Neurology: A Clinician's Approach (Cambridge Medicine (Paperback)), 1st Ed.

17. Back pain, radiculopathy, and myelopathy

Definitions, history, and examination

Although back and neck pain is commonly managed by primary care physicians, it may come to neurological attention when it is refractory to treatment or when it is accompanied by signs or symptoms of radiculopathy, myelopathy, or cauda equina syndrome.


Radiculopathy is the clinical syndrome caused by pathology at the level of what neurologists call the nerve root, a structure that, strictly speaking, is a mixed spinal nerve containing both sensory and motor fibers. The classic history for radiculopathy is back or neck pain that radiates into the arm or leg in a band-like distribution. The pain should have a sharp, burning, or stabbing character, and is often accompanied by paresthesias. Although monoradiculopathy may produce weakness, this is often mild because most muscles are innervated by more than one nerve root (Table 17.1). Sensory loss due to radiculopathy follows a dermatomal distribution, and may also be mild or incomplete due to the overlapping distributions of the cutaneous sensory nerves (Table 17.2 and Chapter 15Figure 15.1). Patients with radiculopathy may have focal weakness (Chapter 11) or sensory disturbances (Chapter 16) in the extremities without accompanying back pain. The two most useful provocative tests for radiculopathy are the straight leg raise test for lumbosacral root lesions and Spurling’s test for cervical root lesions. To perform the straight leg raise test, instruct the patient to lie supine with their leg extended. Leg pain with passive flexion of the hip between 30 and 70° suggests the presence of a herniated disc secondary to L5 or S1 root compression. Anterior thigh pain with passive extension of the hip while the patient is prone suggests L2 or L3 root compression. To perform Spurling’s test, instruct the patient to tip their head to the symptomatic side. The test is positive for cervical radiculopathy if compressing the head from above in that position causes pain and paresthesias to radiate into the symptomatic arm.


Myelopathy is the pattern of sensorimotor deficits produced by damage to the spinal cord. An understanding of spinal cord neuroanatomy is necessary to determine the level of myelopathic deficits. For the purposes of clinical localization, the spinal cord consists of (Figure 17.1):

• The dorsal columns, which contain ascending sensory fibers mediating vibration and proprioception. Dorsal column lesions produce sensory deficits below the level of the lesion on the same side of the body.

• The lateral spinothalamic tracts, which contain ascending sensory fibers mediating pain and temperature. Spinothalamic tract lesions produce sensory deficits in all dermatomes beginning one to two levels below the level of the lesion on the opposite side of the body.

• The lateral corticospinal tracts, which contain descending motor fibers. Corticospinal tract lesions produce weakness and spasticity below the level of the lesion on the same side of the body.

• The dorsal horns, which relay all sensory information from the dorsal root ganglia to the dorsal columns and lateral spinothalamic tracts. Dorsal horn lesions produce loss of all sensory modalities at the level of the lesion on the same side of the body.

• The anterior horns, which contain the lower motor neurons. Anterior horn cell lesions produce flaccid paralysis at the level of the lesion on the same side of the body.

• The ventral white commissure, which contains decussating sensory fibers connecting the pain and temperature information in the dorsal horns to the contralateral spinothalamic tracts. Commissural lesions produce sensory loss one or two levels below the lesion both ipsilaterally and contralaterally.

Table 17.2 Sensory loss organized by dermatomes

Table 17.2

See also Chapter 15Figure 15.1

Table 17.1 Muscle weakness organized by myotomes

Table 17.1

See Chapter 10 for additional details of testing.

Figure 17.1

Figure 17.1 Cross-sectional diagram of the spinal cord showing locations of the clinically important structures on the left and expected clinical deficits on the right.

A complete myelopathy therefore produces sensorimotor loss at myotomes and dermatomes caudal to the level of the lesion, hyperreflexia, and upgoing toes. In addition, cord lesions lead to urgency of both bowel and bladder. Many patients have incomplete lesions, which may lead to patchy sensorimotor problems. In these patients, the distribution of weakness is most helpful in defining the presence of myelopathy.

