The Pain Practitioner - Arthritis by Academy of Integrative Pain Management

Integrative Pain Management for Optimal Patient Care

The Pain Practitioner March/April 2017

Arthritis

Supplements and Botanicals for Arthritis Visible/Invisible Trauma and Chronic Pain Massage Therapy for Arthritis Neuromodulation for Chronic Pain

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OF PAIN OF RELIEF NUCYNTA® ER is the first and only FDA-approved long-acting opioid designed to control both nociceptive pain and the neuropathic pain associated with diabetic peripheral neuropathy (DPN). Not an actual patient.

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INDICATIONS AND USAGE Limitations of Use NUCYNTA ER is an opioid agonist indicated for the management of: • Because of the risks of addiction, abuse, and misuse with opioids, • pain severe enough to require daily, around-the-clock, longeven at recommended doses, and because of the greater risks of term opioid treatment and for which alternative treatment overdose and death with extended-release opioid formulations, options are inadequate reserve NUCYNTA ER for use in patients for whom alternative treatment options (e.g., non-opioid analgesics or immediate• neuropathic pain associated with diabetic peripheral release opioids) are ineffective, not tolerated, or would be neuropathy (DPN) severe enough to require daily, around-theotherwise inadequate to provide sufficient management of pain. clock, long-term opioid treatment and for which alternative treatment options are inadequate. • NUCYNTA ER is not indicated as an as-needed (prn) analgesic. NUCYNTA® ER IMPORTANT SAFETY INFORMATION WARNING: ADDICTION, ABUSE, AND MISUSE; LIFE- THREATENING RESPIRATORY DEPRESSION; ACCIDENTAL INGESTION; NEONATAL OPIOID WITHDRAWAL SYNDROME; INTERACTION WITH ALCOHOL and RISKS FROM CONCOMITANT USE WITH BENZODIAZEPINES OR OTHER CNS DEPRESSANTS See full prescribing information for complete boxed warning. • NUCYNTA ER exposes users to risks of addiction, abuse, and misuse, which can lead to overdose and death. Assess each patient’s risk before prescribing, and monitor regularly for development of these behaviors or conditions. (5.1) • Serious, life-threatening, or fatal respiratory depression may occur. Monitor closely, especially upon initiation or following a dose increase. Instruct patients to swallow NUCYNTA ER tablets whole to avoid exposure to a potentially fatal dose of tapentadol. (5.2) • Accidental ingestion of NUCYNTA ER, especially in children, can result in fatal overdose of tapentadol. (5.2) • Prolonged use of NUCYNTA ER during pregnancy can result in neonatal opioid withdrawal syndrome, which may be lifethreatening if not recognized and treated. If opioid use is required for a prolonged period in a pregnant woman, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available (5.3). • Instruct patients not to consume alcohol or any products containing alcohol while taking NUCYNTA ER because co-ingestion can result in fatal plasma tapentadol levels. (5.4) • Concomitant use of opioids with benzodiazepines or other central nervous system (CNS) depressants, including alcohol, may result in profound sedation, respiratory depression, coma, and death. Reserve concomitant prescribing for use in patients for whom alternative treatment options are inadequate; limit dosages and durations to the minimum required; and follow patients for signs and symptoms of respiratory depression and sedation. (5.4), (7).

Please see additional Important Safety Information, including BOXED WARNING, and Brief Summary on the following pages.

NUCYNTA® ER (tapentadol) IMPORTANT SAFETY INFORMATION (continued) CONTRAINDICATIONS NUCYNTA ER is contraindicated in patients with: • Significant respiratory depression • Acute or severe bronchial asthma or hypercarbia in an unmonitored setting or in the absence of resuscitative equipment • Known or suspected gastrointestinal obstruction, including paralytic ileus • Hypersensitivity (e.g. anaphylaxis, angioedema) to tapentadol or to any other ingredients of the product. • Concurrent use of monoamine oxidase inhibitors (MAOIs) or use of MAOIs within the last 14 days WARNINGS AND PRECAUTIONS Addiction, Abuse, and Misuse NUCYNTA ER contains tapentadol, a Schedule II controlled substance. As an opioid, NUCYNTA ER exposes users to the risks of addiction, abuse, and misuse. Because extendedrelease products such as NUCYNTA ER deliver the opioid over an extended period of time, there is a greater risk for overdose and death due to the larger amount of tapentadol present. Addiction can occur at recommended doses and if the drug is misused or abused. Assess each patient’s risk for opioid addiction, abuse, or misuse prior to prescribing NUCYNTA ER, and monitor all patients receiving NUCYNTA ER for the development of these behaviors and conditions. Risks are increased in patients with a personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression). Abuse or misuse of NUCYNTA ER by crushing, chewing, snorting, or injecting the dissolved product will result in the uncontrolled delivery of tapentadol and can result in overdose and death. Opioid are sought by drug abusers and people with addiction disorders and are subject to criminal diversion. Consider these risks when prescribing or dispensing NUCYNTA ER. Life-threatening Respiratory Depression Serious, life-threatening, or fatal respiratory depression has been reported with the use of opioids, even when used as recommended. Respiratory depression, if not immediately recognized and treated, may lead to respiratory arrest and death. To reduce the risk of respiratory depression, proper dosing and titration of NUCYNTA ER are essential. Overestimating the NUCYNTA ER dosage when converting patients from another opioid product can result in fatal overdose with the first dose. Accidental ingestion of even one dose of NUCYNTA ER, especially by children, can result in respiratory depression and death due to an overdose of tapentadol. Neonatal Opioid Withdrawal Syndrome Prolonged use of NUCYNTA ER during pregnancy can result in withdrawal in the neonate. Neonatal opioid withdrawal syndrome, unlike opioid withdrawal syndrome in adults, may be life-threatening if not recognized and treated, and requires management according to protocols developed by neonatology experts. Observe newborns for signs of neonatal

