The spine is host to a wide range of afflictions causing an array of neurologic and musculoskeletal symptoms. Frequent etiologies encountered by hospital neurologists include degenerative spine disease, infection, autoimmune, and neoplastic, in addition to several spine emergencies. Degenerative diseases of the spine include cervical and lumbar disc herniations causing radiculopathy, axial back pain, and neurogenic claudication. Spondyloarthropathies, particularly ankylosing spondylitis and rheumatoid arthritis, infection, and neoplastic diseases should be well known. Spine emergencies including spinal canal hematomas, cauda equina syndrome, and conus medullaris syndrome should be promptly diagnosed with appropriate imaging and prompt neurosurgical evaluation.
Cervical disc herniation or cervical herniated nucleus pulposus (HNP) occurs as a result of dehydration and fragmentation of the nucleus pulposus (NP).1 As the body ages, hydrophilic proteoglycan molecules in the NP undergo degenerative biochemical changes that lead to decreased viscoelasticity.2 Eventually disc height is lost and the axial load exerted by the body above is translated to the annulus fibrosus, which then thins and fibroses. In chronic HNP, the fibrotic nuclear material stays within the lamellae without penetrating the annulus. However, due to the lamellae being weak, the disc material can dissect through the attachment of the Sharpey’s fibers to the bony edges of the vertebral bodies, leading to reactive bone growth and osteophyte formation.3,4
All discs are dependent on blood diffusion from capillary beds in the vertebral body endplates to acquire nutrients and dispose of metabolites. Chronic hypoxia to the cells of the NP causes its cells to become quiescent, whereas chronic hypoglycemia causes their death.5 These processes occur as a natural part of aging but can also occur due to environmental factors as well as genetic predisposition. The latter has been shown to be implicated in 34–61% of cases depending of the level of disc disease.6,7
In more acute scenarios of HNP, the nuclear material actually dissects through a failed annulus and often the posterior longitudinal ligament (PLL) as well.
A HNP can compress the spinal cord or adjacent nerve rootsat the foramen level. Acute HNP occurs more often in a lateral direction due to the relative weakness of the PLL in this location. Therefore, acute HNP is more likely to cause nerve root compression as opposed to spinal cord compression.1
Acute disc herniations can cause axial neck pain or a more classic radicular pain.2 Axial neck pain is due to the significant innervation of the anterior and posterior aspects of the annulus by the sympathetic trunk/recurrent branches of gray rami communicants and the sinuvertebral nerves, respectively. Radiculopathy may be acute or chronic. Acute radiculopathy manifests as severe pain, and is usually due to a soft disc herniation and occurs in younger patients. Chronic radiculopathy is often associated with sensory complaints and occurs mainly in an older patient population. Radicular pain can be localized based on the distribution of the pain. Radicular pain radiates from the neck to the shoulder/arm/hand. The disc typically causes symptoms in the distribution of the exiting nerve root at that level. A C4–5 HNP is likely to affect all functions of the C5 nerve root, C5–6 will affect the C6 root, etc.
X-rays: Assess overall alignment but of limited utility unless flexion/extension (F/E XR) performed. F/E XRs used to assess for dynamic instability.
Plain computed tomography (CT): Adequate for bone imaging. This is important for preoperative planning to assess for ossification of the posterior longitudinal ligament (OPLL), calcified HNP, and osteophytes.
Magnetic resonance imaging (MRI): Study of choice to visualize the spinal cord and nerve roots as well as other soft tissues. If the patient has a contraindication to MRI, CT myelogram can alternatively be performed to assess for neurologic compression.
Diskography: Controversial and typically not useful. The evidence for utility of diskography is weak.
Axial neck pain due to HNP is treated conservatively. The algorithm begins with nonsteroidal anti-inflammatory drugs (NSAIDs) and can involve opiates and muscle relaxants if the pain becomes severe.8 If medications fail to improve symptoms, further diagnostic study may be warranted. Facet joint injections may diagnose/alleviate symptoms.9 Physical therapy is very useful for axial neck pain due to HNP. In particular, isometric exercises such as cervical traction have been shown to alleviate pain. Unfortunately, even in cases where all conservative measures have failed, there is little to no evidence that cervical fusion for the treatment of axial neck pain improves outcomes. Surgical decompression is indicated in patients who fail to improve and have radicular symptoms or neurologic deficit that is progressive. This can be accomplished via anterior approaches: anterior cervical discectomy and fusion (ACDF) or artificial disc (arthroplasty). If the HNP is sequestered behind a vertebral body, an anterior cervical corpectomy and fusion (ACCF) may be necessary. Posterior approaches are less common for HNP but include posterior cervical laminectomy/foraminotomy with or without fusion.
