Current treatment of chronic pain has led to an opioid crisis. A prime if not the most frequent cause of chronic pain is chronic muscle spasm. Identification of chronic muscle spasm has been hindered by the lack of a diagnostic tool and a characteristic finding. Spontaneous Electrical Activity (SEA) was thought to only be present in denervated muscle. However, the published work of Dr. Coletti indicates that SEA is found in muscle that has suffered an acute or overuse injury resulting in chronic spasm and resulting chronic pain.
Skeletal muscle that develops prolonged spasm, whatever the cause, will limit its own blood supply. When prolonged for 3-4 weeks there is evidence of membrane instability which presents as spontaneous electrical activity (SEA). The presumed sequence of events is inadequate energy to support the Sodium, Potassium and Calcium channels of the cellular membrane. As a result membrane instability occurs and presents as spontaneous depolarization, presenting as SEA. Steroid injections are know to partially stabilize membranes but the duration of action is seldom long enough to allow the muscle cells to return to normal. Opioid medications simply temporarily block the brains recognition of the pain.
SEA represents not only the identifying signature of true chronic muscle spasm but is the proximal that is actual cause of the sustained spasm maintaining the spasm indefinitely. Similar to what is seen in atrial fibrillation in cardiac muscle, no nerve activation, or lack thereof, is responsible for the continued electrical activity and erratic constant contraction of the atria. The most direct treatment of chronic muscle spasm is to suppress the SEA. The CMECD method suppresses the SEA for several months allowing the muscle to return to a normal state and avoids the need for opioid pain medications for relief of chronic pain caused by chronic muscle spasm. Because of its duration of action, the CMECD injection procedure typically requires one or at most two injections to fully treat a muscle or group of muscles in chronic spasm.
Dr. Coletti began his clinical research over 8 years ago. Initially using Botox he found phenoxybenzamine had been tried but abandoned. However, its safety, utility and cost led to its current usage in his protocol to successfully treat chronic spasm and resulting chronic pain. None of the several hundred patients treated by Dr. Coletti w
Dr. Coletti began his clinical research over 8 years ago. Initially using Botox he found phenoxybenzamine had been tried but abandoned. However, its safety, utility and cost led to its current usage in his protocol to successfully treat chronic spasm and resulting chronic pain. None of the several hundred patients treated by Dr. Coletti with the CMECD procedure were given opioid pain medication. He has now begun training other physicians in this technique.
Short for "Coletti Method Emg guided ChemoDenervation" His pioneering work has been now published in half a dozen abstracts in Muscle & Nerve and presented at four annual meetings of the Association of Neuromuscular and Electrodiagnostic Medicine. Its basis represents a paradyme shift in our understanding of muscle pathophysiology. Finall
Short for "Coletti Method Emg guided ChemoDenervation" His pioneering work has been now published in half a dozen abstracts in Muscle & Nerve and presented at four annual meetings of the Association of Neuromuscular and Electrodiagnostic Medicine. Its basis represents a paradyme shift in our understanding of muscle pathophysiology. Finally having a method to identify which muscles are in a state of chronic spasm, it will be possible to correctly tailor treatments for chronic pain.
Dr. Coletti is no longer in clinical practice but wanted to be sure that the technique he developed would be followed if cited. He holds no patent or restrictions on its use. Furthermore, supportive research requires adherence to a fixed protocol. His intent is to give a fixed point of reference for all therapies and developments that may
Dr. Coletti is no longer in clinical practice but wanted to be sure that the technique he developed would be followed if cited. He holds no patent or restrictions on its use. Furthermore, supportive research requires adherence to a fixed protocol. His intent is to give a fixed point of reference for all therapies and developments that may follow. Independent research sites and funds are being sought and a medical school collaboration is in progress.
No epidural injection experience is required as the spine is never penetrated. Joint injections are also not performed. Any office based trigger point injection experience is adequate. With experience a comfort develops in the use of 2.5 to 3 inch EMG injection needles to do deep muscle injections especially in the low back and piriformis. The EMG tracing showing spontaneous electrical activity (SEA) identifies the muscle in chronic spasm. Small doses of the injection cocktail are given to essentially infuse the muscle diffusely. Residual pockets of SEA should be sought and treated. Injection should be extended into adjacent sites of SEA when possible to fully treat the muscles that are functioning together.
While full functioning EMG equipment can be used, smaller hand held units, especially those with sound and screens are adequate. The Myoview by Intronix is pictured above and is entirely adequate. EMG injection needles, such as those supplied by AMBU work well. An alcohol spray to numb and clean the site for injection is useful. Most injections are best performed with the patient is a standard massage chair which allows full relaxation of most muscles potentially being treated including the piriforim. Standard EKG electrode tabs can be used. Phenoxybenzamine can be obtained, sent overnight, compounded with a low dose of dexamethasone from Millers Pharmacy in NJ, shipped to any state, 888-891-3334 for $50 per treatment vial. Onsite dilutions with equal amounts of 2% lidocaine are then performed prior to injection.
It is recommended to have a staff member in the treatment room especially if there is not a patient's relative observing. This is primarily because occasionally patients may become lightheaded or rarely faint from simple needle insertion or the effects of the medication itself. Patient family members in observation often serve to support the patient and later to explain how the procedure was performed. Once demonstrated how the the device identifies sites of spasm, family members not uncommonly take great interest in the search for additional symptomatic sites. Billing personnel need to be trained to use EMG guided chemodenervation codes associated with codes for chronic pain and sites of injection and symptoms. Specific ICD 10 codes need to be identified for each patient interaction
EMG GUIDED CHEMODENERVATION TREATMENT OF SCIATICA presented 2012
Sciatica represents a clinical syndrome for which current treatments have been of limited benefit. Utilization of EMG guided chemodenervation was explored in an attempt to achieve better and more consistent outcomes.
To develop a successful methodology for treatment of sciatica not caused by disc protrusion or spinal stenosis.
Chemodenervation agents including Botox and phenoxybenzamine were utilized in clinical practice for patients presenting with sciatica. EMG identification of spontaneous electrical activity (SEA) was sought in resting muscles including erector spinae and psoas muscles with injection of chemodenervation agents to suppress the SEA in the lumbar-sacral region. Initially Botox was used but lack of insurance coverage led to seeking a less expensive agent. Currently, 0.5% phenoxybenzamine combined with 2% Lidocaine is used and generally requires 10cc injected under EMG guidance in 1/4 cc aliquots to multiple adjacent sites until all SEA is abolished.
Over the last year, approximately 20 patients presented with chronic sciatica and were treated with EMG guided chemodenervation. In patients with ongoing disc issues treatment often improved but did not resolve sciatica. In non disc patients with SEA, treatment resolved sciatica in nearly all patients. Piriformis injections were needed in the remaining few patients. Rare recurrences after several months occurred only in patients who did not adjust their activity to prevent repeat overuse injury.
EMG guided chemodenervation of SEA in the erector spinae and psoas muscles using phenoxybenzamine/Lidocaine resulted in a high degree of success with long term relief of sciatica in selected patients.
Coletti, R.H., EMG Guided Chemodenervation Treatment of Sciatica, Abstract in Muscle & Nerve, Volume 46, Issue 4, October 2012, Pages: 621–679, Article first published online: 14 SEP 2012, DOI: 10.1002/mus.23652
NOVEL INJECTION TECHNIQUE FOR CHEMODENERVATION OF SYMPTOMATIC
CHRONIC MUSCLE SPASM presented 2014
Treatment of chronic muscle spasm with trigger point injections has typically sought to identify a focal trigger point for that muscle. Spontaneous Electrical Activity (SEA) often referred to as end plate noise has been found to be present at trigger points.
Develop an effective injection technique for symptomatic chronic muscle spasm using EMG guided chemodenervation agents.
