Version May 2024
INTRODUCTION — Lumbosacral radiculopathy is a condition in which a disease process impairs the function of one or more lumbosacral nerve roots and often leads to pain, numbness, and weakness in the back, groin, or leg. The most common causes of lumbosacral radiculopathy are compressive intervertebral disc herniation and degenerative spondylosis.
This topic will review the etiologies, clinical features, and diagnosis of acute lumbosacral radiculopathy. The treatment and prognosis of lumbosacral radiculopathy are discussed separately. (See "Acute lumbosacral radiculopathy: Treatment and prognosis".)
The clinical features and management of nonradicular disorders of the lower spine are discussed elsewhere.
●(See "Evaluation of low back pain in adults".)
●(See "Treatment of acute low back pain".)
●(See "Subacute and chronic low back pain: Nonpharmacologic and pharmacologic treatment".)
ANATOMY
●Lumbosacral spine – The lumbar spine consists of five movable lumbar vertebral bodies, numbered L1 to L5. The sacrum is made up of five developmentally fused vertebral levels (S1 to S5), followed by a terminal bony prominence, the coccyx. The entire region is commonly described as the lumbosacral spine.
Directly beneath each lumbar and sacral vertebra, there is a pair of neural foramina with the same number designation, such that the L1 neural foramina are located just below the L1 vertebral body. Neural foramina are bounded superiorly and inferiorly by pedicles, anteriorly by the intervertebral disc and vertebral body, and posteriorly by facet joints (figure 1 and figure 2).
Through each neural foramen passes the same-numbered spinal nerve root, recurrent meningeal nerves, and radicular blood vessels. On each side there are five lumbar, five sacral, and one coccygeal spinal nerve root(s).
●Nerve fibers – All lumbar and sacral spinal nerve roots originate at the T10 to L1 vertebral level, where the spinal cord typically terminates at the conus medullaris (figure 3). For patients with congenital spinal deformities such as spina bifida, the conus medullaris may be displaced more downward toward the middle of the lumbar spine due to tethering to ligamentous or bony structures.
•Spinal nerve roots – A dorsal (somatic sensory) root from the posterolateral aspect of the spinal cord and a ventral (somatic motor) root from the anterolateral aspect of the cord join in the spinal canal to form the spinal nerve root (figure 1).
The nerve roots then course down through the intraspinal canal, forming the cauda equina, until they exit at their respective neural (intervertebral) foramina. Thus, the lumbosacral nerve roots exit the spinal canal at a lower level than where they arise from the spinal cord (figure 3). A potential consequence of this arrangement is that intraspinal pathology may affect roots at higher levels than the level where the roots exit [1,2].
•Cell bodies – Cell bodies of the motor nerve fibers are located in the ventral (anterior) horns of the spinal cord, while those of the sensory nerve fibers are in a dorsal root ganglion (DRG) at each lumbar and sacral level. DRGs tend to be located within the neural foramina and are therefore not strictly speaking intraspinal (ie, within the lumbar canal). However, at the low lumbar and sacral levels, there is a tendency for DRG to reside proximal to the neural foramina, within the intraspinal canal, as found in 11 to 38 percent of cases at L5 and 71 percent at S1 [3,4]. The DRGs are attached to the vertebral body on the transverse process [5]. Compressive radicular disease typically occurs proximal to this.
•Rami – Just distal to the neural foramen, the nerve root divides in two, forming the dorsal and ventral primary rami.
-The small dorsal (posterior) primary ramus supplies motor innervation to the paraspinal muscles and cutaneous innervation to the skin of the trunk and back
-The large ventral (anterior) primary ramus supplies motor and sensory innervation to the legs and trunk, including abdominal wall muscles
The dorsal rami of the spinal nerves also supply the apophyseal joints and the paraspinal muscles. They innervate structures both above and below the level of the nerve. Clinical evaluation of injury to the dorsal rami is difficult because of the overlap in areas innervated by these nerves and the limited ability to clinically evaluate individual paraspinal muscles. However, electromyography (EMG) can be helpful in determining the distribution of disease.
The ventral rami innervate the extremities and the trunk. These branches can be evaluated by assessing the motor and sensory functions of the different myotomes and dermatomes, respectively. However, variability to the dermatomal and myotomal distribution of innervation exists [6,7].
•Myotomes and dermatomes – The collection of muscles with significant innervation from a single root is called a myotome (table 1). Similarly, the sensory distribution of a single root is labeled a dermatome (figure 4).
The primary manifestations of lumbosacral root disease can be broken up into dysfunction of two distinct systems: motor and sensory. Motor dysfunction from a root lesion may cause weakness in some or all muscles innervated by that root. However, many muscles have innervation from multiple roots, which may result in preserved strength despite significant impairment of a single root. Similarly, there is substantial individual variability in the distribution of specific dermatomes. Careful clinical and/or electrodiagnostic evaluation of multiple muscles and sensory regions may be needed to identify the spinal innervation. (See 'Physical examination' below.)
PATHOPHYSIOLOGY OF NERVE ROOT DYSFUNCTION — Radiating pain from a spinal nerve injury is mediated through dysfunction at proximal spinal nerves. Compression of a spinal nerve root by disc, arthritic spur, or inflammation from other processes leads to local edema and ischemia, which impair neuronal transmission. These factors contribute to the production of pain impulses through the spinal nerves. The pain from acute spinal nerve compression reflects a combination of pain generation within the nerve root itself as well as the pain from neighboring tissues whose pain fibers are activated by the effect of disc herniation on dura, ligaments, and surrounding vasculature.
●Spinal sites – Spinal nerve root compression or other injury may occur anywhere from nerve origins at the end of the spinal cord at the T12-L1 level, down the canal (as the cauda equina), until exiting at the neural foramen (figure 3). Specific spinal locations along this pathway include (figure 1):
•Central canal (along the cauda equina)
•Lateral recess
•Neural foramen (nerve root canal)
Lumbosacral nerve roots may be compressed as they exit the spinal canal at the neural foramina below their respective vertebrae or several levels above their respective vertebrae along the central canal. However, lumbosacral nerves are most commonly compressed as they descend in the lateral recess one level above the exiting level. As examples, the L5 root can be compressed by a central disc protrusion at the L2-3 or L3-4 level, a lateral recess disc protrusion at the L4-5 level, or far lateral disc protrusion into the foramen at the L5-S1 level.
Central canal lesions may cause multiple, bilateral radiculopathies due to the presence of multiple spinal nerve roots in the cauda equina.
Nerve root injury may also be complete or partial and thus may involve all or only a subset of root fibers. With a partial injury, incomplete myotomal involvement may result, making the distinction between a radiculopathy and a peripheral nerve injury more challenging.
●Nerve fiber involvement – Like most peripheral nerves, lumbosacral nerve roots are composed of both large and small fibers. Different fiber types play different roles by virtue of the information they carry. Injury to these fibers may result in focal demyelination, as seen initially with compression, or axonal damage, as seen with infarction or a more severe compressive injury.