In the acute stage, weakness from a severe spinal cord lesion is usually flaccid, and does not become spastic for several days to a few weeks following the injury. While severe lesions may produce complete plegia of the limbs, milder paresis with disproportionately greater weakness of the “upper motor neuron” muscles (see Chapter 10Table 10.1) is more common. Be aware, though, that upper motor neuron weakness is a guideline rather than a hard and fast rule, and that many patients with spinal cord lesions do not conform strictly to this pattern.

Cauda equina syndrome

The lumbar and sacral nerve roots emerge from the spinal column to form the cauda equina. Compression or infiltration of the cauda equina produces a distinctive lumbosacral polyradiculopathy characterized by weakness and sensory loss in the lower extremities, sphincter weakness with incontinence of both bowel and bladder, and sensory loss in the perineum. Sphincter tone may be reduced and an anal wink may be absent in patients with cauda equina syndrome. Anal sphincter tone is established by placing the finger inside the anus and asking the patient to bear down. An anal wink is tested by stroking the perianal skin and observing for contraction of the anal sphincter. Cauda equina syndrome is a true neurological emergency, and should be evaluated and treated as quickly as possible. In most cases, it is secondary to a large posterior intervertebral disc herniation or spinal stenosis. Important inflammatory causes of cauda equina syndrome include neoplastic invasion and cytomegalovirus infection.

Back pain due to neurological disease

Red flags

When evaluating back and neck pain, it is critical to seek red flags that point to dangerous conditions such as malignancy, epidural abscess, cord compression, and cauda equina syndrome. Any patient with a history of cancer, fevers, bowel or bladder dysfunction, or rapidly progressive weakness requires urgent imaging of the clinically involved area of the spine, preferentially MRI with and without contrast. Also consider urgent MRI for patients with thoracic-level signs or symptoms, as malignant processes such as epidural cord compression and epidural abscess have a propensity to involve this level of the spine.

Herniated nucleus pulposus

The intervertebral discs lie between the vertebral bodies, provide the spine with structural stability, and allow joint mobility. The discs consist of a tough fibrous annulus fibrosus surrounding a softer, more gelatinous nucleus pulposus. Posterior herniation of the nucleus pulposus is the most common cause of radiculopathy and myelopathy in people between the ages of 30 and 50. Although the precise mechanisms by which disc herniations produce symptoms are not entirely clear, it is likely that the herniated disc incites an inflammatory reaction leading to pain, while physical compression of the nerve root within the neural foramen or the spinal cord within the central canal is mechanistically more important in generating weakness and sensory loss. Trauma or excessive stretching or exercise may immediately precede symptoms, but clear precipitants of intervertebral disc herniation are often absent. Disc herniations are most common at the C5–6, C6–7, L4–5, and L5–S1 levels, and are distinctly uncommon in the thoracic spine. Discs may herniate posteriorly, posterolaterally, or far laterally, compressing different structures in each case. Table 17.3 summarizes the deficits expected with disc herniation at each of the four most common spinal levels.

If there are no red flags, treat patients with suspected herniated intervertebral discs conservatively and defer neuroimaging studies. Because resuming normal activity ultimately should be the goal of patients with intervertebral disc herniation, I usually recommend that patients continue their normal routines rather than beginning programs of bed rest or aggressive “boot camp” physical therapy. Instruct patients with cervical disc disease to wear a soft cervical collar at night, while using a computer, and while driving. Prescribe mild pain relievers including ibuprofen and acetaminophen as the first line of analgesia. Stronger medications including tramadol (50–100 mg bid) and long-acting narcotics (sustained-release oxycodone 10–20 mg bid) may be prescribed cautiously for patients with severe symptoms. Because back pain is often chronic, it is best to delay initiating narcotics for as long as possible. A short trial of corticosteroids (e.g. prednisone 60 mg × 3 days, 40 mg × 3 days, 20 mg × 3 days) is frequently very helpful in reducing the inflammation produced by a herniated disc. Agents for neuropathic pain such as gabapentin and nortriptyline do little for patients with intervertebral disc herniations except make them sleepy.

