Pain Medicine · Supplementary · from Pain Medicine

Case 2: Chronic Low Back Pain with Central Sensitization

Patient Presentation

Demographics: 48-year-old male warehouse supervisor

Chief Complaint: "My back has hurt every day for 5 years and now the pain is spreading everywhere — nothing works anymore."

History of Present Illness: Mr. D.W. presents to the multidisciplinary pain center with a 5-year history of chronic low back pain that has progressively worsened and expanded in distribution. The pain originated after a workplace lifting injury in which he felt a "pop" while moving a 30 kg box. Initial imaging showed a L4-5 disc herniation with left L5 radiculopathy, which was managed with epidural steroid injections and physical therapy with moderate relief over the first 18 months.

Over the past 3 years, the pain has changed in character from well-localized left-sided low back and leg pain to a diffuse, bilateral low back, buttock, and lower extremity pain that he describes as burning, aching, and "electrical." He has developed widespread tenderness — reporting that his thighs, calves, and even upper back now hurt. He notes that activities that previously were not painful (sitting for 20 minutes, riding in a car, light walking) now provoke severe pain flares lasting 2-3 days. Even emotional stress and poor sleep dramatically worsen his pain.

He has undergone two L4-5 epidural steroid injections (last one 2 years ago, minimal benefit), bilateral medial branch blocks at L3-5 (equivocal response), and a trial of physical therapy (4 courses, unable to progress due to pain flares). He was prescribed escalating doses of opioids by his primary care physician and currently takes oxycodone 20 mg QID with minimal analgesic efficacy. He has gained 18 kg since the injury and is largely sedentary.

Past Medical History:

• L4-5 disc herniation (5 years ago, managed non-operatively)
• Major depressive disorder (diagnosed 3 years ago, coinciding with chronic pain)
• Obstructive sleep apnea (diagnosed 1 year ago, non-adherent with CPAP)
• Obesity
• Pre-hypertension

Medications:

• Oxycodone 20 mg QID (80 mg/day = 120 MME/day)
• Duloxetine 60 mg daily
• Cyclobenzaprine 10 mg THS (at bedtime)
• Omeprazole 20 mg daily
• Ibuprofen 800 mg TID (intermittent)

Social History:

• Former smoker (quit 2 years ago, 20 pack-year history)
• No alcohol (quit when started opioids)
• Married, 3 children; reports significant marital strain due to disability
• On long-term disability from work; workers' compensation claim settled
• Spends most of day in recliner watching television
• Previously active: recreational basketball, home renovation projects

Family History:

• Mother: chronic pain (fibromyalgia), opioid use disorder
• Father: alcohol use disorder, depression
• Brother: chronic low back pain

Physical Examination

• Vital Signs: BP 142/90 mmHg, HR 78 bpm, RR 14, SpO2 94% on room air, Temp 36.7°C, BMI 36.2 kg/m²
• General: Obese male in mild distress, moves slowly and guardedly; uses cane for ambulation (no prescription for assistive device)
• Spine: Lumbar paraspinal hypertonicity bilaterally; tenderness to palpation diffusely across lumbar, thoracolumbar, and sacroiliac regions; limited flexion (finger-to-floor distance 45 cm); Waddell signs: 3/5 positive (superficial tenderness, overreaction, regional disturbance)
• Neurological: Straight leg raise negative bilaterally; motor strength 5/5 bilateral lower extremities (give-way weakness pattern noted but full strength when distracted); sensation intact to light touch throughout; reflexes 2+ and symmetric; no clonus; Babinski downgoing bilaterally
• Central sensitization signs:
• Widespread allodynia: mechanical allodynia to light brush over bilateral thighs, calves, and upper back (non-dermatomal)
• Temporal summation: repeated pinprick at same location on forearm produces progressively increasing pain (wind-up)
• Expanded receptive fields: pain from lumbar region referred to bilateral lower extremities and upper back without anatomic correlation
• Psychological screening: PHQ-9: 18 (moderately severe depression); PCS: 42/52 (very high catastrophizing); FABQ-W: 55 (high fear-avoidance); PHQ-15: 14 (high somatic symptom burden); Central Sensitization Inventory (CSI): 58/100 (central sensitization present, score >40)

Workup and Results

Laboratory Studies:

Imaging/Additional Studies:

• MRI lumbar spine (current): L4-5 disc desiccation with mild diffuse bulge; no significant disc herniation; no neural foraminal stenosis; no central canal stenosis; mild facet arthropathy L4-5 and L5-S1; Modic Type II endplate changes at L4-5
• Quantitative sensory testing (QST): Decreased pressure pain thresholds at multiple remote sites (bilateral trapezius, bilateral tibialis anterior); enhanced temporal summation of pain; impaired conditioned pain modulation (CPM deficit — descending inhibitory failure)
• Functional capacity evaluation: Self-limited performance; biomechanical inconsistencies noted; estimated functional capacity: sedentary work with position changes
• Polysomnography review: AHI 28/hr (moderate OSA); minimum SpO2 82%; sleep efficiency 58%

Clinical Image

Diagram illustrating the neurophysiology of central sensitization, showing peripheral nociceptor input, dorsal horn wind-up, loss of descending inhibition, and cortical reorganization leading to widespread pain amplification. Source: Educational illustration.

