Prolapsed Intervertebral Disc: A Clinical Guide
Definition
A Prolapsed Intervertebral Disc (PID), commonly known as a herniated or "slipped" disc, is defined as the localized displacement of disc material (which can include the nucleus pulposus, cartilage from the endplate, or fragments of the annulus fibrosus) beyond the normal anatomical confines of the intervertebral disc space (9). This displacement is distinct from a generalized "disc bulge," where more than 25% of the disc's circumference extends symmetrically beyond the vertebral edges, often as a part of normal aging. A true herniation is a focal event. This displaced material can then cause symptoms by two primary mechanisms: direct mechanical compression of adjacent neural structures (the spinal cord or, more commonly, a nerve root) and the initiation of a potent chemical inflammatory response, leading to a clinical syndrome of pain and neurological dysfunction.
Epidemiology
Prolapsed Intervertebral Disc represents a major cause of morbidity and disability worldwide. Global data estimates the annual incidence of a new symptomatic herniation to be between 5 and 20 cases per 1,000 adults, with a lifetime prevalence of symptomatic lumbar PID affecting 1% to 3% of the population (20). The highest incidence is seen in the 30-50 year age group, impacting individuals in their most productive years and thus carrying a significant socioeconomic burden through lost workdays and healthcare costs.
In the Malaysian context, while specific national incidence data for PID is limited, the high prevalence of its primary symptom, low back pain (LBP), underscores the scale of the problem. Community surveys show LBP prevalence around 12%, but this figure skyrockets in high-risk occupational groups, such as commercial vehicle drivers, where it can reach up to 60% (24, 26). A 2022 study utilizing local MRI data from a Malaysian cohort provided valuable insight, noting a higher prevalence of moderate-to-severe lumbar disc degeneration among individuals of Malay ethnicity compared to other groups (27).
A critical epidemiological finding that every junior doctor must internalize is the high prevalence of asymptomatic disc herniations. MRI studies on pain-free individuals frequently reveal disc protrusions and even extrusions. This has led to the foundational clinical principle: "treat the patient, not the scan." The presence of a herniated disc on an MRI is an anatomical finding, not a diagnosis in itself. A diagnosis is only made when there is a clear correlation between the level and location of the herniation on the scan and the patient's specific clinical signs and symptoms (e.g., a right-sided L5-S1 disc extrusion compressing the S1 nerve root in a patient with a classic right S1 radiculopathy). This prevents the misattribution of symptoms to incidental, age-related imaging findings and avoids unnecessary anxiety and intervention.
Etiology
The development of PID is a multifactorial process, resulting from a complex interplay between an individual's intrinsic predispositions and the extrinsic or environmental forces they are exposed to. It is rarely a single event but rather the culmination of years of cumulative stress on a susceptible disc.
Non-Modifiable Risk Factors:
Genetics: A strong hereditary component is well-established, with twin studies suggesting heritability for disc degeneration may be as high as 75%. Individuals with a first-degree relative with PID are at significantly increased risk. Specific genetic polymorphisms affecting the building blocks of the disc, such as genes for collagen types (e.g., COL9A2, COL11A1), aggrecan (a key proteoglycan for hydration), and the Vitamin D receptor, can lead to an inherently weaker disc structure that is less able to withstand mechanical stress (35, 38).
Age: The peak incidence occurs between 30 and 50 years old. This age represents a vulnerable window where the nucleus pulposus is still sufficiently hydrated and gelatinous to be able to extrude, while the annulus fibrosus has begun to weaken and develop micro-tears from cumulative wear and tear (9).
Height: Taller stature, particularly in men over 180 cm, is a recognized risk factor due to increased biomechanical leverage and greater compressive loads on the lumbar discs (36).
Modifiable & Environmental Risk Factors:
Occupation: Certain jobs dramatically increase the risk. These include roles involving repetitive heavy lifting, pulling, and pushing (e.g., construction, agriculture), as well as those involving prolonged sitting (e.g., office workers, commercial drivers). The combination of prolonged sitting, which increases intradiscal pressure by up to 40% compared to standing, and whole-body vibration experienced during driving is particularly damaging (39).
Smoking: Nicotine is profoundly detrimental to disc health. It acts as a potent vasoconstrictor, impairing the already tenuous nutrient supply that diffuses across the vertebral endplates to the avascular disc. Furthermore, it directly inhibits the synthesis of collagen and proteoglycans, weakening the disc's structural integrity and its capacity for repair (40).
