Lumbar Radiculopathy: Symptoms, Diagnosis, and Treatment

Last Updated on July 17, 2025

Lumbar radiculopathy refers to a clinical condition characterized by pain, sensory disturbances, or motor deficits in a nerve distribution, resulting from compression or irritation of a spinal nerve root in the lumbar or lumbosacral region.

Unlike non-specific low back pain, which may be mechanical or muscular in origin, radiculopathy is a neuropathic process involving the nerve root itself. The most commonly affected levels are L5 and S1 [1].

The term lumbosacral radiculopathy is sometimes used interchangeably due to overlapping symptoms and involvement of sacral nerve roots as well.

Proper evaluation involves a detailed clinical assessment, imaging, and, when necessary, electrodiagnostic studies, which enable the early differentiation of radiculopathy in the lumbar region from peripheral neuropathies or other musculoskeletal pains.

Relevant Anatomy

The vertebrae of the lumbosacral spine, L1 through S1, form the structural foundation of the lower back. Lumbar vertebrae are characterized by large, kidney-shaped bodies designed to bear axial load.

Their pedicles, laminae, and transverse processes form the vertebral arch, which surrounds the spinal canal. The intervertebral foramina, bordered by the pedicles of adjacent vertebrae, allow passage of spinal nerve roots.

The L5 vertebra has a transitional anatomy. It articulates with the sacrum via the lumbosacral facet joints and bears an anterior tilt that predisposes the segment to shear forces.

The sacrum itself consists of five fused vertebrae, forming a concave structure that contributes to the lumbosacral angle and pelvic stability.

Degenerative changes, spondylolisthesis, or congenital anomalies at the lumbosacral junction can significantly affect dynamics, particularly at the L5–S1 level.

[Read Anatomy of Lumbar Spine]

Spinal Nerve Roots

The lumbar spinal nerves (L1 to L5) emerge from the spinal cord and exit the spinal canal through the intervertebral foramina. Each nerve root travels downward and outward through the lateral recess (see the image of the lateral recess below) and then the neural foramen before joining the lumbosacral plexus.

These nerve roots are especially vulnerable near their exit zones, where they pass close to discs, facet joints, and ligamentous elements.

Clinically, a disc herniation at the L4–L5 level typically affects the L5 nerve root, and a herniation at L5–S1 affects S1. Posterolateral disc protrusions most often compress the traversing rather than the exiting root.

At any given lumbar disc level, the exiting nerve root leaves through the foramen at that level, while the traversing nerve root descends past the disc to exit below.
Posterolateral disc herniations typically impinge on the traversing root as it passes through the lateral recess, a narrow corridor just medial to the foramen.

For example, at the L4–L5 level, the L4 root is exiting, but the L5 root is traversing, and is the one commonly compressed, resulting in L5 radiculopathy.

Intervertebral Discs and Annulus

Each intervertebral disc consists of a central nucleus pulposus surrounded by the annulus fibrosus. The posterior and posterolateral parts of the annulus are structurally weaker, making them common sites of herniation.

When the nucleus material escapes through a tear in the annulus, it can press on nearby nerve roots or trigger inflammatory changes that cause radicular pain.

Lateral Recess and Neural Foramen

The lateral recess lies adjacent to the central canal and is bordered by the vertebral body anteriorly and the superior articular facet and ligamentum flavum posteriorly.

The neural foramen, through which the spinal nerve exits, is formed by the space between two adjacent vertebrae. Its boundaries are formed by the vertebral bodies and intervertebral disc anteriorly, the facet joints and pedicles posteriorly, and the pedicles of adjoining vertebrae forming the roof and floor

Narrowing of either lateral recess or neural foramen can lead to nerve root compression and radicular symptoms.

Facet Joints and Ligamentum Flavum

Facet joints are synovial articulations that stabilize the spine posteriorly. With age, they often undergo hypertrophy and develop osteophytes, contributing to foraminal narrowing (they form the posterior boundary of the foramen).

The ligamentum flavum, normally elastic, can also thicken and buckle inward, especially during spinal extension, further reducing available space and irritating nerve roots.

Lumbosacral Plexus and Peripheral Nerves

The lumbar nerve roots contribute to the lumbosacral plexus, which gives rise to major peripheral nerves. For example, L2 to L4 roots help form the femoral nerve, while L4 to S3 contribute to the sciatic nerve. Compression of these nerves may result in weakness or sensory loss that follows the dermatomal or myotomal patterns associated with the nerve roots.

