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Indo-British Advanced Pain Management Recognized and Awarded Pioneer in Pain Medicine, Neuromodulation, and Spinal Cord Stimulation
Chronic Pain Condition

Complex Regional Pain Syndrome (CRPS) The Burning Pain That Has Worn Many Names

Formerly known as RSD, causalgia, Sudeck’s atrophy, and algodystrophy — a complete guide to understanding, diagnosing, and treating CRPS.

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TL;DR — Understanding CRPS at a Glance

Complex Regional Pain Syndrome (CRPS) is a severe, chronic condition where a minor injury triggers a massive nervous system malfunction, resulting in disproportionate burning pain, swelling, and skin changes in the affected limb. Because the condition worsens rapidly over time, early diagnosis is critical. Treatment requires a highly specialized, multidisciplinary approach—such as the one at IBAP Clinics—combining physical therapy with advanced interventions like sympathetic nerve blocks and Spinal Cord Stimulation (SCS) to “reset” the nervous system and restore function.

What Is Complex Regional Pain Syndrome?

Imagine burning your hand on a hot stove. Normally, the pain is intense but predictable it reflects the severity of the injury, and it settles as the burn heals. Now imagine the same burning pain persisting for months or years after a minor sprain of the wrist, intensifying with the slightest breeze or gentle touch, spreading up the arm, turning the skin an unusual colour, and making the affected limb behave as though it belongs to someone else. This is the lived reality of Complex Regional Pain Syndrome (CRPS).

CRPS is a chronic, debilitating pain condition characterised by severe, disproportionate pain usually in one limb  accompanied by a constellation of changes in skin colour and temperature, abnormal sweating, swelling, and impaired movement. What makes CRPS particularly challenging is not just its severity, but its apparent irrationality: the pain far exceeds what any visible injury could justify. For this reason, patients have historically been disbelieved, misdiagnosed, and undertreated for decades  sometimes told the pain is “all in their head.”

It is emphatically not in the head. CRPS involves real, measurable changes in the peripheral and central nervous systems, the immune system, and the vascular system. It is recognised by the International Association for the Study of Pain (IASP), the World Health Organization (ICD-11: MB40.0), and every major pain society worldwide as a serious, biologically driven pain disorder.

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Think of the nervous system as an alarm system in a building. In CRPS, a small power surge — the original minor injury — causes the alarm to malfunction and fire continuously, even after the surge is fixed. The alarm (pain system) is no longer responding to real danger; it has become the problem itself.

A Condition With Many Names: The History of CRPS

Few medical conditions have accumulated as many names as CRPS  each name reflecting the era’s limited understanding of the condition’s true nature. Understanding this history is important not only for historical completeness, but because many patients in India still present with these older diagnoses written in their medical records.

Historical Name Era / Origin Why the Name Changed
Causalgia 1864 — Silas Weir Mitchell (American Civil War physician) Described burning pain after nerve injury in soldiers; from Greek kausos (heat) + algos (pain). Now: CRPS Type 2.
Sudeck's Atrophy 1900 — Paul Sudeck (German surgeon) Described bone demineralisation (osteoporosis) on X-ray in painful post-traumatic limbs. Name limited to the skeletal finding; did not capture full syndrome.
Algodystrophy Mid-20th century — European literature Emphasised pain (algo) and dystrophic (tissue breakdown) changes. Still used in some European countries and older Indian medical records.
Post-Traumatic Dystrophy Mid-20th century Highlighted the trauma trigger; did not account for spontaneous onset or cases without clear injury.
Shoulder-Hand Syndrome 1940s–1970s Described CRPS following myocardial infarction or stroke; now recognised as a subtype rather than a distinct condition.
Reflex Sympathetic Dystrophy (RSD) 1940s–1994 Proposed a reflex arc involving the sympathetic nervous system as the mechanism. Though sympathetic involvement is important, many CRPS cases have pain that is not sympathetically maintained — hence the name was abandoned.
Sympathetically Maintained Pain (SMP) 1980s–1990s Described pain maintained by sympathetic activity; now understood as a feature of some CRPS cases, not a synonym.
Complex Regional Pain Syndrome (CRPS) 1994 — IASP consensus (Stanton-Hicks et al.) Deliberately neutral, descriptive term capturing the complexity, regional distribution, and pain-centred nature without assuming mechanism. Endorsed by IASP, WHO, and all major pain bodies.

📋 For Indian Patients: What This Means for Your Records

If your medical records contain a diagnosis of RSD, Sudeck’s atrophy, algodystrophy, causalgia, or post-traumatic dystrophy, these are older names for what is now called CRPS. The treatment principles are the same. Please bring all old records to your consultation at IBAP Clinics  historical documentation helps us understand your timeline.

