Lower Back and Lower Limb Pain

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Chapter 30 Lower Back and Lower Limb Pain

Lower back pain is one of the most common reasons for neurological and neurosurgical consultation. The cost to society is huge, with estimates of up to $80 billion per year in direct and indirect healthcare costs and loss of productivity. In Switzerland, low back pain consumes 6.1% of the total healthcare budget and up to 2.3% of their GDP (Wieser et al., 2010). In many of the patients who present with lower back pain, the pain either developed or was exacerbated as a result of occupational activity. Lower limb pain is a common accompaniment to lower back pain but can occur independently.

The list of considerations in the differential diagnosis of lower back and lower leg pain is extensive and includes neural, bone, and non-neurological disorders. Although lower back pain usually is thought of as either neuropathic (specifically, radiculopathy-associated) or mechanical in origin, other possible sources of pain, including urolithiasis, tumors, and other intraabdominal processes, must be considered in the differential diagnosis.

Related Anatomy and Physiology

The lumbosacral spinal cord terminates in the conus medullaris at the level of the body of the L1 vertebra (Fig. 30.1). The motor and sensory nerve roots from the lumbosacral cord form the cauda equina. From there, the motor and sensory nerve roots unite at the dorsal root ganglion to form the individual spinal nerves. These anastomose in the lumbosacral plexus (Fig. 30.2), from which run the major nerves supplying the leg (Table 30.1).

Fig. 30.1 Oblique (A) and axial (B) views of the spine showing anatomical relationships between neural and bone elements.

Fig. 30.2 Anatomy of the lumbosacral plexus.

(Reprinted with permission from Bradley, W.G., 1974. Disorders of the Peripheral Nerves. Blackwell, Oxford, p. 29.)

Table 30.1 Motor and Sensory Function of Lumbosacral Nerves

Pain in the lower back can have many origins. A good beginning for the differential diagnosis is determining whether the leg also has pain. A complicating factor in this consideration is that local spine pain can be referred—that is, felt at a distance—because of the common nerve root innervation of the proximal spinal nerves and peripheral nerves supplying distal parts of the leg.

Causes of lower back pain without leg pain include:

Causes of lower back plus lower limb pain include:

Radiculopathy

Plexopathy

Important causes of leg pain without low back pain include:

Sciatic neuropathy

Femoral neuropathy

Peroneal neuropathy

Meralgia paresthetica

Peripheral neuropathies

Isolated tibial neuropathy is uncommon. Individual peripheral nerve lesions usually are caused by local trauma, entrapment by connective tissue, or involvement with mass lesions.

Lower back pain occasionally is caused by non-neurological and nonskeletal lesions. Some of the most important causes are:

Urolithiasis

Ovarian cysts and carcinoma

Endometriosis

Bladder or kidney infection

Abdominal aortic aneurysm

Diagnosis

The first step in diagnosis is localization of the causative lesion. History and examination usually allow differentiation among mechanical, neuropathic, and non-neurological pain.

History and Examination

The history should focus first on features of the back and leg pain:

Mode of onset

Character

Distribution

Associated motor and sensory symptoms

Bladder and bowel control

Exacerbating and remitting factors

History of predisposing factors (e.g., trauma, cancer, osteoporosis)

For example, the acute onset of lower back pain radiating down the leg suggests a lumbosacral radiculopathy. Onset with exertion suggests a herniated disk as a cause of the radiculopathy. Onset following a motor vehicle accident also could be associated with a disk herniation, although contusion of a nerve root without ongoing compression is more common after this type of trauma. Progressive symptom development can be from any expanding lesion, such as a tumor or expanding disk extrusion.

Patients with lower back and leg pain usually have more symptoms than signs of neurological dysfunction. Therefore, if examination shows sensory and motor signs in a specific radicular or neural distribution, a detectable structural lesion is more likely.

The neurological examination is targeted to determine whether the symptoms are accompanied by abnormal neurological signs. General examination of the lower limb is important. Muscle groups that can be tested include:

Sensory examination should include the important nerve roots and peripheral nerve distributions: the femoral, peroneal, tibial, and lateral femoral cutaneous, lumbar roots L2-L5, and sacral root S1. Reflexes to be studied include the Achilles, patellar, and plantar reflexes.

Exacerbation of pain with some maneuvers also can be revealing. Stretch of damaged nerves results in increased pain by deforming the axon membrane, thereby increasing membrane conductance, depolarizing the nerve, and producing repetitive nerve pain action potentials. Straight leg raising augments pain in a lumbosacral radiculopathy. Hip extension exacerbates pain of upper lumbar radiculopathy or that due to damage to the upper parts of the lumbar plexus, such as from carcinomatous infiltration or inflammation.

Armed with the abnormalities recognized from this history and examination, the neurologist may come to a conclusion about the localization of the lesion. This knowledge narrows the differential diagnosis substantially.

Differential Diagnosis of Lower Back and Leg Pain

The differential diagnosis of lower back and leg pain can be addressed as shown in Tables 30.2 through 30.5. Classification into mechanical and neuropathic categories is useful to narrow the scope of diagnostic considerations. The possibility of non-neurological causes should always be kept in mind.

