physical examination. During the medical history, the doctor asks questions about the type and location of symptoms, how long they have been present, and what makes them better and worse.

By knowing the exact location of the patient’s symptoms, the doctor tries to determine the nerve that is responsible for the pain. Neurological tests are performed to determine loss of sensation and motor function. Abnormal reflexes and muscle weakness may indicate a source of the radiculopathy.

Imaging may also be useful for diagnosis. Plain X-rays can often see the presence of trauma or osteoarthritis and early signs of tumor or infection. A magnetic resonance imaging (MRI) or computed axial tomography (CAT) scan looks at the soft tissues (nerves, muscles, etc.) around the spine to determine possible compression of the nerves. In some cases, the doctor may order an electromyogram (EMG) which can show if there is damage to the nerve.

How is radiculopathy treated?

Most radiculopathy symptoms go away with conservative treatment such as anti-inflammatory medications, physical therapy, chiropractic treatment, and avoiding activity that strains the neck or back. Symptoms often improve within 6 weeks to 3 months. If radiculopathy symptoms do not improve with conservative treatments, patients may benefit from an epidural steroid injection (ESI), which reduces the inflammation and irritation of the nerve. Read more about ESIs.

If the symptoms continue despite all the above treatment options, surgery may be an option. The goal of the surgery is to remove the compression from the affected nerve. Depending on the cause of the radiculopathy, this can be done by a diskectomy or microdiskectomy.

A diskectomy removes the part of the disk that has herniated out and is compressing a nerve. In microdiskectomy (or microdecompression) spine surgery, a small portion of the disk and disk material impinging the nerve root is removed to provide more room for the nerve to heal.

In the June 2015 issue of Pain Management and Rehabilitation Journal, three physicians shared differing opinions about treatment for lumbosacral radiculopathy with muscular weakness and loss of reflexes. A patient’s case is presented here, followed by a debate as to the best treatment plan. Drs Sayed Wahezi and Andrew Lederman will argue that a conservative treatment plan will help the patient regain full function. Dr Eric H Elowitz suggests that surgery will provide the best outcome.

Logan’s treatment plan is up for debate because current literature supports both nonsurgical and surgical intervention.

Logan has persistent weakness, and his pain is going away. We recommend an ESI because Logan likely has chemical radiculitis. The painful symptoms already have subsided, and motor recovery will likely follow. If a compressed nerve were the cause, the pain would likely persist.

Logan’s case is an example of a complete herniated disk. The herniated disk is the cause of Logan’s muscle weakness. Understanding the composition of the extruded disk material is critical to understanding our case.

Herniated disk material is primarily the gel-like substance that cushions the vertebrae. Due to its chemical composition, this material promotes inflammation. When it comes into contact with the nerve root, nerve pain occurs. We will demonstrate that Logan’s symptoms indicate chemical radiculitis as the cause of his radiculopathy.

As in Logan’s case, radiculopathy with muscle weakness is likely caused by nerve damage. Chemical radiculopathy causes nerve damage due to the direct contact of the thick disk material with the nerves, causing inflammation and decreasing normal neural transmission [1,2]. The nerve heals as the disk herniation recedes from the nerve and the chemical irritants go away. Chemical radiculopathy usually responds well to conservative treatment, while mechanical radiculopathy may not.

A complete disk herniation, as in Logan’s case, often improves without

surgery because of the absorption of the disk material back into the body. In clinical practice, most disk herniations with muscle weakness are caused by inflamed nerves rather than compression. This is substantiated by most patients whose symptoms improve with conservative treatment alone.

Epidural steroid injections (ESIs), physical therapy, and oral anti-inflammatory medicine are important in treating chemical radiculopathy because they all help reduce inflammation [13]. ESIs decrease the chemical irritation to neighboring nerve roots.

Some investigators have even demonstrated the effectiveness of ESIs without steroids, which supports the theory that diluting or “washing away” inflammation-inducing material adjacent to a nerve also could reduce symptoms [6]. Physical therapy may improve spinal blood flow as well as cerebrospinal flow, adding to the washout concept [7]. Finally, oral anti-inflammatory medicine improves the local inflammation [8].

The decision to perform surgery is a clinical one; we must consider the type of herniation, partial or complete herniation, as well as the patient’s pain state. I believe that current evidence and research suggests that physicians should use conservative therapy in cases of mild weakness before considering surgery.

In Logan’s case, he has chemical radiculitis with mild muscle weakness.

His MRI, which depicts a disk extrusion, and his pain that went away on its own, both support this diagnosis. An ESI may reduce local inflammation, ultimately leading to resolution of his chemical radiculopathy.

We must also consider the cost of the services we offer our patients. A head-to-head cost analysis favors conservative, non-surgical treatments, including ESI, physical therapy, and potentially oral medications, for this patient.

Disk extrusions often improve on their own. A trial of ESI has a better chance of improving short-term outcomes than worsening long-term outcomes [5,9]. Furthermore, Logan’s other factors support conservative therapy; his young age, new symptoms, mild muscle weakness, and the limited number of muscles involved all favor a good prognosis without surgery [3,4].

If we were treating this patient, we would closely monitor Logan’s weakness and schedule Logan for an ESI. At this point, we are comfortable watching Logan’s neurologic function, and if there is no return of strength or even progression of weakness in the ensuing 4-6 weeks, we would then consider surgery.

References

1. Saal JS, Franson RC, Dobrow R, Saal JA, White AH, Goldthwaite N. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine (Phila Pa 1976) 1990;15: 674-678.
2. Mulleman M, Mammou S, Griffoul I, Watier H, Goupille P. Pathophysiology of disk-related sciatica. Evidence supporting a chemical component. Joint Bone Spine 2006;73:151-158.
3. Aono H, Iwasaki M, Ohwada T, et al. Surgical outcome of drop foot caused by degenerative lumbar diseases. Spine (Phila Pa 1976) 2007;32:E262-E266.
4. Matsui H, Kanamori M, Kawaguchi Y, Kitagawa H, Nakamura H, Tsuji H. Clinical and electrophysiologic characteristics of compressed lumbar nerve roots. Spine 1997;22:2100-2105.
5. Dubourg G, Rozenberg S, Fautrel B, et al. A pilot study on the recovery from paresis after lumbar disc herniation. Spine (Phila Pa 1976) 2002;27:1426-1431.
6. Manchikanti L, Singh V, Cash KA, Pampati V, Falco FJ. The role of fluoroscopic interlaminar epidural injections in managing chronic pain of lumbar disc herniation or radiculitis: A randomized, double-blind trial. Pain Pract 2013;13:547-558.
7. Saal JA, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy: an outcome study. Spine 1989;14:431-437.
8. Vane J. The evolution of non-steroidal anti-inflammatory drugs and their mechanisms of action. Drugs 1987;33(Suppl 1): 18-27.
9. Chiu CC, Chuang TY, Chang KH, Wu CH, Lin PW, Hsu WY. The probability of spontaneous regression of lumbar herniated disc: A systematic review. Clin Rehabil 2015;29:184-195.