Treating neuropathic pain

3 Treating neuropathic pain


Although resistant to most medical treatment approaches neuropathic pain responds exceptionally well to frequency-specific microcurrent. The challenge for the practitioner is to recognize that the pain is neuropathic based on history, mechanism of injury, examination findings and response to previous therapies.


Neuropathic pain is typically difficult to treat medically and does not reduce significantly in response to narcotic or opiate medications. This characteristic can be useful in diagnosing pain as neuropathic and distinguishing neuropathic pain from other potential pain generators in the same area. Patients are usually asked to report pain on a 0 to 10 visual analog scale. Nerve pain tends to be moderate to severely painful and is commonly rated between a 5 and 9/10. If the pain is still reported as a 5–7/10 while the patient is being treated with narcotics the pain almost certainly has a strong neuropathic component.


Epidural injections at the nerve root with one of the “caine” class of anesthetics plus an anti-inflammatory steroid can reduce neuropathic pain. These injections, while done routinely, are invasive and expensive, require very specialized training and equipment, have significant risks and are not universally effective or permanent. But if an epidural injection has reduced the patient’s pain, even temporarily, then it is almost certainly neuropathic pain.


Unlike acute pain from trauma which is mediated by the firing of primary afferent nociceptors, chronic neuropathic pain is mediated by inflammation in the nerves through the action of the inflammatory cytokines IL-1, IL-6, TNF-α, and substance P (Meyers 2006, Zieglgansberger 2005, Tal 1999).


FSM has been shown to reduce inflammatory cytokines while treating the pain of fibromyalgia associated with cervical spine trauma which is thought to be neuropathic. One specific frequency combination has been shown to reduce IL-1 (330 to 80pg/ml, p = 0.004), Il-6 (239 to 76pg/ml, p = 0.0008), TNF-α (305 to 78,p=0.002), and substance P (180 to 54pg/ml p = 0.0001) and to increase endorphins (8.2 to 71.1pg/ml, p = 0.003) Pain scores were reduced from an average of 7.3±1.2 to 1.3±1.1 in 45 of 54 patients (p = 0.0001) (McMakin 2005). The treatment that reduced the pain also reduced cytokines.


Studies have shown an association between induction of Cox-2 increased prostaglandin release and enhanced nociception in neuropathic pain. Expression of Cox-1 and Cox-2 in primary afferents and in the spinal cord suggests that NSAIDs act there by inhibiting synthesis of prostaglandins (Zieglgansberger 2005, Tal 1999, Bennett 2000).


A controlled trial using a mouse model for lipoxygenase (LOX) mediated inflammation demonstrated 62% reduction in ear swelling in mice treated with frequency-specific microcurrent (FSM) using 40Hz and 116Hz when compared with the controls. COX mediated inflammation was reduced in the same mouse model by 30% which was equivalent to the prescription anti-inflammatory injectable Toridol when it was tested using the same mouse model. FSM experimentation demonstrated the result to be reproducible, application time dependent, and specific as other FSM frequencies had no effect on the model (Reilly 2004).


An unpublished retrospective study of 20 neuropathic pain patients with a mean chronicity of 6.7 years showed reductions in pain from an average 6.8 ± 1.8 to 1.8 ± 2.1(p < 0.001) during the first treatment. Pain was reduced from 4.8/10 to 0.97/10 during the second treatment (p < 0.001). 13 of the 20 patients had disc injuries as the source of their neuropathic pain, two had nerve traction injuries and the other five patients had dermatomal nerve pain of unknown etiology. 65% (n = 13) of the patients recovered fully in an average of 4.6 treatments. 25% (n = 5) terminated care prior to recovery. One patient required an epidural and one patient uses a HomeCare microcurrent unit for palliative care (Precision Distributing Inc, Vancouver, WA) (McMakin, unpublished work, 2007). The only frequency combination observed to reduce dermatomal neuropathic pain is the frequency to reduce inflammation, found to be effective in the mouse model combined with the frequency for the nerve as a target tissue.


image

Figure 3.1 • Tissue damage stimulates the immune system to produce inflammatory cytokines (IL-1, IL-6, TNF-α) and prostaglandins cyclo-oxygenase (COX) and lipoxygenase (LOX) causing an action potential in a pain nerve.


When the nerve becomes inflamed calcium ions flow into the nerve through voltage gated ion channels (Winquist 2005). The open channels create impulses interpreted as pain, the pain impulses travel up the nerve to the spinal cord and up the spinal cord to the pain processing centers in the brain.


