The intervertebral disk (IVD) is composed of the nucleus pulposus (NP) and the anulus fibrosus (AF), bordered by superior and inferior cartilaginous end plates from the vertebral bodies. The AF is composed of an outer and an inner layer with slightly different biological and mechanical properties. As a functional unit, the IVD provides the spine flexibility and accommodation with bending, twisting, and compression.

The notochord-derived NP is the central portion of the intervertebral disk, providing the majority of the disk height and compressive strength. Composed of proteoglycans and a mesh of type II collagen in a highly hydrated environment, the NP is an elastic, gelatinous structure. The primary source of nutrients to healthy IVD is diffusion through the articular end plates. Innervation, limited to the outer edges of the IVD, is primarily from the sinuvertebral nerve originating at the ventral root.

Factors such as vascular endothelial growth factor (VEGF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) are stimulated by IL-1. This combination of neurovasculature promotion in the setting of an inflammatory state of disk degeneration is thought to contribute to back pain as a result of disk degeneration. Several biomechanical factors may contribute to nociceptive changes with disk degeneration. As the ECM changes, the IVD loses height, which may increase the stress on paraspinal musculature, ligaments, and facet joints, expediting arthritic changes. Loss of disk height also contributes to nerve root compression. With degenerative changes to the matrix of the IVD, the lamellae of the AF may develop small splits, creating an opportunity for NP herniation, further contributing the local tissue inflammation.

Radiographs and MRI are useful for demonstrating degenerative changes; however, they lack specificity and thus cannot themselves prove the source of pain. Diskography has been used to evaluate diskogenic back pain, but it has a high false-positive rate and may contribute to disk degeneration.⁶

While addressing modifiable risk factors such as obesity and smoking may aid in prevention of back pain, current management of diskogenic pain is an evolving field. NSAIDs are commonly used as symptoms dictate; however, the long-term effect on IVD integrity with this modality is debated. Omega-3 fatty acids have been proposed for management and prevention of low back pain because of their anti-inflammatory properties through local competitive inhibitory effects on cytokines. Protein-based therapies aimed at inhibition of TNF-α, IL-1, and MMPs have also been proposed, but their effectiveness will require ongoing investigation. Stem cell therapies and platelet-rich plasma aimed at tissue repair of the IVD have had limited success among small case studies in the management of diskogenic back pain.

Surgical intervention at this time is limited. Lumbar fusions have had mixed results with respect to pain and disability improvement, while subjecting the patient to complications when compared with nonsurgical management. Total disk replacement (TDR) is a possible option for the management of diskogenic pain. A Cochrane review identified short-term success of TDR; however, the authors expressed hesitation toward adoption out of concern for long-term effects on adjacent spinal levels and facet joints.⁷ More recently, an 8-year prospective randomized controlled trial reported a significant decrease in low back pain and disability scores with TDR as compared with a multidisciplinary rehabilitation program, with both cohorts reporting overall improvement.⁸ A recent meta-analysis of small studies comparing TDR to fusion, cognitive behavioral therapy, and physical therapy indicated a trend toward greatest effectiveness of low back pain relief with TDR.⁹

The clinical manifestations of this mechanical and biochemical nerve root irritation most commonly present as low back pain with radiation in a dermatomal pattern, with or without corresponding numbness and/or weakness in correspondence to the involved nerve roots. The location of the herniation dictates the affected nerve, with posterolateral herniations abutting the traversing root, while foraminal and extraforaminal herniations affecting the exiting root. Large central herniations can affect multiple roots. Valsalva maneuvers often exacerbate patient symptoms. Cauda equina syndrome can occur as a result of a large LDH, and symptoms such as urinary retention or overflow incontinence, saddle anesthesia, acute lower extremity weakness, and bilateral leg pain should be investigated emergently. Physical examination should include gait analysis, a comprehensive neurovascular examination, as well as straight leg raise for both the ipsilateral and contralateral limb.

Although nondiagnostic for LDH, imaging should begin with a complete set of weight-bearing lumbar spine radiographs. For those with clinical symptoms that warrant further imaging, MRI is the optimal diagnostic tool with reported sensitivity of 89% to 100%. Disk fragments will appear hypointense on T2 imaging with or without focal intensity with annular rupture (Figure 1). Those who cannot tolerate MRI as a result of implanted medical devices or retained metal can be evaluated with CT myelography.

Up to 90% of individuals with symptomatic LDH will have resolution of symptoms with nonsurgical treatment.¹² NSAIDs and physical therapy are commonly prescribed regimens for symptomatic LDH. Epidural injections can also be used in an effort to target and quell specific nerve root irritation associated with LDH, and they have been shown to be effective in improving patient symptoms.

When surgery is indicated, microdiskectomy, either open or via a minimally invasive technique is the standard intervention. Indications for emergent surgery are suspected cauda equina syndrome or progressive or severe neurological deficits. Indications for surgery also include failure to achieve resolution of symptomatic LDH with nonsurgical management after 6 weeks to 3 months.