•Large fibers – Large fibers carry motor efferent and sensory information involved with vibratory sense as well as conscious and unconscious proprioception. The typical clinical findings of large-fiber involvement in radiculopathies are weakness and diminished or absent stretch reflexes. Clinical testing for proprioception and vibratory sense tends to extend across several dermatomes and thus is often not as helpful in the evaluation of lumbosacral radiculopathies as small-fiber modalities.
•Small fibers – The smaller myelinated A-delta fibers and unmyelinated C fibers carry pain and temperature information. A-delta fibers transmit cold sensation, while C fibers subserve warm sensation. Isolated injury to these fibers is not common in lumbosacral radiculopathies. However, their dermatomal distributions tend to be more specific than those of the large fibers, underscoring the role of small fibers in the clinical evaluation of radiculopathies.
In addition, radicular A-delta and C fiber dysfunction may occur with inflammation, even in the absence of overt nerve root compression. A study of warm and cold sensory thresholds in 32 patients with unilateral L5 or S1 radiculopathy and disc herniation found that warm thresholds (C fiber function) were impaired to a greater extent than cold thresholds (A-delta fibers) [8]. Since it is thought that unmyelinated axons, such as C fibers, are less affected by compression than myelinated ones, this finding suggests that the generation of lumbar radicular pain is mediated by inflammation more than by nerve root compression [8].
●Central pain – Central pain sensitization may result from nerve root compression. Supporting evidence comes from a small study of patients with L5 or S1 radiculopathy that demonstrated a lowered pain threshold in the contralateral root, perhaps mediated by pre- and postsynaptic modulation of opioidergic interneurons [9].
ETIOLOGIES — Lumbosacral radiculopathy is most commonly caused by nerve root compression due to either intervertebral disc herniation or degenerative spondylosis. Other etiologies include nonskeletal causes of nerve root compression and noncompressive mechanisms including infection, trauma, inflammation, neoplasm, and vascular disease.
Disc herniation — Herniation of an intervertebral disc is a common cause of lumbosacral radiculopathy.
●Pathogenesis – Age-related degenerative changes in the spine cause gradual narrowing of the disc space, leading to dysfunction in the intervertebral disc (figure 5). The annulus fibrosis becomes more fibrotic and less elastic, leading to the development of fissures and calcium deposits. The nucleus pulposus becomes desiccated and friable. As the disc shrinks and the intervertebral disc space narrows, the annulus tends to buckle out and/or disc material can be displaced outward and compress a nerve root. These degenerative changes of the intervertebral disc can be classified by appearance and presence of displaced disc material:
•Disc bulge – Buckling of the annulus can involve >90 degrees of the total circumference of a disc. The nucleus pulposus may be intact or partially displaced through a single or multiple layers of the annulus but does not tear through the entire ring with a disc bulge.
•Herniation – Rupture of the nucleus pulposus through the ring of the annulus fibrosus is a true disc herniation. There are two broad categories, protrusion and extrusion.
-Protrusion refers to a rupture of disc material in which the base is broader than the dome. In general, this does not extend above or below the disc space.
-An extrusion is a disc rupture in which the dome is wider than the base, with a dumbbell appearance. Extrusions may extend above or below the disc space.
•Free fragment – When herniated disc material loses its connection with the main disc material, free fragments can migrate from the disc space to produce symptoms at adjacent sites.
●Susceptibility at specific spinal levels – The lumbosacral spine is susceptible to disc herniations because of its mobility from flexion, extension, and torsion. Seventy-five percent of flexion and extension occurs at the lumbosacral (L5-S1) joint [10]. The L5-S1 level, on the other hand, has limited torsion. Twenty percent of flexion and extension occurs at L4-L5. The remaining 5 percent occurs between L1 and L3 [10].
The L4-L5 and L5-S1 levels are most susceptible to injuries from routine movements of the spine; approximately 90 to 95 percent of compressive radiculopathies occur at these levels [11]. The incidence of radiculopathies is split somewhat evenly between L4-L5 and L5-S1, as the lack of torsion at L5-S1 helps to increase its stability despite its higher degree of flexion and extension [12]. Next in frequency is L4. Other levels are uncommon.
Far lateral herniations are seen more often at the L2-4 levels. They may affect the rostral root. This is rare, as only 10 percent of far lateral herniations will result in nerve root compression [4]. Pain from the far lateral disc herniations may be more severe due to compression of the dorsal root ganglia (DRG) [13].
Degenerative spondylosis — Degenerative changes in the joints of the spine (spondylosis) lead to the development of bony overgrowth (osteophytes) that may cause radiculopathy. These degenerative changes occur at three main sites:
●The intervertebral joints
●The uncovertebral joints (cervical spine only)
●The zygapophyseal (facet) joints
Changes at the vertebral body endplates adjacent to the disc accompany disc degeneration (see 'Disc herniation' above). The marrow undergoes fibrovascular change or fatty marrow replacement. Eventually, endplate sclerosis develops. Osteophyte formation occurs at the margins of the vertebral bodies. What triggers osteophyte formation is unclear, although spinal movement at ligamentous attachment sites and loss of buffering tissues between bony surfaces likely play roles. Osteophyte production appears to slow as advancing spondylosis leads to decreasing spinal movement.
Facet joint degeneration may not be directly related to vertebral endplate spondylotic changes but often coexists. Disc degeneration is likely to put additional weight-bearing strains on facet joints, which are not weight-bearing structures. With unnatural movement of the spine, the synovial joint bears more structural burden, degenerates, and develops osteophytes. These osteophytes grow into the posterior aspect of the neural foramen (image 1).
These bony changes may directly impinge on spinal nerve roots or cause instability and misalignment of the spine (ie, degenerative spondylolisthesis) that leads to nerve root pain and neurologic deficits (figure 5). It is not known whether changes in these different structures are causally related or occur independently.
Age-related degenerative spondylosis is more commonly associated with nonradicular low back pain than radiculopathy. It may also cause symptoms of lumbar spinal stenosis from osteophytic compression of multiple nerves within the central canal or in the setting of degenerative spondylitic changes associated with anterior displacement with respect to an adjacent vertebral body (spondylolisthesis). These conditions are discussed in greater detail separately. (See "Evaluation of low back pain in adults", section on 'Nonspecific back pain' and "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Etiologies'.)
Congenital and developmental conditions — Congenital abnormalities of the bony spinal column or its contents occur in 25 to 50 percent of the general population [14]. Congenital narrowing of the canal can be a common substrate upon which spondylosis may result in radiculopathy, especially among younger adults. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Etiologies'.)
Developmental abnormalities may lead to radicular dysfunction due to injuries resulting from traction of the root. These include tethered cord or diastematomyelia and spina bifida. (See "Closed spinal dysraphism: Clinical manifestations, diagnosis, and management" and "Myelomeningocele (spina bifida): Anatomy, clinical manifestations, and complications".)
Other causes — Less common causes of radiculopathy and polyradiculopathy include infection, inflammation, neoplasm, and vascular disease (table 2) [15-18]. These conditions may cause radiculopathy by direct compression, inflammation, or ischemia. Specific etiologies include:
●Diabetes mellitus – Diabetes mellitus can cause lumbosacral radiculopathy as well as other forms of peripheral nerve dysfunction, such as peripheral polyneuropathy, polyradiculopathy, and peripheral mononeuropathies. (See "Epidemiology and classification of diabetic neuropathy".)
