The following turned out to be on of many dead-ends in getting help:
From Deanna to Dr. Eric Williams (11/4/2025)
After sharing: https://davidboulton.com/deanna/
Always desperately searching for more information about my condition and its treatments, I discovered the “CRPS Surgical Success Story | Eric H. Williams, MD & Dr. Lee Dellon | S7 – E7″ by THE POD OF INQUIRY. The doctors make the case that many CRPS patients are misdiagnosed as having brain / central nervous system dysfunction when they may also have trauma-associated nerve compression. The current SOC for CRPS includes lumbar sympathetic blocks that are diagnostically ambiguous in revealing this because they target only part of the pain pathway, their coverage is unpredictable, and CRPS mechanisms are multi-layered—so relief or lack of relief doesn’t definitively locate the pain’s origin (nerve vs. brain). Lumbar sympathetic blocks can confirm that the pain system is hypersensitized, but only nerve-specific lidocaine blocks can confirm that a mechanical nerve lesion is sustaining that sensitization. Using this diagnostic strategy to identify surgical candidates, 70% of selected CRPS patients treated surgically had “excellent” or “good” outcomes (i.e., meaningful improvement).
I want to proceed asap to get the diagnostic tests that will help confirm my candidacy for surgery evaluation.
How can I best proceed? Can you perform the tests? Can you prescribe the candidacy tests to be performed locally? If not, where is the best place to go? If you aren’t sure about the request, could we have an appointment to discuss, or can you direct me to someone who might be interested in helping me?
Thank you!
This is a ChatGpt that contains the entire podcast and our questions. It is primed to be continued by you if helpful.
Below are excerpts: Summary – Key points – Stats – Diagnostic Process
AI Summary: Surgical Strategy and Rationale
Dr. Eric Williams explained his surgical approach, which focused on finding problems he could fix rather than problems to manage [01:00:19]:
- Diagnosis: Alex’s pain pattern correlated to three distinct nerve groups: the common peroneal, the tibial, and the saphenous nerve systems [01:00:19].
- EMG Findings: He noted that Alex had a positive EMG for Tarsal Tunnel Syndrome, a finding that was dismissed by other physicians [01:00:19].
- Nerve Blocks: Diagnostic lidocaine blocks on the lateral cutaneous nerve of the calf and the saphenous nerve provided temporary, area-specific relief, confirming the nerves were entrapped [02:22:30].
- One-Stage Surgery: To prevent the central nervous system from staying “revved up,” it was decided to address multiple compressions in one operation [51:09]. The procedures included:
- Decompression of the common peroneal nerve at the fibular head [41:51].
- Decompression of the proximal tibial nerve (solio sling) [42:25].
- Tarsal Tunnel Release (distal tibial nerve) and decompression of its downstream branches (medial plantar, lateral plantar, calcaneal nerves) [43:58].
- The saphenous nerve and lateral cutaneous nerve of the calf were also addressed through small extensions of the main incisions [44:36].
Dr. Dellon supported this approach, stating that in contrast to nerves that must regrow after a repair, a decompression of an intact but compressed nerve allows it to “wake up almost right away” [42:07]. He also noted that in their experience, 70% of CRPS patients they saw had peripheral nerve problems, and surgery made 80% of that group “largely better” [42:07].
Distilled Statistics on how many Complex Regional Pain Syndrome (CRPS) patients have been treated by surgery in studies from the A. Lee Dellon group (and colleagues) and what their success rates were:
-
In a review of 100 consecutive CRPS (“RSD”) patients (40 upper-extremity, 30 lower-extremity) treated surgically:
-
In a long-term follow-up of 13 of those lower-extremity patients with ≥24 months follow-up: 7 (55 %) excellent, 4 (30 %) good, 2 (15 %) failure. Pure+1
Summary:
-
Roughly in these series ≥ 70 % of selected CRPS patients treated surgically had “excellent” or “good” outcomes (i.e., meaningful improvement) in those cohorts.
-
Failure (poor outcome) rates ranged from ~15-20 %.
-
These are selected patients (with identifiable peripheral nerve or joint pain generators) and not all CRPS cases.
Distilled Key Points — Scientific & Diagnostic Learning Basis for CRPS Surgery
1. Case Overview
- Patient: 15-year-old male (Alex) developed Complex Regional Pain Syndrome (CRPS) after repeated left-leg injuries following a minor car accident.
- Timeline: Misdiagnosed for nearly two years; seen by ~20 specialists across multiple disciplines (orthopedics, vascular, cardiology, pain management) before referral to Dr. Lee Dellon and Dr. Eric Williams, peripheral nerve surgeons.