Table 30.2 Classification of Lower Back and Lower Limb Pain

Type	Examples
Mechanical pain	Facet pain Bony destruction Sacroiliac joint inflammation Osteomyelitis Diskitis Lumbar spondylosis

Neuropathic pain

Polyneuropathy

Radiculopathy from disk disease, zoster, and diabetes

Mononeuropathy including sciatic, femoral, lateral femoral cutaneous, and peroneal neuropathies

Plexopathy from cancer, abscess, hematoma, and autoimmune processes

Non-neurologic pain

Urolithiasis

Retroperitoneal mass

Ovarian cyst or carcinoma

Endometriosis

Table 30.3 Differential Diagnosis of Lower Back and Leg Pain

Disorder	Clinical Features	Diagnostic Findings
Radiculopathy	Back pain radiating into leg in a dermatomal distribution. Sensory loss and motor loss are in a root distribution. Increased pain with coughing or straining.	Suspected when neuropathic pain radiates from back down into leg in a single root distribution. Disk or mass can be seen on MRI or CT. Zoster and diabetes can cause radiculopathy without abnormal studies.
Plexopathy	Back and leg pain with a neuropathic character, dysesthesias, burning, or electric sensation. Back pain can develop when cause is mass lesion in region of plexus.	Suspected when patient has leg pain in more than one peripheral nerve or root distribution. MRI of plexus or CT of abdomen and pelvis can show mass or hematoma.
Spinal stenosis	Pain in lower back, buttocks, and legs, especially with standing, walking, and lumbar spine extension.	MRI or CT shows obliteration of subarachnoid space.

CT, Computed tomography; MRI, magnetic resonance imaging.

Table 30.4 Differential Diagnosis of Isolated Lower Back Pain

Disorder	Clinical Features	Diagnostic Findings
Sacroiliac joint inflammation	Pain lateral to spine where sacrum inserts into top of iliac bone. Pain is exacerbated by movement and pressure but does not radiate down leg.	Clinical diagnosis. Radiographs can show degenerative changes in joint. Bone scan shows increased uptake in region.
Facet pain	Unilateral or bilateral paraspinal pain without radiation. Pain is increased by spine motion, especially extension.	Clinical diagnosis. Radiographs can show facet degeneration.
Ovarian cyst or cancer	Pain in hip and lower back, often but not always extending into lower quadrant. Bowel disturbance may develop with advanced disease.	Abdominal and pelvic CT shows mass lesion in ovary.
Endometriosis	Usually pelvic pain but occasionally pain in back and legs. Pain is often timed to menses.	Diagnosis suspected during pelvic exam. Vaginal ultrasound is supportive. Laparoscopy is diagnostic.
Retroperitoneal mass, abdominal aortic aneurysm, abscess, hematoma	Pain in back. May be bilateral to spine. May be associated with superimposed neuropathic pain in cases with plexus or proximal nerve involvement.	CT or MRI shows hematoma, aneurysm, eroding vertebral bodies, or abdominal mass.
Urolithiasis	Pain in upper to mid-back laterally that may radiate to groin. No radiation into leg.	Radiographs may show stones. Intravenous pyelography typically shows obstruction of flow. Contrasted abdominal CT usually shows the stone and obstruction.
Diskitis	Pain in lower back exacerbated by movement. Some patients may have radiation of pain to abdomen, hip, or leg.	MRI shows characteristic changes in disk and surrounding tissues.

Table 30.5 Differential Diagnosis of Isolated Leg Pain

Disorder	Clinical Features	Diagnostic Findings
Peroneal neuropathy	Loss of sensation on dorsum of foot. Weakness of foot and toe dorsiflexion.	Slowed nerve conduction velocity across region of entrapment, usually at fibular neck. EMG may show denervation in peroneal-innervated muscles, especially tibialis anterior, without involvement of short head of biceps femoris.
Femoral neuropathy	Pain and sensory loss in anterior thigh, often with weakness of quadriceps and suppression of knee reflex.	NCS can sometimes be performed but may be technically difficult. EMG may show denervation in a distribution limited to femoral nerve.
Piriformis syndrome	Pain from back or buttock down posterior thigh. Pain is exacerbated by sitting or climbing stairs. Stretch of piriformis (flexion and adduction of the hip) worsens pain.	Clinical diagnosis. Pain radiating down leg in a sciatic nerve distribution. Exacerbation of pain by flexion and adduction of hip. EMG and NCS may show proximal sciatic nerve damage.
Meralgia paresthetica (lateral femoral cutaneous nerve dysfunction)	Pain and loss of sensation of lateral femoral cutaneous nerve on lateral aspect of thigh.	Clinical diagnosis. NCS is difficult to perform on this nerve.
Claudication	Pain in thigh and lower leg with exertion. Pain does not occur with lumbar spine extension.	Suspected with exertional leg pain without back pain. Ultrasonography or angiography confirms arterial insufficiency.
Plexopathy	Back and leg pain that has a neuropathic character. Dysesthesias, burning, or electric sensation. Plexitis has no associated back pain.	Suspected when a patient has leg pain in more than one peripheral nerve distribution. MRI of plexus or CT of abdomen can show a structural lesion in some patients.
Radiculopathy	Pain largely in one dermatomal distribution. May be motor and reflex loss. Most patients have back pain, but not all.	Suspected with pain radiating down one leg with or without back pain. Best imaged by MRI or postmyelographic CT.

CT, Computed tomography; EMG, electromyography; MRI, magnetic resonance imaging; NCS, nerve conduction studies.

Some basic guidelines for the differential diagnosis of lower back and leg pain are as follows:

Pain confined to the lower back generally is caused by a low back disorder.

Pain confined to the leg usually is caused by a leg disorder, although neuropathic pain from lumbar spine disease can radiate down the leg without back pain in a minority of patients.

Pain in both the low back and the leg usually is caused by lumbar radiculopathy or, less commonly, lumbosacral plexopathy.