If conservative therapy does not improve symptoms after 6 weeks, more aggressive evaluation and treatment is indicated. MRI of the clinically involved level of the spine should be used to confirm the diagnosis, and possibly to plan surgery. Electromyography may be considered, but rarely offers any additional helpful information. Epidural steroid injections may provide short-term relief of pain, but do little to nothing for motor deficits and lack long-term efficacy.1 Surgical referral is indicated for patients with pain that persists despite 6 weeks of conservative therapy, progressive motor deficits, or incontinence of the bowel or bladder.

Figure 17.2

Figure 17.2 Sagittal T2-weighted MRI showing a herniated intervertebral disc (thick arrow) and hypertrophic ligamentum flavum (thin arrow) in a patient with spinal stenosis. Note the disappearance of the hyperintense CSF signal at the greatest level of stenosis. The faint hyperintense signal change in the spinal cord indicates significant cord compression.

Table 17.3 Common intervertebral disc herniation syndromes

Table 17.3

Spinal stenosis

As people age, the intervertebral discs desiccate, and a greater portion of the axial load must be assumed by the facet joints and ligamentum flavum. The combination of disc herniation, facet joint and ligament hypertrophy, and bony spur formation leads to osteoarthritic narrowing of the central spinal canal and neural foramina (Figure 17.2). Like intervertebral disc herniation, spinal stenosis may produce back pain, radiculopathy, myelopathy, or a cauda equina syndrome. Unlike symptoms from disc herniation, those from spinal stenosis typically develop in a subacute to chronic fashion. Spinal stenosis may also be distinguished from disc herniation by its greater tendency to involve the upper lumbar levels.

Neurogenic claudication is a well-known manifestation of spinal stenosis characterized by pain in the back and legs, with fatigue that develops with standing or walking and is relieved by rest and bending over. Neurogenic claudication is often difficult to differentiate from vascular claudication of the lower extremities (Table 17.4). In many older patients, both disorders exist simultaneously. If there is any doubt as to the source of claudication symptoms, referral to a vascular specialist may help to reach the correct diagnosis.

Conservative therapy of spinal stenosis is similar to that described for intervertebral disc herniation. Abnormal neuroimaging findings in patients with spinal stenosis must be interpreted cautiously, as many asymptomatic older people have radiographic evidence of degenerative arthritis. Electromyography is unhelpful in diagnosing spinal stenosis or in planning its treatment. Unfortunately, most patients with spinal stenosis do not improve markedly with physical therapy, medications, or epidural steroid injections. Consider surgery for patients with intractable pain, sphincter dysfunction, progressive weakness, or disabling exercise intolerance. Many spine surgeons are understandably reluctant to perform operations for older patients with spinal stenosis, as these patients frequently require multilevel operations, have medical comorbidities that make them poor surgical risks, and improve modestly at best with surgery.


Neoplastic epidural cord compression, most commonly caused by metastasis, represents a neurological emergency. The most common tumors that produce cord compression are those of the breast, lung, prostate, and lymphoreticular system.2 The most common site of epidural cord compression is the thoracic spine due to both its relatively rich vascular supply and to the greater number of thoracic vertebrae. Back pain, sometimes accompanied by radiculopathic symptoms, is usually the first sign of metastasis, and may go unnoticed for several months, especially in patients with undiagnosed cancer. As cord compression progresses,

Table 17.4 Differentiating between neurogenic and vascular claudication

Table 17.4

weakness develops in a myelopathic pattern and the patient becomes incontinent of bowel and bladder.

Any patient with known cancer who develops back pain should have MRI with and without contrast to look for cord compression. Time is of the essence in diagnosing and treating this condition, as the likelihood of maintaining ambulation and continence of the bowel and bladder is related to the severity of the deficits when treatment begins. Initiate corticosteroids as soon as cord compression is suspected: treat patients with severe weakness with 100 mg dexamethasone orally followed by 24 mg q6h, tapering the dose by 50% every 2–3 days.2 Definitive therapy of metastatic cord compression is determined by the patient’s overall prognosis and the type of primary tumor. Treat patients who are expected to survive for at least 3 months with a combination of surgical decompression and radiotherapy.3 Radiation without surgery is indicated for patients with radiosensitive tumors such as leukemia, lymphoma, and germ cell tumors, or those with otherwise poor prognosis. In patients without a known cancer history who present with epidural cord compression, evaluate for a primary tumor with a torso CT, mammogram for women, and testicular examination and prostate-specific antigen level for men. If these tests do not disclose a primary neoplasm, biopsy of the lesion may aid in diagnosis. Although the overall prognosis of patients who develop metastatic cord compression is poor, the probability of maintaining ambulation is excellent if appropriate measures are taken immediately.