●Trauma – Root avulsion is a rare cause of lumbosacral radiculopathy that may occur with fractures of the sacroiliac joint or with diastasis of the symphysis pubis or the pubic rami [19].
●Infectious diseases – Several infectious agents may cause radiculopathy by neuronal invasion, inflammation, or external compression via epidural abscess [20]. These include:
•Borrelia burgdorferi
•Cytomegalovirus
•Epstein-Barr virus
•Herpes simplex virus
•Human immunodeficiency virus (HIV)
•Mycobacterium
•Mycoplasma
•Syphilis
•Varicella-zoster virus (herpes zoster or shingles)
●Inflammatory conditions – Neuropathic inflammatory conditions typically lead to dysfunction of multiple nerves but may sometimes cause prominent impairment of a single nerve root early in the course of the condition. Inflammatory conditions that may involve lumbosacral nerve roots include:
•Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome)
•Chronic inflammatory demyelinating polyradiculoneuropathy
•Arachnoiditis related to postsurgical changes
•Sarcoidosis
●Mass lesions
•Metastasis (most common) [17]
•Epidural abscess [21]
•Intradural tumor, particularly meningioma, neurofibroma, and ependymoma [15]
•Lymphoma [22]
•Myeloma [23]
•Root sleeve cyst, such as a Tarlov or perineural cyst (though most are asymptomatic and found incidentally on imaging) [24-27]
•Epidural lipomatosis [28]
●Vascular causes
•Arteriovenous malformation
•Vasculitis (nerve root infarction)
•Radiation-induced vascular occlusion
Radiculopathy may also arise in the absence of obvious compression, leading to the hypothesis that the injury may be due to a chemical radiculitis, perhaps caused by the rupture of the annulus fibrosus with subsequent release of inflammatory mediators tracking along the nerve root sheath [29-31]. Electromyography (EMG) may be abnormal even though compression is not observed on imaging studies.
EPIDEMIOLOGY — Lumbosacral radiculopathy is one of the most common problems seen in neurologic consultation. Although data are limited, the estimated lifetime prevalence is approximately 3 to 5 percent for adults, with equal rates among males and females [20].
Risk factors for lumbosacral radiculopathy include increasing age, manual labor (eg, heavy lifting, twisting), obesity, tobacco use, and deconditioning [11,32-34].
CLINICAL PRESENTATIONS — The clinical presentations of lumbosacral radiculopathy vary according to the nerve root or roots involved (table 3). L5 and S1 radiculopathies are the most frequent clinical presentations. Clinical features may also be characterized by the severity and extent of neurologic dysfunction:
●Mild – Radicular pain and a segmental pattern of sensory dysfunction but no other neurologic deficits (figure 4)
●Moderate – Mild nonprogressive segmental motor weakness (table 1) and/or reflex change, often along with radicular pain and sensory dysfunction
●Severe – Marked and/or worsening motor deficits, often along with radicular pain and sensory dysfunction
L1 radiculopathy — L1 radiculopathy is uncommon because flexion/torsion stresses around the L1 level are comparatively modest, and resultant bony degeneration and disc herniation are uncommon at the L1 level. Sensory symptoms predominate [20].
●Pain and sensory symptoms – Pain, paresthesia, and sensory loss is present in the inguinal region.
●Weakness – Mild weakness in hip flexion may rarely be present. However, motor dysfunction in the iliopsoas muscles due to L1 radiculopathy is often absent or difficult to detect because the muscle group is also innervated by lower lumbar nerves.
L2/L3/L4 radiculopathy — There is marked overlap of the L2, L3, and L4 innervation of the anterior thigh muscles, making it difficult to differentiate these spinal nerve root levels based on symptoms, neurologic examination, or neurodiagnostic testing. Thus, these radiculopathies are generally considered as a group. Radiculopathy at these nerve roots most commonly occurs in older patients with symptoms of spinal stenosis.
●Pain and sensory symptoms – Acute back pain is the most common presenting complaint, often radiating around the anterior aspect of the thigh down into the knee and occasionally down the medial aspect of the lower leg as far as the arch of the foot. Sensation may be reduced over the anterior thigh down to the medial aspect of the lower leg.
●Weakness – On examination, there may be weakness of hip flexion, hip adduction, and knee extension. However, substantial weakness of the hip flexors may indicate a proximal lesion (eg, in the spinal canal) involving multiple nerves.
●Reflex loss – A reduced knee (patellar) stretch reflex is common in the presence of moderate weakness.
Nerve conduction studies (NCS) and electromyography (EMG) may reveal abnormalities confined to muscles of the affected root(s), including the quadriceps, leg adductors, and iliopsoas, with associated paraspinal abnormalities. The saphenous sensory response remains normal even if sensory loss is prominent in the distal leg.
L5 radiculopathy — L5 radiculopathy is the most common radiculopathy affecting the lumbosacral spine due to substantial flexion/extension and torsion that occurs at this level. (See 'Disc herniation' above.)
●Pain and sensory symptoms – Classic presenting symptoms of an L5 radiculopathy include back pain that radiates down the lateral aspect of the leg into the foot. Sensory loss is confined to the lateral aspect of the lower leg and dorsum of the foot but may be obvious only when testing pinprick sensation in the web space between the first and second digits.
●Weakness – On examination, weakness may be identified in foot dorsiflexion, toe extension, foot inversion, and foot eversion. Weakness of leg abduction may also be evident in severe cases due to involvement of gluteus minimus and medius.
Atrophy may be present in the extensor digitorum brevis muscle of the foot and the tibialis anterior muscle of the lower leg. In severe cases, there may be "tibial ridging," a condition in which the normal convexity of the anterior compartment of the leg is lost because of atrophy, leaving a prominent sharp contour of the medial aspect of the tibial bone.
●Reflex loss – Reflexes are generally normal, although the internal hamstring reflex may be diminished on the symptomatic side.
NCS and EMG typically show abnormalities in the L5 muscles, including the gluteus medius, tensor fascia lata, semitendinosus, tibialis anterior, tibialis posterior, and the L5 paraspinals. Sensory studies (sural and superficial peroneal responses) are normal since the lesion is almost always proximal to the dorsal root ganglion (DRG).
S1 radiculopathy — S1 radiculopathies are commonly caused by L5-S1 lateral recess disc herniations due to extent of flexion-extension at this site. (See 'Disc herniation' above.)
●Pain and sensory symptoms – Pain radiates down the posterior aspect of the leg from the back to the foot. Sensation is generally reduced on the posterior aspect of the leg and the lateral edge of the foot.
●Weakness – Weakness with an S1 radiculopathy involves the gastrocnemius muscle and is demonstrated on plantar flexion. There may also be weakness of leg extension at the hip (gluteus maximus) and knee flexion (biceps femoris long and short heads).
●Reflex loss – Stretch reflex loss occurs at the Achilles' tendon.
NCS and EMG reveal abnormalities in S1 innervated muscles, including the gluteus maximus, long and short heads of the biceps femoris, gastrocnemius and soleus muscles, and the S1 paraspinals, with intact sensory responses (sural generally tested) [7]. Soleus H reflex is usually absent in patients with significant S1 radiculopathy. Testing should be performed bilaterally to identify asymmetric amplitude loss or latency prolongation on the affected side. (See "Overview of nerve conduction studies", section on 'H reflex'.)