Any inflamed tissue eventually experiences calcium influx and then fibrosis. Inflamed neural tissues are no exception. The concept of mobilizing fibrosed neural tissue and the surrounding fascia or dura has been well explored by Butler (1989a,b, 1991). FSM has well documented success in modifying scar tissue (Huckfeldt 2003) and its use in neural mobilization provides dramatic improvements over manual mobilization techniques both in comfort and in speed of response. The only frequency combinations observed to have an effect on neurofibrosis are those for scar tissue, sclerosis and fibrosis combined with the frequency for the nerve as a target tissue. The frequency to reduce pain does not reduce fibrosis or increase range of motion. If the nerve is traumatized by too vigorous stretching only the frequency to reduce inflammation will reduce the resulting pain.


When treating neuropathic pain with FSM, the practitioner must consider the mechanism of injury to the nerve, the relationships between the nerve and the surrounding or associated tissues, the patient’s general state of health and overall inflammatory status and the possibility of central pain sensitization.


FSM is clinically derived. The frequencies were chosen through 10 years of experience according to the patient’s clinical presentation and response to treatment and not as a result of exploration of the literature describing the pathology of neuropathic pain. It was convenient but not inevitable that the mechanisms of neuropathic pain derived by medical research match the frequencies found to be effective in relieving it.


It is important to remember that the patient is entitled to more than one pain generator and more than one diagnosis. It is not uncommon for a patient to have pain coming from the nerve, from trigger points in the muscles, from inflammation in the spinal facet joints or discs and from inflammation in the peripheral joint such as the shoulder or hip simultaneously and in any combination or proportion. Any and all of these pain generators can cause local pain as well as referred pain in the arms or legs. Being able to make the distinction between overlapping pain generators becomes important when deciding what to treat and assessing prognosis and setting expectations. If the neuropathic component can be treated quickly and easily and removed from diagnostic consideration, it simplifies the challenges of diagnosing and treating all chronic pain.


Frequency-specific microcurrent is low risk, cost effective and widely available – making it an ideal tool for treating neuropathic pain. The preliminary clinical data, cytokine data and collected anecdotal reports suggest that more formal controlled trials should be done to confirm FSM’s benefits in neuropathic pain. Until such studies are completed, considering the low risks associated with its use, FSM can be a valuable adjunct in the treatment of neuropathic pain.



Types of nerve pain


Nerves come out of the spinal cord as nerve roots and describe sensory patterns known as dermatomes; cutaneous nerves are branches of dermatomal nerves and provide sensation to specific areas of the skin. Nerves become pain generators when they are injured. A complete description of all types of neuropathic pain and their mechanisms is beyond the scope of this text and the reader is referred to Neurology in Clinical Practice (Bradley 2000) for a comprehensive treatment of the subject.


This chapter will cover the diagnosis and treatment of dermatomal nerve pain due to spinal disc injuries and traction injuries, two of the compression neuropathies – carpal tunnel syndrome and thoracic outlet – and peripheral neuropathies due to diabetes. Information on more advanced strategies in the treatment of other types of neuropathic pain is available in an FSM seminar setting.


The treatments for different kinds of neuropathic pain are different and the key to successful treatment is an accurate diagnosis. The following sections are intended to help the reader arrive at an accurate clinical diagnosis.



Basic physical examination to evaluate nerve function


A skilled and thoughtful physical examination can reveal almost as much about nerve function as the most sophisticated imaging or electrodiagnostic testing. Sensation for sharp reveals the state of sensory nerve function and spinal cord facilitation. Muscle strength reveals the state of motor nerve function and deep tendon reflexes reveals the relationship between the nerves, the spinal cord, the muscles and the brain. Most practitioners reading this text have been trained to perform a physical examination to evaluate the nervous system. This brief description is meant to be a reminder and a guide to interpretation rather than a comprehensive instruction. The reader who desires more complete instruction is referred to a text on physical examination.



Sensory examination


The sensory nerves and spinal cord pathways for sharp also carry pain information. Gentle stroking of the nerve distribution with a pin or sharp object such as a paper clip or making light contact with a pinwheel as it rolls across the skin is sufficient stimulation to assess sensation for sharp and pain. Test one side and then the other being careful to use the same pressure on both sides. Evaluate the non-painful side first. Check all of the cervical, thoracic and lumbar dermatomes in a similar fashion at both the proximal and distal ends of the nerves. All dermatomes, not just those in the painful area should be tested during the initial evaluation. Any painful area should be tested for cutaneous nerve sensation and sensitization.