EMG guided interrogation was performed of symptomatic chronically spastic muscle. Chemodenervation was performed with dilute OnabotulinumtoxinA 100u/20ml or Phenoxybenzamine 0.25%/Lidocaine 1%. Injection only at the most active sites was found not to provide acute symptomatic relief. Patients were asked to perform movements that caused discomfort at various stages of the injection technique until symptomatic relief was obtained. Injection extending outward from the most active site until all adjacent muscle tissue demonstrating SEA was eliminated provided acute relief and was associated with prolonged relief. For relatively small segments of spastic muscle, redirection of the original needle puncture to cover 360 degree and at various depths and angles was adequate. However, additional skin punctures following the tract of the SEA were commonly required.
Only complete resolution of SEA by EMG guided chemodenervation with various agents provided adequate acute and subsequent prolonged relief of symptomatic chronic muscle spasm.
Novel trigger point injection technique utilizing EMG guided chemodenervation was found to be superior to focal trigger point injection at the site of maximum SEA.
Coletti, R.H., Novel Injection Technique For Chemodenervation Of Symptomatic Chronic Muscle Spasm, Abstract in Muscle & Nerve, Volume 50, Issue 4, October 2014, pages: 626–719, Article first published online: 22 SEP 2014 | DOI: 10.1002/mus.24436
NEEDLE ELECTROMYOGRAPHIC IDENTIFICATION OF CHRONIC MUSCLE SPASM
presented in 2016
Multiple treatments for muscle spasm are utilized without regard to the physiology of the muscle. No systematic differentiation exists to distinguish between temporary and chronic muscle spasm. Muscles in chronic spasm can persist for decades and require specialized treatment.
Patient selection required a pain syndrome of greater than one month. Physical examination of reported sites of muscular pain were evaluated by compression to identify sites of non-compressibility and discomfort. EMG evaluation consisted in identification of Spontaneous Electrical Activity (SEA) also know as "End Plate Noise". Treatment of only those sites with significant SEA was performed with onabotulinumtoxinA or phenoxybenzamine/lidocaine until no residual SEA was present.
More than 100 patients were evaluated and treated. Selective chemodenervation based upon EMG identified SEA activity resulted in long term relief regardless of the duration of the prior pain syndrome with a single treatment. Muscle spasms that did not exhibit SEA were treated with conventional therapies with reported good outcomes.
SEA represents the EMG physiologic identifier and likely etiology of chronic muscle spasm.
EMG of muscle in apparent spasm provides the ability to differentiate and treat selectively muscle that will return to normal function with conventional treatment and muscle that is in a state of chronic spasm requiring selective interventions.
Abstract in Muscle & Nerve, Volume 54, Issue 3, September 2016, pages 525-623, Article first published online: 16 AUG 2016 | DOI: 10.1002/mus.24854.
DEBUNKING THE MYTH: DENERVATED MUSCLE IS THE SOLITARY CAUSE OF MUSCLE SPONTANEOUS ELECTRICAL ACTIVITY presented 2017
Treatment of chronic muscle spasm is confounded by the belief that spontaneous electrical activity (SEA) is only found in denervated muscle. SEA referred to herein is continuous chaotic electrical activity and without evidence of reciprocal inhibition, to be distinguished from the variety of presentations of transient increased insertional activity. Prior reports have shown that needle EMG evidence of SEA is present in acquired chronic muscle spasm which was successfully treated with needle EMG-guided chemodenervation utilizing phenoxybenzamine.
To correct needle EMG misinterpretation of nerve function and muscle pathology.
We present a survey of clinical outcomes of 93 patients with SEA treated with needle EMG-guided chemodenervation.
A steady state of pain relief was achieved within 1 week of the injection procedure; 76% of patients reported having had years of prior pain, 50% of patients reported complete relief of pain. Regarding the impact on overall health, well-being, or ability to function, 55% of patients reported a major impact and 71.4% of patients reported pain relief that lasted over 3 months.
Rapid resolution of pain and disability with a high degree of sustained pain relief is inconsistent with interpretation of SEA in these patients as the result of denervated muscle. Incorrect interpretation of muscle denervation as solitary cause of SEA needs to be abandoned. The clinical impact of this finding will promote further research and treatment of the pathological state of acquired chronic muscle spasm and resultant chronic pain.
Abstract in Muscle & Nerve, Volume 56, Issue 3, September 2017, pages 543-661, Article first published online: 17 AUG 2017, https://www.aanem.org/getmedia/317d32c1-6163-47ff-998e-7046d07ff68f/2017-Abstracts-web.pdf
SUCCESSFUL TREATMENT OF LONGSTANDING CHRONIC MUSCLE SPASM WITH EMG GUIDED CHEMODENERVATION presented 2017
Chronic muscle spasm represents a significant cause for chronic pain. Treatment of chronic pain with opioid medications has led to opioid addiction, and overdose deaths are currently recognized as a national crisis. Treatment modalities are needed to treat truly chronic pain when associated with chronic muscle spasm. Novel treatment modalities utilizing needle EMG-guided chemodenervation have been previously described. Preliminary assessment of the success of such treatments for longstanding chronic muscle spasm can be provided by patient surveys of such treatment.
To identify success rates of needle EMG-guided chemodenervation with phenoxybenzamine in patients with pain duration of greater than 1 year. METHODS: Ninety-three sequential patients treated with this technique were surveyed by mail. Forty-two responded.
Of the respondents, 31 (74%) reported years of pain duration Of those, 50% reported complete relief of pain (81% of which reported relief of pain for greater than 3 months) and 27.4% reported moderate relief of pain (44% of which reported pain relief for greater than 3 months). The average duration of pain when specified was 5 years and the longest was 15 years. A single treated patient, not in this survey, reported near complete pain relief and return of function after 35 years.
Truly longstanding chronic muscle spasm and pain can be successfully treated in a significant portion of patients with stable outcomes utilizing the previously described technique of needle EMG-guided chemodenervation with phenoxybenzamine. In this unselected patient population with longstanding chronic pain, results support further clinical research to establish the utility of this treatment modality.
Abstract in Muscle & Nerve, Volume 56, Issue 3, September 2017, pages 543-661, Article first published online: 17 AUG 2017, https://www.aanem.org/getmedia/317d32c1-6163-47ff-998e-7046d07ff68f/2017-Abstracts-web.pdf
SAFETY OF PHENOXYBENZAMINE CHEMODENERVATION WITH REPEATED INJECTIONS
Chemodenervation with botulinum toxin A is known to cause weakness and atrophy with repeated injections. Alternative medications with a similar duration of action without this side effect would clearly be preferable. Phenoxybenzamine has been shown to be a chemodenervation agent useful in the treatment of chronic muscle spasm. The issue of its safety with repeated use has not been reported. Several hundred patients have been treated without evidence of weakness or atrophy when 1 or 2 injections were delivered to a given muscular region. However, no reports of the outcome of multiple injections have been published.
To document the outcome regarding weakness and atrophy of a single known case of multiple injections to establish parameters of safety for this medication. METHODS: A single patient following a two-level lumbar laminectomy developed severe post-laminectomy syndrome. An MRI at 3 months following surgery was interpreted as worse than pre-surgery. Needle EMG-guided chemodenervation was performed at approximately 2-week intervals with a total of greater than 10 injections for post-laminectomy syndrome to resolve.
A final MRI at 7 months post-surgery showed resolution of neural impingement and resolution of radiculopathy symptoms. No evidence of weakness of atrophy was observed on musculoskeletal physical examination.
Initial results of multiple injections with phenoxybenzamine during needle EMG-guided chemodenervation suggest it may be safely used for repeated interventions. The known mechanism of action indicates this drug should not be toxic to muscle or nerve. Further investigation is needed to determine if the specific dose utilized played a significant role in this outcome.
Abstract in Muscle & Nerve, Volume 56, Issue 3, September 2017, pages 543-661, Article first published online: 17 AUG 2017, https://www.aanem.org/getmedia/317d32c1-6163-47ff-998e- 046d07ff68f/2017-Abstracts-web.pdf
PROPOSED NEW DIAGNOSTIC ENTITY OF ACQURED CHRONIC MUSCLE SPASM
Prior work by this author has demonstrated the ability to identify chronic muscle spasm by the needle EMG finding of spontaneous electrical activity (SEA). Moreover, it was shown that the presence of SEA was not solely the result of denervation of muscle but was present in muscle that had no evidence of denervation. It was further shown that treatment of muscles in chronic spasm without a neurogenic etiology can be successful treated by elimination of the SEA to allow the muscle to return to a normal physiologic state.