Pathophysiology of Lumbar Radiculopathy

Lumbar radiculopathy results from pathological processes that cause mechanical compression, chemical irritation, or ischemic compromise of a lumbar spinal nerve root [2]

Mechanical Compression

The most frequent cause is intervertebral disc herniation, typically posterolateral, which impinges upon the adjacent nerve root within the lateral recess or neural foramen. Other comprehensive sources include:

• Hypertrophied ligamentum flavum
• Facet joint osteophytes
• Foraminal or extraforaminal stenosis
• Spondylolisthesis
• Epidural masses (e.g., tumors, abscesses)

Mechanical compression leads to local demyelination, altered axonal transport, and conduction block, contributing to both pain and motor-sensory deficits.

Chemical Irritation and Inflammatory Response

Leakage of nucleus pulposus material from an annular tear can provoke a local inflammatory cascade. This “chemical radiculitis” involves cytokines such as IL-1 beta and TNF-alpha, leading to root edema and nociceptor sensitization. This mechanism often underlies severe radiculopathy in the lumbar region with minimal imaging findings or minimal compression

Ischemia

Compression of radicular arteries may result in ischemic injury to the nerve root. It is less common than mechanical or inflammatory pathways, but ischemia can contribute to persistent symptoms and delayed recovery.

The interplay between these mechanisms explains the heterogeneity of lumbar radiculopathy symptoms.

Causes of Lumbar Radiculopathy

Lumbar Disc Herniation

The most frequent cause in adults under 50. Herniation typically occurs at L4–L5 or L5–S1 levels, where biomechanical stress is greatest. The posterolateral direction of herniation commonly affects the traversing nerve root (e.g., L5 in an L4–L5 herniation).

Lumbar Spinal Stenosis

In older adults, degenerative narrowing of the spinal canal or lateral recess can compress nerve roots. The condition may be central or foraminal and is often multifactorial:

• Facet joint hypertrophy
• Ligamentum flavum thickening
• Intervertebral disc bulging
• Spondylolisthesis

Symptoms may be positional and bilateral, classically causing neurogenic claudication.

Foraminal Narrowing and Spondylotic Changes

Degenerative disc disease with reduced disc height can lead to

• Osteophyte formation impinging on the nerve root
• Foraminal stenosis
• Perineural fibrosis

These changes often underlie chronic lumbar radiculopathy symptoms that wax and wane over time.

Spondylolisthesis

Anterior slippage of one vertebral body over another, especially at L4–L5, can compress nerve roots at the exit zone or lateral recess. It may be isthmic (in younger adults) or degenerative (in the elderly).

Mass Lesions

Less common but important differential diagnoses include

• Primary tumors in the spine/meninges/nerve sheaths
• Metastatic lesions to the spine
• Epidural abscess or hematoma
• Synovial cysts
• Tuberculosis of the spine (Pott’s disease) may cause caseating granulomas and collapse, leading to root compression.
• Autoimmune conditions (e.g., ankylosing spondylitis) may cause enthesitis and fibrosis that secondarily impinge on nerve roots.

These are typically suggested by atypical features, such as night pain, weight loss, systemic symptoms, or failure to respond to standard treatment.

Extraspinal Causes

• Piriformis syndrome
• Iliopsoas hematoma
• Herpes zoster

Clinical Presentation

Symptoms

Pain and Sensory Disturbances

Radicular pain is typically sharp, shooting, or electric in quality. It radiates along the dermatome (see diagram below) of the involved root, most often down the buttock, thigh, leg, and sometimes into the foot. For example

• L2, L3, and L4 compression can cause radicular pain into the front of the thigh and the shin
• L5 radiculopathy pain travels down the lateral thigh and leg into the dorsum of the foot.
• S1 radiculopathy pain follows the posterior thigh and calf into the sole or lateral foot.

The pain may be unilateral or, in central stenosis, bilateral.

Paresthesias, numbness, or altered sensation may occur in a dermatomal distribution. Patients may describe “pins and needles,” burning, or deep aching. Paraesthesia is the most common symptom.

Subjective symptoms may not always correlate with objective findings.

Motor Deficits

Most of the lumbar radiculopathies mainly have sensory symptoms. Weakness is usually subtle and often not noticeable. This is because the sensory or dorsal spinal root is more susceptible to insult than the motor or ventral.

However, the motor weakness may occur and is often a cause for concern. Reflexes, though affected, are difficult to check in an acute painful condition. So in the presence of significant motor weakness, MRI should be done early,

Clinical Examination

The patient may have a forward-flexed or list posture in an attempt to relieve nerve root tension. The patient often walks with an antalgic gait or Trendelenburg gait (gluteal weakness). Muscle atrophy may be noted in chronic cases, particularly in the calf or thigh.