The examination can be done in any order that flows well and allows the organized gathering of information. The author starts with the patient seated facing the examiner with hands facing palms up on the thighs and tests the C6 dermatome on the thumb and forearm first and then proceeds to the other cervical dermatomes. Ask the patient to report whether the sensation caused by the sharp object feels “normal – just prickly or sharp”, “dull – it feels like pressure but it doesn’t feel sharp”, or “icky or unpleasant”. The patient may ask what “icky” feels like but most patients react strongly to sensory hyperesthesia, which is the medical term for an “icky” sensation. Most male patients cannot bring themselves to say “icky”, but they will react in some way when the hyperesthetic nerve is stimulated. For these patients the distinction becomes sharp, dull and ouch (!). When nerves become inflamed they first become hypersensitive and then progress to numbness.


Occasionally a patient will describe an area as feeling numb but the sensory testing shows an appropriate appreciation of sharp. The patient is describing “paresthesia” or “feels as if it should be numb but it is not”. Paresthesia often appears in the referred pain area for myofascial trigger points and can be mistaken for a description of neuropathic dysfunction.


If nerve function is impaired, the sensory examination may show either hyperesthesia or reduced sensation to sharp in a dermatomal nerve root, cutaneous nerve or in the glove/stocking pattern characteristic of a peripheral neuropathy. Record the findings on the dermatome chart as shown below. The record is a useful way to document progress as the nerves return to normal function with treatment.


image

Figure 3.2 • This dermatome chart is only one of several versions of dermatomal sensory distribution commonly used. There are individual differences among patients and the sensory diagram is an approximation of nerve distribution in any given patient. Record the findings from the sensory examination on the dermatome diagram noting hyperesthesia, normal findings and reduced or absent sensation.



Reflex testing


Reflexes are tested with a quick strike of a reflex hammer or the examiner’s rigid flexed fingers used to create a brisk tendon stretch of a muscle innervated by the nerve root being interrogated. The tendon stretch stimulates a reflex arc in the spinal cord and causes a brisk immediate muscle contraction in the stimulated muscle.


Deep tendon reflexes are rated from +1 to +4 to describe the strength of reflex muscle contraction created by the tendon stretch. A +4/4 reflex involves clonus or rapid repeating involuntary muscle contractions due to complete loss of central descending inhibition in either the brain or the cord.


A normal reflex is graded as +2/4 and is characterized by a small brief brisk muscle contraction.


A reflex will be hyperactive and graded as +3/4 if the spinal cord is inflamed above the level being tested. A normal +2/4 reflex depends on descending inhibitory impulses from brain reaching the tested segment in time to dampen the reflex. Inflammation in the spinal cord slows the descending inhibitory impulses so they cannot reach the stimulated level in time to dampen the muscle contraction but not so much as to create clonus. The muscle contraction will be stronger than it should be and there may be simultaneous contraction of a muscle on the opposite side innervated by the same nerve root. The patellar reflex will be hyperactive if a disc bulge is inflaming the spinal cord above L3. If the cord is sufficiently inflamed the adductors (innervated by L3) will contract on the side opposite the one being tested.


A reduced reflex has little or no contractile amplitude or force and is graded as +1/4. Reduced reflexes may be a sign of nerve compromise caused by disc injury or some other segmental pathology. Reflexes are also reduced in hypothyroid patients and in all patients as they age. If a patient older than age 65 has a +2/4 (normal) patellar reflex it raises suspicion of some spinal cord inflammation above L3 since the patellar reflex is usually reduced in patients of this age.


An absent deep tendon reflex suggests a serious compromise of nerve function as the reflex arc is interrupted and the stretch response is either not conducted to the spinal cord from the tendon or from the spinal cord to the motor fibers.


Note: If the patient has engaged in some sport such as martial arts, racket ball, or sprinting that trains the quick twitch muscle fibers in the legs the patellar reflex may be reduced or absent without pathology. The quick stretch in the tendon should activate the neural arc and cause the quick twitch muscles to reflexively contract. If the quick twitch fibers have been sufficiently trained, they effectively “beat” the reflex arc and the quadriceps muscles do not contract in response to the tendon stretch. In this case the reflex findings must be evaluated in the context of the clinical presentation, the complete physical examination and history.



Muscle testing


To test motor function the examiner isolates a muscle associated with specific cervical and lumbar nerve roots and asks the patient to apply resistance to pressure. The muscle strength is graded from complete paralysis +0/5 to full strength +5/5. For complete instruction in the techniques and interpretation of manual muscle testing the reader should refer to a physical examination text such as Hoppenfeld’s (1976).


If a weakened muscle is innervated by the same nerve root level that has hypersensitive or missing sensation and hypoactive reflexes it completes the clinical picture indicating significant neural compromise.