Clinical abnormalities confined to one nerve root distribution usually are caused by intervertebral disk disease or lumbosacral spondylosis producing radiculopathy.

Clinical abnormalities that involve several nerve distributions usually are caused by plexus lesions, with cauda equina lesions being the alternative diagnosis.

Bilateral lesions suggest proximal damage in the spinal canal affecting the roots of the cauda equina.

Impairment of bladder control indicates either a cauda equina lesion or, less commonly, a bilateral sacral plexopathy.

Presence of more than one lesion may complicate neurological localization.

Non-neurological causes of lower back pain are possible and particularly include urolithiasis, abdominal aortic aneurysm, and other intraabdominal pathological processes.

Multiple lesions can make the differential diagnosis more difficult. For example, radiculopathies at two or more levels may look like a plexopathy or peripheral neuropathic process.

Non-neurological causes of lower back pain include urolithiasis, ovarian cysts, endometriosis, pelvic carcinoma, bladder infection, and other retroperitoneal lesions including tumor, abscess, abdominal aortic aneurysm, and hematoma. These conditions produce pain that does not radiate unless neural structures are involved. Neural involvement in the abdomen and pelvis can produce radiating pain that can be clinically differentiated from radiculopathy only if multiple nerve roots are involved. Early involvement of bowel or bladder function together with abdominal pain suggests one of these non-neurological conditions.

Evaluation

Diagnostic evaluation of lower back and lower leg pain begins with proper clinical localization and classification of the complaint. Diagnostic tests are summarized in Table 30.6 (Russo, 2006). The tests used depend on the clinical presentation, as discussed later (see Clinical Syndromes).

Table 30.6 Diagnostic Studies for Lower Back and Lower Limb Pain

Diagnostic Test	Advantages	Disadvantages
Magnetic resonance imaging (MRI)	Sensitive for identification of lumbar disk herniation, spinal stenosis, paravertebral mass in region of plexus, perineural tumors, and diskitis	May overemphasize structural lesions. May miss vascular lesions of spinal cord. Paravertebral disorders may be overlooked if they are not the focus of interest. Cannot be performed on patients with some implanted metallic and electrical devices.
Non-contrast computed tomography (CT)	Shows osteophytes and lateral disk herniations best. Can show bone fractures and extension of fragments into regions that may contain neural elements.	Cannot identify neural elements without intrathecal contrast. Disk herniations without bone involvement may be missed.
Myelography with postmyelographic CT	Many neurosurgeons consider this the definitive test for identification of lumbar disk herniation, osteophytes, and intervertebral foraminal stenosis. Postmyelographic CT should be routinely performed.	May miss far-lateral herniations. Is invasive with a small risk of serious adverse effects.
Nerve conduction studies (NCS) and electromyography (EMG)	Sensitive for identification of specific nerve root or peripheral neuropathic involvement	Patients may have clinically significant radiculopathy without EMG evidence of denervation (or vice versa if radiculopathy is old).
Diskogram	Can identify disk anatomy in comparison with bony and neural anatomy. May confirm disk level if it produces pain that reproduces patient’s complaints.	Invasive test, but risk of serious complications is low. Seldom performed in routine practice.

Clinical Syndromes

Lower Back and Leg Pain

Lumbar Spine Stenosis

Lumbar spine stenosis is a disorder that affects mainly late middle-aged and older adults. The cause is multifactorial, with disk disease, bony hypertrophy, and thickening of the ligamentum flavum being the most important. Some of the symptoms are undoubtedly caused by direct pressure of these tissues on the cauda equina and exiting nerve roots, but a major contributor appears to be compression of the vascular supply of the nerve roots. Standing is associated with extension of the lumbar spine, which causes anterior bulging of the ligamentum flavum that lies posteriorly. Compression of the vascular supply creates nerve root ischemia, which can produce severe pain and weakness with exertion.

A diagnosis of lumbar spine stenosis should be suspected in patients with leg pain that is exacerbated by standing and walking and relieved promptly by sitting. Lying down, especially in the prone position, may exacerbate the low back pain, again through lumbar extension, a feature that helps differentiate lumbar spine stenosis from lumbar radiculopathy.

Confirmation of the diagnosis is by MRI or CT of the lumbar spine, which shows obliteration of the subarachnoid space at the level of the lesion. The hypertrophied ligamentum flavum and osteophyte formation usually are evident on these studies. If doubt about the diagnosis exists, myelography with postmyelographic CT scanning can be performed, but this invasive test seldom is needed.

Treatment can be conservative in the absence of neurological deficits. Physical therapy and medications can help, but surgical decompression is often required. Weakness of the legs or sphincter disturbance indicates a need for decompression. Although good evidence supports the benefit of surgical decompression in at least the short term, it is not clear that complex spine surgery with instrumentation produces substantial improvement in outcome (Gibson and Waddell, 2005).

Cauda Equina Syndrome and Conus Medullaris Syndrome

Lesions of the lumbar spine can result in damage to the conus medullaris, cauda equina, or both. Cauda equina syndrome is compression of the nerve roots below the termination of the spinal cord. Nerve root dysfunction is due to direct compression by surrounding structures. Important causes include acute trauma, chronic degenerative bony disease with retropulsion of fragments into the spinal canal, lumbar disc disease, infections such as abscess, intraspinal and meningeal tumor, and intraspinal hematoma. This syndrome can be a rare complication of minor and major spinal procedures. Cauda equina syndrome usually develops as an insidious chronic process unless due to acute trauma. Symptoms can include back pain, leg pain, weakness and cramps in the legs. Sensory symptoms can be sensory loss as well as neuropathic pain. Sphincter disturbance is common, especially with progression.

