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Lower back pain is one of the most common reasons for neurological and neurosurgical consultation. 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 is usually thought of as either neuropathic (specifically, radiculopathy-associated) or mechanical in origin, other possible sources of pain, including urolithiasis, tumors, infections, vascular disease, and other intraabdominal processes, must be considered in the differential diagnosis.
The lumbosacral spinal cord terminates in the conus medullaris at the level of the body of the L1 vertebra ( Fig. 33.1 ). 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. 33.2 ), from which run the major nerves supplying the leg ( Table 33.1 ).
Nerve | Origin | Motor Function | Sensory Function |
---|---|---|---|
Femoral | Lumbar plexus, L2–L4 | Extension of knee, flexion of thigh | Anterior thigh |
Saphenous | Distal sensory branch of femoral nerve | None | Inside aspect of lower leg |
Lateral femoral cutaneous | Branch of lumbar plexus, L2–L3 | None | Lateral thigh |
Obturator | Lumbar plexus, L2–L4 | Adduction of thigh | Medial aspect of upper thigh |
Sciatic | Combined roots from lumbosacral plexus, partially separated into tibial and peroneal divisions | Foot plantar (tibial division) and dorsiflexion (peroneal division), foot inversion (tibial) and eversion (peroneal) | Lateral, anterior, and posterior aspects of lower leg and foot |
Tibial | Lumbosacral plexus, L4–S3 | Plantar flexion and inversion of foot | Posterior lower leg and sole of foot |
Peroneal | Lumbosacral plexus, L5–S2 | Dorsiflexion and eversion of foot | Dorsum of foot and lateral lower leg |
Superficial peroneal | Distal sensory branch of peroneal nerve | None | Dorsum of foot |
Sural | Cutaneous branches of peroneal and tibial nerves | None | Lateral foot to sole |
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:
Ligamentous strain
Muscle strain
Facet pain
Bony destruction
Inflammation from many causes
Causes of lower back plus lower limb pain include:
Radiculopathy
Plexopathies
Spinal stenosis
Important causes of leg pain without low back pain include:
Peripheral mononeuropathies
Polyneuropathies
Plexopathies
Select inflammatory conditions
Vascular claudication
Individual peripheral nerve lesions are usually caused by local trauma, entrapment by connective tissue, or involvement with mass lesions.
Lower back pain occasionally is caused by non-neurological and non-skeletal lesions. Some of the most important causes are:
Urolithiasis
Ovarian cysts and carcinoma
Endometriosis
Bladder or kidney infection
Abdominal aortic aneurysm
Visceral ischemia or other aortic ischemic disease.
The first step in diagnosis is localization of the causative lesion. History and examination usually allow differentiation among mechanical, neuropathic, and non-neurological pain.
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. Progressive symptom development can be from any expanding lesion, such as a tumor, infection, or 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:
Hip–girdle muscles:
Hip flexors (psoas, sartorius)
Hip extensors (gluteus maximus, semitendinosus, semimembranosus, biceps femoris)
Hip adductors (adductor group: longus, brevis, magnus)
Hip abductors (gluteus medius, gluteus minimus, piriformis)
Knee muscles:
Knee extension (quadriceps)
Knee flexion (semitendinosus, semimembranosus, biceps femoris)
Ankle and foot muscles:
Foot plantar flexion (gastrocnemius)
Foot dorsiflexion (tibialis anterior)
Foot evertors (peronei)
Foot inverters (tibialis posterior)
Toe extension (extensor digitorum)
Great toe extension (extensor hallucis longus)
Toe plantar flexion (flexor digitorum longus)
Great toe flexion (flexor hallucis longus)
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 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.
The differential diagnosis of lower back and leg pain can be addressed as shown in Tables 33.2 through 33.5 . Classification into mechanical and neuropathic categories is useful for narrowing the scope of diagnostic considerations. The possibility of non-neurological causes should always be kept in mind.
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-neurological pain | Urolithiasis Retroperitoneal mass Ovarian cyst or carcinoma Endometriosis |
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. |
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 examination. 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. |
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. |
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 is usually 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 is usually caused by lumbar radiculopathy or, less commonly, lumbosacral plexopathy.
Clinical abnormalities confined to one nerve root distribution are usually caused by intervertebral disk disease or lumbosacral spondylosis producing radiculopathy.
Clinical abnormalities that involve several nerve distributions are usually 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.
Non-neurological causes of lower back pain are possible and particularly include urolithiasis, abdominal aortic aneurysm, ischemia, 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, visceral ischemia, 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.