Epidural abscess

Bacterial infection of the epidural space occurs either by hematogenous spread from a distant infectious source or by extension of a local infection. The most common organism responsible for epidural abscess is Staphylococcus aureus. Other frequently encountered organisms include Staphylococcus epidermidisEscherichia coli, and Pseudomonas aeruginosa. The well-known clinical triad of back pain, fever, and neurological deficits referable to the spine is present in only a minority of patients, and the diagnosis is most often missed when the triad is incomplete. Failure to detect and treat epidural abscess leads to potentially irreversible weakness, sphincter dysfunction, and distant spread of the infection. MRI of the spine with and without contrast is the diagnostic study of choice in patients with suspected epidural abscess. Unless there are clear signs that the abscess is restricted to a particular vertebral level, the best practice is to image the entire length of the spine in order to detect all possible foci of infection. Patients with epidural abscess and neurological dysfunction require surgical drainage plus a 6-week course of vancomycin (1 g IV bid), ceftriaxone (2 g IV bid), and metronidazole (500 mg IV q8h).

Inflammatory radiculopathies (radiculitis)

The majority of radiculopathies are caused by structural disease of the spine. Inflammatory radiculopathy and polyradiculopathy are less common but important, as they frequently reflect serious and reversible underlying medical conditions. In general, radiculitis should be considered in patients with radiculopathy and normal imaging studies or imaging studies that show inflammation of the nerve roots without obvious structural spinal disease. Spinal fluid analysis is essential to the evaluation of patients with suspected radiculitis. Common causes of inflammatory radiculopathy include Lyme disease, diabetes (especially at the thoracic levels), sarcoidosis, malignant nerve root invasion, and viral infections (most commonly herpes zoster, cytomegalovirus, and herpes simplex).

Musculoskeletal back pain

A wide variety of musculoskeletal conditions may produce back and neck pain. Although such pain is generally self-limited, it may also be chronically disabling and lead to missed work and financial hardship. In addition, because there are no reliable diagnostic tests for musculoskeletal back pain, it is fertile ground for malingerers. Patients with refractory musculoskeletal back pain are frequently referred to neurologists to “rule out a neurological cause.” Thus, it is essential to be able to differentiate between neurological sources of back pain and nonneurological ones. Typical characteristics of nonneurological back pain include tightness, aching, swelling, point tenderness, and a lack of symptom radiation into the extremities. Paresthesias and true motor dysfunction (not give-way weakness, which is frequently the result of pain or poor effort) should be absent. Although most patients with musculoskeletal pain cannot be given a precise diagnosis, the following are some of the exceptions that should be familiar to all neurologists.

Strains and sprains

Muscle strains and ligament sprains are the most common nonneurological causes of back pain. The patient usually describes a history of injury such as lifting a heavy suitcase or moving a piece of furniture, which is followed several hours to a few days later by nonradiating, dull, aching pain. Strains and sprains are usually identified and treated by primary care physicians, but, in some cases, atypical symptoms such as tingling or burning may lead to neurological referral. A combination of rest, ice, and nonsteroidal anti-inflammatory drugs (NSAIDs) generally improves symptoms in a few days.

Spinal fractures

Osteoporosis, trauma, and metastasis are the most important causes of spinal fractures. Fractures due to metastasis are more likely to involve the thoracic levels. Obviously, unstable fractures are a medical emergency and need to be treated with immobilization and possibly with surgical stabilization. Acute compression fractures without compromise of the cord may be treated with immobilization and pain relievers. Vertebroplasty is commonly performed for osteoporotic fractures, but offers no real advantage compared with that provided by conservative measures.4,5

Sacroiliac joint dysfunction

Pain derived from the sacroiliac joints is possibly among the most common causes of lower back pain, but may be unrecognized because it is not a well-defined clinical entity. Patients complain of back pain, which may mimic radiculopathy because it radiates into the groin, hip, thigh, or leg. The mainstay of treatment is NSAIDs and gentle physical therapy. Focal injections are reserved for patients with refractory symptoms.