CASE 39-1
A 56-year-oldright-handed man carpenter presents to your clinic complaining of 1 year of bilateral upper extremity paresthesias. Over time, this has progressed and became constant with increased severity. In the last 6 months, his wife has begun to notice that he has been stumbling when walking, and that he seems stiff. The patient most recently has noticed difficulty completing basic tasks at work. What is your differential? What is the most likely diagnosis?
Cervical spondylotic myelopathy (CSM) results from the same findings of disc dehydration, OPLL, and reactive osteophyte formation that are found in HNP. These processes initiate a cascade of more diffuse cervical degenerative changes known as cervical spondylosis that progresses to CSM. As the disc space becomes more firm and loses height, there is straightening of the normally lordotic cervical spine. This shifts the center of axial loading anteriorly and alters cervical biomechanics, eventually causing hypertrophy or laxity of the ligamentum flavum and facet joints.2 In an attempt to stabilize itself, the cervical spine develops even more osteophytes known as a “cervical bar.” This cycle of laxity and ossification eventually causes a reduction in the sagittal diameter of the cervical spinal canal and causes significant stenosis. Symptoms of spinal cord injury are a result of direct compression, microtrauma due to flexion and extension, as well as vascular injury.2
OPLL is characterized by PLL hypertrophy initially with eventual development of ossification centers and ectopic bone formation. Its frequency increases with age. There is evidence of a strong genetic predisposition with possible autosomal dominant inheritance, but there is no simple inheritance pattern. Metabolic factors are significant contributors as well; many patients are obese and/or diabetic.10
What would you expect on examination?—Patients often initially complain of gait disturbance and weakness of the distal upper extremities, in particular the intrinsic muscles of the hands. Patients often complain they are dropping things. There is frequently stiffness of the lower extremities and difficulty with fine motor skills such as handwriting or buttoning of shirts. Neck pain is also a common complaint. Sensory loss is in a glove distribution in the hands or several levels below. The examination may be notable for hyperreflexia, Hoffmann’s sign (finger flexor reflex), ankle clonus, and/or Babinski signs. A Lhermitte’s sign (barber chair phenomenon) may also be present, but is not needed for diagnosis.
What imaging would you use to evaluate the patient’s complaints?
Flexion-extension (F/E) x-rays: To assess for dynamic instability
Plain CT: Good bone imaging to assess for OPLL, calcified HNP, and osteophytes. This may affect the surgeon’s decision about whether to use an anterior (contraindicated in some cases of OPLL) or posterior approach (Figure 39-1A, B).
Magnetic resonance imaging (MRI): Evaluates spinal cord and nerve roots. Identifies parenchymal changes in the spinal cord on T2-weighted imaging.
CT myelogram can alternatively be performed to assess for neurologic compression if there is a contraindication to MRI or if there is previous spinal instrumentation. The most common absolute contraindications to MRI include pacemaker/defibrillator, metallic foreign bodies in the eye, and deep brain stimulators. While previous metallic spinal instrumentation is not a contraindication to MRI, the artifact from the hardware may obscure the soft tissue and thus myelogram may provide more detail on impingement of the neurologic elements.
What is the natural course of this disease? What would you do next? What would you recommend?—The natural history of CSM is characterized by progression in 20–60% of patients if no surgical intervention is undertaken.11 It typically occurs slowly over time. As such, some practitioners consider nonoperative management for mild myelopathy. This approach should be used with caution, however, as postoperative outcomes correlate with preoperative deficit and functional status.12 Surgical decompression can be accomplished via anterior approaches (ACD, ACDF, ACCF) or posterior laminectomy with or without fusion or cervical laminoplasty if the patient has CSM but no neck pain. While each approach has pros and cons, most neurosurgeons consider posterior approaches to be suboptimal in restoring lordosis in the presence of a kyphotic deformity while anterior approaches accomplish this more easily.
The relative immobility of the thoracic spine compared to the cervical and lumbar spines accounts for the decreased incidence of disc herniation in this region. The incidence is approximately 1 patient per 1 million people.13 While uncommon, thoracic disc herniations can cause significant morbidity when they occur. Seventy-five percent of them occur below T8, with T11–12 being the most common site.14
Laterally herniated discs can cause radicular pain in a dermatomal pattern along the intercostal nerve. These are rare. Centrally located discs are more common and cause symptoms of spinal cord compression and long-tract signs resulting in sensory loss, bilateral lower extremity weakness, spasticity, hyperreflexia, clonus, and, in extreme cases, bowel and bladder dysfunction. Axial back pain is often a component of the patient’s symptomatology as well.
Magnetic resonance imaging (MRI): Evaluates spinal cord and nerve roots as including parenchymal changes (Figure 39-2A–H).
Plain CT: Good bone imaging and assessment of disc calcification.
CT myelogram can alternatively be performed to assess for neurologic compression if there is a contraindication to MRI.
