Physiology · Year 1 · from Physiology

Case 3: Complex Regional Pain Syndrome - Central Sensitization

Clinical Image

Source: Clinical illustration of pain pathway sensitization and CRPS features

Patient Presentation

A 45-year-old female presents to the pain clinic with persistent, severe pain in her right hand 4 months after a Colles fracture that was treated with casting. Although the fracture has healed with good bony alignment on X-ray, she describes burning, throbbing pain that far exceeds what would be expected from the original injury. The slightest touch to her hand causes excruciating pain (allodynia), and even air currents are painful. Her hand is swollen, discolored (alternating between red and blue), and sweats excessively. She cannot use the hand and keeps it wrapped and protected.

Demographics

  • Age: 45 years
  • Sex: Female
  • Precipitating event: Right distal radius fracture 4 months ago

Chief Complaint

Severe persistent burning pain in right hand disproportionate to original injury, swelling, color changes, and hypersensitivity to touch

Physical Examination

  • Right hand/wrist:
  • Severe allodynia: Light touch elicits intense pain (cotton swab causes severe discomfort)
  • Hyperalgesia: Pinprick causes disproportionate pain
  • Skin: Edematous, alternating red/dusky discoloration (vasomotor instability)
  • Temperature: Cooler than left hand by 2C (measured with thermometer)
  • Sweating: Hyperhidrosis compared to left hand
  • Hair/nail changes: Increased hair growth, brittle nails
  • Motor: Weakness and tremor, limited range of motion due to pain
  • Contracture beginning in fingers
  • Left hand: Normal examination

Workup

  • X-ray right hand: Healed distal radius fracture, patchy osteoporosis (spotted demineralization characteristic of CRPS)
  • Three-phase bone scan: Increased uptake in late (delayed) phase in affected hand - consistent with CRPS
  • Thermography: Temperature asymmetry >1C between hands
  • Labs: Normal inflammatory markers (rules out infection, inflammatory arthritis)
  • EMG/NCS: Normal (CRPS Type I - no identifiable nerve injury; Type II has confirmed nerve lesion)

Diagnosis

Complex Regional Pain Syndrome Type I (CRPS-I, formerly reflex sympathetic dystrophy)

Treatment

  1. Early aggressive physical and occupational therapy (most important intervention)
  • Mirror therapy: Patient performs movements with unaffected hand while watching mirror reflection, tricking brain into perceiving affected hand moving painlessly
  • Graded motor imagery
  • Desensitization exercises
  1. Medications for neuropathic pain:
  • First-line: Gabapentin, pregabalin, or duloxetine
  • Topical agents: Lidocaine patches, capsaicin
  • Low-dose naltrexone (emerging evidence)
  1. Interventional approaches if refractory:
  • Sympathetic nerve blocks (stellate ganglion block for upper extremity)
  • Spinal cord stimulation
  • Intrathecal drug delivery
  1. Psychological support: CBT, coping strategies, treatment of depression/anxiety
  2. Vitamin C 500 mg daily (may reduce risk of CRPS after fractures)
  3. Avoid immobilization; encourage functional use within pain tolerance

Physiological Principles Demonstrated

  • Central sensitization: After injury, repeated nociceptor activation causes hyperexcitability of spinal cord dorsal horn neurons. This "wind-up" phenomenon involves NMDA receptor activation and leads to amplification of pain signals.
  • Allodynia mechanism: Central sensitization causes normally innocuous Aβ fiber input (light touch) to activate pain circuits, producing pain from non-painful stimuli. This represents a failure of the gate control mechanism.
  • Hyperalgesia: Enhanced pain from painful stimuli results from both peripheral sensitization (lowered nociceptor thresholds from inflammatory mediators) and central sensitization (amplified spinal cord responses).
  • Autonomic dysregulation: The vasomotor instability (color changes), temperature changes, and sweating abnormalities reflect disordered sympathetic function. Whether this is cause or effect remains debated.
  • Neuroplasticity in pain: Chronic pain can cause maladaptive reorganization of sensory cortex. The affected limb's representation may shrink, and the brain's body schema becomes distorted. Mirror therapy attempts to normalize this cortical representation.
  • Gate control theory application: The theory predicts that enhancing large fiber (Aβ) input should reduce pain transmission. In CRPS, central sensitization disrupts this mechanism, and stimulation (e.g., spinal cord stimulation) at specific frequencies and intensities attempts to restore inhibitory control.

All cases for this lecture as Markdown