Conus medullaris syndrome is due to damage to the terminus of the spinal cord above most of the cauda equina and therefore at a higher spinal level. Etiology can be compression from all the conditions listed above plus occasional infiltrating lesions of the conus medullaris itself, especially by tumor. Conus medullaris syndrome is usually more rapidly progressive, associated with earlier back pain and sphincter disturbance, and is more likely to be associated with preservation of some lower extremity reflexes, usually patellar.

MRI is the preferred diagnostic imaging method. If MRI cannot be performed, many causes of both syndromes can be identified on CT of the spine.

Lumbosacral Radiculopathy

Lumbosacral radiculopathy usually is caused by infringement on the neural foramen by either herniated disk material or osteophytes. Herniated disk is more common in young patients; osteophyte formation is more common in older patients.

Patients present with back pain radiating down the leg in a distribution appropriate to the involved nerve root. The most common lumbosacral radiculopathy is of the S1 nerve root, produced by a lesion at the L5-S1 interspace. Table 30.7 presents the typical motor, sensory, and reflex deficits associated with lumbosacral radiculopathy at individual levels.

Table 30.7 Lumbosacral Radiculopathy

The presence of lower back pain with radiating pain in a nerve root distribution points to a diagnosis of radiculopathy. Motor, sensory, and reflex deficits are not always present, so the diagnosis is suspected on the basis of symptoms without objective signs.

Confirmation of the diagnosis is by MRI, which can show disc protrusion or osteophyte encroachment with nerve root compression. MRI is the diagnostic procedure of choice for most surgeons, although postmyelographic CT is still occasionally used. Myelography with CT also may be used, especially in patients who cannot undergo MRI because of implanted electronic devices and metallic heart valves.

NCS findings usually are normal in patients with lumbosacral radiculopathy, although F-waves may be delayed in the affected root. EMG can reveal evidence of denervation in a nerve root distribution and usually can differentiate peripheral neuropathic processes from radiculopathy. This study also can determine whether denervation is present with radiculopathy.

Management of lumbosacral radiculopathy depends on the severity of symptoms, including pain and weakness. If the symptoms are mild, antiinflammatory agents may suffice. Muscle relaxants can produce short-term relief of muscle spasm and pain.

Surgical options for lumbosacral radiculopathy are considered when the patient has intractable pain refractory to conservative care; when weakness is prominent, especially if it is unresponsive to conservative management; and when sphincter disturbance is present. Sphincter disturbance caused by lumbar disk disease or spondylosis necessitates consideration of urgent surgery. Patients with such deficits should not be given a trial of conservative therapy.

An important management consideration is how long conservative treatment should be continued in patients with weakness before surgical options are considered. In general, weakness should prompt at least consideration of surgery. Patients may have mild and transient weakness that responds to conservative therapy, but if weakness is prolonged or severe, recovery is compromised.

Intractable pain without motor loss and with or without sensory loss can be treated surgically, but treatment effectiveness is limited.

Arachnoiditis

Arachnoiditis is inflammation of the arachnoid membranes surrounding the spinal cord. The inflammation can be caused by a number of processes including trauma to the spinal canal by injury or surgery, chronic compression of spinal nerves, chemicals such as intrathecal chemotherapy or contrast agents, blood products from subarachnoid hemorrhage, infections, or neoplasms. Some clinicians believe that arachnoiditis due to mechanical processes is overdiagnosed. Also, arachnoiditis has been attributed to some conditions for which causation is tentative at best, such as with some intrathecal contrast materials.

There is chronic inflammation of the motor and sensory nerve roots. The inflammation results in fibrinous adhesions between the membranes and nerve roots and between adjacent nerve roots.

Common symptoms include pain in the back and legs which typically has a neuropathic character. Sensory symptoms can be loss of sensation or dysesthesias. Muscle symptoms can include twitching and cramps, and in severe cases, weakness or even paralysis can develop.

Diagnosis of arachnoiditis is suspected in patients with low back and leg pain who have radiological studies which suggest the diagnosis; arachnoiditis is seldom a diagnosis of first consideration during initial evaluation. MRI shows thickened and clumped nerve roots. Careful examination of the imaging shows nerve roots adherent to each other and to the dura. When MRI cannot be performed, myelography can show the same overall appearance.

Diagnosis is confirmed by imaging, with MRI being the principal modality; myelography is typically used only if MRI cannot be performed. EMG can identify denervation spanning single root distributions and document motor dysfunction, but no EMG findings are specific for arachnoiditis. CSF analysis is performed if the differential diagnosis includes meningeal infection or tumor; neoplastic meningitis and chronic infections can produce a similar clinical and radiological appearance. CSF can be normal with noninfectious and non-neoplastic causes of arachnoiditis.

Treatment of arachnoiditis is dependent on the cause. For patients with arachnoiditis due to trauma, instrumentation, chronic nerve root compression, or other mechanical cause, treatment is symptomatic, involving medications and procedures for chronic neuropathic pain. Treatment is also symptomatic for patients with arachnoiditis due to resolved infections, previous chemical administration, or previous subarachnoid hemorrhage. Steroids are often administered to patients receiving some types of intrathecal chemotherapy to reduce the risk of arachnoiditis, although this is not completely protective.

Plexopathy

Neoplastic Lumbosacral Plexopathy

Neoplasms affecting the lumbosacral plexus can be solid or infiltrating. Infiltrating tumors such as lymphoma usually are treated by radiation therapy, which commonly is followed by chemotherapy for the systemic cancer. Solid tumors affecting the lumbosacral plexus rarely can be completely surgically excised without producing severe damage to the plexus.