opioid withdrawal syndrome and manage accordingly. Advise pregnant women using opioids for a prolonged period of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available. Risk from Concomitant Use with Benzodiazepines or Other CNS Depressants Patients must not consume alcoholic beverages or prescription or non-prescription products containing alcohol while on NUCYNTA ER therapy. The co-ingestion of alcohol with NUCYNTA ER may result in increased plasma tapentadol levels and a potentially fatal overdose of tapentadol. Profound sedation, respiratory depression, coma, and death may result from the concomitant use of NUCYNTA ER with benzodiazepines or other CNS depressants (e.g., nonbenzodiazepine sedatives/hypnotics, anxiolytics, tranquilizers, muscle relaxants, general anesthetics, antipsychotics, other opioids, alcohol). Because of these risks, reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate. If the decision is made to prescribe a benzodiazepine or other CNS depressant concomitantly with an opioid analgesic, prescribe the lowest effective dosages and minimum durations of concomitant use. In patients already receiving an opioid analgesic, prescribe a lower initial dose of the benzodiazepine or other CNS depressant than indicated in the absence of an opioid, and titrate based on clinical response. If an opioid analgesic is initiated in a patient already taking a benzodiazepine or other CNS depressant, prescribe a lower initial dose of the opioid analgesic, and titrate based on clinical response. Follow patients closely for signs and symptoms of respiratory depression and sedation. Advise both patients and caregivers about the risks of respiratory depression and sedation when NUCYNTA ER is used with benzodiazepines or other CNS depressants (including alcohol and illicit drugs). Advise patients not to drive or operate heavy machinery until the effects of concomitant use of the benzodiazepine or other CNS depressant have been determined. Screen patients for risk of substance use disorders, including opioid abuse and misuse, and warn them of the risk for overdose and death associated with the use of additional CNS depressants including alcohol and illicit drugs. Risk of Life-Threatening Respiratory Depression in Patients with Chronic Pulmonary Disease or in Elderly, Cachectic, or Debilitated Patients The use of NUCYNTA ER in patients with acute or severe bronchial asthma in an unmonitored setting or in the absence of resuscitative equipment is contraindicated. Patients with Chronic Pulmonary Disease: NUCYNTA ER treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with a substantially decreased respiratory reserve, hypoxia, hypercapnia, or pre-existing respiratory depression are at increased risk of decreased respiratory drive including apnea, even at recommended dosages of NUCYNTA ER.

NUCYNTAÂŽ ER (tapentadol) IMPORTANT SAFETY INFORMATION (continued) Elderly, Cachectic, or Debilitated Patients: Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients because they may have altered pharmacokinetics or altered clearance compared to younger, healthier patients. Alternatively, consider the use of non-opioid analgesics in these patients. Serotonin Syndrome with Concomitant Use of Serotonergic Drugs Cases of serotonin syndrome, a potentially life-threatening condition, have been reported during concomitant use of tapentadol with serotonergic drugs.Serotonergic drugs include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), triptans, 5-HT3 receptor antagonists, drugs that affect the serotonergic neurotransmitter system (e.g., mirtazapine, trazodone, tramadol), and drugs that impair metabolism of serotonin (including MAO inhibitors, both those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue). This may occur within the recommended dosage range. See Warnings and Precautions in full Prescribing Information for a list of symptoms associated with Serotonin Syndrome. Discontinue NUCYNTA ER if serotonin syndrome is suspected. Adrenal Insufficiency Cases of adrenal insufficiency have been reported with opioid use, more often following greater than one month of use. Presentation of adrenal insufficiency may include non-specific symptoms and signs including nausea, vomiting, anorexia, fatigue, weakness, dizziness, and low blood pressure. If adrenal insufficiency is suspected, confirm the diagnosis with diagnostic testing as soon as possible. If adrenal insufficiency is diagnosed, treat with physiologic replacement doses of corticosteroids. Wean the patient off of the opioid to allow adrenal function to recover and continue corticosteroid treatment until adrenal function recovers. Other opioids may be tried as some cases reported use of a different opioid without recurrence of adrenal insufficiency. The information available does not identify any particular opioids as being more likely to be associated with adrenal insufficiency. Severe Hypotension NUCYNTA ER may cause severe hypotension including orthostatic hypotension and syncope in ambulatory patients. There is an increased risk in patients whose ability to maintain blood pressure has already been compromised by a reduced blood volume or concurrent administration of certain CNS depressant drugs (e.g., phenothiazines or general anesthetics). Monitor these patients for signs of hypotension after initiating or titrating the dosage of NUCYNTA ER. In patients with circulatory shock, NUCYNTA ER may cause vasodilation that can further reduce cardiac output and blood pressure. Avoid the use of NUCYNTA ER in patients with circulatory shock. Risks of Use in Patients with Increased Intracranial Pressure, Brain Tumors, Head Injury, or Impaired Consciousness In patients who may be susceptible to the intracranial effects of CO2 retention (e.g., those with evidence of increased intracranial pressure or brain tumors), NUCYNTA ER may reduce respiratory

drive, and the resultant CO2 retention can further increase intracranial pressure. Monitor such patients for signs of sedation and respiratory depression, particularly when initiating therapy with NUCYNTA ER. Opioids may also obscure the clinical course in a patient with a head injury. Avoid the use of NUCYNTA ER in patients with impaired consciousness or coma. Risks of Use in Patients with Gastrointestinal Conditions NUCYNTA ER is contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus. The tapentadol in NUCYNTA ER may cause spasm of the sphincter of Oddi. Opioids may cause increases in serum amylase. Monitor patients with biliary tract disease, including acute pancreatitis, for worsening symptoms. Increased Risk of Seizures in Patients with Seizure Disorders The tapentadol in NUCYNTA ER may increase the frequency of seizures in patients with seizure disorders, and may increase the risk of seizures occurring in other clinical settings associated with seizures. Monitor patients with a history of seizure disorders for worsened seizure control during NUCYNTA ER therapy. Withdrawal Avoid the use of mixed agonist/antagonist (e.g., pentazocine, nalbuphine, and butorphanol) or partial agonist (e.g., buprenorphine) analgesics in patients who have received or are receiving a course of therapy with a full opioid agonist analgesic, including NUCYNTA ER. In these patients, mixed agonists/ antagonists and partial agonist analgesics may reduce the analgesic effect and/or may precipitate withdrawal symptoms. When discontinuing NUCYNTA ER, gradually taper the dose. Do not abruptly discontinue NUCYNTA ER. Risks of Driving and Operating Machinery NUCYNTA ER may impair the mental or physical abilities needed to perform potentially hazardous activities such as driving a car or operating machinery. Warn patients not to drive or operate dangerous machinery unless they are tolerant to the effects of NUCYNTA ER and know how they will react to the medication. Risk of Toxicity in Patients with Hepatic Impairment A study with an immediate-release formulation of tapentadol in subjects with hepatic impairment showed higher serum concentrations of tapentadol than in those with normal hepatic function. Avoid use of NUCYNTA ER in patients with severe hepatic impairment. Reduce the dose of NUCYNTA ER in patients with moderate hepatic impairment. Closely monitor patients with moderate hepatic impairment for respiratory and central nervous system depression when initiating and titrating NUCYNTA ER. Risk of Toxicity in Patients with Renal Impairment Use of NUCYNTA ER in patients with severe renal impairment is not recommended due to accumulation of a metabolite formed by glucuronidation of tapentadol. The clinical relevance of the elevated metabolite is not known. ADVERSE REACTIONS In clinical studies, the most common (â&#x2030;Ľ10%) adverse reactions were nausea, constipation, vomiting, dizziness, somnolence, and headache.