To formulate a proper diagnosis and thereby allow for correct directed treatments for patients with clinical and needle EMG evidence of acquired chronic muscle spasm (ACMS).
ACMS shall be considered to be present when the following conditions are met: (1) Needle EMG tracing demonstrates chaotic SEA in muscles that are or should be at rest given proper body positioning. (2) SEA will not be abated by reciprocal inhibition by activation of competitive muscle groups. (3) No known neurogenic cause for the presence of SEA has been identified. (4) When physically accessible, muscle will demonstrate a resistance to compression and which will typically result in discomfort.
The acceptance and utilization of the proposed new diagnostic entity of ACMS should allow for improved diagnosis of the etiology of chronic muscle spasm. This should allow alternative treatment of the resultant chronic pain.
Abstract in Muscle & Nerve, Volume 58/ No. S2/September 2018, Pages: S1-S120; First Published: 02 October 2018, page S34, https://onlinelibrary.wiley.com/toc/10974598/58/S2
EMG GUIDED CHEMODENERVATION PROCEDURE OF ACQUIRED CHRONIC MUSCLE SPASM DESIGNATED AS CMECD™ presented 2018
Multiple prior abstract publications involving the novel procedure of needle EMG guided chemodenervation of chronic muscle spasm have been presented. Various details of the procedure were contained in each of these abstracts. However, sufficient information for undertaking this procedure was lacking. Clear designation of the described procedure was deemed necessary for physicians seeking complete procedural information with access to references and other supportive documentation.
To make a clear and simple designation of this novel procedure to facilitate online search for procedural information and subsequent published research.
A simple acronym, CMECD™, which represented “Coletti Method EMG Guided ChemoDenervation” was chosen and subsequently trademarked. Internet search under this acronym now readily identifies videos and the CMECD.info site holds all information presently compiled on this procedure.Trademark application was chosen to assure that there was consistency in the procedure if and when undertaken by various practitioners.
Online viewing of the procedural website, CMECD.info, is already allowing hundreds of views per month.
This method of online presentation allows for dissemination of emerging medical treatments in a fashion more readily accessible to physicians and potential patients. Designation of a procedure with a readily searchable acronym, providing procedural, research, and outcome data should be considered a model for providing ready access to detailed information on emerging medical treatments.
Abstract in Muscle & Nerve, Volume 58/ No. S2/September 2018, Pages: S1-S120; First Published: 02 October 2018, Page S36, https://onlinelibrary.wiley.com/toc/10974598/58/S2
LIMITATIONS OF EMG AND NERVE CONDUCTION STUDIES IN CLINICAL PRACTICE
Chronic pain and weakness are significant factors in the onset of disability. Complete needle EMG and NCSs are often required to identify the state of nerve function as it may relate the presenting symptoms. However, recent studies have shown that acquired chronic muscle spasm, identified with simple needle EMG sampling with the presence of spontaneous electrical activity (SEA), is a common causes of both chronic pain and weakness. Current reporting techniques will typically indicate the presence or absence of SEA without indication of its functional significance.
To expand current reporting techniques for needle EMG and NCSs to include precise location by muscle group of the presence and intensity of SEA.
A severity scale of SEA and parameters for reporting is proposed. Several levels of activity are to be discriminated and given point values for any muscle showing or adjacent to muscles demonstrating SEA. Increased insertional activity is included as it has been seen in spasms of intermediate duration. The proposed levels include: (1) No SEA or increased insertional activity, (2) Increased insertional activity whether or not it recurs on repeat insertion, (3) low level SEA, (4) moderate SEA, and (5) high level SEA. Requirements for measurement of SEA require that reciprocal inhibition by contralateral muscle groups cannot be demonstrated and that the muscle should be in a natural state of relaxation based upon body habitus.
Outcome data and correlation with pathophysiology can then be determined.
Proposed addition of SEA reporting should allow for improved assessment of presenting symptoms of chronic pain and weakness.
Abstract in Muscle & Nerve, Volume 58/ No. S2/September 2018, Pages: S1-S120; First Published: 02 October 2018, page S31, Page S36, https://onlinelibrary.wiley.com/toc/10974598/58/S2
NON SKELETAL ETIOLOGY OF FOOT DROP WITH THERAPEUTIC REVERSAL
Foot drop has been long considered the result of neural foraminal compression or spinal stenosis. Therapeutic intervention has focused on epidural injections or laminectomy.
Identify potential etiology of successful cases of foot drop reversal with non-skeletal interventions.
CMECD® denervation procedure, previously described, see also CMECD.info, was performed on 4 cases of foot drop lasting from 3 months to 4 years. Outcomes were classified as immediate, progressive or delayed. Injection was performed of the ipsilataeral erector spinae at the level the lower lumbar vertebrae typically at sites of discomfort on manual focused compression.
An immediate reversal was seen with a case of 3-month foot drop duration. An immediate improvement with full recover was noted in a case with 6 months of foot drop. An improvement but not full reversal was seen in a case 2½ years post laminectomy. Minimal initial with complete progressive recovery was seen after 6 months, including return of knee-jerk reflex, with 4 years of foot drop.
Various responses of non-skeletal muscular intervention indicate that non-skeletal etiologies exist and may be caused by and responsive to treatment of chronic muscle spasm. Time frames of response appear to coincide with the duration of the presenting symptom although at least some immediate response was present in all cases. Nerve recovery with release of compression is known to vary with the extent of nerve injury. Current findings suggest that nerve compression muscular non-skeletal etiologies of foot drop exist and may be potentially treated with therapies to resolve chronic muscle spasm.
Abstracts 2019 AANEM Annual Meeting Abstract Guide Austin, TX, October 16–19, 2019 Muscle & Nerve, Volume 60, Issue S1 First published: 13 August 2019, https://doi.org/10.1002/mus.26647
STAGED HEALING OF WRIST TENDONITIS FOLLOWING CMECD® TREATMENT
CMECD® denervation treatment, previously described, also see CMECD.info, of chronic muscle spasm of forearm muscles with associated wrist tendonitis follows a different pattern of recovery from most other muscles in chronic spasm. The associated muscle spasm and wrist pain is generally considered referred pain or isolated tendonitis.
Objective was to identify underlying pathophysiology.
Initial response to treatment and self-reporting of pain relief in the week following treatment was compared to patients without associated wrist tendonitis.
Patients with forearm pain secondary to chronic muscle spasm without tendonitis reported initial relief of pretreatment pain and 2-5 days of local mild injection site discomfort without recurrence of the presenting pain. Patients with chronic muscle spasm and associated wrist tendonitis reported predominant relief of pretreatment wrist pain associated with motion or stress but typically required 3 days before the wrist motion associated pain fully resolved. Injection site discomfort for 3-5 days was also noted.
Complete relief of wrist tendonitis associated with forearm chronic muscle spasm appears to be time dependent. It is postulated that the tendonitis was the result of the chronic muscle spasm pull on the tendon and that resolution of the chronic muscle spasm pull allowed the tendon to recover. It was notable that one patient had undergone steroid injections of the wrist tendon with only temporary relief but attained long standing relief after the associated chronic muscle spasm was resolved following CMECD® treatment. In contrast to the concept of referred pain, this appears to represent tendinopathy secondary to chronic muscle spasm.
Abstracts, Austin, TX, October 16–19, 2019, Muscle & Nerve Volume 60, Issue S1, page S126 First published: 13 August 2019, https://doi.org/10.1002/mus.26647
PATTERN OF RECOVERY OF ACQUIRED CHRONIC MUSCLE SPASM CONSISTENT WITH ISCHEMIC INJURY MODEL
It is known that the blood supply of cardiac muscle is lessened by cardiac contraction. Flow is significantly less in systole than diastole even though the perfusion pressure is higher in systole. Prior unpublished work by this author demonstrated that with a weakening of the force of contraction, predominant cardiac flow occurred in systole. Microvascular supply of skeletal and cardiac muscle are similar. High heart rates that can occur with atrial fibrillation with near constant contraction can lead to cardiac dysfunction and muscle injury that slowly recovers over a one to two month period. Skeletal muscle in chronic spasm has been shown to have a depleted number of mitochondria that normalize with relief of the chronic spasm.