Clinical example


This basic clinical neurological examination can give a fairly detailed assessment of the condition of the spine and nerves and when combined with the patterns found in the history and the mechanism of injury eventually create a clear picture when all of the elements are analyzed.


For example if the patient was a 44-year-old right handed non-smoking male who exercises regularly and works as a computer programmer, complains of severe right shoulder and midscapular pain rated as 7/10 of two weeks duration that started after he used a pick to dig a trench in hard soil in the back yard, how would the source of his pain be discovered? Is it simply an injury to the shoulder or are the nerves, discs and neck involved?



History and mechanism of injury


The history gives basic parameters and a proposed mechanism of injury. The pain complaints are in the right shoulder in a right handed man and there is pain between the scapulae. Consider the mechanism of injury. The mechanism of injury comes from the ballistic forces of the pick striking the soil while the patient has the neck flexed looking down at the target. The ballistic forces from the impact translate into compressive forces on the disc when the cervical muscles contract forcefully to stabilize the spine. The shoulder muscles and joint structures are also challenged by the impacts. Neck flexion and rotation while the arms are raising the pick for the next impact create additional stress on the disc annulus. Eventually it becomes a “strength of materials” problem when the forces exerted simply overwhelm the structural integrity of the traumatized tissues.


The hypothesis is formed during the history and by observation of the pain diagram: the disc annulus fails, develops small fissures and the inflammatory chemicals in the disc nucleus become exposed to the nerve and the cord. The shoulder joint may also be compromised by the same forces.



Physical examination


The basic physical examination will disclose the condition of the nerves and joints and either confirm or contradict the hypothesis.


In our computer programmer, sensation in the right and left C4 dermatome, and the right C5 and C6 dermatomes were hyperesthetic. All other dermatomes had normal sensation for sharp.


The patellar reflex was hyperactive bilaterally and striking the right patellar tendon caused the left adductors to contract, indicating spinal cord inflammation above L3. The biceps (C5) and brachioradialis (C5–6) reflexes on the right were slightly reduced, and the triceps reflex on the right was slightly more brisk than the triceps on the left. All other deep tendon reflexes were +2/4 or brisk and considered “normal”.


Muscle testing revealed slight weakness in the right biceps and forearm flexors; all other muscles were full strength and rated +5/5.


Palpation of the muscles in the cervical spine and shoulder revealed trigger points and tenderness in most of the shoulder muscles and in the muscles of the anterior cervical spine especially at the C5–6 level.


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Figure 3.3 • The cervical disc annulus refers pain in between the shoulder blades stepwise down the spine according to the levels injured. The presence of mid-scapular pain helps diagnose the presence of an injured disc as the cause of neuropathic pain. It should be kept in mind that there are nine muscles, seven thoraco-costal joints and seven cervical facet joints that also refer to the midscapular area


(adapted with permission from Cloward 1959).



Interpretation and diagnosis


The physical examination suggests that he had a small contained right, paracentral disc herniation at C5–6 brushing the thecal sac at the spinal cord that was not large enough to compress the nerve root since nerve functions were altered but not eliminated.


The central portion of the disc inflamed the cord enough to create hyperactive patellar reflexes bilaterally, crossed adductor contraction and the hyperactive right triceps reflex. The reflex can be hyperactive at any level below the inflammation. The disc was close enough to the nerve and the cord at C5 and C6 on the right to reduce the right C5 and C5–6 reflex arcs and create slight muscle weakness in the biceps. The sensory nerves at C4, C5 and C6 were inflamed by the disc material and became hypersensitive. Muscle palpation revealed myofascial trigger points in the anterior scalenes over the C5 and C6 disc levels and trigger points in most of the shoulder muscles, which are innervated by the C5 and C6 nerve roots.


The history and reported pain pattern suggested a disc injury at C5–6. The ballistic compression damaged the disc annulus which inflamed the nerves and the cord. The midscapular pain is consistent with referred pain from the disc annulus (Cloward 1959).


The MRI confirmed the findings suggested by the history and physical examination. FSM treatment and a home exercise program resolved the pain and normalized the neurological examination in 8 treatments over four weeks.



Dermatomal nerve pain due to disc injuries


Spinal nerve roots most commonly become painful because of exposure to the inflammatory chemicals released by the spinal discs. The central part of the disc, or nucleus pulposus, is rich in a highly inflammatory substance called phospholipase-A2 (PLA2). PLA2 has the ability to turn ordinary membranes into the cellular equivalent of battery acid, damages the nerve and eventually impairs its ability to conduct impulses (Ozaktay 1995, 1998). If the disc ruptures and releases a piece of nucleus material it is said to herniate. If the disc nucleus is injured but remains contained within the disc annulus it is said to be a contained herniation. If the herniated disc material forms a fragment and compresses the nerve it can create serious damage to the nerve including complete loss of sensory and motor function and compromise of deep tendon reflexes which may become permanent if not treated appropriately. A surgical consult is prudent if reflexes or muscle strength is lost even if the patient is to be treated with FSM.