Diagnosis

Chronic Low Back Pain with Nociplastic Pain (Central Sensitization Syndrome), Opioid-Induced Hyperalgesia, and Comorbid Major Depression

Key Diagnostic Criteria:

• Pain disproportionate to identifiable structural pathology (mild disc changes on current MRI without nerve compression)
• Pain spreading beyond original anatomic region to non-dermatomal distribution
• Central Sensitization Inventory score >40 (58/100)
• QST demonstrating: reduced pressure pain thresholds at remote sites, enhanced temporal summation, impaired conditioned pain modulation
• Allodynia and hyperalgesia in areas remote from the lumbar spine
• Features consistent with opioid-induced hyperalgesia: progressive dose escalation with worsening, diffuse pain; expanding pain distribution correlating with opioid dose increases
• Significant psychosocial contributors: depression, catastrophizing, fear-avoidance, deconditioning, disability mindset

Treatment Plan

1. Opioid taper (critical first step):

• Structured taper of oxycodone: reduce by 10% every 2 weeks (target: off opioids in 5-6 months)
• Bridge with buprenorphine transdermal patch if needed (partial agonist — less hyperalgesia risk)
• Address opioid-induced endocrinopathy: testosterone replacement if levels remain low after taper

1. Central sensitization-targeted pharmacotherapy:

• Optimize duloxetine: increase to 90 mg then 120 mg daily (dual SNRI effect for pain and depression)
• Add pregabalin 75 mg BID, titrate to 150 mg BID (calcium channel modulation, reduces central sensitization)
• Discontinue cyclobenzaprine (limited long-term evidence, sedation compounding OSA)
• Low-dose naltrexone 4.5 mg nightly (glial modulator, emerging evidence for nociplastic pain)
• Vitamin D3 5,000 IU daily for 8 weeks then 2,000 IU maintenance

1. Functional restoration program (intensive interdisciplinary):

• 4-week intensive program (4 hours/day, 5 days/week): graded exercise therapy with pain neuroscience education
• Quota-based exercise progression (not pain-contingent): walking, swimming, core stabilization
• Goal: progressive return to function regardless of pain level

1. Pain neuroscience education (PNE):

• Reconceptualize pain: pain ≠ damage; explain central sensitization in patient-accessible terms
• Address threat appraisal and pain catastrophizing
• Shift from biomedical to biopsychosocial model of pain

1. Psychological interventions:

• CBT for chronic pain: targeting catastrophizing (PCS goal <20), fear-avoidance beliefs, behavioral activation
• Mindfulness-based stress reduction (MBSR) program
• Acceptance and Commitment Therapy for values-based functional engagement

1. Sleep optimization:

• Mandatory CPAP adherence for OSA (untreated OSA worsens pain sensitization)
• CBT for insomnia (CBT-I)

1. Follow-up: Monthly during opioid taper; validated outcome measures (PCS, CSI, PHQ-9, PROMIS Pain Interference) at each visit

Key Learning Points

• Central sensitization (now termed "nociplastic pain" per IASP taxonomy) represents a third mechanism of pain distinct from nociceptive and neuropathic pain; it is characterized by augmented CNS pain processing with allodynia, hyperalgesia, expanded receptive fields, and pain spreading beyond the original injury site
• The Central Sensitization Inventory (CSI) is a validated screening tool; quantitative sensory testing (QST) provides objective evidence of altered pain processing including impaired conditioned pain modulation (a measure of descending inhibitory pathway function)
• Opioid-induced hyperalgesia is a paradoxical increase in pain sensitivity caused by chronic opioid use; it is neurobiologically distinct from tolerance and should be suspected when pain worsens or spreads despite dose escalation
• Pain neuroscience education is an evidence-based intervention that reduces pain catastrophizing and fear-avoidance by reconceptualizing pain as a product of neural sensitization rather than ongoing tissue damage
• Interdisciplinary pain rehabilitation programs combining graded exercise, PNE, and cognitive-behavioral therapy demonstrate superior outcomes to unimodal treatments for chronic pain with central sensitization

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