- Outcome: Full recovery and restored function after multi-site nerve decompression surgery.
2. Diagnostic Insights
- Misconception: CRPS = “non-surgical” condition. Conventional teaching warns: never operate on CRPS patients.
- Correction: Many CRPS cases have treatable peripheral nerve entrapments that mimic CRPS Type I (non-nerve injury) but are in fact Type II (causalgia, nerve injury).
- Key lesson: Some “Type I” cases may actually be undiagnosed multi-nerve entrapments.
- Examination Techniques:
- Dellon Test (“tickle test”)—eliciting localized sensory response to detect nerve involvement.
- Tinel’s Sign: Percussion along the nerve to elicit distal tingling, confirming irritation or entrapment.
- Ultrasound Mapping: To visualize entrapment points (e.g., tibial, saphenous, peroneal, sural nerves).
- Lidocaine Block Tests: Immediate relief in distribution = diagnostic confirmation of entrapment.
- Nerve Conduction (EMG): May show focal compressions—but absence of EMG findings doesn’t rule out nerve entrapment.
3. Scientific Basis for Surgical Indications
- Entrapment vs. Severed Nerve:
- Entrapped but intact nerves can “wake up” immediately after decompression—no regrowth required.
- Severed nerves (e.g., gunshot or knife injury) require regeneration across grafts, which is slow and unpredictable.
- Multi-nerve Interaction:
- CRPS-like symptoms may arise when multiple distinct nerves (e.g., common peroneal, tibial, saphenous) are compressed simultaneously, producing diffuse pain, color change, and dystonia.
- Peripheral nerve training enables identifying overlapping sources, explaining full-limb pain.
- “Double Crush” Model:
- Both proximal (e.g., tibial nerve under the soleal sling) and distal (e.g., tarsal tunnel) compressions may coexist.
- Decompressing all implicated sites in one operation reduces persistent nociceptive input and helps reset central sensitization.
4. Surgical Findings & Methods
- Procedures performed:
- Decompression of common peroneal, tibial, saphenous, and lateral cutaneous calf nerves.
- Addressed tarsal tunnel and downstream branches (medial/lateral plantar, calcaneal).
- Used ultrasound-guided localization and intraoperative physical mapping.
- Rationale:
- Multiple entrapments in the same limb can cause chronic pain mistaken for centralized CRPS.
- Early decompression prevents irreversible central sensitization.
5. Physiological & Psychological Correlates
- Pain–Depression Loop:
- Severe peripheral nerve pain induces anxiety, depression, and suicidality; relief after decompression often brings immediate mood recovery.
- Central Nervous System Recalibration:
- Removing all active nociceptive inputs simultaneously (“one-stage multi-site decompression”) helps the CNS recalibrate—avoiding residual hyperactivity if any pain generators remain.
6. Paradigm Conflict
- Pain Management vs. Surgical Lens:
- Pain specialists aim to manage symptoms pharmacologically (gabapentin, ketamine, etc.).
- Peripheral nerve surgeons aim to eliminate the source when anatomical lesions exist.
- The divide persists due to training silos and differing conceptual frameworks: “CRPS = central” vs. “CRPS = peripheral plus central.”
- Clinical Heuristic:
- “You only see what you look for.” Many physicians fail to detect entrapments because they aren’t trained in peripheral nerve examination.
7. Clinical & Educational Takeaways
- For clinicians:
- Always evaluate for anatomical entrapments in CRPS-like syndromes, especially when history involves local trauma.
- Use targeted diagnostic blocks before ruling surgery out.
- Consider multidisciplinary collaboration rather than categorical avoidance of surgical options.
- For researchers:
- Study correlation between multi-site nerve entrapments and central sensitization reversal post-decompression.
- Quantify long-term neuroplastic changes after peripheral relief.
- For patients/families:
- Persistence and second opinions are vital.
- Nerve surgery, when anatomically justified, can restore life quality even after years of CRPS diagnosis.
Core Learning Principle:
CRPS is not always a central mystery—it can be a peripheral problem misunderstood through central bias. Accurate nerve-based diagnostics and decompression can sometimes convert “untreatable” CRPS into curable nerve compression syndromes.
Diagnostics
Principle: Trauma–Distribution Correlation
There is usually a predictable, narrowing relationship between:
-
The kind of trauma,
-
The mechanical path of force, and
-
The nerve(s) most likely entrapped or stretched.