CRPS Type 1 and Type 2: What Is the Difference?

In 1994, the IASP divided CRPS into two subtypes based on whether a peripheral nerve injury can be identified:

CRPS Type 1

(formerly Reflex Sympathetic Dystrophy / RSD): Develops after a noxious event  commonly a fracture, sprain, surgery, or immobilisation without confirmed damage to a named peripheral nerve. This accounts for approximately 90% of CRPS cases.

CRPS Type 2

 (formerly Causalgia): Develops following confirmed injury to a peripheral nerve (e.g., median nerve injury after wrist fracture, sciatic nerve injury after hip surgery). The clinical features are identical to Type 1; only the history of nerve injury distinguishes them.

Both types are managed with the same interventions. The distinction is primarily academic and matters for mechanistic research rather than clinical treatment decisions.

What Goes Wrong in CRPS? Understanding the Mechanism

CRPS is not a simple problem with a single cause. It arises from a perfect storm of dysregulation across multiple biological systems an exaggerated and self-perpetuating response to injury that refuses to switch off. Understanding these mechanisms helps explain why treatment must target multiple systems simultaneously.

1. Peripheral Sensitisation

After injury, peripheral nerve endings (nociceptors) become hypersensitive. In CRPS, this sensitisation persists and amplifies far beyond the normal healing period. Sodium channels on nerve fibres multiply abnormally, reducing the threshold needed to fire a pain signal. Even a light touch like a gentle breeze or the weight of clothing activates pain fibres that should only respond to genuinely damaging stimuli. This is allodynia: pain from a stimulus that should not cause pain.

2. Central Sensitisation

The spinal cord and brain also reorganise abnormally in CRPS. The dorsal horn of the spinal cord the pain relay station  becomes “wound up,” amplifying every incoming signal. This is central sensitisation. Functional MRI studies show that in established CRPS, the brain’s somatosensory cortex  the area that maps the body  actually shrinks and reorganises the representation of the affected limb. This explains why CRPS patients often feel that the affected limb “doesn’t feel like mine”  the brain has literally altered its map of the body.

3. Sympathetic Nervous System Dysregulation

The sympathetic nervous system controls blood vessel tone, sweating, and skin temperature. In CRPS, abnormal coupling develops between sympathetic nerve fibres and pain fibres  essentially, the body’s “fight-or-flight” system starts directly driving pain signals. This produces the characteristic skin colour changes (red, blue, or mottled), temperature differences between the affected and unaffected limb, and abnormal sweating (hyperhidrosis or anhidrosis).

4. Neuroinflammation and Immune Dysregulation

CRPS involves elevated levels of pro-inflammatory neuropeptides  particularly Substance P and calcitonin gene-related peptide (CGRP)  in the affected tissues and spinal fluid. Mast cell activation and microglial sensitisation perpetuate local and central inflammation. Elevated autoantibodies against adrenergic receptors have been identified in some CRPS patients, suggesting a potential autoimmune component.

5. Motor System Involvement

The motor cortex is also affected in CRPS. Patients commonly experience difficulty initiating movements, involuntary tremor, dystonia (fixed abnormal postures), and weakness disproportionate to any structural cause. Brain imaging studies show reduced cortical motor representation of the affected limb.

Symptoms of CRPS: What Patients Experience

CRPS presents differently in every patient, but the following features are the hallmarks. The severity can range from manageable to profoundly disabling.

The Cardinal Symptom: Disproportionate Pain

The defining feature of CRPS is pain that is out of all proportion to the original injury. Patients describe it as burning, searing, or electric in quality often compared to having the limb constantly held over a flame. Even the gentlest contact, a change in ambient temperature, emotional stress, or loud noise can trigger or intensify a pain episode.

Sensory Abnormalities

  • Allodynia pain from stimuli that should not be painful (light touch, breeze, clothing)
  • Hyperalgesia exaggerated pain response to stimuli that are mildly painful
  • Hypaesthesia reduced sensation in the affected area
  • Hyperpathia delayed, exaggerated response after repeated stimulation

Vasomotor Changes

  • Skin colour changes: red, blue, purple, mottled, or pale often changing within minutes
  • Skin temperature differences: affected limb noticeably warmer or cooler than the other side

Sudomotor Changes and Oedema

  • Abnormal sweating  either excessive (hyperhidrosis) or absent
  • Swelling of the affected limb

Motor and Trophic Changes

  • Weakness, stiffness, and difficulty initiating movement
  • Tremor, dystonia (fixed abnormal posture), or involuntary movements
  • Changes in nail growth (brittle, ridged, or accelerated nails)
  • Changes in hair growth (coarse, increased, or decreased)
  • Skin texture changes (shiny, thin, atrophic skin)
  • Osteoporosis visible on X-ray (classic finding — Sudeck’s atrophy)

The Three Stages of CRPS

While not all patients progress through all stages, the classical description of CRPS evolution remains clinically useful as a framework.