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 33.6 ( ). The tests used depend on the clinical presentation, as discussed later (see the section Clinical Syndromes).
Diagnostic Test | Advantages | Disadvantages |
---|---|---|
Magnetic resonance imaging | 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. |
Noncontrast 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 and 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. |
Magnetic resonance imaging (MRI) commonly is performed to assess the lumbosacral spine and lumbosacral plexus. It also can be used to evaluate the peripheral nerves in the pelvis and lower limbs.
MRI of the lumbosacral spine has the highest yield when the patient has back pain associated with radicular distribution of pain. Isolated back pain with no clinical symptoms or signs in the leg seldom is associated with significant findings on MRI. Intraspinal disorders that may not be revealed by MRI without contrast enhancement include neoplastic meningitis, epidural abscess, diskitis, and some chronic infectious meningitides ( ).
Techniques for MRI of the lumbosacral plexus and peripheral nerves have greatly improved, so this modality can reveal masses, infiltration, and some inflammatory lesions, but MRI can miss disorders that are without a structural defect.
With the advent of MRI, myelography has been performed less commonly. If adequate information is not obtained from noninvasive studies, myelography occasionally may be indicated. Modern uses of myelography are not only for patients who cannot have MRI due to size or implanted devices ( ).
For myelography, lumbar puncture is performed, and radiopaque dye is infused into the cerebrospinal fluid (CSF). Conventional radiographs are obtained as the dye is manipulated through the CSF pathways. Postmyelographic computed tomography (CT) is performed in most instances.
Nerve conduction studies (NCS) and electromyography (EMG) are performed for four principal purposes:
Assist localization of the lesion(s)
Assist in evaluating the severity of the lesion(s)
Determine whether the lesion is acute, subacute, or chronic
Determine whether the lesion is neuropathic, axonal, or demyelinating
Axonal damage seen with radiculopathy or entrapment neuropathy suggests consideration of surgical decompression. Of note, signs of denervation may not appear on EMG until up to 4 weeks after onset of axonal damage.
Entrapment neuropathy, or nerve root compression which can be responsible for lower limb pain, is likely to slow conduction velocity across the region of compression. Conduction velocities proximal and distal to the compression are usually normal, so conduction across the affected nerve segment must be studied.
Radiculopathy typically is associated with normal NCS findings in the peripheral branches of the nerves but with slowing of the F-wave. Asymmetry of tibial H-reflexes can suggest S1 radicular process on the side with the prolonged H-reflex Absence of abnormalities on NCSs and EMG does not rule out the presence of a radiculopathy.
Mechanical lower back pain is associated with no EMG or NCS alterations, so these studies are not usually indicated unless symptoms or signs of neural involvement are present.
Plain radiographs are obtained in patients with acute skeletal trauma and in almost all patients with isolated lower back pain. Among the potential findings are degenerative joint disease, vertebral body collapse, bony erosion, subluxation, and fracture. Radiographs of the pelvis and long bones also are obtained and may show fractures and destructive lesions.
Bone scan is especially important for examining multiple bone regions in cases of suspected neoplastic bone involvement. Multifocal involvement makes a neoplastic cause more likely than an infectious cause for the destruction.
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 are usually evident on these studies. If doubt about the diagnosis exists, myelography with postmyelographic CT scanning can be performed, but this is seldom needed.
Treatment can be conservative in the absence of neurological deficits. Physical therapy and medications can help, but surgical decompression may be required. Weakness of the legs or sphincter disturbance indicates a need for decompression. Although good evidence supports the benefit of surgical decompression at least in the short term, it is not clear that complex spine surgery with instrumentation produces substantial improvement in outcome especially when the etiology of the pain is not related to fracture or instability ( ).
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 disk 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, and 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, is 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 but contrast may be required.
Lumbosacral radiculopathy is usually 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 33.7 presents the typical motor, sensory, and reflex deficits associated with lumbosacral radiculopathy at individual levels.
Root | Motor Deficits | Sensory Deficits | Reflex Deficits |
---|---|---|---|
L2 | Psoas, quadriceps | Lateral and anterior upper thigh | None |
L3 | Psoas, quadriceps | Lower medial thigh | Patellar (knee) |
L4 | Tibialis anterior, quadriceps | Medial lower leg | Patellar (knee) |
L5 | Tibialis anterior, peroneus longus, gluteus maximus | Lateral lower leg | None |
S1 | Gastrocnemii, gluteus maximus | Lateral foot, digits 4 and 5, outside of sole | Achilles (ankle) |
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 disk 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 certain implanted electronic devices and metallic heart valves.
NCS findings are usually 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 can usually 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.
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