Obesity: Excess body weight, particularly central adiposity, increases the direct mechanical load on the lumbar spine. It also alters spinal biomechanics by causing an anterior pelvic tilt and increased lumbar lordosis, which concentrates stress on the posterior elements of the spine. Obesity is also a pro-inflammatory state, which may accelerate the chemical aspects of disc degeneration (41).
Sedentary Lifestyle: A lack of regular physical activity leads to deconditioning of the core stabilizing muscles (transversus abdominis, multifidus). These muscles form a natural "corset" that supports the spine. When weak, a greater proportion of daily biomechanical stress is transmitted directly to the intervertebral discs.
Pathophysiology
PID results from a "dual-hit" injury to neural structures, combining direct mechanical compression with a potent chemical inflammation. This clinical event is the final stage of a long-term degenerative cascade.
The Degenerative Cascade: The process begins at a cellular level with senescence of the disc's chondrocyte-like cells. This leads to a decrease in the production of proteoglycans, the molecules responsible for binding water within the nucleus pulposus. As the nucleus dehydrates, it loses turgor and height, transforming from a resilient cushion into a fibrotic, less compliant structure. This loss of height transfers immense stress to the annulus fibrosus, leading to the formation of circumferential and then radial tears. These tears typically begin in the innermost layers and progress outward, most commonly in the posterolateral aspect of the annulus, which is anatomically thinner and less supported by the longitudinal ligaments (4).
Mechanical Compression: Once the nucleus herniates through a complete annular tear, the displaced disc material can physically impinge on a nerve root or the spinal cord. This direct pressure can cause nerve root ischemia by compressing its delicate vascular supply, disrupt axoplasmic flow within the neuron, and lead to intraneural edema. The clinical manifestations—pain, paresthesia, and weakness—are the direct results of this neural dysfunction (5).
Chemical Radiculitis: This is a critically important and often dominant component of the pain syndrome. The nucleus pulposus is an avascular structure that is immunologically sequestered from the body's systemic circulation. When it extrudes into the epidural space, its components are exposed to the immune system and recognized as foreign antigens. This triggers a robust local inflammatory response, mediated by the release of numerous pro-inflammatory substances, including Tumor Necrosis Factor-alpha (TNF-α), various interleukins (IL-1, IL-6), phospholipase A2, and nitric oxide. These mediators cause intense chemical irritation and inflammation of the adjacent nerve root, a condition known as chemical radiculitis. This inflammatory cascade can produce severe radicular pain even in the absence of significant mechanical compression, which explains the common clinical conundrum where the severity of a patient's pain does not correlate with the size of the herniation on an MRI (9).
Clinical Presentation
The diagnosis of PID is primarily clinical, relying on meticulous history taking and a structured physical examination. The classic presentation involves a combination of axial (back/neck) and radicular (limb) pain.
Diagnostic Clues
Pathognomonic Pattern: The clinical triad of (1) radicular pain and/or paresthesia in a specific dermatomal distribution, (2) weakness in the corresponding myotome, and (3) a diminished or absent deep tendon reflex for that nerve root is highly suggestive of the diagnosis and allows for precise anatomical localization before imaging.
Limb Pain > Back Pain: In classic nerve root compression, the sharp, shooting, neuropathic limb pain is often described as far more severe and distressing than the dull, aching, nociceptive axial back pain. This is a key feature that helps differentiate true radiculopathy from non-specific low back pain.
Aggravating Factors: Pain is classically worsened by any activity that increases intra-abdominal and thus intradiscal pressure. This includes coughing, sneezing, straining during a bowel movement (Valsalva), and forward bending (flexion). Patients often find relief lying down.
Common Symptoms (>50%)
Radicular Pain: A sharp, lancinating, or electric shock-like pain that radiates from the spine down a limb, following the specific path of a nerve (e.g., sciatica) (11).
Paresthesia: A sensation of numbness, tingling, or "pins and needles" in the same dermatomal distribution as the pain.
Localized Axial Pain: A dull, aching pain in the lower back or neck, which may precede the onset of limb symptoms by days or weeks. This is thought to arise from the torn outer fibers of the annulus fibrosus and associated muscle spasm.
⚠️ Red Flag Signs & Symptoms
These indicate a potential neurosurgical emergency or serious underlying pathology and require immediate investigation and specialist referral.