Stage 1: Acute (0–3 Months)

  • Severe burning pain
  • Warm, red, swollen limb
  • Increased hair and nail growth
  • Allodynia prominent
  • Most responsive to treatment

Stage 2: Dystrophic (3–6 Months)

  • Pain becomes constant
  • Skin becomes cool, shiny, mottled
  • Swelling persists; oedema hardens
  • Muscle wasting begins
  • Early osteoporosis on X-ray

Stage 3: Atrophic (>6 Months)

  • Irreversible tissue changes possible
  • Contractures of joints
  • Severe muscle atrophy
  • Marked osteoporosis
  • May spread to other limbs
⚡ Time Is Critical in CRPS

CRPS responds dramatically better when diagnosed and treated in Stage 1. Every month of delay allows central sensitisation and neuroplastic changes to become more entrenched. If you or a family member has burning, disproportionate pain in a limb after injury or surgery — do not wait. Seek specialist assessment immediately.

How Is CRPS Diagnosed? The Budapest Criteria

There is no single blood test, scan, or investigation that diagnoses CRPS. It is a clinical diagnosis made by a specialist who carefully evaluates the pattern of symptoms and signs. The internationally validated Budapest Criteria (Harden et al., 2010) are used worldwide and require the following:

Prerequisite: Pain that is disproportionate to the inciting event, affecting part or all of a limb.

Required: At least one symptom in three of the four categories, AND at least one sign in two of the four categories (a sign must be observed at the time of clinical examination).

Supporting investigations  though not diagnostic alone  include triple-phase bone scintigraphy (bone scan), thermography, plain X-rays showing Sudeck’s osteoporosis, and skin temperature testing. MRI may reveal bone marrow oedema in early CRPS.

🌡️ Sensory
  • Allodynia (pain to light touch)
  • Hyperalgesia (to pinprick)
  • Hypaesthesia
🩸 Vasomotor
  • Skin colour asymmetry
  • Skin temperature
    asymmetry (>1°C)
💧 Sudomotor / Oedema
  • Oedema (swelling)
  • Abnormal sweating
  • Sudomotor asymmetry
🤲 Motor / Trophic
  • Reduced range of motion
  • Motor dysfunction (tremor, dystonia)
  • Trophic changes (hair, nail, skin)

Treatment of CRPS: A Multidisciplinary Approach

CRPS demands a multimodal strategy — no single treatment is sufficient. At IBAP Clinics, the treatment ladder is staged from conservative through to advanced interventional therapies, guided by response at each step.

Rehabilitation: The Foundation of All CRPS Treatment

Physiotherapy and graded motor imagery (GMI) form the cornerstone of CRPS management. Pain-free movement desensitises peripheral nerves, reverses central sensitisation, and reconstructs the brain’s cortical map of the affected limb. Mirror therapy using a mirror to create the visual illusion that the affected limb is moving normally has Level II evidence for reducing CRPS pain and is a key component of the GMI programme at IBAP Clinics.

Pharmacological Management

  • Neuropathic pain agents: Gabapentin, pregabalin, duloxetine, amitriptyline
  • Anti-inflammatory agents: NSAIDs, oral corticosteroids (useful in early stage)
  • Bisphosphonates: Alendronate, zoledronic acid  reduce bone resorption and have evidence for reducing CRPS pain
  • Vitamin C: Evidence supports prophylactic use after wrist fracture to reduce CRPS incidence (500 mg/day for 50 days)
  • Topical agents: Lidocaine patches, capsaicin cream, EMLA
  • Low-dose naltrexone: Emerging evidence for neuroinflammation modulation