NUCYNTAÂŽ ER (tapentadol) IMPORTANT SAFETY INFORMATION (continued) Select Postmarketing Adverse Reactions Anaphylaxis, angioedema, and anaphylactic shock have been reported very rarely with ingredients contained in NUCYNTA ER. Advise patients how to recognize such reactions and when to seek medical attention. Panic attack has also been reported. DRUG INTERACTIONS Alcohol See BOXED WARNING. Benzodiazepines and Other Central Nervous System (CNS) Depressants See BOXED WARNING. Serotonergic Drugs See Warnings and Precautions. Monoamine Oxidase Inhibitors (MAOIs) See Contraindications. Mixed Agonist/Antagonist and Partial Agonist Opioid Analgesics May reduce the analgesic effect of NUCYNTA ER and/or precipitate withdrawal symptoms. Avoid concomitant use. Muscle Relaxants See BOXED WARNING and Warnings and Precautions. Diuretics Opioids can reduce the efficacy of diuretics by inducing the release of antidiuretic hormone. Monitor patients for signs of diminished diuresis and/or effects on blood pressure and increase the dosage of the diuretic as needed. Anticholinergic Drugs The concomitant use of anticholinergic drugs may increase risk of urinary retention and/or severe constipation, which may lead to paralytic ileus. Monitor patients for signs of urinary retention or reduced gastric motility when NUCYNTA ER is used concomitantly with anticholinergic drugs. USE IN SPECIFIC POPULATIONS Pregnancy Pregnancy Category C. NUCYNTA ER should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Prolonged use of opioid analgesics during pregnancy may cause neonatal opioid withdrawal syndrome. Labor or Delivery Opioids cross the placenta and may produce respiratory depression in neonates. NUCYNTA ER is not recommended for use in pregnant women during and immediately prior to labor, when use of shorter-acting analgesics or other analgesic techniques are more appropriate. Opioid analgesics, including NUCYNTA ER, can prolong labor through actions that temporarily reduce the strength, duration, and frequency of uterine contractions. Lactation Because of the potential for serious adverse reactions including excess sedation and respiratory depression in a breastfed infant, advise patients that breast feeding is not recommended during treatment with NUCYNTA ER.

Females and Males of Reproductive Potential Infertility Chronic use of opioids may cause reduced fertility in females and males of reproductive potential. It is not known whether these effects on fertility are reversible. Pediatric Use The safety and efficacy of NUCYNTA ER in pediatric patients less than 18 years of age have not been established. Geriatric Use Elderly patients (aged 65 or older) may have increased sensitivity to tapentadol. In general, use caution when selecting a dosage for an elderly patient. Respiratory depression is the chief risk for elderly patients treated with opioids, and has occurred after large initial doses were administered to patients who were not opioid-tolerant or when opioids were co-administered with other agents that depress respiration. Titrate the dosage of NUCYNTA ER slowly in geriatric patients and monitor closely for signs of central nervous system and respiratory depression. Hepatic Impairment Use of NUCYNTA ER in patients with severe hepatic impairment is not recommended. In patients with moderate hepatic impairment, dosage reduction of NUCYNTA ER is recommended. Renal Impairment Use of NUCYNTA ER in patients with severe renal impairment is not recommended. DRUG ABUSE AND DEPENDENCE See BOXED WARNING OVERDOSAGE In case of overdose, priorities are the reestablishment of a patent and protected airway and institution of assisted or controlled ventilation, if needed. Employ other supportive measures (including oxygen, vasopressors) in the management of circulatory shock and pulmonary edema as indicated. Cardiac arrest or arrhythmias will require advanced life support techniques. Please see Brief Summary, including BOXED WARNING, on the following pages.

BRIEF SUMMARY OF FULL PRESCRIBING INFORMATION This does not include all the information needed to use NUCYNTA® ER safely and effectively. See full Prescribing Information for NUCYNTA® ER. INDICATIONS AND USAGE NUCYNTA® ER is indicated for the management of: • pain severe enough to require daily, around-the-clock, long-term opioid treatment and for which alternative treatment options are inadequate • neuropathic pain associated with diabetic peripheral neuropathy (DPN) in adults severe enough to require daily, around-the-clock, long-term opioid treatment and for which alternative treatment options are inadequate. Limitations of Usage • Because of the risks of addiction, abuse, and misuse with opioids, even at recommended doses, and because of the greater risks of overdose and death with extended-release opioid formulations, reserve NUCYNTA® ER for use in patients for whom alternative treatment options (e.g., nonopioid analgesics or immediate-release opioids) are ineffective, not tolerated, or would be otherwise inadequate to provide sufficient management of pain. • NUCYNTA® ER is not indicated as an as-needed (prn) analgesic. WARNING: ADDICTION, ABUSE, AND MISUSE; LIFE-THREATENING RESPIRATORY DEPRESSION; ACCIDENTAL INGESTION; NEONATAL OPIOID WITHDRAWAL SYNDROME; AND INTERACTION WITH ALCOHOL See full prescribing information for complete boxed warning. • NUCYNTA® ER exposes users to risks of addiction, abuse, and misuse, which can lead to overdose and death. Assess each patient’s risk before prescribing, and monitor regularly for development of these behaviors or conditions. (5.1) • Serious, life-threatening, or fatal respiratory depression may occur. Monitor closely, especially upon initiation or following a dose increase. Instruct patients to swallow NUCYNTA® ER tablets whole to avoid exposure to a potentially fatal dose of tapentadol. (5.2) • Accidental ingestion of NUCYNTA® ER, especially in children, can result in fatal overdose of tapentadol. (5.2) • Prolonged use of NUCYNTA® ER during pregnancy can result in neonatal opioid withdrawal syndrome, which may be life-threatening if not recognized and treated. If opioid use is required for a prolonged period in a pregnant woman, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available. (5.3) • Instruct patients not to consume alcohol or any products containing alcohol while taking NUCYNTA® ER because co-ingestion can result in fatal plasma tapentadol levels. (5.4) CONTRAINDICATIONS Significant respiratory depression; acute or severe bronchial asthma or hypercarbia in an unmonitored setting or in the absence of resuscitative equipment; known or suspected paralytic ileus; hypersensitivity (e.g., anaphylaxis, angioedema) to tapentadol or to any other ingredients of the product; concurrent use of monoamine oxidase inhibitors (MAOIs) or use within the last 14 days. WARNINGS AND PRECAUTIONS Addiction, Abuse, and Misuse: NUCYNTA® ER contains tapentadol, a Schedule II controlled substance. As an opioid, NUCYNTA® ER exposes users to the risks of addiction, abuse, and misuse. As modified-release products such as NUCYNTA® ER deliver the opioid over an extended period of time, there is a greater risk for overdose and death due to the larger amount of tapentadol present. Although the risk of addiction in any individual is unknown, it can occur in patients appropriately prescribed NUCYNTA® ER and in those who obtain the drug illicitly. Addiction can occur at recommended doses and if the drug is misused or abused. Assess each patient’s risk for opioid addiction, abuse, or misuse prior to prescribing NUCYNTA® ER, and monitor all patients receiving NUCYNTA® ER for the development of these behaviors or conditions. Risks are increased in patients with a personal or family history of substance abuse (including drug or alcohol addiction or abuse) or mental illness (e.g., major depression).The potential for these risks should not, however, prevent the prescribing of NUCYNTA® ER for the proper management of pain in any given patient. Patients at increased risk may be prescribed modified-release opioid formulations such as NUCYNTA® ER, but use in such patients necessitates intensive counseling about the risks and proper use of NUCYNTA® ER along with intensive monitoring for signs of addiction, abuse, and misuse. Abuse or misuse of NUCYNTA® ER by crushing, chewing, snorting, or injecting the dissolved product will result in the uncontrolled delivery of tapentadol and can result in overdose and death. Opioid agonists such as NUCYNTA® ER are sought by drug abusers and people with addiction disorders and are subject to criminal diversion. Consider these risks when prescribing or dispensing NUCYNTA® ER. Strategies to reduce these risks include prescribing the drug in the smallest appropriate quantity and advising the patient on the proper disposal of unused drug. Contact local state professional licensing board or state controlled substances authority for information on how to prevent and detect abuse or diversion of this product. Life-Threatening Respiratory Depression: Serious, life-threatening, or fatal respiratory depression has been reported with the use of modified release opioids, even when used as recommended. Respiratory depression from opioid use, if not immediately recognized and treated, may lead to respiratory arrest and death. Management of respiratory depression may include close observation, supportive measures, and use of opioid antagonists, depending on the patient’s clinical status. Carbon dioxide (CO2) retention from opioid-induced respiratory depression can exacerbate the sedating effects of opioids. While serious, life-threatening, or fatal respiratory depression can occur at any time during the use of NUCYNTA® ER, the risk is greatest during the initiation of therapy or following a dose increase. Closely monitor patients for respiratory depression when initiating therapy with NUCYNTA® ER and following dose increases. To reduce the risk of respiratory depression, proper dosing and titration of NUCYNTA® ER are essential. Overestimating the NUCYNTA® ER dose when converting patients from another opioid product can result in fatal overdose with the first dose. Accidental ingestion of even one dose of NUCYNTA® ER, especially by children, can result in respiratory depression and death due to an overdose of tapentadol.