Pain in the coccygeal region may mimic sacral radiculopathy or lead to evaluation for cauda equina syndrome. Although there may be a history of trauma, coccygodynia may be the result of nothing more than prolonged sitting. The diagnosis is confirmed by finding tenderness with direct manipulation of the coccyx. Treat patients with coccygodynia with cushioned seating and local steroid injections.

Painless myelopathy

A variety of processes, most of which are intrinsic to the cord, lead to painless subacute or chronic myelopathy.

Transverse myelitis and multiple sclerosis

These are two of the most common causes of myelopathy caused by intrinsic cord disease, and are discussed further in Chapter 22.

Vitamin B12 deficiency

Vitamin B12 deficiency may affect the myelin of the cerebrum, optic nerves, spinal cord, or peripheral nerves. The most common presentation is subacute-to-chronic myelopathy with prominent numbness and paresthesias in the hands and feet. Causes of vitamin B12 deficiency include vegetarianism, pernicious anemia, and gastric bypass. The diagnosis is straightforward when the serum B12 level is low. If the B12level is more than the laboratory-defined lower limit of normal but still relatively low (e.g. <500 pg/ml), look for elevated levels of homocysteine and methylmalonic acid to diagnose subtle B12 deficiency.6Although high-dose oral and intramuscular formulations are presumably equivalent, most patients with myelopathy secondary to B12 deficiency should be treated with intramuscular B12, starting at 1 mg daily for 1 week, 1 mg weekly for 1 month, and then 1 mg monthly thereafter.


Adrenoleukodystrophy (ALD) is an X-linked disorder that usually causes cognitive decline, blindness, and quadriparesis in young boys. Both men and women between their second and fourth decades may develop adrenomyeloneuropathy (AMN), a milder form of the disease characterized principally by myelopathy.7 The majority of these patients have adrenal dysfunction, and some also have cerebral involvement, which preferentially involves the parietal and occipital lobes. Nerve conduction studies characteristically show slow nerve conduction velocities reflective of demyelination. The diagnosis is established by finding elevated levels of very long chain fatty acids in the plasma. There is no cure for ALD, but affected patients may be referred for a clinical trial of Lorenzo’s oil.

Metachromatic leukodystrophy

Metachromatic leukodystrophy (MLD) is an autosomal recessive disorder that presents uncommonly in adults as a painless myelopathy, spastic paraparesis, or a neuropsychiatric disorder.8 Brain MRI usually shows symmetric, periventricular cerebral white matter changes that spare the subcortical U-fibers. Nerve conduction studies characteristically show nerve conduction velocities in the demyelinating range. The disorder is diagnosed by finding low levels of leukocyte arylsulfatase A. Unfortunately, there is no cure for MLD.

Tropical spastic paraparesis

Human T-cell leukemia virus (HTLV) is endemic to the Caribbean, Japan, and Africa. It is transmitted through sexual contact, blood transfusion, or intravenous drug use. However, fewer than 5% of patients infected with the virus develop tropical spastic paraparesis.9 This disorder is a slowly progressive, painless myelopathy characterized by gait instability, hyperreflexia, and sphincter dysfunction. All myelopathic patients from endemic regions or with risk factors for infection with the virus should undergo serum HTLV polymerase chain reaction (PCR) testing. Although treatment of tropical spastic paraparesis is of limited benefit, diagnosis and counseling are important to prevent further transmission of the virus.

Dural arteriovenous fistula

Dural arteriovenous fistula (AVF) is an uncommon but important cause of slowly progressive, usually painless myelopathy. In general, the presentation is identical to that of other chronic myelopathies, although some patients may report that their symptoms characteristically worsen with exercise. The diagnosis is often elusive, and symptoms may progress for years before the condition is identified correctly. If dural AVF is suspected, MRI and magnetic resonance angiography (MRA) of the spine should be performed first, as they help to guide conventional angiography. Embolization of the fistula cures a minority of patients, and most will ultimately require surgical treatment.10

Copper-deficiency myelopathy

Copper-deficiency myelopathy, identified only recently, is characterized by slowly progressive lower extremity weakness and spasticity.11 Patients who use excessive amounts of zinc-containing denture cream or zinc supplements (zinc competes with copper for intestinal absorption) are at risk of developing the disorder. The diagnosis is established by finding low serum copper levels. Copper supplementation may help patients with copper-deficiency myelopathy, but the response is usually modest.