A classic study evaluating surgical outcomes for lumbar herniated nucleus pulposus demonstrated that at 1-year follow-up, the surgical cohort had statistically better outcomes than the nonsurgical cohort. However, at 4 years, the difference was no longer significant, and at 10 years, there was no difference in outcomes between the cohorts.¹³ A 10-year follow-up of the Maine Lumbar Spine Study reported that those treated surgically had improved leg pain, function, and satisfaction; however, work status and disability were not significantly different between groups.¹⁴ The Spine Patient Outcomes Research Trial (SPORT) reported at 8-year follow-up that patients surgically treated for symptomatic LDH had better relief of pain, function, decreased disability, and better satisfaction compared with the nonsurgical cohort.¹⁵ Improvement with surgery has been associated with more severe symptoms preoperatively, married status, and absence of diabetes or other joint problems.^16,17 It has been suggested that delay in treatment greater than 6 months may decrease the therapeutic effect and symptomatic improvement of surgery for LDH.^18,19

Recurrent LDH is a well-known complication after surgical intervention. In the United States, revision surgery occurs in 13.4% of patients at 5 years. SPORT had a 15% revision surgery rate overall, and 85% of those patients were treated for recurrent LDH. Although revision surgery does yield symptomatic improvement, subjective outcomes are significantly worse after revision surgery as compared with primary surgery.²⁰

Thoracic disk herniations (TDHs), while much less common than lumbar herniated nucleus pulposus, present with axial pain, possibly accompanied by radicular pain in a thoracic dermatomal pattern with or without paresthesias. Myelopathic symptoms can coexist as a presenting symptom and are important considerations during physical examination. Although TDH is not an uncommon finding on MRI, symptomatic TDH is rare, occurring in only one in one to two million people. Most instances of TDH (50% to 75%) occur between T8 and L1 at the junction of the stiff thoracic spine and the more flexible lumbar spine with the highest prevalence at T11-12 and T12-L1. Plain radiography of the thoracic and lumbar spine should be obtained for all patients with concern for TDH; however, MRI is the most useful diagnostic imaging tool to identify symptomatic TDH. CT is also useful, as the presence of calcification may alter treatment.

If surgery is required for refractory pain, increasing neurologic deficit or myelopathic symptoms, a variety of techniques exist. Traditionally, an anterior approach via thoracotomy has provided excellent exposure. Posterior approaches to the disk through a transpedicular or costotransversectomy route are alternatives but are technically demanding and carry significant neurologic risk. Recently, there has been increased focus on thorascopic and other minimally invasive techniques aimed at decreasing morbidity associated with thoracic spine surgery. A calcified TDH has an increased risk of dural tear and should be noted preoperatively along with preexisting pulmonary disease, as these particular findings may preclude thoracoscopic options.

Depending on the location of the stenosis, patients present with a combination of neurogenic claudication with decreased walking tolerance, radiculopathy, and low back pain. In a prospective trial analyzing patients with symptomatic LSS, 95% of patients endorsed some degree of lumbar pain, 91% endorsed claudication symptoms, and 70% reported sensory disturbance in the legs.²³

Neurogenic claudication classically presents as bilateral buttock and proximal thigh heaviness, fatigue, and pain, and it tends to worsen with prolonged standing or walking. These symptoms should be differentiated from vascular claudication, which typically begins distally and causes predominantly calf pain and burning.

There is often a dynamic component to the symptoms. Because the spinal canal diameter changes between flexion and extension, patients notice exacerbation or relief of symptoms often based upon positioning. Leaning forward, such as walking uphill, can provide relief of symptoms, and thus patients frequently find using a walker or holding onto a stroller to be easier. Walking downhill and extension activities narrow the canal dimensions and therefore exacerbate symptoms. Lying down is frequently more comfortable than sitting or standing.

Physical examination is often normal in patients with lumbar spinal stenosis, and therefore, the history is crucial to the diagnosis. In SPORT, only 50% of patients had physical examination findings including depressed reflexes, sensory or motor deficits, or positive nerve tension signs.²⁴ Therefore, it is also crucial to perform an examination of the lower extremities to rule out alternative causes for pain, as lumbar spine pathology and lower extremity joint dysfunction, especially the hip, are common. AP and lateral radiographs of the lumbar spine, with consideration for dynamic radiographs are important to evaluate alignment and evidence of instability. MRI has become the benchmark for identifying spinal pathology. T2-weighted sagittal and axial images can demonstrate disk bulges, facet hypertrophy, ligamentum flavum hypertrophy, cysts, and other causes of stenosis, whereas sagittal T1-weighted images best show foraminal stenosis (Figures 2 and 3). Although imaging is an important modality, it cannot replace a history and physical examination, as radiographic findings of spinal stenosis increase with age, yet many patients never become symptomatic. In a study of asymptomatic individuals, one study found that over 20% of patients older than 60 years had MRI evidence of lumbar spinal stenosis.⁴ For those patients who cannot undergo MRI, CT myelography can also demonstrate compression although with less detail than MRI. Electrodiagnostic studies can be used to help rule out a peripheral neuropathy; however, their role in diagnosis of spinal stenosis is unclear.