To record patterns of clinical recovery of chronic muscle spasm to find potential consistency with an ischemic injury model.
Muscles identified as acquired chronic muscle spasm by EMG according to criteria previously described, were treated with the CMECD® procedure, see CMECD.info.
Relief of pain occurred early but the capacity of the muscle to perform work, without return to spasm, gradually increased. The severity and extent of the spasm appeared to correlate with the length of time to full recovery noted to occur within a two month span.
Clinical findings are supportive of an ischemic injury model of chronic muscle spasm. Expectations of full recovery and physical therapy interventions should be informed by consideration of this model. Assessment of treatment success or failure viewed within the context of this model may improve treatment outcomes.
Abstracts, 2019 AANEM Annual Meeting Abstract Guide Austin, TX, October 16–19, 2019 Muscle & Nerve Volume 60, Issue S1, page S126, First published: 13 August 2019, https://doi.org/10.1002/mus.26647
CMECD® Experience Regarding Apparent Failed Pain Treatments
Experience with the CMECD® procedure, previously described, see also CMECD.info, has led to frequent findings that represent important elements in understanding apparent failed treatment responses to pain relief techniques.
Categorize and determine etiology of secondary pain responses.
Results: Several patterns of secondary pain were identified. An immediate alternate pain symptom in neighboring muscle group or occasionally at a distant site. A latent response and noted a new site of pain within hours of the injection as patient resumed normal activities. New sites of pain within days or weeks of the procedure.
Summary/Conclusion: It appeared that with the immediate reaction, the initial pain suppressed awareness of a less severe pain. The latent response appeared to be caused by use of muscles that did not cause as much pain as the presenting pain but were now noted to be painful when put to use. The delayed response appeared to be the result of new overuse injury resulting from muscle use in response to change in gait or increased use. Pain awareness appears to follow a hierarchy such that the most significant pain limits awareness of less severe pains. As one pain is relieved, one becomes aware of lesser site of pain. The immediate and latent responses follow a hierarchy of pain. The delayed response is unrelated to this hierarchy of pain but is important to consider in evaluating pain relief techniques. Pain relief assessment tools should identify specific treatment site relief noting potential confounding effects of this Hierarchy of Pain.
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Background of CMECD®
CMECD® is an acronym for “Coletti Method Emg ChemoDenervation”. It was based upon the finding that chronic muscle spasm was caused by chronic spontaneous electrical activity (SEA). SEA is actually muscle membrane instability caused by chronic muscle ischemia. It has been known that muscle contraction limits blood supply and chronic muscle spasm is likely to lead to impaired muscle function as is seen in cardiac muscle. Hibernating myocardium in the heart is a model that speaks to the findings in skeletal muscle. It has been found the chronic skeletal muscle spasm leads to a decrease in mitochondrial density that tends to normalize with therapy to relive the chronic muscle spasm. While EMG identification of SEA has not been used for treatment of skeletal muscles prior to description of the CMECD®, it has been used for Botox injection of the vocal cords for spasmodic dysphonia.
The following is a step by step instruction regarding the use of the CMECD® procedure.
1. Patient evaluation
CMECD® is for the treatment chronic muscle spasm. No other condition is known to be an appropriate use at this time. However, not all muscle spasm can be identified clinically by palpation. Some of the deeper paraspinal muscles may not show tenderness even on deep palpation. However, most muscles in chronic spasm can be identified manually with the presence of tenderness on compression and the appreciation of a non-compressible muscle group.
In many cases it is useful to review any prior CT or MRI studies when available. The severity of the findings is what is most important to identify. Mild and moderate degrees of foraminal narrowing, disc herniation or spinal stenosis are not usually associated with a clinical presentation of pain or radiculopathy. However, with severe findings, the etiology of the symptoms may well be secondary to vertebral abnormalities. Secondary, chronic muscle spasm may aggravate spinal etiologies and in some cases treatment of paraspinal muscle spasm has alleviated symptoms even when severe vertebral abnormalities were present.
Generally, the patient should be asked to point to the site of pain and examination of that site should include compression to elicit symptoms of tenderness. Moderately deep compression may be necessary for lumbar back muscles. However, in the case of radiculopathy, dermatome evaluation should be use to find a potential site of muscle spasm that may be responsible for nerve compression. Paraspinal muscles have also been found to be involved in disc herniation. One documented case by MRI actually showed the resolution of disc herniation after paraspinal muscle injection.
Pain at a distance, unrelated to vertebral abnormalities is seen with peripheral nerve compression by chronic muscle spasm such as may occur in the lower leg at various sites. Cervical brachial syndrome is another instance where chronic spasm of the scaline muscles presents with a typical pattern of thoracic outlet syndrome by compression of the brachial plexus travelling between the mid and posterior scaline muscles. Cases of tendonitis, such as tennis elbow can also be attributed to chronic muscle spasm of various muscles above and below the elbow. Writer’s cramp has been found to be resulting from chronic muscle spasm of various forearm muscles and has been shown to be resolved with careful identification of the particular muscle in spasm and with CMECD® treatment.
2. Patient discussion and Consent
At this point in time the CMECD® is a procedure performed under the guidance of FDA regulations for the off label use of an FDA approved medication. This must be explained to the patient and note that many current treatments are off label. The known possible side effects should be verbally mentioned. They primary side effects are site discomfort that may last up to a week and lowering of blood pressure for up to 48 hours. Atypical known side effects include absent ejaculation for up to 48 hours and hiccups for 24 to 36 hours noted in only one case. In a small patient it may not be appropriate to use a full ampoule of medication especially if they have low blood pressure to start with. Be aware that phenoxybenzamine was FDA approved as an anti hypertensive agent with a 24hour half-life. Lowering of blood pressure medications may be needed for the first 24 hours. Whenever possible, the patient should be accompanied by a family member as post procedure hypotension does occasionally occur especially with a full dose in a small patient. As with any injection procedure, the occurrence of vasovagal syncope can occur. Keeping tract of the development of and skin dampness should help prevent an unexpected vasovagal event. It is useful to ask patients if they have a tendency or history of syncope with or without needle insertions. Some of those patients may not give any warning prior to syncope. Patients with low blood pressure many need to be encouraged to increase their salt and water consumption through the following day.
It should be made clear to the patient that the injection needle may come in contact with unseen nerve roots. Occasional sharp pain may occur. Patients should be told that the needle will then been quickly retracted and that nerve damage has not been found to occur in conscious patients. The highest risk of hitting a nerve is in treatment of a piriformis syndrome. Contact with the sciatic nerve will undoubtedly cause sharp discomfort to the patient. Thus when injecting the piriformis muscle, a slower than normal insertion technique should be used. During the procedure itself, injection of very small aliquots of medication also minimize patient discomfort. The procedure as distinct from typical Botox injections requires the entire muscle that is in chronic spasm to receive small amounts of medication such that by the completion of the procedure, no residuals spontaneous electrical activity (SEA) can be found in the treated muscle.
A consent form can be found on the CMECD.info web site. It is on the long side, was the original consent form used and can be modified to the comfort of the treating physician, especially as experience with the treatment is obtained. The patient should be asked to review the consent form prior to signing.
Anticoagulants have been only a relative contraindication to injections with the CMECD® procedure. No episodes of significant bleeding occurred. Even when a vascular structure was punctured, local control was easily achieved. It is relatively easy to identify the problem by virtue of blood entering the syringe or rapid local swelling. Compression for up to 10 minutes has been successful to date in all cases. Fortunately, there is apparently little chance of hitting a significant vascular structure when injecting the deep muscles of the back. This was the most common procedure performed and no evidence of bleeding occurred, except for an occasional small skin vessel. As a precaution it would be advised to have a patient hold off but not omit a dose of anticoagulant prior to the procedure. It is recognized that holding a dose of warfarin will have little effect for that day. There it is recommended to seek a recent INR to be sure there is not over anticoagulation.