Diagnosis is suspected with pain and often weakness in a leg associated with a known neoplasm. In such patients, the differential diagnosis often includes plexus infiltration, compression, and radiation plexopathy. MRI of the lumbar spine and plexus may show plexus involvement by tumor. EMG can help with differentiation of radiation plexopathy from neoplastic infiltration (Jaeckle, 2010).

Radiation therapy is given initially. Pain often is relieved shortly after the radiation therapy has begun. During initial treatment, anticonvulsants can be used to relieve the neuropathic pain. Pure analgesics also may be used, and sustained-release opiate formulations are effective in treating this condition.

Plexus Injury from Retroperitoneal Abscess

Retroperitoneal abscess usually is caused by peritonitis from gastrointestinal neoplasms or following surgery. Retroperitoneal abscess can affect the lumbosacral plexus. Patients present with abdominal and flank pain, often with overt signs of systemic infection, with fever, malaise, elevated white blood cell counts, and elevated C-reactive protein (CRP) concentration. The diagnosis is confirmed by CT of the abdomen. Management typically begins with surgical drainage followed by prolonged antibiotic treatment. Narcotics usually are needed for the pain of retroperitoneal abscess.

Plexus Injury from Retroperitoneal Hematoma

Retroperitoneal hematoma usually is caused by a bleeding disorder, a pelvic fracture, or abdominal surgery. Occasionally, bleeding from the site of arteriography can result in tracking of blood into the region of the lumbosacral plexus, especially after thrombolytic therapy or anticoagulation. Hematoma has also been described in patients after lumbar plexus block and may be delayed (Aveline and Bonnet, 2004).

This diagnosis should be suspected in patients with leg motor and sensory symptoms who are at risk for intraabdominal hemorrhage; abdominal and leg pain are common. Confirmation of the diagnosis is by CT of the abdomen, which can show blood in the region of the plexus.

Treatment of plexus hematoma is supportive. Evacuation of the hematoma is seldom needed, and surgery commonly is reserved for patients with continued blood loss, which must be arrested.

Leg Pain without Lower Back Pain

Peripheral Nerve Syndromes

Peripheral nerve palsy is commonly the result of sustained compression. Peroneal palsy is the most common lower-extremity syndrome, usually caused by pressure at the fibular neck. Femoral neuropathy commonly results from intraabdominal causes and can be difficult to differentiate from upper-lumbar plexopathy.

The diagnosis of peripheral nerve palsy is clinical, with symptoms and signs confined to one neural distribution. Patients usually present with neuropathic pain and sensory loss. Dysesthesias and paresthesias in the affected distribution are common. Reflex abnormalities depend on the individual nerves affected.

Definitive treatment of peripheral nerve entrapment is surgical release. Surgery is not always necessary, and conservative management may be successful. Tumor compression of peripheral nerves can be treated surgically, but radiation therapy can shrink the tumor, thereby relieving pain. Conservative management includes physical therapy to maximize comfort and improve function, antiinflammatory agents and anticonvulsants to alleviate pain, and counseling on methods to avoid subsequent damage. The counseling should address prevention of nerve compression and nerve stretch. For example, to prevent peroneal nerve compression at the fibular neck, the patient can avoid pressure on the posterior knee while the leg is extended and also can avoid squatting with the knee acutely bent.

Femoral Neuropathy

The femoral nerve usually is injured in the pelvis as it passes beneath the inguinal ligament or in the leg. Intraabdominal disorders including mass lesions and hematoma are commonly implicated. Femoral artery puncture for angiography also may be a cause, either directly or via the resultant hematoma.

Patients present with weakness that is most easily detected in the psoas, because the quadriceps is so strong. Sensory loss is over the anterior thigh and medial aspect of the calf and has a saphenous nerve distribution (the terminal sensory branch of the femoral nerve). This distribution of sensory loss is helpful to differentiate femoral neuropathy from lumbar radiculopathy. The patellar reflex usually is depressed.

The diagnosis can be supported by EMG evidence of denervation in the quadriceps but not in the lower leg or posterior thigh muscles. The adductors are especially important to test because they are innervated by the same nerve roots as for the femoral nerve but instead are innervated by the obturator nerve. Normal EMG findings cannot rule out this diagnosis, because many patients do not have active or chronic denervation. NCS of the femoral nerve is difficult, especially in large patients, who are predisposed to development of femoral neuropathy.

Treatment is seldom surgical, except for the removal of a massive psoas or iliacus hematoma or mass lesion. Weight loss and avoidance of marked hip flexion can reduce the chance of persistent damage. Physical therapy will aid recovery of motor power. Femoral neuropathy usually resolves.

Meralgia Paresthetica

Dysfunction of the lateral femoral cutaneous nerve commonly is caused by compression as it passes beneath the inguinal ligament. Obesity and pregnancy predispose to this disorder, as does intraabdominal surgery of a variety of types. Recent reports have even described soldiers with body armor having meralgia paresthetica. This problem is likely underdiagnosed and assumed to be a lumbar radiculopathy or atypical femoral neuropathy.

Meralgia paresthetica is the sensory syndrome of pain and sensory loss on the lateral thigh. Patients present with numbness and often pain on the lateral thigh. Motor deficits are not a feature. Meralgia paresthetica is differentiated from femoral neuropathy by the lateral distribution of the sensory findings and the absence of motor and reflex abnormalities.