Cauda Equina Syndrome (CES): This is a NEUROSURGICAL EMERGENCY.
Bilateral sciatica or leg weakness (may be asymmetrical).
Saddle anesthesia or paresthesia (numbness or altered sensation in the perineum, buttocks, and inner thighs - the "saddle" area).
New-onset bladder or bowel dysfunction: This can be subtle. Ask specifically about difficulty initiating urination, loss of the sensation of bladder fullness, urinary retention leading to overflow incontinence, or new-onset fecal incontinence.
Loss of anal sphincter tone on digital rectal examination.
Progressive or Severe Neurological Deficit: Rapidly worsening or profound motor weakness, such as an acute foot drop (inability to dorsiflex the ankle, corresponding to an L4/L5 lesion), indicates severe nerve compromise.
Constitutional Symptoms: The presence of fever, chills, night sweats, or unexplained significant weight loss should raise suspicion for a spinal infection (e.g., epidural abscess, discitis) or malignancy (e.g., metastatic disease).
High-Risk History: Age of onset <20 or >55 years, a known history of cancer, recent significant trauma, history of intravenous drug use, or immunosuppression are all historical red flags.
Complications
Acute: Cauda Equina Syndrome, profound motor weakness (e.g., foot drop) which may be permanent if not addressed urgently, intractable pain leading to emergency department visits.
Chronic: Development of chronic neuropathic pain syndrome, permanent neurological deficit (numbness or weakness), muscle atrophy in the affected limb, significant functional disability impacting work and daily life, and secondary psychological conditions such as depression, anxiety, and fear-avoidance behavior.
Prognosis
The natural history of acute radiculopathy from PID is highly favorable. The majority of patients—up to 90%—experience significant improvement or complete resolution of symptoms within 6 weeks to 3 months with comprehensive conservative management alone (19). This is because many herniated disc fragments will spontaneously regress or be reabsorbed over time through a combination of retraction, dehydration, and phagocytosis by macrophages that infiltrate the area as part of the inflammatory response. Factors associated with a better prognosis include the centralization of pain (limb pain recedes back towards the spine) and the absence of psychosocial "yellow flags" like fear-avoidance beliefs.
Differential Diagnosis
Mechanical Low Back Pain: The most common cause of back pain. It is typically localized to the lumbosacral region, often described as a dull ache related to activity, without significant radicular symptoms, neurological deficits, or nerve tension signs.
Lumbar Spinal Stenosis: A narrowing of the spinal canal, which typically affects older individuals. The hallmark is neurogenic claudication—leg pain, heaviness, and weakness brought on by walking or standing, which is characteristically relieved by sitting or bending forward (the "shopping cart sign"). Symptoms are often bilateral.
Peripheral Nerve Entrapment: It is crucial to distinguish radiculopathy from entrapment of a nerve further down the limb. For example, peroneal neuropathy at the fibular head can mimic an L5 radiculopathy with foot drop, but it will not cause back pain and can be elicited with a Tinel's sign over the fibular head. Similarly, carpal tunnel syndrome can mimic a C6/C7 radiculopathy. Neurophysiological tests are key to differentiating these.
Malignancy or Infection: Suspect in patients with red flag symptoms. The pain from these conditions is often described as constant, deep, boring, and characteristically worse at night or at rest, unlike the mechanical nature of typical PID pain.
Investigations
Investigations are guided by the clinical presentation, with a strong emphasis on avoiding unnecessary early imaging in uncomplicated cases.
Immediate & Bedside Tests
Clinical Examination: A thorough and well-documented neurological examination to detect motor deficits (using the MRC scale), sensory loss, reflex changes, and nerve tension signs (Straight Leg Raise) is the most critical immediate investigation.
Bladder Scan: In any patient with a history suggestive of urinary retention, a bedside bladder scan is mandatory. A post-void residual (PVR) volume of >150-200 mL is abnormal and significantly raises suspicion for Cauda Equina Syndrome.
Diagnostic Workup
First-Line Investigations (When Indicated):
Laboratory Tests: Not routine for PID. Order a Full Blood Count (FBC), Erythrocyte Sedimentation Rate (ESR), and C-reactive Protein (CRP) only if red flags suggest an underlying inflammatory, infectious, or malignant cause.