S2/S3/S4 radiculopathy — Structural radiculopathies at these lower levels are less common than other lumbosacral radiculopathies but may be caused by a large central disc compressing the nerve roots intrathecally at a higher level (eg, L5). (See 'Pathophysiology of nerve root dysfunction' above.)
●Pain and sensory symptoms – Patients can present with sacral or buttock pain that radiates down the posterior aspect of the leg or into the perineum.
●Weakness – Weakness of somatic muscles may be minimal. However, patients may report urinary and fecal incontinence as well as sexual dysfunction.
The utility of NCS and EMG for the evaluation of S2, S3, and S4 radiculopathy is limited. However, EMG investigation of the low paraspinal muscles may be helpful. In addition, abnormalities may be identified in gluteus maximus and gastrocnemius. Sensory studies are normal. Prolongations in latency when performing electrical bulbocavernosus reflex testing may indicate a lesion in the region, although this is not specific for radiculopathy.
EVALUATION AND DIAGNOSIS — Acute lumbosacral radiculopathy should be suspected in patients with lower extremity pain or neurologic deficits in a radicular distribution. The diagnosis of acute lumbosacral radiculopathy is clinical, made in patients with compatible symptoms and examination findings.
Diagnostic testing is typically reserved for selected patients with high-risk features for suspected structural or inflammatory conditions and those with progressive or severe weakness who are at risk for permanent neurologic impairment. (See "Acute lumbosacral radiculopathy: Treatment and prognosis", section on 'Identifying patients who need urgent diagnostic evaluation'.)
Our approach — We perform a careful history and physical examination, including neurologic examination, for all patients with suspected lumbosacral radiculopathy (see 'Clinical diagnosis' below). Acute lumbosacral radiculopathy may often be painful but is frequently self-limited when due to disc herniation or degenerative spondylosis, common causes of the condition.
Patients with severe or progressive weakness and those with high-risk clinical features warrant diagnostic testing to exclude structural (ie, neoplastic, infectious, inflammatory) etiologies such as cauda equina syndrome, epidural abscess or hematoma, or acute disc rupture (algorithm 1) (see 'Diagnostic testing for selected patients' below). Such features include patients with acute lumbosacral radicular symptoms associated with [20]:
●Bilateral radicular signs/symptoms
●Progressive weakness
●Urinary retention
●Fever
●Night sweats
●Immunosuppression (eg, concurrent chemotherapy or immunosuppressive therapy)
●History of HIV infection
●Active anticoagulant therapy
●Malignancy
●Unintentional weight loss
●Age ≥60 years
●Pain that is prominent at night, severe with palpation of the spinous process, or unchanged despite change in body position
In addition, diagnostic testing is also warranted for other patients with milder symptoms and low-risk features when symptoms do not respond to initial conservative therapy. (See "Acute lumbosacral radiculopathy: Treatment and prognosis", section on 'Management for patients with persisting symptoms'.)
Clinical diagnosis
History — Pain and sensory symptoms that involve a specific lumbosacral dermatome are suggestive of a radicular process. This may include paresthesia, dysesthesia, hyperesthesia, or anaesthesia. Paresthesia occurs in 63 to 72 percent of cases, radiating pain in approximately 35 percent, and numbness in approximately 27 percent [35,36].
Similarly, weakness confined to the muscles in a particular lumbosacral myotome should raise suspicion for radiculopathy, though few people spontaneously report such specific complaints. Instead, patients may report functional impairments suggestive of a specific muscle and nerve root dysfunction. As examples:
●L2/L3/L4 – Inability to get up from a chair suggests iliopsoas or quadriceps weakness.
●L3/L4 – Buckling of the knee is consistent with quadriceps weakness.
●L5 – Dragging of the toe points to tibialis anterior weakness.
●S2/S3/S4 – Urinary and/or fecal incontinence may be due to impaired urinary and/or rectal sphincter motor function.
Triggers and alleviating factors may also help to suggest a radicular cause to symptoms. Radicular pain that worsens with Valsalva or improves while lying down suggests a compressive etiology. Conversely, radicular pain that worsens with lying down may suggest an inflammatory or neoplastic etiology. However, such symptoms have not been shown to be sensitive or specific for these conditions.
The acute onset of symptoms with bending, lifting, or trauma may herald a radiculopathy. In large series, approximately 30 to 50 percent of patients identify an inciting event, most commonly nonlifting activities (eg, bending, slipping without falling, vacuuming, recreational sports), heavy lifting, falls, and motor vehicle accidents [37,38]. However, none of these factors are specific for radiculopathy.
Physical examination — Evaluation for lumbosacral radiculopathy requires a careful general and neurologic examination. Additional procedures (eg, straight leg raising, reverse straight leg raising) may be useful, but their specificity, sensitivity, and reproducibility are variably limited. Vertebral tenderness is suggestive of infection but is not specific enough to be clinically useful [11].
●General examination – The spine should be evaluated for any cutaneous abnormalities, such as tufts of hair, nevi, or pores that may be suggestive of a neural tube developmental abnormality.
Patients with lumbosacral radiculopathy from herpes zoster may have an erythematous vesicular maculopapular rash or a history of a rash that precedes onset of dermatomal allodynia [39].
●Neurologic examination – The localization of pain, sensory loss, weakness, and reflex loss can help identify dysfunction at specific nerve root levels (table 3).
Muscle weakness must be distinguished from ineffective voluntary effort, such as may occur in the setting of severe pain. A radicular pattern of weakness suggests involvement of the ventral root or severe impairment of the nerve. Weakness is a common feature of radiculopathy due to nerve infarction or diabetic amyotrophy. Long-standing radicular weakness may also lead to muscle atrophy.
Muscle stretch reflexes should be tested to identify hyporeflexia or areflexia. Side-to-side asymmetries are usually significant. Commonly tested muscle stretch reflexes include the quadriceps (L2/L3/L4) and Achilles (S1). The internal hamstring reflex can be useful in assessing a suspected L5 radiculopathy [40], but its correct performance requires experience. It is sometimes difficult to elicit in patients with obesity. An experienced clinician may try to elicit this reflex by tapping the semitendinosus and semimembranosus (internal hamstring muscles) tendons just proximal to the popliteal fossa.
The sensory examination is more subjective than other parts of the neurologic examination and is further confounded by dermatomal overlap and variability [6,7]. However, there are areas that are exclusively served by individual nerves (autonomous zones). The most important of these in the evaluation of lumbosacral radiculopathies include the sole of the foot (S1), dorsum of the foot (L5), medial calf (L4), and anterior thigh (L2 and 3) [41]. We suggest testing the relevant lumbosacral dermatomes for light touch, pain, and temperature. Vibratory sensation and proprioception are usually not useful for evaluating radiculopathies.
●Provocative maneuvers – Specific bedside maneuvers can be helpful in determining whether symptoms are radicular in nature. These include the straight leg raise, the contralateral straight leg raise, and the reverse straight leg raise (also referred to as femoral stretch).