Interventional Treatments at IBAP Clinics

Procedure Mechanism Evidence Level Best For
Stellate Ganglion Block Interrupts sympathetic activity to the upper limb Level II–III Upper limb CRPS, sympathetically maintained pain
Lumbar Sympathetic Block Interrupts sympathetic supply to the lower limb Level II Lower limb CRPS with vasomotor features
IV Ketamine Infusion NMDA receptor antagonist; reverses central sensitisation Level II Severe, refractory CRPS; high allodynia
Spinal Cord Stimulation (SCS) Modulates dorsal horn pain processing via epidural electrodes Level I–II Established CRPS unresponsive to other measures; CRPS Type 1 and 2
Dorsal Root Ganglion Stimulation (DRG-S) Targets specific nerve roots at DRG level; more focal than SCS Level II CRPS with focal limb distribution; foot and knee CRPS
IV Immunoglobulin (IVIG) Modulates autoimmune component; anti-nociceptive Level III Refractory CRPS with autoimmune features
⚡ Spinal Cord Stimulation (SCS) — The Gold Standard for Established CRPS

The landmark RSDSA-sponsored RCT (Kemler et al., NEJM 2000) demonstrated that SCS combined with physiotherapy was significantly superior to physiotherapy alone for CRPS pain and global perceived effect. Subsequent studies, including the ACCURATE trial for DRG stimulation, confirm neuromodulation as the most powerful tool available for severe, established CRPS. At IBAP Clinics, our Fellowship in Neuromodulation training ensures patients receive the full breadth of stimulation options — from conventional SCS to advanced waveforms and DRG-S.

Your CRPS Patient Journey at IBAP Clinics

CRPS presents differently in every patient, but the following features are the hallmarks. The severity can range from manageable to profoundly disabling.

Before Your Procedure: Preparation

Pre-Procedure Checklist

  • Attend a thorough consultation. Bring all records  including those with old diagnoses (RSD, algodystrophy). Take time to understand the proposed procedure, its rationale, realistic expectations, and alternatives before you consent.
  • Disclose all medications, particularly anticoagulants and blood thinners (warfarin, rivaroxaban, apixaban, clopidogrel, aspirin). These must be managed before any invasive procedure. Stopping them requires coordination between your pain specialist, cardiologist, and GP — never stop these independently.
  • For sympathetic nerve blocks, no special fasting is required for a pure local anaesthetic block performed under sedation; however, follow the specific instructions provided at your clinic appointment.
  • For spinal cord stimulator implantation, standard pre-operative fasting, blood tests, ECG, and medical review apply as for any day surgical procedure.

On the Day of the Procedure

Day-of Checklist

  • Follow fasting instructions precisely. If you take weight-loss or diabetes medications including GLP-1 agonists such as Ozempic (semaglutide) or Mounjaro (tirzepatide), your fasting period must be extended. Inform the team in advance.
  • Bring all imaging and investigation reports relevant to your condition — MRI, bone scans, thermography reports, nerve conduction studies.
  • Inform the team if you have any current fever, infection, or systemic illness. Procedures must be deferred in the presence of active infection. Inform the team of any recent antibiotics or corticosteroid use.
  • Arrange for a responsible adult to accompany you and take you home.

During the Procedure

After changing into an OT gown, you will have an intravenous cannula placed, vital signs and blood glucose monitored, and the injection site prepared under sterile conditions. For sympathetic blocks, fluoroscopic guidance confirms correct needle placement at the stellate ganglion (C6 level, anterior approach) or lumbar sympathetic chain (L2–L3 vertebral level). You will receive local anaesthesia and mild sedation if required. Full general anaesthesia is neither necessary nor desirable — remaining responsive allows you to report any unusual sensations that guide the procedure safely.

Immediately After & Post-Procedure

  • After a stellate ganglion block, expect temporary Horner’s syndrome (drooping eyelid, small pupil, nasal congestion on the injected side)  this is expected and confirms correct placement. It resolves as the local anaesthetic wears off.
  • After a lumbar sympathetic block, expect temporary warmth and increased blood flow to the treated leg.
  • Vital signs are monitored until stable. You will be discharged with written instructions.
  • Contact IBAP Clinics immediately for: fever, progressive neurological symptoms, severe headache, or any signs of allergic reaction.
  • Continue your physiotherapy programme the procedure opens a window of reduced pain; rehabilitation must follow without delay.

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Our - Treatment Process

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Medical History Review

We review your medical history and relevant reports for a clear understanding.

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Personalized Consultation

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Advanced Imaging

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Our team identifies the root cause and key trigger points for treatment.

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Some quick information

CRPS duration is highly variable. In children and adolescents, remission rates are high (up to 90%) with aggressive physiotherapy. In adults, outcomes vary: some achieve remission, particularly with early intervention; others develop chronic CRPS requiring long-term management. Duration is significantly influenced by time to diagnosis and initiation of appropriate treatment.