Nerve conduction testing of the lateral femoral cutaneous nerve, although feasible, is technically difficult even in the best circumstances. It is even more difficult in obese patients, who are at particular risk for entrapment of the nerve.

Treatment is conservative. Weight loss usually is effective in preventing recurrence. Anticonvulsants and tricyclic antidepressants are effective for control of the neuropathic pain. A nerve block may be supportive of the diagnosis in patients unresponsive to conservative measures. Surgery is rarely performed, and controversy about its indications and effectiveness is ongoing (Harney and Patijn, 2007; Haim, et al., 2006).

Sciatic Neuropathy

The sciatic nerve is most likely to be injured as it leaves the sciatic notch and descends into the upper leg. Compression can occur in patients in prolonged coma, especially those who are very thin. The sciatic nerve also is susceptible to injury from pelvic and sacral fractures, hip surgery or dislocation, needle injection injuries, and any penetrating injury.

Patients present with pain that usually is localized close to the level of the sciatic nerve lesion, although substantial radiation of the pain may be a feature. Loss of sensation is prominent below the knee, sparing the medial lower leg (the territory of the saphenous branch of the femoral nerve). Weakness can affect all muscles of the lower leg, but peroneal-innervated muscles are more likely to demonstrate weakness for two reasons. First, tibial-innervated foot extensors are so strong that substantial weakness would have to be present for weakness to be evident on examination. Second, the peroneal division of the sciatic nerve is more susceptible to compression injury than the tibial division, even high in the thigh.

Sciatic neuropathy is a clinical diagnosis, although the EMG can show evidence of denervation in sciatic-innervated muscles; signs of denervation may not be seen until 4 weeks after injury. NCS findings usually are normal, but F-wave study may show slowing.

Treatment of sciatic compression is supportive, with avoidance of recurrent compression. Tricyclic antidepressants and anticonvulsants commonly are used for the neuropathic pain. In some patients with acute sciatic injury, opiates are needed to deal with the pain in the short term. Surgical exploration and decompression are performed only in patients with clear evidence of a structural lesion such as neural or perineural tumor.

Piriformis Syndrome

Piriformis syndrome is an uncommon condition in which the sciatic nerve is compressed by the piriformis muscle in the posterior gluteal area. Hypertrophy of the piriformis muscle and other anatomical variants predispose affected persons to development of the syndrome. This condition may affect not only the main sciatic trunk but also the superior gluteal nerve. The diagnosis and even existence of this as a singular condition is controversial (Halpin and Ganju, 2009).

Patients present with pain in the buttock that radiates down the leg and is exacerbated by adduction and flexion of the hip. Pain tends to be aggravated by prolonged sitting, climbing steps, and other maneuvers that irritate the piriformis muscle.

Piriformis syndrome is a clinical diagnosis. A patient with symptoms of sciatic neuropathy has typical clinical features on examination but no signs of radiculopathy or spinal stenosis on imaging. Spinal claudication can be confused with piriformis syndrome, so imaging of the spine usually is warranted. MRI neurography may show the lesion in many patients (Filler et al., 2005).

Piriformis syndrome usually is managed with antiinflammatory agents for acute exacerbations and with physical therapy, which can be tailored to address the specific problems and any associated limitations. Local injections of corticosteroids are given occasionally, but these are unlikely to produce long-term improvement. Surgical treatment is rarely performed, and controversy is ongoing about the indications and expected effectiveness of surgical treatment.

Peroneal Neuropathy

Peroneal neuropathy commonly is caused by compression of the nerve as it passes from the popliteal fossa across the fibular neck into the anterior compartment of the lower leg. Patients often present with foot drop from weakness of the tibialis anterior muscle. The diagnosis is confirmed by NCSs and EMG, with slowing of peroneal nerve conduction across the region of entrapment, usually across the fibular neck. The EMG shows evidence of active and chronic denervation in many patients, in keeping with the axonal damage indicated by the foot drop (Marciniak et al., 2005).

Peroneal neuropathy may be secondary to prolonged bed rest, or it may result from hyperflexion of the knee, usually from an occupational activity. The condition also may accompany peripheral neuropathy, predisposing to pressure palsy, or may be the result of a fibrous band attached to the peroneus longus, predisposing to nerve compression (Dellon, Ebmer, and Swier, 2002). In addition, pressure in obstetrical stirrups, prolonged sitting with crossed legs, cast on the lower leg for sprain or fracture, and stretch and compression by the contracted tibialis anterior muscle in ballet dancers all have been implicated. A fibrous band beneath the superficial head of the peroneus longus is found in a much larger proportion of patients with peroneal entrapment than in normal persons.

Polyneuropathy

Peripheral neuropathy is a common cause of lower-extremity pain. The differential diagnosis for this condition is broad in scope, as would be expected. Among the most common causes are diabetes mellitus, familial neuropathy, metabolic neuropathies, and vasculitis. Pain is the presenting manifestation and differs in character according to the type of neuropathy. Small-fiber neuropathies manifest with burning pain that often is worse in the evening. Large-fiber neuropathies manifest with dysesthesias and paresthesias, often with electric shock–like pains.

Diagnosis usually is confirmed by NCS and EMG. Axonal neuropathy is more common than demyelinating neuropathy. Occasionally, patients with a predominantly small-fiber sensory neuropathy have normal NCS findings. Laboratory studies for peripheral neuropathy typically are performed as outlined in Chapter 31.