Neonatal Opioid Withdrawal Syndrome: Prolonged use of NUCYNTA® ER during pregnancy can result in withdrawal signs in the neonate. Neonatal opioid withdrawal syndrome, unlike opioid withdrawal syndrome in adults, may be life threatening if not recognized and treated, and requires management according to protocols developed by neonatology experts. If opioid use is required for a prolonged period in a pregnant woman, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available. Neonatal opioid withdrawal syndrome presents as irritability, hyperactivity and abnormal sleep pattern, high pitched cry, tremor, vomiting, diarrhea and failure to gain weight. The onset, duration, and severity of neonatal opioid withdrawal syndrome vary based on the specific opioid used, duration of use, timing and amount of last maternal use, and rate of elimination of the drug by the newborn. Interactions with Central Nervous System Depressants: Patients must not consume alcoholic beverages or prescription or non-prescription products containing alcohol while on NUCYNTA® ER therapy. The co-ingestion of alcohol with NUCYNTA® ER may result in increased plasma tapentadol levels and a potentially fatal overdose of tapentadol. Hypotension, profound sedation, coma, respiratory depression, and death may result if NUCYNTA® ER is used concomitantly with alcohol or other central nervous system (CNS) depressants (e.g., sedatives, anxiolytics, hypnotics, neuroleptics, other opioids). When considering the use of NUCYNTA® ER in a patient taking a CNS depressant, assess the duration of use of the CNS depressant and the patient’s response, including the degree of tolerance that has developed to CNS depression. Additionally, evaluate the patient’s use of alcohol or illicit drugs that cause CNS depression. If the decision to begin NUCYNTA® ER is made, start with NUCYNTA® ER 50 mg every 12 hours, monitor patients for signs of sedation and respiratory depression, and consider using a lower dose of the concomitant CNS depressant. Use in Elderly, Cachectic, and Debilitated Patients: Life-threatening respiratory depression is more likely to occur in elderly, cachectic, or debilitated patients as they may have altered pharmacokinetics or altered clearance compared to younger, healthier patients. Therefore, closely monitor such patients, particularly when initiating and titrating NUCYNTA® ER and when NUCYNTA® ER is given concomitantly with other drugs that depress respiration. Use in Patients with Chronic Pulmonary Disease: Monitor for respiratory depression those patients with significant chronic obstructive pulmonary disease or cor pulmonale, and patients having a substantially decreased respiratory reserve, hypoxia, hypercarbia, or pre-existing respiratory depression, particularly when initiating therapy and titrating with NUCYNTA® ER, as in these patients, even usual therapeutic doses of NUCYNTA® ER may decrease respiratory drive to the point of apnea. Consider the use of alternative non-opioid analgesics in these patients if possible. Hypotensive Effect: NUCYNTA® ER may cause severe hypotension. There is an increased risk in patients whose ability to maintain blood pressure has already been compromised by a reduced blood volume or concurrent administration of certain CNS depressant drugs (e.g., phenothiazines or general anesthetics). Monitor these patients for signs of hypotension after initiating or titrating the dose of NUCYNTA® ER. In patients with circulatory shock, NUCYNTA® ER may cause vasodilation that can further reduce cardiac output and blood pressure. Avoid the use of NUCYNTA® ER in patients with circulatory shock. Use in Patients with Head Injury or Increased Intracranial Pressure: Monitor patients taking NUCYNTA® ER who may be susceptible to the intracranial effects of CO2 retention (e.g., those with evidence of increased intracranial pressure or brain tumors) for signs of sedation and respiratory depression, particularly when initiating therapy with NUCYNTA® ER. NUCYNTA® ER may reduce respiratory drive, and the resultant CO2 retention can further increase intracranial pressure. Opioids may also obscure the clinical course in a patient with ahead injury. Avoid the use of NUCYNTA® ER in patients with impaired consciousness or coma. Seizures: NUCYNTA® ER has not been evaluated in patients with a predisposition to a seizure disorder, and such patients were excluded from clinical studies. The active ingredient tapentadol in NUCYNTA® ER may aggravate convulsions in patients with convulsive disorders, and may induce or aggravate seizures in some clinical settings. Monitor patients with a history of seizure disorders for worsened seizure control during NUCYNTA® ER therapy. Serotonin Syndrome: Cases of life-threatening serotonin syndrome have been reported with the concurrent use of tapentadol and serotonergic drugs. Serotonergic drugs comprise Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs), tricyclic antidepressants (TCAs), triptans, drugs that affect the serotonergic neurotransmitter system (e.g. mirtazapine, trazodone, and tramadol), and drugs that impair metabolism of serotonin (including MAOIs). This may occur within the recommended dose. Serotonin syndrome may include mental-status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular aberrations (e.g., hyperreflexia, incoordination) and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea) and can be fatal. Use in Patients with Gastrointestinal Conditions: NUCYNTA® ER is contraindicated in patients with GI obstruction, including paralytic ileus. The tapentadol in NUCYNTA® ER may cause spasm of the sphincter of Oddi. Monitor patients with biliary tract disease, including acute pancreatitis, for worsening symptoms. Avoidance of Withdrawal: Avoid the use of mixed agonist/antagonist (i.e., pentazocine, nalbuphine, and butorphanol) or partial agonist (buprenorphine) analgesics in patients who have received or are receiving a course of therapy with a full opioid agonist analgesic, including NUCYNTA® ER. In these patients, mixed agonists/antagonists and partial agonist analgesics may reduce the analgesic effect and/or may precipitate withdrawal symptoms. When discontinuing NUCYNTA® ER, gradually taper the dose. Driving and Operating Heavy Machinery: NUCYNTA® ER may impair the mental or physical abilities needed to perform potentially hazardous activities such as driving a car or operating machinery. Warn patients not to drive or operate dangerous machinery unless they are tolerant to the effects of NUCYNTA® ER and know how they will react to the medication. Hepatic Impairment: A study with an immediate-release formulation of tapentadol in subjects with hepatic impairment showed higher serum concentrations of tapentadol than in those with normal hepatic function. Avoid use of NUCYNTA® ER in patients with severe hepatic impairment. Reduce the dose of NUCYNTA® ER in patients with moderate hepatic impairment. Closely monitor patients with moderate hepatic impairment for respiratory and central nervous system depression when initiating and titrating NUCYNTA® ER. Renal Impairment: Use of NUCYNTA® ER in patients with severe renal impairment is not recommended due to accumulation of a metabolite formed by glucuronidation of tapentadol. The clinical relevance of the elevated metabolite is not known.

