Figure 16 USG showing muscle regeneration at 12 days

Row 1:

Right hand with CRPS swollen warm and painful cant bend the finges at all.  Pinch gauge for finger shows very low pressure and dynamometer  zero pressure.

Row 2:

The USG images on 6^th December show that there are no clear outlines for muscles which are hyper echoic. The same hand on December 18^th after 6 sessions of USGDN shows return of clear muscle outlines, with islands of hypoechoic muscle tissue in the hyperechoic fibrotic mass.

Row 3:

He is now able tp flex the fingers, generates 1 PSI pressure, is able to turn doorknobs and write legibly

This led to a lot of queries by the reviewers which had to be satisfactorily answered point by point, but the saving grace was that there were 31 pictures which told their own convincing story in irrefutable black and white. Even now in 2025, 12 years later, all the publications on this topic have come exclusively from the Ashirvad group. No other research group has explored the USG changes of muscle in CRPS either to refute or corroborate our findings, though it has been cited >32 times by different authors.

Another problem was the highly unusual nature of this topic which dealt with the potential of USG as a diagnostic investigation in CRPS where there had been no investigation to clinch the diagnosis. MRI as a diagnostic investigation had been proposed but was refuted shortly thereafter as being inconsistent.  X-ray does show osteopenia and osteoporosis in later stages but by that time the diagnosis would have been already established.

The addition of USG into our armamentarium opened the door to the hitherto unexplored world of muscle pathology in CRPS which provided many answers to explain the enigma of not only CRPS but a related but much milder pathology of co-contraction, the writer’s cramp. (49-60,75)

How co-contraction explains the inflammatory symptoms and signs of CRPS:

Inflammation has always been cited in CRPS literature as an important finding (76) but never with reference to muscles. The inflammation has been attributed to nerves as a neuroinflammation to explain the increased levels of inflammatory mediators that have been demonstrated in the cerebrospinal fluid of CRPS patients as well as in the blood collected from the veins of CRPS limb as compared to the normal limb. The proposed explanation for this is that inflammation is supposed to involve the nervous system at all levels right from the spinal cord down to the peripheral nerves of hand and is supposed to express itself peripherally as the inflamed red swollen hand of CRPS. This concept of neuroinflammation neither acknowledges nor attempts to explain the muscle stiffness. Instead the stiffness and disability of the CRPS hand is attributed to the Central nervous system which somehow decides to “neglect” the CRPS hand and eventually joints of the hand get fused after a few years.   However, neither the medications that address the nervous system ( neuromodulators) or the interventions that address this hypothetical neuroinflammation may or may not produce beneficial results. Nerve blocks (with injection of anti-inflammatory drugs like steroids) may not work at all or may relieve CRPS symptoms temporarily. We have seen that SGB works only in patients with sympathetically maintained pain but not in those with sympathetically independent pain.  Single shot or short-term blocks of somatic nerves work temporarily. In our 40 patients with CBPB, the block had to be continuous 24/7 and maintained for 40-60 days for physiotherapy to be effective. Those patients with accidental extrusions at 10-15 days or earlier there was a full-blown recurrence of CRPS symptoms before we introduced USGDN as an additional treatment (after our east African patient in 2006). In retrospect it is obvious that once USGDN was introduced even those patients with accidental catheter extrusions within the first 2 weeks went on to recover completely from CRPS.  This data indicates that the nerve blocks play a secondary role in addressing the CRPS symptoms, their effects confined to partial and temporary relief of only pain and sensory symptoms. Thus, neuroinflammation does not seem to comprehensively explain CRPS.

In contrast, the Ashirvad understanding explains that while the inflammation of hand is very real, it is not neuroinflamamtion from spinal nerves which somehow mysteriously expresses itself in the hand but is actually a localized tenosynovial inflammation consequent to involvement of muscles and their tendons.

CRPS patients have a very clear and specific description of their pain. They seldom complain of any significant pain in the forearm where the co-contracted muscles are but always point to their fingers and wrist as the painful areas. It was a perplexing observation to solve. So how and why does co-contraction of muscle in forearm produce pain in the fingers and why exactly does the relaxation of forearm muscle relieve the pain, swelling, redness and warmth of CRPS hand?