Yes — surgical procedures are one of the most common triggers, particularly orthopaedic surgery (wrist fracture fixation, knee surgery, hip replacement) and nerve injury during procedures. This does not mean surgery caused negligence; some individuals have a biological predisposition to developing CRPS. Vitamin C supplementation after wrist surgery reduces incidence.

No — while both are chronic pain conditions involving central sensitisation, they are distinct diagnoses. CRPS is regional (affecting one or two limbs), associated with autonomic and trophic changes, and usually follows a specific injury or trigger. Fibromyalgia is widespread, associated with fatigue and sleep disturbance, and has different diagnostic criteria. However, some patients have features of both conditions.

SCS does not cure CRPS — it significantly reduces pain intensity and improves quality of life, allowing better engagement with physiotherapy and rehabilitation. The KEMLER trial (NEJM) showed that SCS produced at least 50% pain reduction in over 60% of CRPS patients at 6 months. Some patients achieve long-term excellent control; others may require reprogramming or supplementary treatments over time.

Some prevention strategies have evidence: Vitamin C (500 mg/day for 50 days) after wrist fracture reduces CRPS incidence. Early mobilisation after injury or surgery, minimising immobilisation, and prompt management of neuropathic pain features after injury or surgery are key preventive strategies. If you have had CRPS before, inform your surgeon before any planned procedure.

Yes — epidemiological studies report a female-to-male ratio of approximately 3:1 for CRPS. The peak incidence is in middle-aged adults (40–60 years), although CRPS can occur at any age, including in children. The reasons for the sex disparity are not fully understood but may relate to hormonal influences on pain processing.

Yes, absolutely. RSD (Reflex Sympathetic Dystrophy) is one of the former names for what is now called CRPS Type 1. The condition, its symptoms, and its treatment are identical. The name changed in 1994 because the older term implied a mechanism (reflex sympathetic involvement) that does not apply to all patients.

Dr. Vijay Bhaskar Bandikatla

Founder IBAP Clinics, Pain Physician

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References & Evidence Base

  • Harden RN, Bruehl S, Perez RS, et al. Validation of proposed diagnostic criteria (the “Budapest Criteria”) for Complex Regional Pain Syndrome. Pain. 2010;150(2):268–274.
  • Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. New England Journal of Medicine. 2000;343(9):618–624.
  • Perez RS, Zollinger PE, Dijkstra PU, et al. Evidence based guidelines for complex regional pain syndrome type 1. BMC Neurology. 2010;10:20.
  • Mitchell SW, Morehouse GR, Keen WW. Gunshot wounds and other injuries of nerves. Philadelphia: JB Lippincott; 1864. (Original description of causalgia.)
  • Sudeck PHM. Über die akute entzündliche Knochenatrophie. Archiv für klinische Chirurgie. 1900;62:147–156. (Original description of Sudeck’s atrophy.)
  • Bruehl S. Complex regional pain syndrome. BMJ. 2015;351:h2730.
  • Lunden LK, Kleggetveit IP, Jørum E. Delayed diagnosis and worsening of pain following orthopedic surgery in patients with complex regional pain syndrome (CRPS). Scandinavian Journal of Pain. 2016;11:27–33.
  • Zollinger PE, Tuinebreijer WE, Breederveld RS, et al. Can vitamin C prevent complex regional pain syndrome in patients with wrist fractures? Journal of Bone and Joint Surgery. 2007;89(7):1424–1431.
  • Deer TR, Levy RM, Kramer J, et al. Dorsal root ganglion stimulation yielded higher treatment success rate for complex regional pain syndrome and causalgia at 3 and 12 months: a randomized comparative trial. Pain. 2017;158(4):669–681. (ACCURATE trial.)
  • Moseley GL. Graded motor imagery is effective for long-standing complex regional pain syndrome: a randomised controlled trial. Pain. 2004;108(1–2):192–198.
  • Stanton-Hicks M, Jänig W, Hassenbusch S, et al. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain. 1995;63(1):127–133. (IASP taxonomy consensus.)
  •  
  • Dr. Vijay Bhaskar Bandikatla
Founder IBAP Clinics, Pain Physician

MBBS, DA, FRCA (UK), FFPMRCA (Pain Medicine, RCOA, UK)
CCT (Anesthesiology And Pain Management)
Neuromodulation & Advanced Pain Research Fellowship (London), MBA (HM)

  • Dr. Vijay Bhaskar Bandikatla
Founder IBAP Clinics, Pain Physician
MBBS, DA, FRCA (UK), FFPMRCA (Pain Medicine, RCOA, UK)
CCT (Anesthesiology And Pain Management)
Neuromodulation & Advanced Pain Research Fellowship (London), MBA (HM)

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