ADVERSE REACTIONS The following serious adverse reactions are discussed elsewhere in the labeling: • Addiction, Abuse, and Misuse [see Warnings and Precautions (5.1)] • Life-Threatening Respiratory Depression [see Warnings and Precautions (5.2)] • Neonatal Opioid Withdrawal Syndrome [see Warnings and Precautions (5.3)] • Interaction with Other CNS Depressants [see Warnings and Precautions (5.4)] • Hypotensive Effects [see Warnings and Precautions (5.7)] • Gastrointestinal Effects [see Warnings and Precautions (5.11)] • Seizures [see Warnings and Precautions (5.9)] • Serotonin Syndrome [see Warnings and Precautions (5.10)] Clinical Trial Experience Commonly-Observed Adverse Reactions in Clinical Studies with NUCYNTA® ER in Patients with Chronic Pain due to Low Back Pain or Osteoarthritis The most common adverse reactions (reported by ≥10% in any NUCYNTA® ER dose group) were: nausea, constipation, dizziness, headache, and somnolence. The most common reasons for discontinuation due to adverse reactions in eight Phase 2/3 pooled studies reported by ≥1% in any NUCYNTA® ER dose group for NUCYNTA® ER- and placebo-treated patients were nausea (4% vs. 1%), dizziness (3% vs. <1%), vomiting (3% vs. <1%), somnolence (2% vs. <1%), constipation (1% vs. <1%), headache (1% vs. <1%), and fatigue (1% vs. <1%), respectively. Commonly-Observed Adverse Reactions in Clinical Studies with NUCYNTA® ER in Patients with Neuropathic Pain Associated with Diabetic Peripheral Neuropathy The most commonly reported ADRs (incidence ≥ 10% in NUCYNTA® ER-treated subjects) were: nausea, constipation, vomiting, dizziness, somnolence, and headache. Postmarketing Experience: The following adverse reactions, not above, have been identified during post approval use of tapentadol. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Psychiatric disorders: hallucination, suicidal ideation, panic attack. Anaphylaxis, angioedema, and anaphylactic shock have been reported very rarely with ingredients contained in NUCYNTA® ER. Advise patients how to recognize such reactions and when to seek medical attention. DRUG INTERACTIONS Alcohol: Concomitant use of alcohol with NUCYNTA® ER can result in an increase of tapentadol plasma levels and potentially fatal overdose of tapentadol. Instruct patients not to consume alcoholic beverages or use prescription or non-prescription products containing alcohol while on NUCYNTA® ER therapy. Monoamine Oxidase Inhibitors: NUCYNTA® ER is contraindicated in patients who are receiving monoamine oxidase inhibitors (MAOIs) or who have taken them within the last 14 days due to potential additive effects on norepinephrine levels, which may result in adverse cardiovascular events. CNS Depressants: The concomitant use of NUCYNTA® ER with other CNS depressants including sedatives, hypnotics, tranquilizers, general anesthetics, phenothiazines, other opioids, and alcohol can increase the risk of respiratory depression, profound sedation, coma and death. Monitor patients receiving CNS depressants and NUCYNTA® ER for signs of respiratory depression, sedation and hypotension. When combined therapy with any of the above medications is considered, the dose of one or both agents should be reduced. Serotonergic Drugs: There have been post-marketing reports of serotonin syndrome with the concomitant use of tapentadol and serotonergic drugs (e.g., SSRIs and SNRIs). Caution is advised when NUCYNTA® ER is coadministered with other drugs that may affect serotonergic neurotransmitter systems such as SSRIs, SNRIs, MAOIs, and triptans. If concomitant treatment of NUCYNTA® ER with a drug affecting the serotonergic neurotransmitter system is clinically warranted, careful observation of the patient is advised, particularly during treatment initiation and dose increases. Muscle Relaxants: Tapentadol may enhance the neuromuscular blocking action of skeletal muscle relaxants and produce an increased degree of respiratory depression. Monitor patients receiving muscle relaxants and NUCYNTA® ER for signs of respiratory depression that may be greater than otherwise expected. Mixed Agonist/Antagonist Opioid Analgesics: Mixed agonist/antagonist analgesics (i.e., pentazocine, nalbuphine, and butorphanol) and partial agonists (e.g., buprenorphine) may reduce the analgesic effect of NUCYNTA® ER or precipitate withdrawal symptoms. Avoid the use of mixed agonist/ antagonist analgesics in patients receiving NUCYNTA® ER. Anticholinergics: The use of NUCYNTA® ER with anticholinergic products may increase the risk of urinary retention and/or severe constipation, which may lead to paralytic ileus. USE IN SPECIFIC POPULATIONS Pregnancy Clinical Considerations Fetal/neonatal adverse reactions Prolonged use of opioid analgesics during pregnancy for medical or nonmedical purposes can result in physical dependence in the neonate and neonatal opioid withdrawal syndrome shortly after birth. Observe newborns for symptoms of neonatal opioid withdrawal syndrome, such as poor feeding, diarrhea, irritability, tremor, rigidity, and seizures, and manage accordingly. Teratogenic Effects - Pregnancy Category C There are no adequate and well-controlled studies in pregnant women. NUCYNTA® ER should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Labor and Delivery: Opioids cross the placenta and may produce respiratory depression in neonates. NUCYNTA® ER is not for use in women during and immediately prior to labor, when shorter acting analgesics or other analgesic techniques are more appropriate. Opioid analgesics can prolong labor through actions that temporarily reduce the strength, duration, and frequency of uterine contractions. However this effect is not consistent and may be offset by an increased rate of cervical dilatation, which tends to shorten labor. Nursing Mothers: There is insufficient/limited information on the excretion of tapentadol in human or animal breast milk. Physicochemical and available pharmacodynamic/toxicological data on tapentadol point to excretion in breast milk and risk to the breastfeeding child cannot be excluded. Because of the potential for adverse reactions in nursing infants from NUCYNTA® ER, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother. Withdrawal symptoms can occur in breast-feeding infants when maternal administration of