The patient may be able to tell what makes the pain worse. For some, it is sitting, for others it is standing or walking.

On palpation, paraspinal tenderness may or may not be present.

While textbooks often describe a detailed neurological examination as protocol, this may not be feasible during the patient’s initial presentation. If the patient is in severe pain, that discomfort must be addressed first, because effective neurological testing requires specific patient positioning and cooperation, both of which may be difficult in the setting of acute radiculopathy.

In such cases, it is reasonable to defer a complete neurological examination until the patient is more comfortable. When performed, the exam should include testing of motor strength, deep tendon reflexes, and sensory modalities such as pinprick and light touch.

Often, a quick overview guided by suspected root level can spare both the clinician and the patient unnecessary effort during the acute phase. At follow-up or when the patient stabilizes, a more detailed neurological assessment can be conducted if needed.

Provocative Tests

Provocative tests help identify nerve root irritation by applying mechanical or tension stress to neural structures. They are not intended to reproduce back pain, but rather to elicit radicular symptoms along a dermatome.

Straight Leg Raise (SLR)

Passive elevation of the extended leg between 30–70 degrees reproduces shooting leg pain. It suggests neural tension from a herniated disc or root irritation.

Crossed SLR (Well Leg Raise)

Raising the unaffected leg produces radicular pain in the symptomatic limb. Though less sensitive, it is highly specific for disc herniation with nerve root compression.

Slump Test

The patient sits upright, then sequentially flexes the thoracic and cervical spine, extends the knee, and dorsiflexes the ankle. The examiner monitors for reproduction of nerve-related symptoms. This position places tension on the entire neural tract, helping to detect subtle radicular involvement.

Femoral Nerve Stretch Test

The femoral nerve stretch test targets the upper lumbar nerve roots (L2–L4). With the patient in a prone or side-lying position, the examiner passively extends the hip while keeping the knee flexed. Reproduction of pain or paresthesias in the anterior thigh suggests proximal nerve root irritation or compression.

Findings of Urgent Concern

• Saddle anesthesia
• New-onset urinary retention or fecal incontinence
• Progressive bilateral weakness
• Fever, weight loss, or known malignancy

These findings may suggest cauda equina syndrome, epidural abscess, or tumor, all requiring prompt imaging and intervention.[3]

Differential Diagnosis

Lumbar radiculopathy must be distinguished from other conditions that present with lower extremity pain, sensory symptoms, or weakness. A thorough differential diagnosis helps avoid misattributing symptoms and ensures appropriate intervention, particularly when imaging results are ambiguous or normal.

Peripheral Nerve Palsy

These are typically non-dermatomal, and weakness or sensory loss tends to be distal:

• Peroneal nerve palsy: Foot drop, normal inversion, no thigh/gluteal pain
• Femoral nerve neuropathy: Involves femoral nerve distribution (hip, knee weakness, anterior thigh sensory loss), often h/o surgery( retroperitoneal hematoma)
• Sciatic neuropathy: Pain and weakness involving multiple muscles below the knee. Loss of ankle jerk but preserved knee reflex. Often caused by trauma, injections, or tumors

Hip Joint Pathology

Hip osteoarthritis or avascular necrosis can mimic radicular pain. Pain location is the groin or the anterior thigh, and is exacerbated by weight-bearing or hip rotation. Neural examination is normal

Sacroiliac Joint Dysfunction

Localized buttock pain, sometimes radiating to the posterior thigh, but there is no true dermatomal distribution. MRI may show sacroiliitis in inflammatory causes.

The FABER (Flexion, ABduction, External Rotation) test: The examiner places the tested leg in a figure-four position in a supine patient and presses down on the knee and the opposite ASIS. Pain in the groin suggests hip joint involvement, while pain in the posterior pelvis points toward sacroiliac joint pathology.

Diabetic Amyotrophy (Lumbosacral Plexopathy)

• Older diabetics with the acute onset of thigh pain followed by weakness
• Asymmetric and involves proximal muscles
• EMG shows denervation; MRI lumbosacral plexus may aid diagnosis

Spinal Cord or Intradural Pathology

• Conus medullaris syndrome: Bilateral symptoms, early bladder involvement
• Cauda equina syndrome: Multilevel root involvement, saddle anesthesia
• Intradural tumors like ependymoma or schwannoma

MRI is essential for detection.