Examples:
| Trauma Mechanism | Commonly Affected Nerves | Diagnostic Block Sites |
|---|---|---|
| Direct lateral impact to knee or fibular head | Common peroneal, lateral cutaneous calf | Peroneal head, lateral calf |
| Ankle twist / inversion or tight boot | Tibial (tarsal tunnel), medial/lateral plantar | Behind medial malleolus |
| Medial knee impact or valgus strain | Saphenous (below medial condyle) | Along medial tibial plateau |
| Deep posterior calf contusion or immobilization | Tibial (soleal sling entrapment) | Posterior proximal calf |
| Dorsal foot crush / tight lacing | Superficial peroneal | Dorsolateral ankle |
| Surgical scar / orthopedic fixation | Nearby cutaneous branch (sural, saphenous, peroneal) | Adjacent to scar line |
Thus, the pattern of sensory pain and prior trauma localizes the target zone for diagnostic nerve blocks—just as dermatome mapping localizes radiculopathy.
Functional Logic of the Lidocaine Test
-
Lidocaine blocks test reversibility of pain from a specific nerve.
-
If pain immediately disappears in that nerve’s sensory territory:
→ Confirms that a peripheral nerve generator exists before central sensitization. -
If no effect:
→ Suggests central sensitization dominates or the target nerve was incorrect.
In Dellon-style protocols:
-
Each nerve suspected from history + exam is sequentially tested.
-
The pattern of relief (partial, full, none) creates a map of compressions—what Dellon called “nerve topography.”
Predictive Value
-
The relationship between type/location of trauma and likely nerve compression is semi-predictable, not absolute:
-
Roughly 70–80 % of chronic post-traumatic neuropathic pain cases can be correlated to identifiable nerve entrapments when mapped this way (Dellon et al.).
-
The rest reflect diffuse injury, secondary fibrosis, or central pain dominance.
-
Hence:
→ Diagnostic blocks are targeted but individualized.
→ The targets are predictable once you analyze the mechanical and sensory pattern.
→ There is no single “set of universal nerve block sites” for CRPS evaluation.
Learning Takeaway
Lidocaine block diagnostics are not about where to inject, but about how well one can listen to the story the nerves are telling.
Trauma history, sensory geography, and immediate relief response together form the most precise predictor of surgical success.
Summary Line:
The method—mapping trauma to pain distribution and confirming by focal lidocaine relief—is universal. The actual block sites are variable but predictable once the trauma path and sensory pattern are carefully traced.
Two Diagnostic Philosophies — and Why They Diverge
| Diagnostic Mode | Physiologic Target | Information It Yields | Limitation |
|---|---|---|---|
| Lumbar sympathetic block | Autonomic plexus (T12–L3 chain) | Tests whether pain is sympathetically maintained (SMP) — i.e., whether blocking sympathetic efferents reduces pain. | It does not reveal which peripheral afferent nerves are structurally compressed or injured. Relief ≠ anatomical localization. |
| Targeted peripheral lidocaine block | Specific sensory/mixed nerve (peroneal, tibial, saphenous, etc.) | Tests whether pain arises from conduction within that exact nerve — i.e., whether local compression/irritation is the generator. | Requires anatomical skill; if mis-localized, gives false negatives. |
So:
-
Sympathetic blocks tell you how the pain is modulated.
-
Peripheral blocks tell you where it originates.
They operate on entirely different layers of the nervous system.
Why Lumbar Sympathetic Blocks Mislead in Compression-Based CRPS
-
The lumbar chain carries autonomic traffic, not somatic afferents from the distal limb.
-
When you anesthetize that chain, you’re quieting downstream vasomotor and nociceptive amplification loops — but not the injured afferent fibers themselves.
-
If the underlying driver is a trapped saphenous or tibial branch, the sympathetic block cannot reveal it; it only blunts the global signal transiently.
-
Hence the “diagnostic ambiguity”: a positive sympathetic response doesn’t differentiate between a centrally sensitized pain and a peripherally compressed nerve that is sympathetically over-coupled.
In Dellon/Williams logic, CRPS pain may present as sympathetically maintained, but persist because of unresolved afferent compression.
“Listening to the Story the Nerves Are Telling”
That line means:
-
Instead of starting from a generic spinal level and diffusing anesthetic over broad nerve traffic, you map backward from the symptoms — color change, allodynia zone, mechanical trigger — to the precise nerve trajectory that could explain them.
-
Each nerve “tells its story” through the geography of pain and the mechanical history of trauma.
-
A single drop of lidocaine at that point becomes a conversation with one nerve, not a broadcast over a highway of fibers.
Thus, diagnostic precision grows from pattern recognition, not protocol repetition.
Resulting Principle
Sympathetic blocks = top-down “is this modulated?” test.
Peripheral blocks = bottom-up “is this caused?” test.
When CRPS is perpetuated by peripheral compression, the former mislocates its inquiry, anesthetizing the wrong traffic lanes; only the latter isolates the generator.