Figure 39-2
(A, B) MRI thoracic spine T2 sagittal and axial weighted images demonstrating severe spinal cord compression from a thoracic disc herniation. There is evidence of abnormal T2 cord signal change. (C, D) CT thoracic spine sagittal and axial images reveal that the disc herniation is calcified. (E, F): Postoperative MRI thoracic spine T2 sagittal and axial weighted images demonstrating decompression of the spinal cord following discectomy. (G, H) Postoperative CT thoracic spine sagittal and axial images demonstrating decompression of the spinal cord following discectomy.
The natural history of thoracic disc herniations is not completely known. Brown et al15 found that 77% of patients with thoracic disc herniations did not require surgery to return to work. Perhaps some patients with minimal findings such as axial back pain and sensory loss can be managed conservatively with rest, physical therapy, oral NSAIDs, and even injections, but patients with myelopathy or persistent symptoms following nonoperative treatment warrant surgical intervention. Due to the narrow diameter of the thoracic canal and the need to avoid manipulation of the spinal cord, thoracic disc herniations can be treated via anterior approaches as well and posterolateral approaches. Laminectomy alone is not recommended, as it does not address the primary pathology that lays ventral to the spinal cord. Central calcified discs should not be removed via a posterior laminectomy approach. These cases necessitate anterolateral techniques such as a thoracotomy. Transpedicular and costotransversectomy techniques are the posterolateral approaches used in cases when the disc herniation is soft.
Lumbar disc disease results from a similar degenerative process as the one described for cervical HNP. Again, these changes maybe a result of natural aging, environmental factors, or genetic predisposition. These changes maybe asymptomatic in some patients and can be found incidentally on imaging obtained for other reasons. It is important to consider etiologies for the pain and weakness that can be seen in lumbar radiculopathy including diabetic amyotrophy, osteoarthritic conditions, and synovial cysts. MRI helps differentiate these conditions.
As degenerative changes in the spine can be asymptomatic, correlation between patient complaints, physical examination, and radiographic findings is key. Some patients are able to cite a specific inciting event that was associated with sudden onset of pain but this is not always the case. Patients often complain of sharp, electric-like, shooting pain in a specific dermatomal distribution but the pain can also be characterized as aching and dull. There may also be associated weakness, paresthesias, and diminished reflexes. Paracentral disc herniations affect the traversing nerve root, whereas far lateral discs affect the exiting nerve root at that level.
Diskography: As with cervical HNP, typically not useful.
X-rays: Flexion-extension XR helps identify dynamic instability that may be contributing to disc herniation.
Plain computed tomography (CT): Identifies pars defects, osteophytes, and disc calcification.
Magnetic resonance imaging (MRI): Study of choice.
There have been no worthwhile randomized clinical trials (RCT) to date that have offered useable evidence of surgery versus conservative management. The SPORT trial that was published in 2006 was plagued by a poor design and high crossover rate that made it difficult to accept as true any recommendations from the paper. Therefore, unless there is a progressive neurologic deficit or loss of bowel, bladder, or sexual function, patients should undergo a trial of nonsurgical interventions17 Pain can be initially managed with NSAIDs, narcotics, and muscle relaxants combined with physical therapy (PT) for 6–8 weeks. A short trial of steroids may also be indicated in the acute setting. Epidural or transforaminal steroid injections are the next step if pain is persistent18–20 Patients who have unremitting pain after conservative measures (ie, PT and spinal injections) should be considered for surgical intervention. The procedure depends on the patients’ overall structural alignment and other pathologies, but the goal is always neurologic decompression while maintaining good biomechanical alignment and structural stability. All patients with neurologic deficits should be referred for neurosurgical evaluation, and patients with acute findings should be referred urgently.
The etiology of back pain due to disc disease is the same as that for lumbar radiculopathy. Axial low-back pain does not preclude lumbar radiculopathy, and in fact, the two are often coexistent.
Patients complain of back pain that worsens with activity and improves with rest and recumbency. Classical teaching is that back pain due to lumbar disc degeneration is exacerbated on examination by asking the patient to bend forward and relieved with extension, although this criterion is far from universal. Neurologic examination is normal. This is typically a diagnosis of exclusion, and it is important to rule out other pathologies that may account for the patient’s symptoms.
Flexion-extension XR: Rule out dynamic instability and spondylolisthesis.
MRI: It evaluates the discs and surrounding structures.
Diskography It is only used when diagnosis is truly in question, and even then its usefulness is debatable.
As for lumbar radiculopathy, all patients should initially be managed with conservative therapies. Patients with discogenic axial low-back pain do not show significant improvements with surgery compared to their conservatively managed counterparts.21 Unless there is other pathologies such as dynamic instability to account for the disc pathology, isolated axial back pain due to an intervertebral disc does not always respond well to surgery, although there are authors who find surgery to be beneficial.22
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