NUCYNTA® ER is stopped. Pediatric Use: The safety and efficacy of NUCYNTA® ER in pediatric patients less than 18 years of age have not been established. Geriatric Use: Of the total number of patients in Phase 2/3 double-blind, multiple-dose clinical studies of NUCYNTA® ER, 28% (1023/3613) were 65 years and over, while 7% (245/3613) were 75 years and over. No overall differences in effectiveness or tolerability were observed between these patients and younger patients. In general, recommended dosing for elderly patients with normal renal and hepatic function is the same as for younger adult patients with normal renal and hepatic function. Because elderly patients are more likely to have decreased renal and hepatic function, consideration should be given to starting elderly patients with the lower range of recommended doses. Renal Impairment: The safety and effectiveness of NUCYNTA® ER have not been established in patients with severe renal impairment (CLCR <30 mL/min). Use of NUCYNTA® ER in patients with severe renal impairment is not recommended due to accumulation of a metabolite formed by glucuronidation of tapentadol. The clinical relevance of the elevated metabolite is not known. Hepatic Impairment: Administration of tapentadol resulted in higher exposures and serum levels of tapentadol in subjects with impaired hepatic function compared to subjects with normal hepatic function. The dose of NUCYNTA® ER should be reduced in patients with moderate hepatic impairment (Child-Pugh Score 7 to 9). Use of NUCYNTA® ER is not recommended in severe hepatic impairment (Child-Pugh Score 10 to 15). DRUG ABUSE AND DEPENDENCE Controlled Substance: NUCYNTA® ER contains tapentadol, a Schedule II controlled substance with a high potential for abuse similar to fentanyl, methadone, morphine, oxycodone, and oxymorphone. NUCYNTA® ER can be abused and is subject to misuse, addiction, and criminal diversion. The high drug content in the extended release formulation adds to the risk of adverse outcomes from abuse and misuse. Abuse: All patients treated with opioids require careful monitoring for signs of abuse and addiction, because use of opioid analgesic products carries the risk of addiction even under appropriate medical use. Drug abuse is the intentional non-therapeutic use of an over-the-counter or prescription drug, even once, for its rewarding psychological or physiological effects. Drug abuse includes, but is not limited to the following examples: the use of a prescription or over-the-counter drug to get “high,” or the use of steroids for performance enhancement and muscle build up. Drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that develop after repeated substance use and include: a strong desire to take the drug, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to drug use than to other activities and obligations, increased tolerance, and sometimes a physical withdrawal. “Drug-seeking” behavior is very common to addicts and drug abusers. Drug-seeking tactics include emergency calls or visits near the end of office hours, refusal to undergo appropriate examination, testing or referral, repeated claims of loss of prescriptions, tampering with prescriptions and reluctance to provide prior medical records or contact information for other treating physician(s). “Doctor shopping” (visiting multiple prescribers) to obtain additional prescriptions is common among drug abusers, and people suffering from untreated addiction. Preoccupation with achieving pain relief can be appropriate behavior in a patient with poor pain control. Abuse and addiction are separate and distinct from physical dependence and tolerance. Physicians should be aware that addiction may not be accompanied by concurrent tolerance and symptoms of physical dependence in all addicts. In addition, abuse of opioids can occur in the absence of true addiction. NUCYNTA® ER, like other opioids, can be diverted for non-medical use into illicit channels of distribution. Careful record-keeping of prescribing information, including quantity, frequency, and renewal requests, as required by law, is strongly advised. Proper assessment of the patient, proper prescribing practices, periodic re-evaluation of therapy, and proper dispensing and storage are appropriate measures that help to limit abuse of opioid drugs. Dependence: Both tolerance and physical dependence can develop during chronic opioid therapy. Tolerance is the need for increasing doses of opioids to maintain a defined effect such as analgesia (in the absence of disease progression or other external factors). Tolerance may occur to both the desired and undesired effects of drugs, and may develop at different rates for different effects. Physical dependence results in withdrawal symptoms after abrupt discontinuation or a significant dose reduction of a drug. Withdrawal also may be precipitated through the administration of drugs with opioid antagonist activity, e.g., naloxone, nalmefene, mixed agonist/antagonist analgesics (pentazocine, butorphanol, nalbuphine), or partial agonists (buprenorphine). Physical dependence may not occur to a clinically significant degree until after several days to weeks of continued opioid usage. NUCYNTA® ER should not be abruptly discontinued. If NUCYNTA® ER is abruptly discontinued in a physically-dependent patient, an abstinence syndrome may occur. Some or all of the following can characterize this syndrome: restlessness, lacrimation, rhinorrhea, yawning, perspiration, chills, piloerection, myalgia, mydriasis, irritability, anxiety, backache, joint pain, weakness, abdominal cramps, insomnia, nausea, anorexia, vomiting, diarrhea, increased blood pressure, respiratory rate, or heart rate. Infants born to mothers physically dependent on opioids will also be physically dependent and may exhibit respiratory difficulties and withdrawal symptoms. OVERDOSAGE Clinical Presentation: Acute overdosage with opioids can be manifested by respiratory depression, somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, constricted pupils, and sometimes pulmonary edema, bradycardia, hypotension and death. Marked mydriasis rather than miosis may be seen due to severe hypoxia in overdose situations. Treatment of Overdose: In case of overdose, priorities are the re-establishment of a patent and protected airway and institution of assisted or controlled ventilation if needed. Employ other supportive measures (including oxygen, vasopressors) in the management of circulatory shock and pulmonary edema as indicated. Cardiac arrest or arrhythmias will require advanced life support techniques. Rx Only