It is possible for the disc to be minimally damaged with a small tear in the annulus that allows the PLA2 in the nucleus to leak out and create chemical inflammation in the nerve (Olmarker 1993, 1995). This has been called “chemical neuritis” (Marshall 1977). Inflammation in the posterior joints of the spine called facet joints can diffuse out to the nerve roots and create neuropathic pain and osteophytes from the facet joints can both inflame and mechanically compress dermatomal nerves. Any condition or pathology that creates an inflammatory response in the vicinity of the nerve can contribute to or cause neuropathic inflammation and pain.



Diagnosing neuropathic pain from disc injuries


The history will include a mechanism that would explain a disc injury usually involving flexion, flexion combined with rotation, a whiplash movement from an auto accident or a fall with ballistic compressive impact to the spine. Lifting or postural strain involving repetitive flexion of the neck or trunk, especially when flexion is combined with rotation, can injure a disc. Prolonged static position that places the weight loaded spine in combined flexion and rotation, such as falling asleep for four hours with the head on chest, can weaken the disc annulus through connective tissue creep. A disc does not have to be herniated to cause neuropathic pain. When there is a temporal association between onset of dermatomal pain symptoms and some trauma or change in activity that involves flexion and rotation, common sense suggests the connection and the need for treating both the nerve and the disc.



Diagnosing dermatomal nerve pain due to nerve traction injuries


Nerves can be injured mechanically by forces that cause traction or pull on the nerve, damaging the nerve membrane, creating inflammation from glial activation, pain, sensory changes and even motor weakness. Look for a mechanism of injury that involves one end of the nerve being held stationary while the other end of the nerve is stretched or pulled away.


Nerve traction injuries are typically created in auto accidents, falls, and contact sports and by positioning or procedures during surgery. The brachial plexus is particularly vulnerable to traction injuries since the C5 through C8 nerves are tethered to the vertebra as they leave the spine by ligaments while the distal ends of these nerves are free to move. Patient position during a surgery in which the nerve is statically stretched for a prolonged period such as a cardiac bypass procedure or a cervical tumor dissection can create nerve traction injuries. Surgery in which the nerve is stretched acutely along with the soft tissue to make room for a knee or hip replacement can also create persistent neuropathic pain. Nerve traction injuries may heal without treatment over time as the nerve lining slowly repairs itself but many nerve traction injuries remain painful for years after the trauma and never become pain free on their own.


The diagnosis of a nerve traction injury is made on the basis of the pain pattern, the history and the neuro-sensory examination. The patient will describe pain that matches one or more dermatomal nerves. The history will include a mechanism of injury that could stretch a nerve. The physical examination will show sensory hyperesthesia or sensory loss in a dermatome that matches the patient’s pain complaint. The reflexes will be +2/4 or brisk and considered normal unless the mechanism of injury included a flexion and rotation component that caused a disc bulge as well as the nerve traction injury. The patient, as always, is entitled to more than one complaint.



Examples of nerve traction injuries


The auto accident patient holding the steering wheel with both hands when the air bag deployed into her chest rapidly stretching the thoracic nerve roots, had nerve traction injuries to the thoracic intercostal nerves. She was diagnosed with “costochondritis” for 20 months following the accident. The sensory examination showed hyperesthesia from T2 to T6 nerve roots and the “costochondritis” resolved permanently in a single 60 minute treatment for neuropathic pain from a nerve traction injury.


The police officer who landed on the ground under the suspect with his trunk left rotated and his right arm stretched around the torso of the DCS (drunken combative suspect) was diagnosed with a “chronic thoracic sprain strain” for three years following the injury. In all that time no one had done a sensory examination. The sensory examination revealed hyperesthesia in the right T4 through T7 dermatomes and the patellar reflex was hyperactive on the right only. The MRI showed a small disc bulge (contained herniation) at T5. The injury resolved in three 60 minute treatments for the nerve and an additional three treatments for the disc.