3. Dose preparation
Preparation of the phenoxybenzamine/dexamthasone solution can be obtained sent overnight and refrigerated from Miller’ pharmacy in New Jersey. This pharmacy has licenses to send sterile compounded medications to all 50 states. The cost has been $50 per vial plus the cost of shipping. Patient information is required for each dose that is prepared. An order form can be found on the CMECD.info site. The 10 ml vials of phenoxybenzamine 0.5mg/ml and Dexamethasone 1.5mg/ml are to be diluted on a 1:1 basis with 2% Lidocaine just prior to use. This results in a 0.25% phenoxybenzamine/0.75mg/ml dexamethasone/1% Lidocaine solution. Typically, 3ml syringes are used and 1.5 ml of each is drawn up with simple agitation by means of adding a half cc of air and inverting the syringe several times. The resulting liquid should be clear and not cloudy. If the medication is still cold there may be a degree of suspension rather than solution. Warming the syringe by rolling it between your hands normally warms the liquid adequately and leads to clearing of the cloudy appearance. Should it not clear for whatever reason, it should not be used as the phenoxybenzamine is not known to be effective if it is in suspension rather than solution. Phenoxybenzamine is not a very soluble drug and the addition of 1.5 mg/ml of dexamethasone was the highest concentration possible without phenoxybenzamine coming out of solution. Although no documentation has been obtained, use of frozen 10ml ampoules of solution with defrosting at room temp or assisted by hand warmth has seemed to be effective. Testing of long term frozen samples is being planned and the results will be added to the Website when this has been accomplished.
4. Injection needles
Typically, Ambu EMG injection needles were used. Needles of 3” were commonly used even if the muscle was rather superficial such that repositioning of the needle could treat a longer segment of muscle without additional skin penetration. The 3” needle is of a slightly larger caliber than the 2” or 2.5” needled but has not seemed to have much clinical import. There can also be found a 5” needle that may be necessary for treatment of piriformis syndrome in patients who are exceptionally large in that area. Generally, the 3“ needle can reach the piriformis by indenting the skin of the buttocks. Care should be taken in that case not to over manipulate the needle when inserting it deeply as it could break off at the hub. To date this has not occurred but should be considered when used in piriformis injections.
While standard full function EMG devices can be used, the smaller hand held devices such as the Intronix Myoguide are entirely adequate and simpler to use. For that device the setting that has been used was at 7 for volume and signal amplitude. Other settings may work just as well but that is the setting that was used for all patients that were treated in the published reports. Standard EKG skin electrodes worked quite adequately and special EMG electrodes were not needed.
EMG findings that are typical of SEA are loud and chaotic tracings and are most apparent at the center of the muscle spasm. On approach to that site, progressive increase in activity is noted. Following injections, no residual activity should be found. It is critical that there is no purposeful activity at the time of injection. If a patient tenses up a muscle, it will provide a false signal, as purposeful activity is difficult if not impossible to distinguish from SEA. A typical massage chair is normally used for back and neck injections as they are designed to put the patient in a position of full relaxation. Portable and foldable massage chairs are easily obtained. For injections at other sites it is necessary to find a comfortable position of the patient such that the limb, for example, is at complete rest. Injections to the scaline muscles may be easiest by putting the patient in a prone position.
EMG findings aside from SEA can also be of use. Increased insertional activity of various forms is not uncommonly seen in muscle that has some degree of abnormality but not in full chronic spasm. These sporadic runs are usually quite brief and cannot normally be seen but once. In some cases where increased insertional activity was seen, just the act of dry needling, i.e. in the process of looking for SEA, led to clinical benefit in cases without SEA. Classically, injection with the phenoxybenzamine cocktail was only performed when typical SEA was found, however several cases with typical clinical pictures of chronic muscle spasm revealed only increased insertional activity. Excellent short and long term results with resolution of the clinical chronic muscle spasm were achieved. This variation in muscle electrical activity as it is related to the perseverance of chronic muscle spasm lies outside of the currently proposed hypothesis and warrants further research to expand or modify current thinking. While there has been only very limited experience in such instances to date, treatment of otherwise clinically classic chronic muscle spasm should be considered. The major limitation here is the inability to verify the suppression of the SEA at those sites. Therefore, limited injectate should be used.
6. Procedural Process
Alcohol cleansing of the skin has been found to be adequate sterilization. This is consistent with standard EMG procedure. As the injection needles are of larger diameter than the diagnostic EMG needles, freezing the skin with ethyl alcohol spray may be used as well. In sites such as the low back, some patient prefer not to have the very cold ethyl alcohol spray and prefer simple quick insertion of the needle.
The use of Lidocaine, which on it own suppresses SEA, serves the purpose of knowing that adequate phenoxybenzamine had been injected into the muscle. Phenoxybenzamine is known not to have full effect for up to one hour. There would be significant pain if phenoxybezamine alone were injected as it has a pH of 3. Fortunately, Lidocaine mitigates against that. However, given the near immediate effect of Lidocaine, it is possible to verify that the treatment has had clinical effect. Typically, the patient would be asked to stand up and move about in the middle of the procedure such that it could be determined if the right location had been treated.
We have found that there is an apparent hierarchy of pain such that as soon as the most significant pain is treated, the next most significant pain is noted. A most notable case was when immediately following injection of one arm, the patient complained of pain in the other arm. In one case following successful treatment of a piriformis syndrome the patient complained of another hip rotator that was then successfully injected. Yet another hip rotator was then noted to be painful and fortunately following injection of that third muscle the patient, who was a dance instructor, could then do all of her gymnastic moves without discomfort. Long term relief was obtained at all three sites.
Several cases of writer’s cramp were treated successfully. Careful examination of the forearm will help identify the likely muscle or muscles that are resulting in the overuse injury known as writer’s cramp. A single muscle is commonly the source although multiple muscles may be involved. Examination of the muscles on the dorsum plantar aspect of the muscle by compression will typically identify a tender muscle that is non-compressible. Injection technique here is no different from other sites but usually requires a relatively small volume of medication to be injected. In one case, transient lack of the hand contraction ability occurred but resolved as the Lidocaine wore off. Presumably, diffusion of Lidocaine to a peripheral nerve was the culprit. The writer’s cram was successfully resolved in that case. No recurrence was reported in any of those cases treated. It was important to identify the cause of the overuse injury to prevent its recurrence. Hand injections are not needed for treatment of writer’cramp as the responsible muscles are in the forearm. Only muscles of thumb compressive activity would be likely candidates for injection. However, it should be kept in mind that the hand is essentially a closed space and swelling can lead to the typical closed space complication. Aggressive treatment to limit swelling may be needed in this situation.
Tennis elbow is a common presentation of chronic muscle spasm leading to a tendonitis with symptoms at the elbow. Muscles above or below the elbow may be causative depending upon the acute or chronic overuse injury that was responsible. Tennis players do, in fact, get tennis elbow. Early symptoms may respond to classic treatment with massage and stretching, however, stretching of muscles that insert into the elbow is a bit difficult. Since the pain syndrome is actually a tendonitis, it generally takes about 3 days following the injection for the tendonitis to significantly improve. The patient may well be left with discomfort at a site away from the elbow for 3-5 days but with progressive relief of the elbow symptoms. For athletes, especially active or professional tennis players, it will be important to slowly return to full activity and it can take a month or more for the muscle to recover and be able to sustain repeated high impact use. Tennis elbow symptoms, indicating tendonitis from prolonged tension on the tendon, suggest that the muscle has already been in chronic spasm for a long time. Consequently, early treatment with CMECD® should be considered if local therapy does not readily resolve the symptoms.