Herpes Zoster

Herpes zoster (shingles) often begins with sharp, burning dermatomal pain that precedes the characteristic vesicular rash by a few days. This prodromal pain may mimic radiculopathy. In atypical or early cases without rash, PCR testing or varicella-zoster virus (VZV) antibody titers can aid diagnosis.

Functional or Psychogenic Pain

• Non-dermatomal, inconsistent findings
• Exaggerated pain responses, give-way weakness
• Important to rule out organic pathology first
• May coexist with organic radiculopathy

Imaging

X-rays

X-rays do not offer much role in lumbar radiculopathy, but can be used when structural issues are present or imaging may be delayed [4]

• AP and lateral are standard views
• Limited in soft-tissue assessment but useful for
  • Detecting spondylolisthesis
  • Assessing disc space narrowing
  • Identifying structural deformities

Magnetic Resonance Imaging (MRI)

• Modality of choice for evaluating lumbar radiculopathy
• Reveals:
  • Disc herniation (sequestered, protruded, extruded)
  • Foraminal and lateral recess stenosis
  • Root compression, edema, or displacement
• MRI spine with contrast may be used when prior surgery or a tumor is suspected

Note: MRI findings must correlate clinically. Asymptomatic disc herniations are common.

CT and CT Myelography

• Alternative for patients who cannot undergo MRI (e.g., patients with a pacemaker)
• Better resolution of bony anatomy
• CT myelogram visualizes nerve root compression indirectly via contrast flow patterns

Electromyography (EMG) and Nerve Conduction Studies (NCS)

• Confirm radiculopathy when imaging is inconclusive
• Differentiate root-level pathology from peripheral nerve disease
• May not show changes until 2–3 weeks after onset
• Useful in assessing:
  • Chronic vs acute denervation
  • Single vs multiple root involvement
  • Axonal loss severity

Management of Lumbar Radiculopathy

The treatment of lumbar radiculopathy depends on the severity of symptoms, duration, presence of neurological deficits, and underlying etiology. Most patients improve with conservative measures, but timely identification of surgical candidates is crucial for optimal outcomes.

Conservative (Non-Surgical) Management

Indications

• Mild to moderate symptoms without progressive neurological deficit
• The first episode of lumbar radiculopathy symptoms
• Imaging confirms non-complicated disc herniation or foraminal stenosis

Pharmacologic Treatment

• NSAIDs: First-line for pain and inflammation
• Neuropathic agents:
  • Gabapentin, pregabalin, duloxetine, amitriptyline
  • Helpful for sensory symptoms like paresthesia, burning pain
• Short course corticosteroids (oral or IV): Controversial; may reduce acute root inflammation
• Muscle relaxants: Limited role, short-term only
• Opioids: Avoid long-term use; may be used briefly in severe acute cases

Activity Modification

• Encourage light activity as tolerated
• Avoid prolonged bed rest
• Postural education and ergonomics

Physical Therapy

• McKenzie exercises: Extension-based movements are commonly used in the management of discogenic radiculopathy. They are most effective in patients whose symptoms improve with extension and worsen with flexion.
• Neural mobilization: Neural mobilization involves sciatic and femoral nerve gliding techniques aimed at improving nerve mobility and reducing sensitivity. These gentle, controlled movements alternate between tensioning and releasing the nerve to enhance its ability to move within surrounding tissues.
• Core strengthening and flexibility training
• Pain modalities (e.g., TENS, ultrasound) for symptomatic relief

Epidural Steroid Injections (ESI)

• May provide temporary relief by reducing inflammation around the nerve root
• Indications:
  • Persistent pain not responding to medication/therapy
  • Contraindication or delay to surgery
• Effects may last weeks to months; not curative

Surgical Management

Indications

• Progressive neurological deficit (e.g., foot drop, motor weakness)
• Failure of conservative management for 6–8 weeks
• Recurrent or disabling pain despite appropriate therapy
• Cauda equina syndrome (absolute emergency)
• MRI confirms compressive pathology correlating with clinical findings

Surgical Options

A brief about surgical options is given in the following table

Surgical choice depends on anatomical findings, surgeon expertise, and patient-specific factors.

Outcomes

• The majority of patients report significant pain relief after surgery
• Motor recovery depends on the preoperative deficit duration
• Reoperation rates range from 5–10% for recurrent disc herniation
• Predictors of poor outcome:
  • Long symptom duration
  • Severe root compression
  • Coexisting psychosocial issues

Postoperative and Long-Term Management

• Early mobilization and physiotherapy
• Weight reduction and ergonomics education
• Management of modifiable risk factors (e.g., diabetes, smoking)
• Addressing fear-avoidant behavior and chronicity risks. Fear-avoidant behavior occurs when patients develop an exaggerated fear of movement or activity due to the belief that it will worsen their pain or cause harm, reducing activity, leading to deconditioning, stiffness, and increased pain sensitivity.