•Straight leg test – The straight leg raise test is done with the patient supine. The examiner raises the patient's symptomatic leg at the hip with the knee extended and the foot dorsiflexed, being careful that the patient is not actively "helping" in lifting the leg. Straight leg raising results in an increase in dural tension in the lower lumbar and upper sacral levels. Pain that occurs or worsens during testing or improves after testing suggests radiculopathy (positive straight leg test). By contrast, radicular pain is absent or unchanged when the hip is flexed with the leg in flexion at the knee. Additional maneuvers may be performed during the straight leg test to help identify radiculopathy:
-Lasègue's sign is the presence or worsening of radicular pain (not just low back pain or hamstring pain) with the straight leg maneuver (ie, hip flexion with the leg extended at the knee). A positive Lasègue's sign usually occurs when hip flexion is between 30 and 60 degrees, though positive tests can also occur at smaller and larger degrees of hip flexion.
-The bowstring sign refers to the relief of radicular pain when the knee is flexed during a positive straight leg raise.
The straight leg raise test is more sensitive but less specific than the contralateral straight leg raise for the diagnosis of radiculopathy due to disc herniation [42]. It is most helpful in the evaluation of radiculopathy at the L5 and S1 levels. In a prospective study of 100 patients, Lasègue's sign was positive in 83 percent [43]. One study of patients with acute low back pain found that the combination of radiating pain into the leg, sensory loss in the foot, and a positive straight leg raise test was predictive of a herniated disc with nerve root compression [44].
•Contralateral straight leg test – The contralateral (crossed) straight leg raise test refers to passive elevation of the unaffected leg by the examiner. The test is positive (abnormal) when lifting the unaffected leg reproduces radicular pain in the affected leg. It is relatively specific for radiculopathy due to disc herniation but has poor sensitivity [44,45].
•Reverse straight leg test – The reverse straight leg raise (femoral stretch) test is performed by placing the patient prone on the table and passively extending the hip and leg straight up off the plane of the table. This maneuver is most useful for evaluating the L2, L3, and L4 roots. However, the value of this test is limited by inadequate information on its sensitivity and specificity.
•Patrick's test – Patrick's test is a maneuver during which the hip is externally rotated with the ipsilateral knee flexed at 90 degrees and placed on the opposite knee. The test is positive if it elicits hip or buttock pain. A positive test raises suspicion for hip or sacroiliac disease. However, it is nonspecific for a radicular process [16,39]. (See "Musculoskeletal examination of the hip and groin", section on 'Tests for acetabular pathology'.)
Diagnostic testing for selected patients — We perform diagnostic testing for patients with a suspected high-risk mechanism for progressive or permanent disability, those with severe or progressive weakness, and when symptoms do not improve with initial conservative therapy (algorithm 1). We typically start with neuroimaging to assess for structural causes. Neurodiagnostic and other testing may be warranted if neuroimaging is nondiagnostic.
Neuroimaging — Multiple spinal imaging modalities may be used for patients with lumbosacral radiculopathy. Magnetic resonance imaging (MRI) is typically used as an initial test to identify bony and soft tissue abnormalities. Computed tomography (CT) is commonly used as an alternative to MRI.
●MRI – Lumbosacral MRI with contrast is the preferred routine initial diagnostic test for most patients with suspected lumbosacral radiculopathy. MRI can identify soft tissue and bony abnormalities and does not involve the use of radiation. Lumbosacral MRI is a sensitive imaging modality to identify soft tissue abnormalities such as a disc herniation or a compressed nerve root (image 1 and image 2 and image 3). MRI with intravenous contrast is performed to help identify other intraspinal pathologies, including inflammatory, malignant, and vascular disorders.
●CT – CT of the lumbosacral spine may be performed as an alternative test including for patients unable to obtain an MRI. CT may also be the preferred study to identify bony pathology such as an osteophyte. However, CT alone is unable to visualize nerve roots, so it is not helpful in the direct imaging of a radicular process.
●CT myelography – Spinal myelography is typically reserved for patients unable to obtain an MRI when CT with contrast is nondiagnostic. Myelography can be used to visualize spinal nerve roots and their trajectory through the neural foramina. In addition, CT myelography is preferred for patients who have surgically placed spinal hardware that produces magnetic artifacts.
●Others – Other imaging modalities have limited utility in the diagnostic evaluation of lumbosacral radiculopathy. These include:
•Plain radiographs of the lumbar spine can visualize bony structures but do not detect herniated discs. Thus, plain radiographs are not recommended in the work-up of lumbosacral radiculopathy unless there is a need to evaluate for infection, fracture, malignancy, spondylolisthesis, degenerative changes, disc space narrowing, or prior surgery. However, normal plain films do not exclude malignancy or infection in patients with a suspicious history. (See "Evaluation of low back pain in adults".)
•Discography is a controversial technique of uncertain utility that involves the injection of contrast under fluoroscopy into the nucleus of a disc thought to be the cause of a patient's low back pain. The test is considered positive if it demonstrates an annular disruption and reproduces the patient's usual low back pain symptoms. It is not helpful in the evaluation of lumbosacral radiculopathy.
Neuroimaging results should be correlated with clinical features on examination. There is a high prevalence of disc herniations and other abnormal neuroimaging findings in asymptomatic individuals, including some who have what appears to be frank nerve root compression [46]. As an example, one study of 98 people without back pain found MRI evidence of disc herniation in 27 percent [47]. Furthermore, lumbar spine abnormalities on MRI in asymptomatic patients do not appear to be predictive for the future development or duration of low back pain [48].
Neurodiagnostic testing — Neurodiagnostic testing is typically performed for patients with suspected lumbosacral radiculopathy when the diagnosis is uncertain despite neuroimaging. The primary neurodiagnostic procedures are nerve conduction studies (NCS) and electromyography (EMG). Together, they provide insight into the integrity of spinal nerve roots and their connection with the muscles they innervate. These tests are most commonly considered in patients with persistent disabling symptoms of radiculopathy in whom neuroimaging findings are nondiagnostic or inconsistent with the clinical presentation (algorithm 1).
Somatosensory evoked potentials (SEPs) are another neurodiagnostic procedure used infrequently in patients with lumbosacral radiculopathy to help localize sensory nerve dysfunction.
Nerve conduction studies and electromyography — NCS and EMG can localize the specific spinal nerve root that is damaged, distinguish between old and new axon loss nerve damage, and provide indirect support for the presence of injury, such as demyelinating conduction blocks at the root level [7,49]. Neurodiagnostic testing also can identify conditions that mimic radiculopathy, such as more distal mononeuropathies of the leg or lumbosacral plexopathy.
NCS and EMG also provide physiologic information, which complements the anatomic information provided by neuroimaging [50,51]. When there is uncertainty in the relationship between abnormal neuroimaging findings and neurologic deficits, NCS and EMG are useful to support or refute this relationship. In particular, EMG may provide objective evidence of denervation when there is no motor deficit or uncertain motor deficit. In addition, EMG findings may help determine the timing of the denervation (eg, distant past versus ongoing). This is particularly useful in patients with past surgery and residual pain. For patients with nonspecific spine pain, EMG can help to distinguish pain-related reduced muscular effort from true neurogenic weakness.