Academy of Integrative Pain Management

www.aapainmanage.org

The Pain Practitioner

ACADEMY BOARD OF DIRECTORS President Joanna Katzman, MD, MSPH Past President Robert A. Bonakdar, MD, FAAFP Vice President W. Clay Jackson, MD, DipTh Secretary Paul Christo, MD, MBA Treasurer Kevin T. Galloway, BSN, MHA, Colonel, US Army (Retired) Directors-at-Large Alfred V. Anderson, MD, DC George D. Comerci, Jr, MD, FACP John Garzione, DPT Christian D. GonzĂĄlez, MD Michael Kurisu, DO, ABIHM Joseph Matthews, DDS, MSc Liaison to the Board Maggie Buckley

MARCH/APRIL 2017

To access the virtual magazine, go to newsstand.aapainmanage.org

PAGE 9

10 EDITORIAL Common, but Confounding, Osteoarthritis By W. Clay Jackson, MD, DipTh, Editor-in-Chief 11 ANNUAL MEETING/EDUCATION Annual Meeting

STAFF AND CONSULTANTS Executive Director Robert Twillman, PhD, FAPM Director of the State Pain Policy Advocacy Network (SPPAN) Amy Goldstein, MSW Assistant Director of Education Cathleen Coneghen SPPAN Assistant Director for Legislative and Regulatory Affairs Katie Duensing, JD Member Services Manager Whitney Oâ&#x20AC;&#x2122;Donnell Account Managers Rosemary LeMay Professional Development Project Manager MacKenzie Davis Content Consultant Debra Nelson-Hogan

NOTES FROM THE FIELD Paying Lip Service to Integrative Pain Management By Bob Twillman, PhD, FAPM, Executive Director

PAGE 13x

12 ADVOCACY State policies Related to Demonstrations and Access to Non-pharmacological, Integrative Pain Care By Amy Goldstein, MSW, Director, State Pain Policy Advocacy Network 13 Supplements and Botanicals for Arthritis By Rob Slater, MD, MPH, and Victor Sierpina, MD 17 Massage Therapy for Arthritis By Dolly Wallace 18 Visible/invisible Traumas and Chronic Pain By Robert J. Gatchel, PhD, ABPP, and Nancy D. Kishino, OTR/L, CVE

PAGE 18

22 The Interior World of the Pain Patient By Rachel B. Aarons, MSW, Phd 24 Acoustical Neuromodulation for Chronic Pain Management By John E. Garzione, PT, DPT, DAAPM, and L. Richard Bruursema

THE PAIN PRACTITIONER STAFF AND CONSULTANTS Editor-in-Chief W. Clay Jackson, MD, DipTh Editor Debra Nelson-Hogan Advertising and Sales Leslie Ringe Managing Editor Cathleen Coneghen Clinical Editor Christine Rhodes, MS Art Director Peter McKinley, Pak Creative Copy Editor Rosemary Hope

The Pain Practitioner is published by the Academy of Integrative Pain Management, P: 209-533-9744, F: 209-533-9750, Email: aapm@aapainmanage.org, website: www. aapainmanage.org. Copyright 2017 Academy of Integrative Pain Management. All rights reserved. Send correspondance to: Debra NelsonHogan at dhogan@aapainmanage.org. For advertising opportunities, media kits, and prices, contact: Leslie Ringe, 209-288-2207, leringe@verizon.net The Pain Practitioner is published by the Academy of Integrative Pain Management solely for the purpose of education. All rights are reserved by the Academy to accept, reject, or modify any submission for publication. The opinions stated in the enclosed printed materials are those of the authors and do not necessarily represent the opinions of the Academy or individual members. The Academy does not give guarantees or any other representation that the printed material contained herein is valid, reliable, or accurate. The Academy of Integrative Pain Management does not assume any responsibility for injury arising from any use or misuse of the printed material contained herein. The printed material contained herein is assumed to be from reliable sources, and there is no implication that they represent the only, or best, methodologies or procedures for the pain condition discussed. It is incumbent upon the reader to verify the accuracy of any diagnosis and drug dosage information contained herein, and to make modifications as new information arises. All rights are reserved by the Academy to accept, reject, or modify any advertisement submitted for publication. It is the policy of the Academy to not endorse products. Any advertising herein may not be construed as an endorsement, either expressed or implied, of a product or service.

PAGE 24

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NOTES FROM THE FIELD

Paying Lip Service to Integrative Pain Management By Bob Twillman, PhD, FAPM, Executive Director

I’ve remarked a number times about the recent spate of guidelines that recommend that non-opioid medications and non-pharmacologic interventions be used before initiating opioid therapy for chronic pain. I’ve also remarked about the fact that these recommendations fail to provide much guidance at all about which non-pharmacologic interventions should be used, and about how patients can access them, considering the uniformly poor reimbursement supported by third-party payers, including Medicare and Medicaid. I’ve seen a continuing stream of these lip-service recommendations, and it recently was pointed out to me that one very important guideline actually weakened its recommendation in its final draft. I think it’s time for us to call out the people who draft these recommendations, to demand that they work with us on more helpful language, and to enlist their support in lobbying for increased reimbursement for non-pharmacologic treatments. Here are some examples: •

I’ve previously written here, and our immediate past-president, Robert Bonakdar, MD, has written in USAToday, about the letter from the US Surgeon General to all physicians in the United States, urging them to curtail opioid prescribing for chronic pain. This letter, and supporting materials with it, make a passing mention of the importance of non-pharmacologic interventions, but don’t do much more than that.

•

In January 2017, the Centers for Medicare and Medicaid Services issued its 2016 Opioid Misuse Strategy (Yes, those dates are correct!). This 30-page document lists four priority areas for grappling with the opioid problem. Strategy No. 4 reads, “Increase the use of evidence-based practices for acute and chronic pain management.” The document then provides expanded discussion of each of the four priorities. On page 21, it states Objective 4-2: “Encourage the use of non-pharmacologic therapies, non-opioid pharmaceuticals, and multi-modal analgesia (MMA) as first options for pain management.” The discussion of this objective is one three-sentence paragraph—in a 30-page document!

can access those interventions without paying out of pocket.

