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 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. 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 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
LIMITATIONS OF EMG AND NERVE CONDUCTION STUDIES IN CLINICAL PRACTICE-2018-top (pdf)Download
LIMITATIONS OF EMG AND NERVE CONDUCTION STUDIES IN CLINICAL PRACTICE - 2018 -bottom (pdf)Download
EMG GUIDED CHEMODENERVATION PROCEDURE of ACQUIRED CHRONIC MUSCLE SPASM DESIGNATED as CMECD® - 2018 -Top (pdf)Download
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PROPOSED NEW DIAGNOSTIC ENTITY OF ACQUIRED CHRONIC MUSCLE SPASM -2018- TOP (pdf)Download
PROPOSED NEW DIAGNOSTIC ENTITY OF ACQUIRED CHRONIC MUSCLE SPASM - 2018 - BOTTOM (pdf)Download
DEBUNKING THE MYTH 2017- - TOP (pdf)Download
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LONGSTANDING CHRONIC PAIN - 2017 - TOP (pdf)Download
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SAFETY OF PHENOXYBENZAMINE - 2017- TOP (pdf)Download
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