USG provided the answer by showing that the hand swelling in CRPS patients was actually a collection of fluid around the tendons(effusion) of the extensor muscles at the back of the hand. There is no swelling at all in the soft tissues of the hand superficial to the tendons. (figure-21). The flexor tendons in front of the hand and wrist are inflamed and USG shows effusion around these tendons as well but the swelling on dorsum(back) of hand is much more obvious.

Figure 17- Ultrasound appearance of the inflammation around tendons

The first image shows the diagrammatic representation of tendons of the hand and the synovial covering around it. The 2^nd image is from a non CRPS patient where the swollen hand shows collection of fluid under the skin (subcutaneous) as irregular black spaces but the tendons are normal. The 3^rd  image shows the collection of black fluid around the white round tendons in a CRPS patient while the subcutaneous tissues have no fluid. The 4^th  image shows the same patient after treatment where the effusion has disappeared and the tendons are normal.

The tendons of the flexor and extensor muscles of the fingers have a very thin covering (synovial sheath) with an extremely rich supply of nerves. Any overstretching/ pull/friction between the tendons and this sheath produces local inflammation called tenosynovitis. Once USG showed this tenosynovial effusion, I understood that the straining and struggling of co-contracted muscles with attempts to move the hand or make a fist causes repeated friction between the tendons and their tendons causing inflammation. (tenosynovitis) This releases inflammatory mediators which lead to increasing pain, warmth and swelling which can be visualized by USG around the tendons. This inflammatory tenosynovitis in turn reciprocally worsens the spasm of the already co-contracted flexor and extensor muscles which in turn worsens the pull on the tendons and further inflammation forming a vicious circle.

Exercises of the fingers and hand of CRPS feed into this vicious circle to increase the friction and hence the repeated exacerbations. It is as if the limb affected by CRPS-1 experiences a trauma every time the patient attempts physical therapy or tried to use the hand and hence experience an exacerbation of their symptoms when they did physiotherapy. It is also a common finding that patients have no symptoms of CRPS as long as their hand is immobilized in a plaster cast and the problems of pain and swelling start only during the mobilization phase after removal of plaster cast. They also complain that it is their fingers that hurt most and later swell, when they try to make a fist.

Pain during the needling appeared to vary directly with the resistance encountered by the needle in the CRPS muscles. This resistance is caused by intense co-contraction in the initial phases of CRPS and by fibrosis of muscle in later phases. Patients report that they are happy to cooperate for USGDN despite this pain because of the exquisite relief of their original pain after needle removal. Even more important to them is the returning ability to use the hand and the ability to sleep undisturbed by the pain. All of them comment on the difference in pain and movement restriction before and after DN.

The movement restriction seen as a distinctive feature in every patient of CRPS, is of such severity that even considerable passive effort by a physiotherapist fails to mobilize these muscles to increase the ROM. Without USGDN, there prevails a yo-yo situation of minuscule improvement with physiotherapy followed by recurring restrictions of movement due to resistance by the abnormal muscle and pain which impede all such efforts at mobilization. Successive, incremental muscle relaxation and pain relief by USGDN allows better passive stretches to achieve coordinated movements. The active ROM follows more slowly because the patient has to regain the requisite power with strengthening exercises. Systematic alternate needling of the antagonist/ agonists followed by passive physiotherapy provided us with the ideal treatment to overcome the motor disability of CRPS with demonstrably improved ROM of 4-5⁰ with each USGDN session. Needling the antagonists and agonists specific to any remaining restriction restored the ROM. This needling technique is based on anatomy of muscles around the joints, physiology of muscle contraction/relaxation and dynamics of movement. Utilizing it for the first time in CRPS, we found that USGDN is the much-needed ideal tool to optimize the effects of Physiotherapy.