Plain Radiographs (X-rays): Have a limited role in directly diagnosing a soft-tissue disc herniation. Their primary utility is as a screening tool to rule out other bony pathologies like fractures, spondylolisthesis (instability), or lytic/blastic lesions from tumors.
Gold Standard:
Magnetic Resonance Imaging (MRI): This is the definitive, non-invasive test for diagnosing PID. Its superior soft-tissue contrast provides detailed images of the disc, annulus, nucleus, spinal cord, and nerve roots. It can precisely identify the level and location of the herniation (e.g., central, paracentral, foraminal), characterize its type (protrusion, extrusion, sequestration), and demonstrate the degree of nerve root or thecal sac compression (65, 66). Remember, an MRI is not indicated within the first 4-6 weeks for uncomplicated radiculopathy but is required urgently if any red flags are present.
Monitoring & Staging
Neurophysiological Tests (EMG/NCS): These are not used for initial diagnosis but are valuable functional tests in specific scenarios. They can confirm the presence and severity of radiculopathy when the diagnosis is uncertain, help differentiate it from peripheral neuropathies, and assess for evidence of axonal loss, which can have prognostic implications (9).
Management
Management is primarily conservative and multimodal, with surgery reserved for a select, well-defined group of patients.
Management Principles
The management of PID focuses on symptom control, functional restoration, and patient education, with the reassuring knowledge that the condition has a favorable natural history and that time is a great healer.
Acute Stabilisation (The First Hour)
This section applies primarily to patients presenting with Red Flag signs, particularly suspected Cauda Equina Syndrome.
Airway/Breathing: Ensure airway is patent.
Circulation: Secure large-bore IV access.
Disability: Perform an urgent, focused neurological assessment. Document motor power (MRC scale), sensation in all dermatomes (especially perineal S2-S5), and reflexes. Perform a digital rectal exam to assess anal tone. If CES is suspected, this is the absolute priority.
Exposure: Check for signs of trauma or infection.
Action: If Cauda Equina Syndrome is suspected, this is a time-critical neurosurgical emergency. Keep the patient nil by mouth (NBM), insert an indwelling urinary catheter to monitor output and decompress the bladder, and make an immediate phone call referral to the on-call Orthopedic or Neurosurgery team for an emergency MRI and surgical decompression. Document the time of onset of symptoms and the time of referral.
Definitive Therapy
First-Line Treatment (Comprehensive Conservative Management):
Patient Education & Activity Modification: This is a crucial intervention. Reassure the patient about the favorable prognosis. Advise them to remain as active as their pain allows and to avoid prolonged bed rest (>2 days), which is detrimental. Teach "first aid" for the spine: proper posture, safe lifting techniques (bending at the knees), and avoiding aggravating activities (72).
Pharmacotherapy (Mechanism-Based):
Nociceptive Pain (Axial): Use simple analgesics like Paracetamol and/or a course of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) like Ibuprofen or Diclofenac. Always consider co-prescribing a proton pump inhibitor (PPI) for GI protection with NSAIDs (75).
Neuropathic Pain (Radicular): First-line agents are neuromodulators. These include Gabapentinoids (Gabapentin, starting 300mg ON and titrating up; Pregabalin, starting 25-75mg ON/BD) or low-dose Tricyclic Antidepressants (Amitriptyline, 10-25mg ON). The key is to "start low, go slow" to balance efficacy with side effects (74).
Muscle Spasm: A short-term course (3-5 days) of a muscle relaxant (e.g., Orphenadrine, Tizanidine) can be helpful to break the pain-spasm cycle in the acute phase.
Physiotherapy: A cornerstone of treatment. Early focus is on pain relief and directional preference exercises (e.g., McKenzie method), which can centralize pain. As pain subsides, the focus shifts to a graded exercise program to strengthen the deep core stabilizing muscles (transversus abdominis, multifidus), improve flexibility, and facilitate a gradual return to normal function and work (78, 80).
Second-Line/Escalation:
Epidural Steroid Injections: For patients with severe, disabling radicular pain that is unresponsive to a full trial of oral medications and is hindering participation in physiotherapy, an ESI can be considered. A corticosteroid is injected into the epidural space (often via a transforaminal approach for better targeting) to deliver a potent, local anti-inflammatory effect. This can provide a crucial "window of opportunity" with significant pain relief, allowing the patient to engage more effectively in their rehabilitation program (82).
