Complex Regional Pain Syndrome

Neuropathic Pain

Complex Regional Pain Syndrome (CRPS) Treatment in Hyderabad

Complex Regional Pain Syndrome (CRPS) is a severe, chronic, and often progressive neurological pain condition characterised by disproportionately intense, burning pain; sensory, motor, and autonomic abnormalities; and trophic changes in the affected limb — all out of proportion to any identifiable tissue injury. CRPS is considered one of the most painful conditions known to medicine — often rated higher than childbirth, amputation, and cancer on pain severity scales. It affects approximately 26 per 100,000 people per year, with a significant female predominance (3:1). Despite being a devastating condition, CRPS has a poorly understood pathophysiology and has historically been dramatically undertreated in India. SurgiPartner’s specialist pain management team in Hyderabad provides expert CRPS assessment and evidence-based interventional treatment. 

CRPS Type I vs Type II

Feature CRPS Type I (Formerly RSD) CRPS Type II (Formerly Causalgia)
Trigger Tissue injury WITHOUT definable nerve damage (fracture, surgery, soft tissue injury, immobilisation) Injury WITH confirmed peripheral nerve damage (partial nerve transection, nerve injury during surgery or trauma)
Prevalence ~90% of CRPS cases ~10% of CRPS cases
Pain character Same as Type II — burning, allodynia, hyperalgesia; pain distribution may exceed the nerve territory Same but clearly in the distribution of the injured nerve
Electrophysiology No nerve conduction abnormality on EMG/NCS Confirms nerve injury on EMG/NCS
Treatment Identical — sympathetic interventions, SCS, desensitisation physiotherapy Identical; nerve repair or decompression additionally considered in selected cases

Budapest Diagnostic Criteria for CRPS

The Budapest Criteria (2007, revised) are the current international standard for CRPS diagnosis. CRPS is diagnosed when the following are all present:

  1. Continuing pain disproportionate to any inciting event
  2. At least one symptom in 3 of 4 categories:
    • Sensory: hyperaesthesia and/or allodynia
    • Vasomotor: temperature asymmetry and/or skin colour changes and/or skin colour asymmetry
    • Sudomotor/oedema: oedema and/or sweating changes and/or sweating asymmetry
    • Motor/trophic: decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. At least one sign in 2 or more categories (same categories as above, confirmed on examination)
  4. No other diagnosis better explains the signs and symptoms

Phases of CRPS

  • Acute phase (0–3 months): Severe burning pain; warm, red, sweaty limb; significant oedema; allodynia; loss of function; bone scan shows increased uptake (phase 1–3); MRI shows periarticular oedema. Most responsive to treatment — early intervention is critical.
  • Dystrophic phase (3–12 months): Pain continues; skin becomes mottled, cool; hyperhidrosis; progressive loss of movement; muscle atrophy; bone scan shows periarticular uptake.
  • Atrophic phase (12+ months): Cool, pale, dry, atrophic skin; irreversible joint contractures; osteoporosis (Sudeck’s atrophy on X-ray); some pain reduction but severe functional impairment; less responsive to interventional treatment — prevention of this phase by early aggressive treatment is the primary therapeutic goal.

Pathophysiology — Why CRPS Is So Complex

CRPS involves multiple interacting pathophysiological mechanisms:

  • Neurogenic inflammation — substance P and CGRP release from sensitised peripheral C fibres causes vasodilation, oedema, and tissue sensitisation — explaining the warm, red, swollen acute phase
  • Sympathetic nervous system dysregulation — coupling between the sympathetic nervous system and pain fibres (sympathetically-maintained pain) explains the colour, temperature, and sweating changes; and why sympathetic nerve blocks are therapeutic
  • Central sensitisation — spinal cord and cortical hyperexcitability drives the allodynia, hyperalgesia, and spread of pain beyond the original injury site
  • Autoimmune component — autoantibodies against autonomic receptors have been found in a proportion of CRPS patients; supported by the higher prevalence in women and post-infective triggers in some cases
  • Cortical reorganisation — somatosensory and motor cortex reorganisation (expansion of the affected limb representation) contributes to the body image disturbance, motor dysfunction, and maladaptive pain perception

Treatment of CRPS — A Multidisciplinary Approach

Physiotherapy — The Cornerstone of CRPS Treatment

Despite the severe pain, movement rehabilitation is the single most important long-term treatment for CRPS — targeting the central cortical reorganisation and the motor dysfunction that perpetuate the syndrome. The physiotherapy approach must be carefully graded to avoid the post-activation worsening that can occur with aggressive early mobilisation:

  • Graded Motor Imagery (GMI) — a three-stage programme: laterality recognition (discriminating left from right body images without moving); motor imagery (imagining movement without actually moving); and mirror visual feedback (using a mirror box to provide visual feedback of the unaffected limb moving, “tricking” the brain into accepting movement). GMI targets the cortical reorganisation of CRPS — multiple RCTs demonstrate significant pain and function improvement.
  • Desensitisation therapy — graded exposure to increasingly varied sensory stimuli (textures, temperatures, vibration) in the allodynic area — gradually recalibrating the hypersensitive sensory system
  • Graded activity and CRPS-specific physiotherapy — gentle range of motion exercises, stress loading (carrying activities that create compressive/tensile loads on the limb — scrubbing and carrying exercises), gradual resistance training

Sympathetic Nerve Blocks — Targeting the Autonomic Component

Stellate ganglion block — for upper limb CRPS; the stellate ganglion (a sympathetic ganglion at C7–T1) is blocked under ultrasound or fluoroscopic guidance — interrupting sympathetically-maintained pain and vasospasm in the arm and hand. Provides diagnostic confirmation (if significant relief follows, sympathetically-maintained pain is confirmed) and therapeutic benefit.

Lumbar sympathetic block — for lower limb CRPS; the lumbar sympathetic chain (at L2–L4) is blocked under fluoroscopic guidance — providing sympathetic interruption to the lower limb. A series of blocks can provide significant, cumulative relief. For sustained effect, radiofrequency ablation of the lumbar sympathetic chain (lumbar sympathectomy) provides 3–12 months of sympatholysis from a single procedure.

Intravenous Ketamine

Ketamine — an NMDA receptor antagonist — is one of the most effective treatments for severe, refractory CRPS. Low-dose ketamine infusions (subanaesthetic doses 0.2–0.5mg/kg/hour over 3–5 days as an inpatient) produce significant, sustained reduction in CRPS pain — typically lasting 3–6 months — through normalisation of NMDA receptor-mediated central sensitisation. Multiple case series and some RCT data support ketamine for CRPS. Side effects during infusion: dissociative symptoms (manageable with benzodiazepine premedication), mild elevation in blood pressure and heart rate, nausea. Available at specialist pain centres with appropriate monitoring facilities — SurgiPartner coordinates ketamine infusion protocols with partner hospitals in Hyderabad. Call +91 9030053009 for assessment.

Spinal Cord Stimulation (SCS) — For Refractory CRPS

Spinal cord stimulation is the most evidence-based interventional treatment for refractory CRPS, with Level I evidence from a landmark Dutch randomised controlled trial (Kemler et al., NEJM 2000) and subsequent long-term follow-up studies. Epidural electrodes placed at the thoracic level (for upper limb CRPS) or lumbar level (for lower limb CRPS) deliver electrical stimulation to the dorsal columns — replacing the painful sensation with paraesthesia and significantly reducing allodynia and spontaneous pain. A 7–10 day trial stimulation period allows assessment of benefit before permanent implantation. Studies show 60–75% of CRPS patients achieve >50% pain reduction with SCS, with sustained benefit at 5-year follow-up in many patients.

Bisphosphonates — For Bone Involvement

Intravenous bisphosphonates (pamidronate, alendronate) reduce bone oedema and nociception in CRPS through inhibition of osteoclast activity and direct analgesic effects. Multiple RCTs demonstrate significant pain reduction with IV bisphosphonate infusions. Effective particularly when bone scintigraphy or MRI confirms bone involvement.

Pharmacological Management

Gabapentinoids (gabapentin, pregabalin) — reduce central sensitisation and neuropathic pain in CRPS; widely used as first-line adjuvant medication. Low-dose amitriptyline — addresses sleep disruption and neuropathic pain. Topical treatments — EMLA cream (topical anaesthetic) reduces allodynia pain from touch; capsaicin 8% patch (specialist application) defunctionalises C fibres. Calcitonin — nasal or intranasal calcitonin has evidence for CRPS pain relief and bone protection. Free radical scavengers (vitamin C 500mg/day for 50 days) have evidence for preventing CRPS after wrist fracture — an important preventive strategy.

💡 Most critical CRPS principle: Time is tissue — the earlier CRPS is treated, the better the outcome. Acute CRPS (<3 months) treated aggressively with physiotherapy, sympathetic blocks, and appropriate medications frequently resolves completely. CRPS present for years with joint contractures and atrophic changes is far more refractory. If you suspect CRPS, call SurgiPartner on +91 9030053009 for an urgent assessment — do not wait.

Frequently Asked Questions — CRPS Treatment Hyderabad

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