The patient was the seat-belted driver with her trunk turned to the right at the time of a side impact collision. The car spun to the left creating traction of the left side of her neck and left arm. Fourteen months after the accident she still complained of left shoulder and chest pain, left arm weakness, tingling in her fingers and lower arm. She had been diagnosed with thoracic outlet syndrome. Her sensory examination showed hyperesthesia of the left C5 through T1 nerve roots and completely normal reflexes at all levels. Her pain was reduced from 6/10 to 2/10 with the first 60 minute treatment and she was pain free with full strength and range of motion after six treatments.


Once it becomes possible to resolve nerve traction injuries the clinician is more likely to diagnose and treat them.



Treating nerve traction injuries with FSM


FSM treatment for nerve traction injuries uses the frequencies to reduce inflammation, reduce fibrosis between the fascia and nerve and to improve secretions in the nerve. Nerve traction injuries respond very well to FSM as long as the nerve is not torn because there is no perpetuating factor. The sensory distribution of the injured nerves may be hypersensitive or it may have reduced or absent sensation to sharp as tested with a pin or a pinwheel. If the nerve is not torn the pain and sensory changes should resolve in two to four treatments. Motor weakness may require more treatments and may take longer to resolve than pain and sensory changes.


In one case involving a professional football player who lifted a tackle off of his back using his neck, the pain and sensory changes resolved with treatment for the nerve traction injury created by the forceful lateral flexion of his neck. But the motor weakness in the external rotators would not resolve even after three treatments. The weak muscles were all innervated by the subscapular nerve which travels through a small foramen on the scapula immediately adjacent to the attachment of the levator scapulae. It became apparent eventually that the swelling caused by the muscle strain injury to the levator was compressing and inactivating the motor nerve. Treating the injured muscle and using Russian stim to make it contract and then treating the motor nerve resolved the muscle weakness in less than an hour.


If the nerve root is torn the area of sensory loss may become smaller during treatment but the numbness does not resolve. If the nerve is torn, the pain will be reduced but not eliminated during treatment and returns within hours. The treatment is so consistently effective that a lack of response to FSM treatment suggests that the nerve root is torn and suggests the need for a neurology consult and medical management.



Note on the C2 nerve root


The C2 nerve root exits the spine at C1–C2 and innervates the posterior portion of the scalp up to an imaginary line drawn across the top of the head between the ears and provides sensation along a thin stripe on the lower portion of the jaw and upper neck. This nerve can be tractioned or crushed during whiplash injuries. The key to diagnosis will be complaint of an intense headache at the back of the skull. If the patient says, “I have had a migraine every day since the accident that doesn’t respond to migraine medication”, check sensation in the C2 nerve root. In cases such as this the C2 dermatome will be strongly hyperesthetic. If C2 should happen to be numb it usually means that the nerve has been crushed and may not respond well to treatment. Treat with the protocols for any nerve traction injury. The prognosis is guarded if the nerve is numb initially and optimistic if the nerve is hyperesthetic.



Treating dermatomal nerve pain




image Hydration




• The patient must be hydrated to benefit from microcurrent treatment.


• Hydrated means 1 to 2 quarts of water consumed in the 2 to 4 hours preceding treatment.


• Athletes and patients with more muscle mass seem to need more water than the average patient.


• The elderly tend to be chronically dehydrated and may need to hydrate for several days prior to treatment in addition to the water consumed on the day of treatment.


• DO NOT accept the statement, “I drink lots of water”


• ASK “How much water, and in what form, did you drink today before you came in?”


• Coffee, caffeinated tea, carbonated cola beverages do not count as water.


• Water may be flavored with juice or decaffeinated tea.




Channel A: condition frequencies


The frequencies listed are thought to remove or neutralize the condition for which they are listed except for 81 and 49 / which are thought to increase secretions and vitality respectively. They are listed alphabetically not in order of use or importance. Frequencies rationale is explained in the treatment protocol.







































• Calcium ions

 91 /


• Chronic inflammation

 284 /


• Emotional shock

 970


• Histamine

 9/


• Inflammation

 40 /


• Paralysis

 321 /


• Scarring

 13 /


• Sclerosis

 3 /


• Secretions (Increase)

 81 /


• Trauma

 94 /


• Vitality

 49 /


Channel B: tissue frequencies




• Dermatomal or Peripheral Nerve: ___ / 396


image Any nerve outside the spinal cord

• Fascia: ___ / 142


image Fascia is the thin connective tissue covering surrounding the muscles and virtually all visceral tissue. Nerves travel in a fascia–nerve–fascia sandwich. Any time a nerve is inflamed or injured the fascia becomes inflamed to some extent and adhesions will develop between the nerve and the fascia.

• Disc Annulus: ___ / 710


image The well innervated disc annulus is the most pain sensitive and most easily injured portion of the disc. It consists of coiled layers of sturdy connective tissue wrapped around the gel like nucleus.