Specific abnormal findings on NCS and EMG vary according to the nerve root involved. (See 'Clinical presentations' above.)
●Technique – NCS are carried out by applying an electrical stimulus to the skin overlying a nerve trunk, followed by the recording of the generated electrical response over either the nerve trunk or muscle innervated by it, at some distance from the stimulation. EMG records the electrical potentials generated in a muscle belly through a needle electrode inserted in the muscle. Both methods are discussed in detail separately. (See "Overview of electromyography" and "Overview of nerve conduction studies".)
●Timing – NCS and EMG have a high diagnostic utility for radiculopathy when neurologic weakness is present for at least three weeks. However, the diagnostic yield is lower in patients with only pain or sensory loss as the manifestation of radiculopathy.
For patients with acute symptoms of less than three weeks' duration, EMG and NCS provide limited but potentially important information. The needle EMG examination is more sensitive and provides better localizing information than NCS but is not likely to show prominent features of acute axon loss until three or more weeks after symptom onset. This is due to a two- to three-week delay in the development of fibrillation potentials after acute motor axon loss. In the face of marked weakness from acute radiculopathy, NCS can show loss of amplitude of compound muscle action potentials by day 8 after injury.
●Evidence of efficacy – EMG and imaging studies have a comparable diagnostic sensitivity for lumbosacral radiculopathy, varying between 50 to 85 percent, depending on the patient population [50,52,53]. In a retrospective comparison of 47 patients who had a clinical history suggestive of either cervical or lumbosacral radiculopathy, there was congruence between EMG and MRI findings in 60 percent of patients [50]. Agreement between EMG and MRI was highest for patients with clearly abnormal examination findings consistent with radiculopathy.
In a systematic review of evidence published through mid-2006, the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) assessed the utility of neurodiagnostic testing for patients with lumbosacral radiculopathy [54]. The AANEM noted that the available data are limited by the lack of a universally accepted "gold standard" definition for the diagnosis of lumbosacral radiculopathy, thus preventing comparison of sensitivities and specificities reported by the included studies. With this caveat in mind, the AANEM concluded that the H reflex on NCS and peripheral limb EMG probably aid the clinical diagnosis [54].
Somatosensory evoked potentials — SEPs are another neurodiagnostic procedure that is performed by repetitively stimulating the tibial nerve at the ankle and recording the propagated sensory potentials as they ascend the leg, through central sensory pathways in the spinal cord and brain, and then to the sensory cortex. SEPs may be used as adjunct testing when the neuroanatomic site of sensory abnormalities is uncertain, such as for patients with suspected spinal cord or cerebral localization to symptoms. However, SEPs are not a routine part of the evaluation of most patients with radiculopathy. In addition, the available evidence is conflicting regarding the ability of SEPs to localize specific nerve root compression [55-57]. A systematic review found insufficient evidence to reach a conclusion about the utility of dermatomal/segmental SEPs of the L5 or S1 dermatomes [54].
Cerebrospinal fluid analysis — A lumbar puncture for cerebrospinal fluid (CSF) evaluation of lumbosacral radiculopathy is typically reserved for instances when there is suspicion for a neoplastic or infectious cause for radiculopathy and the etiology cannot be determined by neuroimaging or other methods (algorithm 1).
Common infectious causes of lumbosacral radiculopathy include Lyme disease, herpes zoster, and mycobacterium species. (See 'Other causes' above.)
Typical findings consistent with an infectious cause of lumbosacral radiculopathy include elevated protein and leukocytosis. The specific infectious agent may be identified by culture of the CSF. (See "Aseptic meningitis in adults", section on 'Cerebrospinal fluid' and "Clinical features and diagnosis of acute bacterial meningitis in adults", section on 'Cerebrospinal fluid examination'.)
However, there are theoretical risks with lumbar puncture in the setting of epidural abscess or other epidural infectious processes. One is that lumbar puncture in the presence of complete canal obstruction by the infectious mass could cause a differential in CSF pressure above and below the obstruction, leading to stretching of neural elements (ie, herniation). Another is that infection could be inadvertently carried into the intrathecal space by the lumbar puncture needle. In addition to these concerns, the diagnostic yield of lumbar puncture for epidural abscess is low, as discussed separately. (See "Spinal epidural abscess", section on 'Diagnosis'.)
For patients with a known primary tumor, evaluation of the CSF may be indicated if contrast-enhanced MRI is nondiagnostic. In addition, CSF sampling should be done for patients with an unknown source of primary cancer when neuroimaging is nondiagnostic, particularly those who fail to improve, have progressive neurologic deficits, and/or have involvement of multiple roots. CSF cytology can be diagnostic in patients with leptomeningeal carcinomatosis, but it may be negative in 10 percent of cases [18]. In such patients, CSF testing should be repeated if there is clinical suspicion for cancer. Other abnormalities in the CSF include a monocytic pleocytosis, decreased glucose, and increased protein. (See "Clinical features and diagnosis of leptomeningeal disease from solid tumors", section on 'Cerebrospinal fluid'.)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of lumbosacral radiculopathy most commonly includes nonspecific (eg, musculoskeletal) low back pain and other neurologic conditions that involve lower extremity nerves. These neurologic conditions include lumbar spinal stenosis, cauda equina syndrome, diabetic amyotrophy, lumbosacral plexopathy, and mononeuropathies of the leg such as femoral, sciatic, peroneal, and tibial nerve lesions. (See 'Low back pain' below and 'Neurologic conditions' below.)
In addition, systemic infections and disorders such as cancer or rheumatologic conditions and some abdominal or pelvic conditions can also cause or refer pain to the lumbosacral region. These conditions vary according to the location of pain in lumbar, sacral, or inguinal regions or in the lower extremities. (See 'Systemic conditions and referred pain' below.)
Low back pain — Low back pain is one of the most common symptoms causing patients to seek medical attention. Most patients with lumbosacral radiculopathy will also have symptoms of low back pain. However, the majority of cases of low back pain are not due to radiculopathy or another neurologic cause. Disc disease proves to be the underlying etiology in <5 percent of patients [58]. Furthermore, a specific etiology cannot be reliably established for most patients with low back pain.
Nonradicular low back pain may be misdiagnosed as a lumbosacral radiculopathy due to the use of nonspecific nomenclature such as the term "sciatica." Sciatica is often applied to conditions involving low back pain with or without radiation into the leg regardless the cause. Because of its nonspecific use, the term "sciatica" should be avoided when referring to radicular pain.
●Pain generators in the lumbosacral spine – Several other tissues within the low back contain nerve fibers with pain receptors (table 4). Of note, intervertebral disc material does not contain significant numbers of pain fibers.
Localized lumbosacral pain is thought to arise from intraspinal structures. These pain impulses arise from the blood vessels, dura mater, and longitudinal ligaments, and travel in the sinuvertebral nerves through the neural foramina, connecting via rami communicantes with the extraspinal sympathetic chain.
Nonlocalized, nonradiating pain is thought to arise from muscle, bone, and ligament outside the spinal canal. Interconnected ventral and dorsal nerve plexuses surround the vertebral column [59]. The ventral nerve plexus serves the anterior longitudinal ligament and has bilateral innervation. Many branches from the sympathetic trunk, rami communicantes, and perivascular nerve plexuses join to form the ventral nerve plexus. The dorsal nerve plexus arises from the sinuvertebral nerves and serves the posterior longitudinal ligament.