Variations in frozen shoulder are excellent candidates for the CMECD® procedure. The deltoid muscle is the most common player and typically one or more bands of the deltoid can be palpated and found to be tender and non-compressible. Injection of the most tender and largest band should be injected first. The patient should then be asked to perform as much range of motion as possible and then point to the spot that then is most uncomfortable. Aside from the eventual relief of sustained spasm by the effects of phenoxybenzamine, the multiple effects of Lidocaine with pain relief and blocking of SEA will allow the patient to find the next most significant site to be injected. Further rehabilitation in these cases needs to be carefully considered. Not uncommonly the prescribed physical therapy exercises only lead to maintaining the chronic spasm. Only range of motion activities should be encouraged. The most useful is using the opposite hand to hold the hand of the affected limb and gradually over time raise the affected arm until the upper arm is able to touch the ear on the affected side. As this post procedure activity progresses, it may be found that there are additional sites of chronic spasm that are limiting movement and that may be in need of injection. The coricobrachialis muscle is one such muscle. In one case of an orchestra conductor, the supraspinatus was the only involved muscle limiting shoulder movement. In severe cases where there is such compression of the joint that the joint lubrication is essentially absent, it will take time with daily range of motion activity for the joint space to be able to recover and the natural joint lubrication to return. Such cases are readily recognized when attempt to raise the arm by the practitioner result in the sensation of crepitus in the joint. No active exercises that are painful have been found to be beneficial over the long run. Maintaining range of motion activity and return to normal function is what has been found to be most useful following CMECD® treatment.
Head & Neck
Injection of strap muscles of the posterior neck is not likely to hit a vascular structure. These muscles, even as they extent to insertion onto the skull, have been implicated in posterior migraine headaches. Significant experience has been gained with long lasting relief of posterior migraines when all SEA has been eliminated from these muscles. The temporalis muscle was injected in one patient for relief of anterior migraine headaches. Marked SEA was found and the treatment was effective. However, the irritant effect of the medication led to swelling of the temporal area and was unacceptable to the patient. In summary, SEA seems to be present and likely causative in anterior migraine headaches but use of phenoxybenzamine would not be a first choice for treatment. It does however raise the question of whether EMG with a search for SEA should be used with Botox treatment of only the temporalis muscle rather than the 31-injection sequence now being used. Since Botox is used to treat muscle contraction and for chronic muscle spasm, it is unknown why no research has been done to identify sites of chronic muscle spasm by EMG to inform the injection procedure. Furthermore, if a patient has neither the adequate insurance coverage or funds to undertake Botox injection for chronic migraines but is willing to accept temporary temporal swelling, this may be an alternative treatment.
Scaline muscle injection for the treatment of cervical brachial syndrome requires a bit of creativity regarding the angle of approach and placement of the patient. While injection the scaline muscles in a patient place in a massage chair is possible, it is nonetheless awkward. In any case the patient must not have any voluntary neck muscle activity. Treatment of a small section of one of the scaline muscles may bring temporary relief, but experience has shown that the length of the muscle of at least one of the mid or posterior scaline muscles needs to be treated for long term relief.
Using post surgical issues as an example of the potential duration of chronic muscle spasm, one particular case is relevant. Following cervical surgery, this patient could turn her head to the right but not to the left for years following surgery. This became particularly problematic upon the death of her husband who accompanied her when she was driving, as he looked left for her when needed. Following, a single injection but with fuller effect after a second injection she was finally able to look left. What is most impressive is that this had gone on for 37 years. No recurrence or need for further treatment was necessary. A large number of patients successfully treated had suffered the effects of chronic muscle spasm for 5 years or more.
When injecting the trapezius it is important to realize that the dome of the lung can be penetrated leading to a pneumothorax. Injections for most of the back above the lumbar vertebrae need to be done with a very low angle from the skin surface. As SEA is found, one can proceed deeper so long as there continues to be classic SEA. Don’t be fooled by the respiratory electrical signal, which is phasic, so long as the patient is not holding their breath. Above the trapezius, when injecting the posterior muscles of the neck, a direct angle perpendicular to the skin can be used. It is possible, but fortunately highly unlikely, to hit the carotid or vertebral arteries if the practitioner is especially unlucky. Any evidence of swelling, whether or not blood is aspirated or enters the syringe, should be an assumed hit to an artery. Direct pressure over the puncture site held continuously for 10 minutes should normally be enough to seal the puncture. The degree of pressure to be exerted need not and should not be excessive. A good measure is that it should be considered firm but not painful to the patient. Pressure applied to the neck can always cause a vagal reaction so placing the patient in a recumbent position is always a good idea in such situations. Any question of control should require the patient to be transported to a local ER with pressure continuing to be applied. Obviously, that is when the procedure is to end for the day.
As is known from EMG literature, the serratus anterior muscle is the site with the greatest risk of entering the pulmonary space. As with any muscle injection, palpation of the muscle to best identify its exact location prior to needle entry is the best protection. Superficial muscles that are not tender to compression are not likely to be harboring evidence of chronic spasm. The higher the risk of lung penetration the more certain there should be a high likelihood of chronic spasm before attempted treatment of that muscle. A flat approach here is definitely warranted.
The muscles of the back below the trapezius and above the lumbar vertebrae each require a well thought out approach. Looking at the cross section of a typical CT scan of the chest will inform the practitioner where the greatest caution needs be taken. Again, respiratory phasic signals must not be confused with SEA and should warn of closer approximation to the lung parenchyma. Injection of the central posterior thoracic muscles requires patience and caution but has been found to successfully relieve chronic pain when secondary to chronic muscle spasm typically as a result of overuse injury. Small scapular muscles such as the rhomboids are often very painful despite their small size. A flat injection technique should be use.
A very common source of chronic back pain is from the levator scapulae. Pain is felt at the insertion into top of the scapulae. However, that is not where the muscle should be injected, different from other subscapular muscle spasms. The site of pain is actually a tendonitis from chronic pulling of the levator scapulae muscle. Insertion of the diagnostic EMG needle should be started in the mid portion of that long muscle and follow and eradicate the SEA throughout the length of the muscle body. Since this is an example of a tendonitis, it then usually takes about 3 days following the treatment for the burning pain at the insertion site onto the scapulae to resolve.
When injecting the low back it may be found that the trail of SEA extends in directions not anticipated. If not all the SEA can be reached with a single skin insertion of a 3” needle, then a second or third skin insertion may be needed. If not the full area on one side has been treated, the patient will still be aware of discomfort on that side and may report a poor outcome. Not uncommonly one side had much stronger SEA than the other side and even with bilateral pain, not both sides will exhibit SEA. As one patient put it, “It starts on this side and then goes to the other side” Only one side of this patient had SEA. Crossover nerve fibers can also confound the injection procedure as contralateral sensation can occasionally be noted.
Low back muscles overlying the sacrum can often be the source of chronic low back pain. Most are superficial and can be readily injected. At times very significant SEA was found more deeply in that region. It turned out that needle penetration through the sacral ostea and found it way into the what was most likely the lower portion of the iliopsoas muscle. Treatment of that SEA did lead to symptomatic relief. It is unknown if any of that treatment had any effect on the sacro-iliac joint or sacroilitis. No attempt to explore the sacro-iliac joint was undertaken.
When injecting the deep muscles of the back at the lumbar level, there may be concern that the peritoneum may be entered. Fortunately, even if this did occur, it would most likely cause no significant harm. When a practitioner has significant experience with the procedure, they will be able to know if it is appropriate to insert the needle deeper when SEA has not yet been found at a more superficial level. SEA at a distance has a characteristic sound that will alert the practitioner that there is SEA at some distance from the needle tip. A multidirectional search with the needle at that level of insertion should then be made before making a much deeper insertion.
Flank muscles of the back such as the latissimus dorsi require a flat injection approach. Review of a CT scan of the mid and lower back in a cross sectional view will inform the practitioner as to how much caution is required when injecting these muscles. There is a higher chance of peritoneal puncture but as noted above the risk is small.
Symptomatic failure following surgical procedures such as laminectomy is unfortunately common. Post laminectomy syndrome has been reported in 20-40% of patients. The use of phenoxybenzamine in post laminectomy syndrome differs from its use elsewhere when there has been muscle disruption of frank cutting of the muscles during the procedure. The action of phenoxybenzamine is to form a covalent bond on the muscle neurotransmiter receptor. The effect is permanent for that receptor and the muscle must over time grow new receptor for the effect of the injection to wear off. This is why the effect of phenoxybenzamine is for 2-3 months. However, in the case of muscle disruption, the muscle in a state of regeneration is forming new receptors at a much faster rate. Hence the duration of the effect of phenoxybenzamine is typically only 2-3 weeks in that situation. This aside, the CMECD® procedure is extremely useful in relieving pain and radiculopathy when caused by muscle spasm. Treatments may need to be done several times over the 2-3 month post surgical period for relief and eventual full resolution of the post laminectomy syndrome. The author was one such patient and fortunately had the availability of this procedure.