• Disc Nucleus: ___ / 330


image The gel like disc nucleus fills the center of the disc and absorbs water to become a cushion for the vertebral bodies in the spine. It is very high in PLA2 and very inflammatory.

• Disc as whole: ___ / 630


image This frequency is thought to address the entire disc structure.

• Muscle Tissue as a tissue type: ___ / 46


image This frequency is rarely used and is thought to possibly represent the sarcomere or some contractile portion of the muscle. Combining the frequency to “increase secretions” in the nerve and “muscle tissue” has been observed to eliminate neuropathic atrophy in numerous cases. This protocol has no effect on disuse atrophy.


Treatment protocol



Channel A condition / Channel B tissue



Reduce the pain



40 / 396



• Reduce inflammation / in the nerve


• 40 / 396 polarized positive is consistently effective in reducing nerve pain.


• Current polarized positive +


• Positive leads at the spine – Negative leads at the distal end of the nerve. See photos for details of set up.


• Treatment time. Use 40 / 396 until the pain has been reduced to approximately 2/10 on a 0 to 10 VAS scale. In most cases of dermatomal nerve pain this will take approximately 20–30 minutes but it may take up to an hour. Pain reduction usually begins distally and progresses proximally. If the patient is on narcotics or is dehydrated or has low essential fatty acid levels due to poor diet or lack of supplementation, response may be slow or poor. See the notes on what to do if response to treatment is slow.


• It is essential to reduce the pain by using 40 / 396 before treating the nerve for any other pathology.



image Stenosis precaution


If there is dense scar tissue or bony stenosis of the nerve root or spinal cord or if a disc fragment is compressing the nerve root or cord at the involved level the patient’s pain may increase when polarized positive current is applied. If the patient is positioned comfortably, it is the only time the pain will increase during polarized positive treatment for nerve inflammation. It may increase in the dermatome or at the spine or both. Assess patient position to determine whether it is contributing to the pain increase.


Stop treating immediately if pain goes up during treatment. Move the patient to a seated position if possible. Move the contacts slightly up the spine superior to the nerve root being treated, reduce current levels and change the current from polarized positive to alternating. If this is going to reduce the reaction it will do so in 5 to 10 minutes. If the pain continues to increase, stop treating with current. The pain should go back down in a few hours although it may take up to 24 hours to reduce to base line.


This reaction is diagnostic. If physical examination findings of reduced sensation and deep tendon reflexes at the involved level or hyperactive deep tendon reflexes below the involved level are present this reaction suggests the need to x-ray or perform an MRI to confirm the presence of compression.



Remove the basic pathologies / from the nerve



970, 94, 321, 9 / 396



• Remove the emotional component, remove nerve trauma, restore function, and remove histamine / from the nerve


• This sequence comes from Van Gelder’s concept of concussion as discussed in Chapter 10. In Van Gelder’s model, emotional shock and trauma leads to “paralysis” which leads to “allergy reaction” and reduction in secretions and vitality.


• “Emotional shock” from an injury or trauma changes tissue function; 970 / takes the “fact of” this emotional shock out of the membrane.


• “Trauma” stuns the nerve, overloading it rather like a power surge that trips a circuit breaker causing it to switch into something like a “safe mode.” The “safe mode” preserves the most important critical functions and allows for repair and recovery at some later time.


• “Paralysis” does not refer to complete loss of function or true medical paralysis. The analogy to the loss of function when a computer “locks up” and loses the ability to move to the next step is most apt. The fact of the trauma interferes with the smooth transfer of information within the tissue that allows it to know what to do next. The frequency to remove “paralysis” is Van Gelder’s conceptual equivalent of the computer command “control–alt–delete” that reboots the computer system.


• “Allergy Reaction” refers to the body’s first response to any dysfunction which is to release histamine as a way of starting the inflammatory cascade. Removing the allergy reaction allows the tissue to complete the return to normal function.


• Note: These four frequencies are known collectively as “The Basics”. They are usually used in sequential order as a group combined with the channel B frequency for the injured tissue but each can be used individually as needed based on the patient’s condition.


• Treatment time. Use each frequency for 1 to 2 minutes each. Current polarized positive.