●Distinguishing nonradicular pain – Radicular low back pain is typically associated with pain that radiates down one or both legs. There may be associated nerve root dysfunction resulting in sensory loss and/or weakness that may or may not be overtly symptomatic. Symptoms may also be associated with a loss or diminution of stretch reflexes.
Nonradicular low back pain is not associated with other neurologic symptoms or signs. Symptoms are generally localized to the spine and paraspinal regions and may radiate into the leg. However, some patients have pain that radiates from the lower back into the buttocks and upper leg in a manner that mimics radiculopathy even though it is not due to nerve root impingement.
●Causes of low back pain – Low back pain may be caused by injury of nonneurologic structures such as bone, muscle, tendon, ligament, or fascia that does not affect nerve roots.
•Musculoskeletal strain – Musculoskeletal causes of low back pain, such as muscle or tendon strain, probably account for the majority of cases. Patients may have muscle tenderness on palpation or worsening pain with muscle activation. Musculoskeletal low back pain often improves spontaneously or with treatment within a few weeks. (See "Evaluation of low back pain in adults", section on 'Nonspecific back pain'.)
Diagnostic testing for nonspecific (musculoskeletal) low back pain is often equivocal or may even show findings suggestive of radiculopathy that do not correlate to symptoms [60-62]. (See "Evaluation of low back pain in adults", section on 'Limited utility of imaging'.)
•Other lumbosacral causes of low back pain may be distinguished from radiculopathy by specific risk factors or characteristic clinical findings. These conditions include:
-Osteoarthritis – Patients with osteoarthritis or risk factors for its development (eg, older age, prior joint injury, obesity) may also develop low back pain due to involvement of the intervertebral or facet joints of the lumbar spine. Common symptoms of osteoarthritis include pain that worsens with joint use and improves with rest. Knees, hips, and hands are common sites for osteoarthritis. (See "Clinical manifestations and diagnosis of osteoarthritis".)
Osteoarthritis of the spine may also lead to spinal stenosis. (See 'Spinal stenosis' below.)
-Ankylosing spondylitis – Primary inflammatory arthropathies such as ankylosing spondylitis commonly cause low back pain. Characteristic features include onset <40 years old, morning stiffness, and improvement with activity. Extra-articular features are common, such as anterior uveitis and inflammatory bowel disease. (See "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)
-Osteoporotic compression fracture – A history of osteoporosis should raise suspicion for vertebral body fracture as a cause for acute back pain. Onset may be after bending, coughing, or stretching. Pain may radiate to the flank or abdomen but does not typically radiate to the legs. (See "Osteoporotic thoracolumbar vertebral compression fractures: Clinical manifestations and treatment".)
-Osteomyelitis and epidural abscess – Back pain associated with fever should raise suspicion for an infection of the spine, such as discitis, osteomyelitis, or epidural abscess. Pain may be localized and progressive. (See "Vertebral osteomyelitis and discitis in adults" and "Spinal epidural abscess".)
Epidural abscesses adjacent to nerve roots may also cause radiculopathy. (See 'Other causes' above.)
-Psychological distress – Pain associated with psychological distress (eg, stress, depression) may contribute to or cause low back pain in some patients. (See "Somatic symptom disorder: Epidemiology and clinical presentation".)
Neurologic conditions — Neurologic disorders of the spinal cord or peripheral nerves beyond the nerve roots may mimic symptoms of lumbosacral radiculopathy. They may be discriminated clinically when abnormalities on neurologic examination extend beyond the distribution of a single nerve root. Neuroimaging and electrodiagnostic testing may also be used to localize these conditions as the cause of symptoms.
Spinal stenosis — Lumbar spinal stenosis is a common condition that causes narrowing of the intraspinal canal. It can be caused by a variety of congenital or acquired conditions. The most common etiology is degenerative spondylosis that leads to facet joint arthropathy and osteophyte formation. The major manifestation is neurogenic claudication, which is a syndrome of bilateral, often asymmetric pain, sensory loss, and/or weakness affecting the legs. The symptoms are produced or exacerbated by walking or prolonged standing in an erect posture. These symptoms represent intermittent mechanical and/or ischemic disruption of lumbosacral nerve root function. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis".)
Lumbar spinal stenosis can also cause lumbosacral radiculopathy in some patients when degenerative spondylitic changes impact a single lumbar nerve root at the lateral recess, neural foramen, or (occasionally) central canal. Severe lumbar spinal stenosis, such as caused by spondylolisthesis, may produce both neurogenic claudication and lumbosacral radiculopathy and can also rarely cause cauda equina syndrome or conus medullaris syndrome.
Cauda equina syndrome — The cauda equina syndrome is caused by an intraspinal lesion caudal to the conus that injures two or more of the 18 nerve roots constituting the cauda equina within the lumbar spinal canal. (See "Anatomy and localization of spinal cord disorders", section on 'Cauda equina syndrome'.)
The cauda equina syndrome is typically associated with marked neurologic disability. The clinical presentation is dominated by bilateral leg weakness in multiple root distributions (L3-S1) and may be associated with perineal sensory symptoms as well as bowel, bladder, and sexual dysfunction due to involvement of the S2-4 spinal nerve roots.
Potential etiologies include developmental abnormalities such as neural tube defects, infectious or inflammatory conditions, or mass lesions such as tumors. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)
The cauda equina syndrome is a rare presentation of lumbar spinal stenosis. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis".)
Diabetic amyotrophy and other lumbosacral plexopathies — Diabetic amyotrophy typically involves the L2, L3, and L4 roots, at least at onset, and presents with leg pain and dysesthesia followed by weakness primarily in the proximal leg, which progresses over days to weeks. Symptoms typically become bilateral and symmetric over time and may also be associated with autonomic symptoms such as orthostatic hypotension and tachycardia as well as unintentional weight loss. Diabetic amyotrophy may be diagnosed with MRI of the lumbosacral plexus and electrodiagnostic studies. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
Lumbosacral plexopathies may also be caused by several other conditions, including inflammatory conditions such as vasculitis or compressive lesions such as tumor and retroperitoneal hematoma. Patients may present with weakness of hip abduction, knee flexion, and ankle flexion/extension, similar to symptoms in patients with L5 and S1 radiculopathies. Plexopathies may be suspected when weakness is patchy, involving selective muscles innervated by multiple roots. However, clinical overlap with radiculopathy may be substantial and electrodiagnostic studies may be needed to discriminate between radiculopathy and plexopathy. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Lumbosacral plexopathy'.)
Peripheral mononeuropathies — Some peripheral mononeuropathies may be mistaken for lumbosacral radiculopathy due to prominence of shared sensory or motor symptoms. Careful evaluation to identify features corresponding to a specific nerve root or peripheral nerve distribution can help distinguish between a radicular and a more peripheral process. (See "Overview of lower extremity peripheral nerve syndromes".)