Piriformis syndrome is the result of chronic spasm of the piriformis muscle pressing on the sciatic nerve. In approximately 5% of cases the sciatic nerve actually passes through the piriformis muscle. It is not known what percentage of piriformis syndrome cases are associated with this structural variant. Treatment of piriformis syndrome the CMECD® procedure is essentially no different from treatment of any other chronic muscle spasm. However, here the muscle is not in view and not palpable. Tenderness over the sciatic notch is suggestive but the muscle location cannot be found by palpation. Interrogation of the muscle should begin at the sciatic notch. Typically needle insertion should begin 2-3”lateral to the top of the gluteal cleft. A 3” needle is minimal and in large patients a 5” EMG injection needle may be needed. Generally, the 3” needle can be inserted and with indentation of the buttocks, the piriformis muscle can be reached. The full length of the muscle should be examined for SEA and injected until the SEA is fully resolved. Track the muscle laterally toward the hip and all the way medially to the sacrum where it inserts. It is clearly possible to touch the sciatic nerve and cause sharp pain. Fortunately, it is a natural reaction of the practitioner to instinctively pull back the needle on such occasions and no damage to the sciatic nerve has been recorded in this procedure. Ultrasound guidance is possible for general guidance, was not used by this author, has recently been found to identify likely cases of piriformis syndrome but has no value in identifying SEA and its resolution after injection. Injection under X-ray guidance falls short in identifying the true depth at which the muscle lies and not useful to identify chronic spasm. As always with the CMECD® procedure, multiple small injections of one half ml or less at every site of SEA until full resolution of SEA is required.
IT band syndrome (Illio Tibial Band Syndrome) is a rather peculiar case of action at a distance. Pain is felt at the lateral aspect of the knee and sometimes by the hip. The causative muscle is the tensa fascia lata. It is found on the high anterior aspect of the thigh. Here a lateral approach a few inches below the groin crease seems to work best. It is not a large muscle but in classic cased of IT band syndrome, exhibits very significant SEA that when abolished resolves the IT band syndrome and its accompanying symptoms. In one case of bilateral IT band syndrome, x-rays of the knees demonstrated outward tilting of both knee caps. Following treatment, both knee caps returned to their normal position and the accompanying knee pain resolved.
Injection of the lower leg is more complex than most other sites. For one thing, the presence of at least one muscle in chronic spasm in the calf is found in a high percentage of adults with no clear complaints. Multiple different pain symptoms of the feet are caused by various calf and anterior/lateral lower leg muscles. A very useful reference manual, especially for the lower leg is The Trigger Point Therapy Wookbood by Clair and Amber Davis, now in third edition. This inexpensive book is extremely useful for identifying muscles responsible for various sites of pain. The complexities of the lower leg make it all the more useful here. Diagrams showing the pain distribution in the lower leg and foot can be shown to the patient to match up with their particular symptoms. When a match is made then go looking for the presumptive muscle at cause and look for SEA in that muscle.
Another reason for stopping mid procedure is to assess any hypotension caused either by a vasovagal effect or direct effect of the phenoxybenzaine. Note that while the effect on the muscle at the receptor level may take up to one hour, it may occur that the spread of the medication via the blood stream may affect blood pressure more rapidly. Yet another reason to pause mid procedure, aside from the potential hypotensive effect, is to assure that there is enough medication left for treatment of any residual sites. Clearly, only a limited number of sites can be successfully treated with one 10 ml vial which upon dilution with Lidocaine give 20ml. Therefore, it is important to get the most significant relief of pain with what medication may still remain. Six and a half 3-ml syringes can be filled for use before starting to inject the patient.
Several cases of drop foot were successfully treated with the CMECD® procedure. In one case where the duration of the symptom was only a few months, the drop foot resolved at the time of injection and has not recurred. Another case that had gone on for 5 years required a few injections and resolved at 6 months with recovery of the knee jerk reflex. This highlights the action of chronic muscle spasm on nerve compression symptoms. Gradual recovery of long standing lack of sensation of portions of the legs was also seen in other cases.
In the thigh, the sartorius and gracillis muscles can be responsible for medial knee pain. Both can be successfully injected but require generally injection at multiple sites along the length of the muscles and invariably lead to large areas of ecchymosis. Knee pain just below the knee cap from the patellar tendon is usually the result of spasm on anterior thigh muscles. Local therapy with a rolling pin may be adequate for relief with adjustment of the activity causative for the overuse injury. However, lacking success of that therapy, injection can be undertaken with improvement of symptoms. Recurrent painful night cramps involving the gracillis were treated in one patient. It was found that the gracillis exhibited SEA at rest and this likely had predisposed the night cramps to occur. Partial injection of the gracillis markedly decreased the occurrence of the night spasms. Potentially, a fuller treatment of the gracillis would have prevented their recurrence completely.
Another muscle in the thigh that underwent successful treatment was the vastus lateralis. In this case post hip replacement, there was concern that the prosthesis had become loose based upon great pain on walking. Examination revealed spasm of the vastus lateralis and an initial injection attempt failed to find significant SEA to treat. However, further research revealed that the likely site of SEA was two thirds down the muscle and close to the bone. Fortunately, the second attempt found marked SEA at that site and following injection the patient carried his crutches over his shoulder as he walked out of the office without pain. No further treatment was required. This case was a good example of post surgical muscle spasm seen also as noted previously in Post Laminectomy Syndrome and the case of cervical spasm for 37 years following cervical surgery. There are likely multiple other sites of post surgical spasm that did not present for treatment over the 10 year period that the CMECD® procedure was being developed and treatment applied. Save it to say that chronic pain in the post surgical period should consider the possible presence of chronic post surgical spasm.
No cases of plantar fasciitis were treated with CMECD®. Based upon the likely cause of chronic spasm of plantar foot muscles, this would be a potentially useful therapy. The marked sensation of the plantar aspect of the foot, thick skin and the potential for several days following the procedure what would impede walking as a result of local tenderness were consideration in not attempting treatment in this location. However, if severe symptoms are not relieved by other therapies, CMECD® treatment should be a consideration.
This author has used sterile technique for all injections. However, neither sterile or non-sterile gloves were utilized. This rightly has been challenged. However, with gloves on there is no immediate opportunity to sense skin dampness that would precede vasovagal syncope. Use of one glove rather than two is an option or having another staff person monitor the patient’s skin is yet another. However, when performing the procedure with only a single practitioner in the room, sterile technique performed without gloves has warded off unwanted syncope and no instances of infection have occurred.
7. Post Procedure
The patient should be made to stand and walk about for few minutes before letting them out the door. Generally, it is recommended for a friend or family member to drive the patient home. Experience to date has always been with the family member and/or friend in the room during the procedure. This has led to better understanding by the patient of what had taken place as the friend or family member will normally explain afterwards what was seen and was done. Also the obvious nature of hearing the SEA and its resolution leads to a better understanding of the nature and outcome of the procedure.
8. Recording Outcomes
Keep in mind that the sequence of pain relief is different from other treatments. Relief of the muscle spasm pain or muscle spasm compression of a nerve will be noted during the procedure. In some cases the Lidocaine alone is giving relief. Should that be the case, then the original discomfort will return as the effects of the Lidocaine wear off in 30minutes to 2 hours. A curious fact is that true red heads metabolize Lidocaine about twice a fast as non red heads. Furthermore, the effects of phenoxybenzamine have been shown to take up to an hour to have full effect. One patient who was a red head had the Lidocaine wear off before the phenoxybenzamine took hold.