Hereditary spastic paraplegia

Hereditary spastic paraplegia (HSP) is a heterogeneous group of conditions causing lower extremity weakness, spasticity and hyperreflexia.12 It may be inherited in any fashion, although autosomal dominant forms are the most common. The diagnosis of HSP may be straightforward in patients with a suggestive family history. Simple HSP is characterized by spastic paraparesis, while complicated HSP includes additional dysfunction of other parts of the nervous system.

Spinal cord infarction

Spinal cord infarction is much less common than cerebral infarction. The two main varieties of spinal cord infarction are the anterior spinal artery syndrome and transverse spinal cord infarction. Both varieties tend to affect the mid-thoracic spine, as this is the vascular watershed territory between the upper thoracic arteries and the artery of Adamkiewicz (which enters the cord from T10–L1 and supplies the lower thoracic and lumbar regions). The typical clinical history of spinal cord infarction is sudden-onset back pain (although pain may be absent in many patients) followed by weakness and sensory loss in the trunk and legs. Because the anterior spinal artery supplies the ventral two-thirds of the cord, patients with anterior spinal artery syndrome lose motor and spinothalamic function below the level of the lesion while maintaining dorsal column sensibilities. Transverse cord infarction produces a state of spinal shock characterized by flaccid weakness, areflexia, and sphincter dysfunction. Etiologies of spinal cord stroke include emboli that result from cardiac or aortic surgery, spinal vascular malformations, and vasculitis. Unfortunately, imaging of spinal cord stroke is not as reliable as is imaging of cerebral stroke: diffusion-weighted imaging protocols for the spine are not yet solidified, and the characteristic MRI changes (T2 hyperintensity within the cord with T1 showing evidence of cord edema) are usually not visible for several days. Treatment options for spinal cord stroke are somewhat limited. In addition to supportive care and modification of risk factors for vascular disease, the mainstays of therapy include steroids and CSF drainage. Unfortunately, there are few rigorous data to recommend any particular medical therapy.


1. Koes BWScholten RJMens JMBouter LM. Efficacy of epidural steroid injections for low back pain and sciatica: a systematic review of randomized clinical trials. Pain 1995;63:279–288.

2. DeAngelis LMPosner JBNeurologic Complications of Cancer. Oxford: Oxford University Press; 2009.

3. Patchell RATibbs PARegine WF, et al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised trial. Lancet 2005;366:643–648.

4. Kallmes DFComstock BAHeagerty PJ, et al. A randomized trial of vertebroplasty for osteoporotic spine fractures. N Engl J Med 2009;361: 569–579.

5. Buchbinder ROsborne RHEbeling PR, et al. A randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med 2009; 361:557–568.

6. Savage DGLindenbaum JStabler SPAllen RH. Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies. Am J Med1994;96:239–246.

7. Moser HW. Adrenoleukodystrophy: phenotype, genetics, pathogenesis and therapy. Brain 1997; 120:1485–1508.

8. Rauschka HColsch BBaumann N, et al. Late-onset metachromatic leukodystrophy. Genotype strongly influences phenotype. Neurology 2006;67:859–863.

9. Orland JREngstrom JFridey J, et al. Prevalence and clinical features of HTLV neurologic disease in the HTLV Outcomes Study. Neurology 2003;61:1588–1594.

10. van Dijk JMCTerBrugge KGWillinsky RAFarb, RIWallace, MC. Multidisciplinary management of spinal dural arteriovenous fistulas: clinical presentation and long-term follow-up in 49 patients. Stroke 2002; 33:1578–1583.

11. Kumar NGross JBAhlskog JE. Myelopathy due to copper deficiency. Neurology 2003;61:273–274.

12. Salinas SProukakis CCrosby AWarner TT. Hereditary spastic paraplegia: clinical features and pathogenetic mechanisms. Lancet Neurol 2008; 7: 1127–1138.