This understanding of CRPS inflammatory process has increased my respect for physiotherapists tremendously because hitherto they were managing to produce some improvement in CRPS patients even though it was a tightrope walk for both the patients and physiotherapists. Less movements mean more stiffness, deterioration and no improvement, and little more exercises and the patient deteriorates with exacerbations of inflammation. This exacerbation is double edged in that not only is there inflammation around the hand tendons but also an increase in stiffness of muscles and worsening co-contraction. It was a testament to their dedication, patience and perseverance as well as the determination and endurance of CRPS patients that historically physiotherapy has been the consistent mainstay of CRPS treatment. Unfortunately, there appears to be little uniformity amongst physiotherapy techniques utilized for CRPS. (77) ‘Physiotherapy’ appears to be an umbrella term to be interpreted as mobilization exercises of various kinds according to the knowledge of CRPS or lack thereof of the physiotherapist.

USGDN, by reducing the co-contraction reduces both the problems of taut muscles and the consequent tenosynovial friction/inflammation and actually makes physiotherapy much easier. Any exacerbation of co-contraction by an intensive but productive session of physiotherapy can be reversed by the very next session of USGDN which invariable reduces the tenosynovitis symptoms. This predictable relief of pain makes the patients gain the confidence to work with the physiotherapist making graded reduction of co-contraction accompanied by return of normal coordination and disability improvement an achievable goal. It has been our routine observation that,

• The most significant benefit of USGDN to the patient is the reduction of both rest and movement pains with restoration of sleep disturbances within 2-3 sessions of USGDN. Once pain and stiffness relief is achieved, these symptoms do not recur at the original intensity even after intense physiotherapy.
• Next are the sensory symptoms like numbness, hypersensitivity, allodynia (normal touch of clothes, breeze perceived as pain) insect crawling sensations, shocks etc are reduced with each session and relieved within 3- 4 sessions. Once relief is achieved these symptoms do not recur. There are very fine muscle fibres (dermal motor elements) in the skin and erector pili muscles which cause goosebumps on exposure to cold. These muscle elements in the skin go into spasm in CRPS and are involved in the causation of sensory manifestations of CRPS. When needles are introduced through the skin to reach to the deeper muscles, they relieve the spasm of these dermal muscles.
• The warmth of CRPS limb is invariably reduced by USGDN as documented by skin temperature readings before and after a session. This is one of the most obvious and consistent findings in all CRPS patients. (figure 18) Warmth as a symptom does recur after intensive physiotherapy but subsides after the next USGDN. After about 5-7 sessions the recurrence of warmth does not occur.
• The sudomotor symptom of swelling takes about 7-14 to disappear completely. Initially swelling takes 1-2 days to reduce after USGDN. The patients present the next day with an obvious reduction of swelling. However excessive use of the hand, or intense physiotherapy can cause a recurrence of swelling and warmth in the first fortnight, but this is usually relieved by next session. We routinely observe that the initial tenosynovial effusion in the hands disappears for good after 10-15 days and does not recur thereafter.
• The color changes take about a 1-2weeks to normalize and do not recur thereafter.
• The motor improvement keeps happening with each USGDN session all along the treatment period of 20-40 days. It is the motor symptoms that take the longest to recover. The dystonia is replaced by purposeful movements, the range of motion improves at various joints by a few degrees as measured by goniometer after each session of USGDN. Since the whole limb and the neck are addressed at every session of USGDN, major changes are seen after each session at several joints, at the wrist, at the proximal middle and distal interphalangeal joints, supination and extension at elbow and all the movements at shoulder.

Once we understood that the clinical diagnostic criteria (Budapest criteria) of CRPS were actually manifestations of tenosynovitis (synovium of tendon) the mechanism of action of USGDN in specifically targeting the pathophysiology of CRPS became clear. It is actually the most specific treatment for CRPS, more than medications, sympathetic ganglion blocks, or CBPB or spinal cord stimulator which is a presently recommended treatment.