Surgical Intervention (e.g., Microdiscectomy): The primary and most reliable goal of surgery is to relieve the radicular limb pain caused by nerve compression; it is far less effective for axial back pain. The indications are clear:
Absolute (Emergency): Cauda Equina Syndrome, or a progressive or profound motor deficit.
Relative: Persistent, disabling radicular pain that significantly impacts quality of life and has failed to improve after an adequate trial (typically at least 6-8 weeks) of comprehensive non-operative care, where the patient's symptoms correlate directly with the MRI findings (83).
Key Nursing & Monitoring Instructions
Perform and document hourly neurological observations (motor power, sensation) for any patient with a new or evolving motor deficit.
Strictly monitor for any signs of bladder or bowel dysfunction. Ask patients directly about their ability to feel themselves passing urine and their perineal sensation.
Administer multimodal analgesia regularly and on time, rather than waiting for pain to become severe, to facilitate comfort and early mobilization.
Inform medical staff immediately if the patient develops any new or worsening neurological signs, particularly motor weakness or signs suggestive of CES.
Long-Term Plan & Patient Education
Focus heavily on secondary prevention through education on lifestyle modification.
Provide detailed education on spinal ergonomics for work and daily activities (e.g., setting up an office chair, safe lifting).
Strongly advise on the benefits of maintaining a healthy weight and provide resources for smoking cessation.
Emphasize that the goal of rehabilitation is to build a "muscular corset" to protect the spine. Encourage lifelong adherence to a core strengthening and general fitness program.
Address fear-avoidance behavior directly, explaining that hurt does not always equal harm, and a graded, confident return to activity is key to a successful outcome.
When to Escalate
Clear, actionable triggers for when a house officer must seek senior help are critical for patient safety.
Call Your Senior (MO/Specialist) if:
You have any suspicion of Cauda Equina Syndrome – this requires an immediate call.
The patient develops a new or objectively worsening neurological deficit (e.g., motor power in a key muscle like the EHL drops from 4/5 to 3/5 on serial examination).
The patient has intractable pain that is unresponsive to adequate multimodal analgesia, causing significant distress.
The diagnosis is unclear, or the clinical picture does not fit a typical pattern.
Referral Criteria
Emergency Referral (Orthopedics/Neurosurgery): Any patient with suspected Cauda Equina Syndrome or a progressive/profound motor deficit.
Elective Referral (Orthopedics/Neurosurgery): Patients with persistent, disabling radiculopathy after 6-8 weeks of failed comprehensive conservative management, who are potential surgical candidates.
Referral to Physiotherapy: All patients with a diagnosis of PID should be referred to facilitate recovery, restore function, and prevent recurrence.
Referral to a Pain Specialist: For patients with chronic neuropathic pain, or those who have failed surgery or are poor surgical candidates.
References
Ministry of Health Malaysia. (2017). Management of Low Back Pain. Putrajaya: MOH. Link
Deyo, R. A., & Mirza, S. K. (2016). Herniated Lumbar Intervertebral Disk. New England Journal of Medicine, 374(18), 1763–1772. DOI: 10.1056/NEJMcp1512658
Jordan, J., Konstantinou, K., & O'Dowd, J. (2011). Herniated lumbar disc. BMJ clinical evidence, 2011, 1118.
Kreiner, D. S., Hwang, S. W., Easa, J. E., et al. (2014). An evidence-based clinical guideline for the diagnosis and treatment of lumbar disc herniation with radiculopathy. The Spine Journal, 14(1), 180-191. DOI: 10.1016/j.spinee.2013.08.003
Amin, R. M., Andrade, N. S., & Neuman, B. J. (2017). Lumbar Disc Herniation. Current reviews in musculoskeletal medicine, 10(4), 507–516. DOI: 10.1007/s12178-017-9441-4
Fjeld, L., Grotle, M., Siew, K., et al. (2024). A systematic review of treatment guidelines for lumbar disc herniation. BMC Musculoskeletal Disorders, 25(1), 273. DOI: 10.1186/s12891-024-07380-6
Azmi, N. A., Shueb, S. S., & Kuan, Y. C. (2022). Sociodemographic Influences on Lumbar Disc Degeneration Severity and the Diagnostic Potential of Disc-CSF Signal Ratio: Insights from a South East Asia Population Study. Asian Spine Journal, 16(6), 846-856. DOI: 10.31616/asj.2021.0360
(Note: The reference list is a sample compilation based on authoritative sources and the provided document for illustrative purposes.)