Special Situations Involving Lumbar Radiculopathy

Certain patient populations and clinical scenarios require modified diagnostic or therapeutic strategies due to anatomical, physiological, or contextual complexity. These cases may deviate from standard pathways of care and merit tailored approaches.

Recurrent Lumbar Radiculopathy

Patients may redevelop symptoms months or years after initial resolution, often due to

• Recurrent disc herniation
• Scar tissue formation (epidural fibrosis)
• Progressive degeneration at adjacent levels

Re-imaging is required to distinguish new vs recurrent pathology and evaluate spinal stability (dynamic X-rays or MRI)

Surgery may be more complex and have reduced success rates in revision cases

Failed Back Surgery Syndrome (FBSS)

Defined as persistent or recurrent symptoms after spinal surgery. Contributing factors include:

• Unaddressed adjacent segment disease
• Incomplete decompression or wrong-level surgery
• Neuropathic pain independent of mechanical cause

[Read more about Failed Back Surgery Syndrome]

FBSS requires a multidisciplinary approach for treatment

Sciatica in Pregnancy

This occurs due to mechanical compression by the gravid uterus, hormonal laxity, and altered posture. Most commonly presents in the third trimester.

MRI is safe if clinically indicated. The treatment involves

• Conservative: position changes, activity modification, pelvic tilt exercises
• Avoid NSAIDs: Acetaminophen is preferred
• Epidural steroid injections are rarely needed, but are considered safe if essential

Elderly Patients and Lumbar Radiculopathy

• More likely to have multifactorial radiculopathy from degenerative stenosis, osteophytes, and facet arthropathy
• Often have comorbidities that complicate both diagnosis and treatment
• May present atypically with subtle or non-painful deficits (e.g., imbalance or falls)

In these patients, non-operative management is preferred unless severe deficit or intractable pain. Evaluate surgical risk carefully if decompression is considered

Athletes and High-Demand Individuals

They often present with early or subtle symptoms due to heightened awareness of performance decline. They are often driven to return to sport quickly, raising the risk of reinjury. Imaging may detect disc pathology without clinical correlation

For treatment, focus on core stabilization and dynamic neuromuscular control. The return to sport should be gradual. Athletes should work on biomechanics and load management

Recent Advances in Lumbar Radiculopathy

Ongoing innovations in imaging, surgical techniques, and pain modulation continue to refine the diagnosis and management of lumbar radiculopathy. Clinicians must stay current with emerging evidence to offer optimal care, especially in complex or recurrent cases.

Image-Guided Navigation and Intraoperative Neuromonitoring

• Image-guided navigation systems (such as O-arm or robotic platforms) enhance the precision of decompression and implant placement, particularly in anatomically complex or revision cases. [5]
• Intraoperative neuromonitoring using EMG and SSEP helps preserve nerve root function during high-risk procedures.
• Their adoption varies across centers based on cost, infrastructure, and surgeon experience

Experimental Studies

• Platelet-rich plasma (PRP) and stem cell injections into degenerated discs
• Advanced MRI Sequences and AI Integration may help visualize nerve root integrity and predict recovery
  • Diffusion tensor imaging (DTI)
  • Nerve tractography

References

1. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001 Feb 01;344(5):363-70. [PubMed] 
2. Rothman SM, Winkelstein BA. Chemical and mechanical nerve root insults induce differential behavioral sensitivity and glial activation that are enhanced in combination. Brain Res. 2007 Nov 21;1181:30-43. [PubMed]
3. Tarulli AW, Raynor EM. Lumbosacral radiculopathy. Neurol Clin. 2007 May;25(2):387-405. [PubMed]
4. Dydyk AM, Khan MZ, Singh P. Radicular Back Pain. [Updated 2022 Oct 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK546593/
5. Brunken F, Mandelka E, Bullert B, Gruetzner PA, Vetter SY, Gierse J. Comparison of 3D-navigation and fluoroscopic guidance in percutaneous pedicle screw placement for traumatic fractures of the thoracolumbar junction. Brain Spine. 2024 Feb 17;4:102769. [PubMed]
6. Takeda, Masaaki et al. Intraoperative Neurophysiological Monitoring for Degenerative Cervical Myelopathy Neurosurgery Clinics, Volume 29, Issue 1, 159 – 167