●Meralgia paresthetica – Pain and sensory loss in the lateral or anterolateral thigh down to the knee may be due to impingement of the lateral femoral cutaneous nerve, similar to sensory symptoms of an L3/4 radiculopathy [63,64]. However, radiculopathy may also present with weakness, such as of hip flexion and knee extension. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)".)
●Femoral neuropathy – Femoral neuropathy may occur from a hip fracture or other compressive lesion at the proximal anterior thigh. Symptoms include weakness of knee extension and numbness of the anterior thigh, similar to those of an L2/3/4 radiculopathy [65,66]. However, these radiculopathies may also present with weakness of hip flexion and adduction. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Femoral nerve'.)
●Fibular (common peroneal) neuropathy – A peroneal neuropathy, commonly due to compression at the fibular head, may present with weakness of ankle eversion and foot dorsiflexion (foot drop), similar to an L5 radiculopathy [67,68]. Patients may also have sensory loss over the lateral shin and foot. However, L5 radiculopathy may also present with weakness of ankle inversion because the tibialis posterior muscle is innervated by the tibial nerve. Hip abduction and knee flexion may also be seen in severe L5 radiculopathy [69]. Ankle inversion, hip abduction, and knee flexion are preserved in patients with a peroneal neuropathy. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Fibular (peroneal) nerve'.)
●Sciatic neuropathy – Compression of the sciatic nerve in the gluteal region may be caused by muscle strain or tendinopathies, hip fracture, or prolonged bed rest. Inflammatory or infiltrative lesions from vasculitis or tumors may also produce a sciatic neuropathy. Patients may present with weakness of knee flexion and ankle flexion/extension, similar to symptoms found with an S1 (or L5 plus S1) radiculopathy [70]. However, patients with an S1 radiculopathy may also have weakness of internal rotation and abduction at the hip, due to involvement of gluteal nerve innervating the gluteus medius/minimus and tensor fascia latae. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Sciatic nerve'.)
Electrodiagnostic testing may also help discriminate peripheral mononeuropathies when clinical features are equivocal.
Systemic conditions and referred pain — Abdominal or pelvic conditions that cause or refer pain and/or sensory loss at a specific lumbosacral level of innervation may mimic lumbosacral radiculopathy (table 3). Organs that can potentially refer pain to the spine include the aorta, pancreas, duodenum, colon, rectum, kidney, ureter, bladder, pelvic organs, and peritoneum. Systemic conditions that may mimic radicular pain include [71-74]:
●Nephrolithiasis
●Abdominal aortic aneurysm
●Ovarian cyst
●Hip bursitis or osteoarthritis
●Acetabular impingement syndrome
Systemic infections and other disorders such as cancer or rheumatologic conditions can also refer pain to the bony spine or produce bony diseases that generate spine pain. The major categories and clues to their diagnosis are listed in the table (table 5).
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Lower spine disorders" and "Society guideline links: Radiculopathy".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Herniated disc (The Basics)" and "Patient education: Radiculopathy of the neck and back (including sciatica) (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Anatomy – Lumbar (L1 to L5) and sacral spinal (S1 to S5) nerve roots originate at the T10 to L1 vertebral level, where the spinal cord ends. The roots then course down through the intraspinal canal, forming the cauda equina, until they exit at their respective neural (intervertebral) foramina (figure 1). Spinal nerve roots within the same numbered neural foramina pass directly below each numbered vertebrae (figure 3). (See 'Anatomy' above.)
Each lumbosacral nerve root innervates a specific sensory region, called a dermatome (figure 4) and a group of muscles, called a myotome (table 1).
●Etiologies – Lumbosacral radiculopathy is most commonly caused by nerve root compression due to either intervertebral disc herniation or degenerative spondylosis. Other etiologies include nonskeletal causes of nerve root compression and noncompressive mechanisms such as infection, trauma, inflammation, neoplasm, and vascular disease. (See 'Etiologies' above.)
Lumbosacral nerve root compression may occur in the central canal, lateral recess, or nerve root canal (figure 1). While lumbosacral nerve roots exit the spinal canal at the neural foramina below their respective vertebrae, they are most commonly compressed as they descend in the lateral recess one level above the exiting level. (See 'Disc herniation' above.)
●Specific radicular presentations – The clinical presentations of lumbosacral radiculopathy vary according to the nerve root(s) involved (table 3). L5 and S1 radiculopathies are the most frequent clinical presentations. (See 'Clinical presentations' above.)
•L1 radiculopathy is uncommon. Symptoms typically involve pain, paresthesia, and sensory loss in the inguinal region (figure 4). (See 'L1 radiculopathy' above.)
•L2, L3, and L4 radiculopathies are considered as a group because there is marked overlap of the innervation of the anterior thigh muscles and the L2, L3, and L4 myotomes (table 1). Acute back pain is the most common presenting complaint, often radiating around the anterior aspect of the thigh down into the knee (figure 4). Weakness of hip flexion and knee extension along with a reduced knee (patellar) stretch reflex may be seen in severe cases. (See 'L2/L3/L4 radiculopathy' above.)
•L5 radiculopathy often presents with back pain that radiates down the lateral aspect of the leg into the foot (figure 4). Weakness may be present in foot dorsiflexion, toe extension, foot inversion, and foot eversion. Reflexes are generally normal. (See 'L5 radiculopathy' above.)
•In S1 radiculopathy, pain radiates down the posterior aspect of the leg into the foot from the back. Sensation is generally reduced on the posterior aspect of the leg and the lateral edge of the foot (figure 4). Weakness may be present in leg extension (gluteus maximus), knee flexion (biceps femoris), and plantar flexion (gastrocnemius). Achilles' tendon (ankle) reflex loss is typical. (See 'S1 radiculopathy' above.)
•S2, S3, and/or S4 radiculopathies are uncommon radiculopathies that may coexist in the setting of a large central disc herniation at a higher level. Patients typically present with sacral or buttock pain that radiates down the posterior aspect of the leg or into the perineum (figure 4). Weakness may be minimal, but urinary and fecal incontinence as well as sexual dysfunction may be present. (See 'S2/S3/S4 radiculopathy' above.)
●Diagnosis – The diagnosis of acute lumbosacral radiculopathy is clinical, made in patients with compatible symptoms and examination findings (table 3). (See 'Evaluation and diagnosis' above.)
Diagnostic testing with a contrast-enhanced lumbosacral MRI is typically reserved for selected patients with high-risk features for suspected structural or inflammatory conditions and those with progressive or severe weakness who are at risk for permanent neurologic impairment (algorithm 1). Neurodiagnostic and other testing may be warranted if neuroimaging is nondiagnostic. (See 'Diagnostic testing for selected patients' above.)
●Differential diagnosis – The differential diagnosis of lumbosacral radiculopathy most commonly includes nonspecific (eg, musculoskeletal) low back pain as well as other neurologic conditions that involve lower extremity nerves, including lumbar spinal stenosis, cauda equina syndrome, diabetic amyotrophy, lumbosacral plexopathy, and mononeuropathies of the leg such as femoral, sciatic, peroneal, and tibial nerve lesions. Systemic infections and other disorders such as cancer or rheumatologic conditions and some abdominal or pelvic conditions may also cause or refer pain to the lumbosacral region (table 5). (See 'Differential diagnosis' above.)
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