SCS modulates the pain sensation but does nothing to the muscle, hence these patients may get some pain relief which has been described in one review thus “up to 60% improvement in pain in 60% of patients 60% of the time”. (35-37)

Figure 18 – Temperature changes with USGDN

Temperature measured with a skin thermometer shows 37-38⁰ centigrade before USGDN, 37⁰ C with needles in situ and 35⁰ C within 30 minutes after needle removal. These findings are uniformly observed in all patients.   Clinically, patients report a reduction of warmth and a sense of coolness in the hand post USGDN, and also report a sensation of relaxation and easier movement after needle removal

Figure 19- Color changes in CRPS and their reversal by USGDN

Figure 19-This patient with CRPS of right hand with a dark skin and swelling over the little and ring fingers which became normal after treatment.

In our practice USGDN has become the sole therapy which produces 100% relief of rest pain within the first week and movements pains after 30-45 days of treatment AND 90-100% relief of disability at the completion of treatment. CBPB which we started out with, has become a secondary treatment being more of a complementary therapy reserved for specific indications like

1. Patients who have a fear of needles,
2. Patients in extremely severe pain who just cannot think of having needles inserted into them.
3. Patients with severe dystonic movements where needles provoke an initial worsening of movements before the later quiescence. The co-contraction locks the agonist and antagonist muscles in severe cramps. In these patients the pain relief from CBPB becomes very useful for the first few sessions of USGDN.
4. Patients who have come with a short time frame for treatment usually from other countries or other parts of India.

Hitherto out of a total 220 CRPS reversals, our first 8 patients had only CBPB and physiotherapy, 40 patients received combination of CBPB, USGDN and physiotherapy and 119 patients received only USGDN for Upper extremity CRPS. We have also successfully reversed lower extremity CRPS in 53 patients with involvement of ankle, knee and hip. For lower extremity CRPS, 32 out of 53 patients received a combination of USGDN, physiotherapy and a complementary neural interventions like continuous sciatic block, Lumbar plexus block and pulsed radiofrequency of entire innervation of knee and 21 patients received only USGDN.  Thus 119 patients of Upper extremity CRPS and 21 patients of lower extremity CRPS have had successful reversal of CRPS with USGDN as the sole treatment modality at Ashirvad.

A striking feature of our CRPS reversal is an unequivocal pain relief within the first 10 days and  gradual but ongoing disability relief over the next 3-6 weeks. We believe that this success is because of a paradigm shift in our understanding of CRPS; that the central pathology of CRPS is an abnormal co-contraction of the agonist /antagonist muscles of movements. Movements of the severely co-contracted muscles lead to secondary digital Teno synovial friction and inflammatory tendinosis in the hand, or ankle or knee. It is this Teno synovial inflammation which gives rise to pain, sensory, sudomotor and vasomotor manifestations which form the Budapest criteria of CRPS.

The abnormal co-contraction of CRPS affected muscles responds with exquisite sensitivity to ultrasound guided dry needling (USGDN) which accurately targets the co-contracted agonist/antagonist muscle combinations to relax them and restore their normal co-ordinated function. This automatically reduces the synovial friction and resolves the inflammatory tendinoses in the hand, or ankle or knee thereby reversing the pain, vasomotor, sudomotor and sensory features. Furthermore, the post needling muscle relaxation reduces the stiffness, weakness and dystonia with restoration of normal coordinated movements with dramatic improvement of disability.

Musculoskeletal ultrasonography (MSKUSG) has been of immense importance in corroborating our hypothesis by demonstrating the primacy of muscle pathology in CRPS.  The disruption of muscle sonoanatomy in CRPS affected muscles is objective evidence that is uniformly demonstrable with ultrasonography, and we have described the importance of MSKUSG as a diagnostic investigation in upper extremity CRPS (51) and is very useful in distinguishing neuropathic pain from CRPS. (52) We have also described the restoration of the initial muscle structure disruption and motor function recovery that occurs after USGDN. (53)

To summarize, CRPS  remains an unsolvable enigma in pain clinics of the world because the importance of muscle pathology has not been explored. At Ashirvad we have focussed on this problem to get an unequivocal and predicatble  resolution of not just pain but also the disability associated with CRPS

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