Treatment is with tricyclic antidepressants or anticonvulsants. Amitriptyline commonly is used for patients with small-fiber neuropathic pain. Anticonvulsants are used predominantly for patients with large-fiber neuropathic pain. When patients have symptoms of both, treatment with gabapentin, pregabalin, or oxcarbazepine can be helpful. Combination therapy with a tricyclic and anticonvulsant may be beneficial. Pure analgesics occasionally are used on a nightly basis to assist with sleep (Singleton, 2005).

Plexopathy

Lumbosacral Plexitis

Lumbosacral plexitis is similar to brachial plexitis, a presumed autoimmune process, but is less common. This entity is differentiated from radiculitis, which can be an inflammatory disorder of autoimmune or infectious origin (Tyler, 2008).

Management of idiopathic lumbosacral plexitis is supportive, with no medical intervention known to alter the course of the disease. Anticonvulsants commonly are used for pain management. Corticosteroids and high-dose intravenous immunoglobulin also are used occasionally, although it is not clear that their benefits outweigh the risks. Lumbosacral plexitis constitutes an indication for the use of pure opiates, because the duration of the pain usually is weeks rather than months. As the pain abates and the weakness is more prominent, the analgesics usually can be tapered and discontinued. Sustained-release opiates are especially helpful for patients with plexitis.

Diabetic Amyotrophy

Diabetic amyotrophy is lumbosacral plexopathy occurring in persons with diabetes mellitus. The disorder is thought to be an inflammatory vasculopathy, with damage that probably is immune mediated. Patients present with pain in the hip and thigh associated with weakness of the quadriceps, psoas, and adductors. The plexopathy is more often unilateral than bilateral.

A diagnosis of diabetic amyotrophy is suggested by proximal pain and weakness in a patient with known diabetes. This disorder must be differentiated from lumbar radiculopathy and other structural lesions in the region of the plexus. NCSs and EMG show coexistent peripheral polyneuropathy denervation in proximal muscles including quadriceps, psoas, and adductors. MRI and CT do not show a structural lesion.

Treatment is symptomatic. Immune-modulating treatment with immunoglobulin may reduce the duration of the deficit but is not routinely administered. Most patients improve, although recovery is incomplete for most. The pain abates before recovery of muscle strength.

Herpes Zoster

With reactivation of varicella-zoster virus infection, the presenting symptom is pain in a single nerve root distribution. In most patients, a vesicular rash develops in the same cutaneous distribution, but the pain often begins before development of skin changes, and the skin changes are variable. Eventually the rash crusts over, leaving some pigmentary changes. The pain abates as the inflammation recedes, although the patient may be left with sensory or motor deficit. Weakness can be evident in muscle innervated predominantly by a single nerve root.

The diagnosis is based on clinical findings, and when the rash is present at onset, structural imaging usually is not necessary. NCSs and EMG often are not needed, but they may show denervation in affected muscles in cases with persistent nerve root damage. The differential diagnosis is broader in scope before development of the rash, and considerations include radiculopathy from other causes including disk disease and osteophytes.

Treatment with antiviral agents such as acyclovir or famciclovir should begin within 72 hours of symptom onset. Early treatment may help hasten recovery and reduce the incidence of postherpetic neuralgia. Corticosteroids often are used, and the chance of disseminated zoster is not appreciably higher in immune-competent patients. Corticosteroids reduce acute neuropathic pain and may decrease the incidence of postherpetic neuralgia. Use of corticosteroids is more important for zoster ophthalmicus than for lower-limb zoster.

Claudication of Leg Arteries

Arterial claudication is discussed here because it is an important element in the differential diagnosis of spinal stenosis. Vascular disease of the iliac arteries and terminal branches results in marginal perfusion of lower-limb muscles. Walking and other moderate activities exacerbate the ischemia, producing pain and weakness with exertion. The clinical picture may resemble that in spinal stenosis, but the lack of back pain with claudication, lack of exacerbation of leg pain with recumbent lumbar extension, and vascular changes in the leg are features that should be absent in spinal stenosis.

Claudication is diagnosed by vascular imaging. Ultrasound examination can be a good screening test, but angiography can provide a definitive diagnosis and in some patients can be the means for definitive treatment by angioplasty.

Lower Back Pain without Leg Pain

Mechanical Lower Back Pain

Mechanical lower back pain usually is caused by strain of paraspinal muscles and ligaments, with local inflammation. Muscle tears also may cause acute lower back pain. Therefore, mechanical lower back pain usually is a combination of bone, muscular, and connective tissue pain. Patients present with pain in the lower back without radicular symptoms and show no motor, sensory, or reflex abnormalities on examination. Any weakness or gait disturbance is due to pain and not neurological deficit.

Diagnosis is based on the clinical features and exclusion of other causes. In the absence of objective neurological deficits, spinal MRI usually is not needed initially, but radiography may be performed to look for bony fractures or erosion. NCSs and EMG usually are not needed. In the absence of signs of bony or neural destruction, conservative management may begin. If the patient does not respond to initial treatment, further study with MRI can be performed.

Mechanical lower back pain usually is treated by an initial period of rest of approximately 2 days, followed by an increase in activity. Physical therapy can be very helpful during this initial treatment period. After the initial treatment, self-help guidelines are followed to reduce the likelihood of recurrent lower back pain. Muscle relaxants can help reduce the tightness of the muscles, which impedes movement and can detract from successful physical therapy.

Patients who do not respond to conservative management may benefit from epidural blocks. Surgery for “bulging disks” occasionally is performed in patients who have clinically apparent mechanical back pain, but the likelihood of response is not high.

