By definition, FBS implies previous surgery. Therefore the first priority in the evaluation of these patients is to understand the indication for the original operation. It is often helpful to ask the patient to compare current symptoms with those experienced prior to surgery in terms of location, frequency, and intensity. A patient who fails to improve at all following surgery is more likely to have been misdiagnosed than a patient who improves for a period of time. If the original indication for surgery is suspect, it is extremely unlikely that further surgical intervention will be helpful.

Patients who do not improve or worsen immediately after surgery may have suffered a technical error during surgery. These errors include inadequate decompression, wrong level surgery, or nerve root injury. Frank instability of the operated level may also worsen if an unstable spinal motion segment such as a mobile spondyllolisthesis is not stabilized or fused at the time of decompression.

A patient who experiences identical recurrent symptoms after a postoperative period of significant improvement will likely harbor recurrent pathology. Disc herniations, for example, carry a lifelong risk of recurrence because the majority of the anatomical intervertebral disc remains after a discectomy and the annular tear that permits the herniation never completely heals. An infection may also be present, frequently becoming apparent within the first 4 weeks of surgery. Infections may cause recurrent symptoms as well as the new onset of significant back pain. These infections can be occult, and imaging studies should be performed to determine if endplate erosion or a fluid collection is present.

Surgical procedures of the lumbar spine are commonly performed for degenerative diseases. Spondylosis, or bony overgrowth of the facet joints and intervertebral endplates, in association with soft tissue ligamentous hypertrophy can cause significant stenosis. Spondylolisthesis, or malalignment of the spine, can progress after decompression alone, causing recurrent nerve root entrapment. Additionally, progression of degenerative changes at a level adjacent to a lumbar fusion may occur, resulting in stenosis and/or spondylolisthesis.

is a pain that shoots like a jolt of electricity and follows a particular dermatomal distribution. This is most often caused by a herniated disk, but not exclusively so. Many times there is associated sensory loss in the same dermatome. The associated myotome can manifest weakness in some cases. Abnormal reflexes can also help to localize the level of involvement in the spinal canal.

1. Imaging is helpful in this context to confirm the level implicated by the history and physical examination findings. However, it has been well-shown that healthy persons without back pain can harbor disks that would be concerning from a purely radiographic perspective. Therefore, imaging findings without a clinical correlate can typically be ignored.

2. The most common cause of the pathogenesis of radiculopathy is herniation of a disk followed closely by degenerative foraminal stenosis. Other entities, such as synovial cyst, are distinctly less common.

3. Whatever the cause, surgery for radiculopathy is focused on decompressing the affected nerve root. The prognosis is quite good; early good results are achieved in >95% of cases.

4. When this type of surgery is unsuccessful, strong consideration should be given to the possibility that the diagnosis was incorrect, the wrong level was operated on, or the patient has secondary issues that are preventing improvement.

5. Radiculopathy can be confused with hip disease in some cases. A positive Patrick’s test should be followed with an evaluation to rule out hip arthrosis.

is a cramping pain or sense of fatigue in the legs caused by exertion. Most patients report the onset of symptoms after walking a particular distance. The pain typically abates after several minutes of rest, such that the person can continue.

1. It is important not to confuse neurogenic and vascular claudication. Patients with neurogenic claudication exhibit a “shopping cart sign,” which is the ability to walk further when leaning forward. This flexed position slightly diminishes the ligamentous compression of the cauda equina, allowing the patient to walk further. For the same reason, a patient with neurogenic claudication will do much better on exercising bicycle than they would on walking. Patients with vascular claudication show no such improvement.

2. Neurogenic claudication is most commonly managed with lumbar laminectomy over the stenotic levels. The goal of surgery is to decompress the thecal sac by removing hypertrophied ligamentum flavum, the medial facet, and occasionally disc material. Foraminotomies are required to decompress the exiting nerve roots, and this may result in iatrogenic instability causing some patients to require fusion as well.

3. Imaging with either MRI or CT myelography shows a markedly compressed thecal sac with a characteristic trefoil configuration and amputation of the exiting nerve root sleeves.

is another common indication for lumbar surgery. From both a theoretical and a practical standpoint, instability is distinct from stenosis and radiculopathy. Management of radiculopathy and stenosis is decompression; management of instability is fusion. The success of fusion operations is distinctly less than that of decompression. For this reason, many patients with FBS have experienced failed fusion.

1. Instability is defined as the ability of the bony components of the spine to withstand physiologic loads without mechanical pain or compromise of nerve root function.

2. Although instability often is thought of in a binomial way as either present or absent, in clinical practice there is a spectrum of instability ranging from gross instability, most often the result of trauma, to microinstability, which is found in the context of degenerative disease.

3. The underlying hypothesis in offering fusion to patients with degenerative spondylosis is that instability represents a painful dysfunctional motion segment. The pain is characteristically exacerbated by prolonged sitting or standing and often is relieved by recumbency. Because the pain does not radiate, it is not possible to localize the responsible spinal level by means of history or physical examination.

4. The pathogenesis of mechanical back pain is controversial and likely is multifactorial. There is evidence implicating the disk space as well as the facet joints. Many patients who improve after lumbar fusion fail to demonstrate overt instability on preoperative dynamic studies. Therefore, the specific pain generator is unknown, and the lumbar segment inclusive of the disc and facet joints is thought to be dysfunctional.

5.If flexion-extension radiographs (dynamic radiographs) show movement of >4 mm, the diagnosis is more certain. However, a large number of patients with movement in excess of 4 mm also do not have mechanical pain. Plain radiographs can provide indirect evidence of instability in the form of traction spurs that result from the tension placed on the bone from Sharpy’s fibers of the annulus or loss of disk height indicative of disk degeneration. MRI often shows Modic’s changes at the interspace thought to represent inflammatory reaction in the adjacent vertebral bodies secondary to disk disruption. Many of these findings are present in patients who are pain free, and therefore their utility is suspect.

6. In an attempt to better determine whether instability is present in a particular patient and whether it is responsible for the back pain being reported, several strategies have emerged. The trial use of a temporary external orthosis or percutaneous pedicle screws before surgical fusion has fallen out of favor.