Remove pathologies from the nerve



284 / 396



• Chronic Inflammation / Nerve


• Treatment time: Use 284 / 396 for 2 to 5 minutes after treating with 40 / 396 when the pain is down to a 2–3/10 and when the nerve pain has been present for longer than 3 months. Acute and chronic inflammation coexist and 284 / has a different but complementary affect on chronic nerve pain.



image Precaution: induced euphoria


Treating inflammation and chronic inflammation in the nerve has a curious effect on affect and cognitive function. Most, but not all, patients will experience an “induced euphoria” that is characteristic of this treatment. It is most pronounced while using 40 / 396 and the practitioner may want to reassure the patient that it is a normal effect as it begins. The first sign will be a reduction in the rate of blinking, respiration and speech that starts within 10 to 15 minutes. Some patients fall asleep and some get so “stoned” that they do not wish to or simply cannot speak.


This is a temporary effect and will wear off as the other frequencies are used.


The patient will remain relaxed but will come to full function within an hour or so after treatment. Most patients are in full possession of their faculties by the time they are dressed and ready to leave the clinic. The practitioner should take care to ensure that the patient is safe to drive. In extreme cases patients have been warned against making important financial decisions until the effect has worn off. The effect is most profound in the first few treatments.



Treat the disc – if nerve pain is discogenic



40 / 330, 630, 710



• Remove inflammation / in the disc nucleus, the disc as a whole and the disc annulus


• If the pain is from a nerve traction injury it is not necessary to treat the disc


• Treatment time: 4 minutes each



Soften the tissue



91 / 396



• Remove Calcium Ions / from the Nerve



91 / 142



• Remove Calcium Ions / from the Fascia


The frequency 91Hz was originally thought to remove calcium from “stones” in the kidney or bile duct as indicated by its description on Van Gelder’s list of frequencies. In July 2003, it was used for the first time to treat “hardening in the fascia” in the legs of a professional football player because his muscles and fascia felt like “stones” as they were being treated; 91Hz produced remarkable softening in the fascia. Its usefulness in treating nerve pain was a late accidental discovery and its effectiveness was a pleasant surprise.


As it turns out, calcium ions flow into nerve and fascial membranes during nerve depolarization and inflammation (Winquist 2005). Using 91/396, 142 seems to remove the calcium influx that perpetuates nerve pain and hardens the fascia around the nerve although there are no biopsy findings to confirm this. Clinically these frequency combinations produce profound softening of the tissue and reductions in pain and the exact mechanism of these changes is yet to be discovered.



• Treatment time: Use these combinations for 2 to 5 minutes each or until the softening response slows or stops. Current Polarized Positive +.



Treatment application



Current level




• 100–300μamps for the average healthy patient.


• Use lower current levels of 20–60μamps for very small or debilitated patients. Current levels above this will be irritating and may make the patient restless or agitated.


• Use higher current levels of 300–500μamps for larger or very muscular patients.


• In general, higher current levels reduce pain more quickly and improve response.


• Do not use more than 500μamps as animal studies suggest that current levels above 500μamps reduce ATP formation.


• Current Polarized Positive +: Current is polarized positive for most nerve treatments except for shingles (see Chapter 9) and peripheral neuropathies which require alternating DC current. Nerves respond very well and very quickly to polarized positive current.


• Waveslope: The waveslope refers to the rate of increase of current in the ramped square wave as it rises in alternating mode from zero up to the treatment current level every 2.5 seconds on the Precision Microcurrent and the automated family of FSM units. Other microcurrent instruments may have slightly different wave form choices. A sharp waveslope has a very steep leading edge on the square wave shape indicating a very sharp increase in current. A gentle waveslope has a very gradual leading edge on the waveform indicating a gradual increase in current.


image Use a moderate to sharp waveslope for chronic pain.

image Use a gentle waveslope for acute pain or new injuries. A sharp waveslope is irritating in new injuries.


Lead placement




• Positive leads. The positive leads contact wraps around the neck or is placed along the spine at the exiting nerve root. The positive contact must cover at least the foramenal area where the nerve exits the spine


• Negative leads. The negative leads attached to an adhesive electrode or wrapped in the warm wet fabric towel are placed at the end of the dermatome or nerve being treated. The placement is shown in the photographs.


• Electrode Contacts. FSM typically uses graphite gloves to conduct the current but any conductor can be used as long as it has low resistance and can be wrapped around the spine at the exiting nerve root and have good contact with the distal end of the nerve being treated.


• Adhesive electrode pads can be used if they are long enough (3 inches) to encircle the foramenal area where the nerve exits the spine and to give good contact at the distal end of the nerve.

Related posts:

The theoretical foundation for frequency-specific microcurrent Treating concussion, central pain and emotions Treating ligaments and sprain injuries Treating fibromyalgia associated with spine trauma Treating muscles, fascia and myofascial trigger points Treating the discs

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Jun 14, 2016 | Posted by in PAIN MEDICINE | Comments Off on Treating neuropathic pain

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