Facet Joint Pain Syndrome

Pain from the facet joints of the lumbosacral spine usually is not an isolated entity but rather a component of mechanical back pain. Pain results from long-term degenerative changes in the facet joints, usually caused by strain. Repetitive strenuous activity, excessive weight, and abnormal posture may predispose affected persons to the development of facet pain. Acute trauma to the back may produce active joint inflammation that can be self-limited.

Facet pain usually is lateral to the spine and exacerbated by extending the spine or bending toward the affected side. Facet pain often is bilateral. Prolonged sitting or walking up steps, as well as retaining one position for a prolonged time, tends to exacerbate the pain. Patients present with pain without motor, sensory, or reflex deficit unless radiculopathy or spinal stenosis is also present.

Results of diagnostic studies usually are normal. Chronic degenerative changes may be seen on radiographs, but with acute facet damage, even the radiographic appearance may be unremarkable.

Facet pain usually is treated with antiinflammatory agents and physical therapy. Avoidance of exacerbating activity usually is helpful. Facet blocks can be performed but often are not necessary, and effectiveness in terms of long-term relief is controversial (Varlotta et al., 2011). As part of physical therapy, traction can change the character of weight bearing on the joints. Physical therapy can strengthen paraspinal muscles and improve posture.

Lumbar Spine Osteomyelitis

Vertebral osteomyelitis is most common in the lumbar region and may develop as a sequela of trauma, urinary tract infection, respiratory infection, and other causes of sepsis. Patients present with lower back pain, which may develop weeks after the inciting infection has abated. Limitation of the motion of the spine and tightness of the paraspinal muscles are additional features. Local lumbar spine pain with tenderness to percussion is characteristic.

The diagnosis of vertebral osteomyelitis is suggested by lower back pain in a patient who has not received radiation therapy, associated with systemic signs of infection—fever, elevated CRP concentration, and elevated white blood cell count (An and Seldomridge, 2006). MRI shows changes in the vertebral body and often in adjacent psoas muscle. Radiographs show degeneration of the disk margin of the vertebral body and disk space narrowing. Needle biopsy can reveal the causative organism in most cases. Open biopsy usually is not necessary. The diagnosis can easily be missed initially, since it can occur in patients with preexisting lumbar spine pain, and inflammatory signs may not be marked early on (Mylona et al., 2009).

Treatment is with antibiotics and bed rest. Surgical débridement is needed in patients who do not respond to antibiotics.

Lumbar Spine Compression

Compression of the lumbar vertebral bodies occurs in the setting of acute trauma, osteoporosis, infection, or tumor. Presence of a tumor may predispose the lumbar vertebrae to collapse with minimal trauma or stress. Patients present with severe lower back pain, usually without radicular symptoms. If the collapse results in compression of the nerve roots by bone, radicular pain may develop in addition to the lower back pain. With compression of the cauda equina, diffuse weakness of the legs and sphincter disturbance can develop.

The diagnosis of lumbar spine compression is suggested by a clinical presentation of lower back pain that is exacerbated by movement, jarring, or certain postures such as bending or twisting. Radiographs and CT scans can easily show the associated bone destruction. Bone scan confirms the damage and can screen for other regions of damage. These studies, however, usually cannot pinpoint the cause of the compression. MRI is better able to make this differentiation, but it is not exact.

Treatment consists of immobilization of the fracture site, which may include bracing. Pure analgesics often are needed, especially at night. Corticosteroids should be avoided if the cause is osteoporotic but can be very helpful for malignant vertebral collapse. Malignant collapse usually is treated by radiation therapy; surgery is performed if the spine is unstable because of the destruction or in the absence of a known primary tumor in a patient with presumed neoplastic vertebral involvement. The benefits of acute surgical decompression for neoplastic cauda equina compression are controversial.

Lumbar Diskitis

Diskitis is an inflammatory process affecting the intervertebral disks of any level, often occurring in the lumbar spine. In adults, Staphylococcus aureus and mycobacteria are important causes, although the list of potential pathogens is large. The causative organism typically reflects the source from which the bacteria spread—for example, skin infection, urinary tract infection, or intestinal infection. Diskitis associated with recent lumbar surgery is likely to be caused by resistant bacteria. In children, diskitis is also usually due to S. aureus, but extraspinal manifestations of infection are less likely (Early, Kay, and Tolo, 2003).

Patients present with lower back pain with marked restriction of flexion of the spine, because flexion increases pressure on the disk and disk space. Patients with postoperative diskitis usually have systemic symptoms, but overt signs of infection with fever and chills may be absent.

A diagnosis of lumbar diskitis is suggested by the presence of severe lower back pain without a radicular component, with tenderness and spasm of the paravertebral muscles associated with willingness of the patient to flex the hips but not the spine (Mikhael et al., 2009). Erythrocyte sedimentation rate (ESR) and CRP concentration usually are increased. The diagnosis can be confirmed by MRI, which shows decreased signal intensity of the disk on T1-weighted images and increased signal intensity on T2-weighted images, often with changes in the end-plates of the adjacent vertebrae. Bone scan shows increased uptake in the region of the infected disk. Radiographs show disk space narrowing.

MRI is the most sensitive test for diskitis. Biopsy often is needed to identify an organism. Treatment begins with bed rest and antibiotics (Grados et al., 2007). Extensive surgery usually is not necessary; even tuberculous diskitis is successfully treated with antibiotics in more than 80% of cases (Bhojraj and Nene, 2002).

In some patients, diskectomy with fusion of the adjacent vertebral bodies may be required for relief of symptoms. Use of this management approach usually is restricted to adults; progression leading to surgery is less common in children.

References

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