Next to keep in mind is that the injection itself will cause tissue irritation that takes on average 3 to 5 days to resolve. Not much has been seen over one week but some patients are more sensitive than others. Some have no injection complaints at all. In other words expect some discomfort especially after day 2 as the dexamethasone will have word off by then. For patients that can tolerate it, the use of Aleve twice daily for the first week post injection is what is usually recommended.
Given all the above, an estimation of pre and immediately post injection pain should be recorded. The patient should be told that whatever relief is noted 2 hours after the injection is the effect of the phenoxybenzamine. It would be useful to have a chart for patients to fill out as they leave the office and record their pre, post and 2 hour post pain scale symptoms. Day 4 and day 7 symptoms would also be useful to record. Follow up patients visits at 2 weeks post injection are recommended to verify or to assess the degree of success or failure of the procedure.
Paramount in recording pain relief is clear documentation of the exact site of the original pain as well as the site of discomfort from the injection which in some cases may be at a distance from the site of the original pain. The patient optimally should be given a figure of the appropriate part of the body and be able to mark the site of each. The principle previously stated of hierarchy of pain may cause pain to be felt at a different or “not so far from the treated site” when there is relief of the original pain.
The appropriate type of pain scale used will obviously vary depending upon the site of pain. In some cases a simple 0-10 scale will suffice. In other cases the use of functional scales such as what could you do before and what can you do now. Multiple such scales are available online.
A follow up visit, survey or at least a phone call from your office at 3 months post procedure would be quite useful as that time frame is suggestive of true resolution of the symptom complex when successful.
Unfortunately not all record keeping as suggested above was being done as the procedure was being developed. However, early and retrospective long term data was obtained and has since been published.
The CMECD.info Website contains information as how to bill as far as ICD codes and CPT codes. Patient visit and evaluation codes should be added to the procedural codes as both are usually done at the time of the procedure. The appropriate ICD codes deal with the presence of chronic pain, its location and if it was post surgical pain. The CPT codes deal with how many sites and the location of the sites that were injected. Experience with insurance companies and Medicare has been variable. It may require submission of treatment success to the medial director to have the procedure approved for payment. In one such case a patient wrote directly to a major insurance company medial director stating all the previously failed treatments that that insurance company had paid for and citing his final relief of symptoms. That did the trick. In nearly all cases Medicare and Medicaid in Delaware paid for the procedure. The medication was not reliably paid and the patient had been told that if it were not covered, they would be charged $50. An ABN was signed when necessary for the medication. This was never a problem given the small cost. The cost of injection needles, syringes and electrode tabs are considered to be included in the payment of the overall procedure. Trying to bill for the phenoxybenzamine is not recommended at this point. It tends to confuse the payor and hold up payment for the procedure. It was my experience that patients would rather pay the $50 and you get paid promptly than find themselves with some automatic balance billing.
As one of the early users of the CMECD® procedure, there will be instances where the insurance companies will need to be convinced of the value by citing the outcome of the procedure. As of the date of this writing, 9 abstracts have been published in Muscle & Nerve and presented at the national yearly meeting of the American Association of Neuromuscular and Electrodiagnostic Medicine and 3 more have recently been accepted for publication and presentation. The Website CMECD®.info is available for any medical director to examine and learn of the benefit to patients that has been documented. Emerging medical procedures do require a certain amount of perseverance in being accepted by a wide medical audience. The AANEM was chosen as the most technically critical organization that dealt with EMG interpretation. It was chosen as a site for publication for that reason. Their acceptance of the 12 abstracts that together describe both the scientific basis and clinical successes with this procedure should be enough to convince insurance companies that this is not a hoax to charge for a procedure. In fact the cost benefit far outweighs virtually any other procedure that deals with chronic muscle spasm and the resultant chronic pain.
10. Relationship to Opioid Crisis
Currently, there are only a handful of physicians that are trained to do this procedure. It is clearly not the optimal procedure for all conditions and other treatments may ultimately be found to be equal or superior. However, for the present, treatment of chronic pain resulting from chronic muscle spasm by the CMECD® procedure appears to be the most effective, least costly and has the least chance of setting a patient on a course of chronic opioid use. For that reason, an alternative URL for the CMECD®.info Website is OpioidNO.com to highlight that advantage.
11. Management of Pain Medications Post Procedure
Experience to date has been with making no change in a patient’s pain medication regimen. Unless the practitioner doing the procedure is a pain management physician with a contract regarding the use of opioid medications, they should not be the ones to withdraw pain mediations from the patient if and when the CMECD® procedure results in abolition or marked reduction in the patient’s pain symptoms. Many patients reported a marked reduction or cessation in the use of pain medications following the procedure. So long as the pain medications were of relatively minor status, the patient was stated to carefully and gradually withdraw the medication. Abrupt cessation of pain medication by a patient in one instance did lead to a state of withdrawal that had to be treated with resumption of the medication and gradual withdrawal.
12. Recurrence of Symptoms
The typical cause of chronic muscle spasm was overuse injury or an acute stress on the muscle as may have occurred in a car accident or a fall. When the symptoms have not recurred for a 3 month period following the procedure, it is assumed that there is a full recovery from the presenting muscle injury. A small number of patients have been treated for recurrence after 3 months following the procedure. In virtually all cases the recurrence could be traced to a repetition of the overuse injury or injury.
Preventing recurrence requires that aside from correctly diagnosing and treating the presenting condition, the physician needs to also seek information as to what was responsible for the condition in the first place. Hopefully, recurrent car accidents will not occur. However, overuse injuries do recur. Often simple issues as having the patient change the position of a keyboard or computer monitor will prevent recurrence. Unfortunately, athletic trainers and even physical therapists are often at fault pushing the individual to do what the muscle is not ready to sustain.
13, Recommendations for Physical Activity Following CMECD® treatment
Especially following symptomatic relief of symptoms, the amount of exercise that affects the treated muscle must be modified. Understanding that the chronically spastic muscle has impaired blood supply and is injured, return to full potential activity should be strongly cautioned against. Research has shown that muscle in chronic spasm has reduced mitochondria presumably secondary to chronic ischemia. Return of mitochondria and normalization of other microstructural changes not yet described takes time. Based upon clinical observation, this may take one to three months and potentially longer in severe cases. As a general rule of thumb, the patient should be advised not to exercise past a point of muscle soreness and if that occurs to use simple measures such as massage and heat to relax the muscle. With overuse of a recently treated muscle, it is entirely possible to put the muscle back into a state of spasm. Inability to provide adequate energy with depleted mitochondria is a setup for recurrent spasm. Remember that the muscle requires energy to relax, not to contract.
The CMECD® procedure has the possibility to resolve chronic pain and chronic muscle spasm in arguably half of all patients who suffer from chronic pain. Other treatments may be found to be less invasive, less expensive and not require direct physician intervention. However, as of the date that this was written, there is an opioid crisis, and the number of patients with unsuccessful surgical procedures for relief of pain has been reported as 20-40%. The CMECD® procedure requires access to an EMG device that can likely be obtained for about $2,000 for a hand held device. The medication is available and inexpensive. The technique while not optimized, has stood the test of time in the current configuration. Variations on concentration of drug or the use of an equally effective drug with fewer side effects may be possible. Physician training has hopefully been accelerated by the CMECD.info Web site and this essay is designed to fill in the gaps in the information provided there.
When a patient has not gotten successful relief of chronic pain by multiple other modalities, a physician has a responsibility to consider emerging treatments. The lack of serious negative side effects from this procedure make it a good candidate for a final attempt to provide relief. Arguably, it does take time to be fully confident with treatment of chronic spasm in the wide variety of muscle sites that have been shown to cause chronic pain and have been successfully treated. Starting with the most common site, chronic low back pain, should be the initial site chosen. Understandably, chronic low back pain is a complex situation and not all treatments will be successful. However, the occurrence of SEA is nearly always identified and at least some improvement is symptoms is likewise nearly always achieved.
Most importantly, the satisfaction gained by relieving a patient from their chronic pain stacks up with saving a life. The author spent a lifetime career in interventional cardiology taking on high risk patients but also had the satisfaction of treating patients with chronic pain. As there is great satisfaction in extending a patient’s life, there is also great satisfaction in providing a life without chronic pain.
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