•

Finally, we have the CDC Guideline for Prescribing Opioids for Chronic Pain. We twice provided 20 pages of comments on draft versions of this guideline. You may recall that its first recommendation is that non-opioid medications and non-pharmacologic interventions should be preferred first-line interventions for chronic pain. What we failed to notice is that, in its discussion of this recommendation, the second draft (p. 17), from December 2015, included the following language: “Based on contextual evidence, many nonpharmacologic therapies, including physical therapy, weight loss for knee osteoarthritis, complementary and alternative therapies (e.g., manipulation, massage, and acupuncture), psychological therapies such as CBT, and certain interventional procedures can ameliorate chronic pain.” By the time the final guideline was issued, one portion of this sentence had been deleted: “… complementary and alternative therapies (e.g., manipulation, massage, and acupuncture).” Not only did CDC fail to help clinicians identify ways to access these effective therapies, but they actually removed any mention of them from the final guideline! One wonders which of the more than 4,000 comments received on this draft of the guideline recommended deleting complementary and alternative therapies.

Through our policy advocacy efforts, we have kept up a steady stream of comments to policymakers regarding the importance of non-pharmacologic treatments and the ways in which they can facilitate accessing those treatments. At times, it feels like we are starting to gain some traction in those efforts, and some jurisdictions (e.g., Oregon’s Medicaid program) have begun to take steps to improve access. But until we get all the policymakers to make informed statements when they issue guidelines or recommendations, and until they put their money where their mouth is and improve reimbursement for these therapies, all we really have in most cases is lip service to integrative pain management. We are at a critical period in the development of integrative pain management. Never before have we had an opportunity to bring our knowledge to policymakers and present it as the solution to not just one, but to two, major public health crises in the United States. And no one is as well-positioned to bring that message as AIPM—which has been working on these issues for 29 years. On behalf of the organization, I pledge to you that we will redouble our efforts, but I also invite you to support us by educating your legislators and regulators about the importance of integrative pain management, and about what is needed to improve access to it. Let us know if you have connections to policymakers, and what we can do to support you when you talk to them. And, when we reach out to ask you to contact your policymakers, please take a few minutes to do so. We’ll make it as easy as possible for you to do that, and it is vital that they hear from as many of us as possible. Maybe then we can move past lip service into real, meaningful, action.❏

The theme here is obvious—policymakers feel compelled to suggest treating chronic pain with non-pharmacologic interventions, but they don’t seem to know which interventions to recommend, and they don’t seem to have the foggiest idea about how a clinician and patient

TH E PAIN PRACTITION ER

Bob Twillman, PhD, is the executive director for the Academy of Integrative Pain Management. Dr. Twillman is responsible for overseeing federal and state pain policy developments and advocating for those supporting an integrative approach to managing pain. He also serves as Chair of the Prescription Monitoring Program Advisory Committee for the Kansas Board of Pharmacy.

| VOLUME 27, NUMBER 2 |

EDITORIAL

Common, but Confounding, Osteoarthritis Pain W. Clay Jackson, MD, DipTh, Editor-in-Chief

ment with me was her functional limitation. Barbara was finding it increasingly difficult to keep up with her work. She was also very concerned as to her continuing ability to care for her aging father. As for activities for enjoyment’s sake—well, that was out of the question.

“So, Doc, what can you do for me?” Barbara—polite, well-resourced, arthritis-bearing Barbara—awaited my response.

Barbara looked okay. Compared to many of my patients, she was rather welldressed, smiled a good bit, and seemed to have it together. She was a professional in her mid-fifties, with a great career and not many health problems. On second glance, though, her smile leveled off at the corners, and the eyes didn’t twinkle normally. Barbara was in pain. She told me a story, the way patients always do. This one was fairly straightforward, though, without a lot of twists and turns. She had developed pain in both knees, but more so on the left than on the right. She had been diagnosed with osteoarthritis, and at age 54, had had a left total knee replacement (TKR). Things hadn’t gone well, though. The left knee still gave her a good deal of trouble, and the right knee ached a good bit. Despite treatment with non-steroid antiinflammatory medications (NSAIDs) and physical therapy, she was finding the pain intolerable. The subjective symptoms were difficult, but the real driver behind her seeking treat-

We briefly explored further orthopedic intervention. Given her difficult postoperative course with the first TKR, and the suboptimal results, however, Barbara really wasn’t willing to “go back down that road.” I offered her duloxetine, a serotoninnorepinephrine reuptake inhibitor (SNRI) that was then newly approved by the FDA for the treatment of chronic pain as a result of osteoarthritis of the knee. I was rather proud of myself for offering what was then cuttingedge pharmacologic help, and was hopeful that she would find relief. She tried it, with a little improvement subjectively, but no great shift in functional ability. The same results came with topical NSAID therapy of various stripes—some help, but nothing that moved the functionality needle.

“What’s next, Doc?” What came next was a miracle. Not the bombastic, instantaneous kind that people build a shrine for, but the slow, fraught-withdifficulty-and-challenges kind that people come to a clinic for. We started a longacting opioid for baseline pain control, with a limited amount of breakthrough opioid medication as needed. Barbara’s pain was reduced—not gone, mind you—but reduced by about 20% (which is about what we would expect from an oral opioid regimen for chronic, non-malignant pain) (1). By starting opioids, I had a decent idea that we were committing to long-term opioid therapy; recent data from the CDC (2) have confirmed this to be the general case. For Barbara, though, that didn’t bother her a bit. Having gone through non-pharmacologic interventions (surgery and physical therapy) without significant relief, and having tried and failed non-opioid pharmacologic therapy (NSAIDs and SNRIs), she felt that

| T HE PA I N P R AC TI TI O NE R | M A R C H / A P R I L 2 0 1 7

her quality of life was unacceptable without additional therapy, and opioids offered the help she needed. More important to her than the symptom relief, however, was the functional improvement she received. Although the evidence base for functional improvement in opioids for chronic nonmalignant pain is poor, in Barbara’s case, the medications worked. She was able to continue working for many years, until she retired on her own terms. Barbara’s proudest moment in her personal life was captured in a picture she brought for me. She and her father are proudly standing side by side—on the Great Wall of China. Their dream trip involved lots of food, fun, sight-seeing—and lots of walking. Osteoarthritis is common, non-exotic, but nonetheless debilitating. Patients like Barbara deserve our best efforts to restore comfort and functionality, which often takes an open-minded, multidisciplinary, and multimodal approach. Whether the goal is a journey to the Great Wall or a trip to the grocery store, you—the clinicians of the Academy of Integrative Pain Management— help tens of thousands of patients with osteoarthritis every day to take the steps to wellness. That, friends, is good news. ❏ W. Clay Jackson, Editor-in Chief, is clinical assistant professor of family medicine and psychiatry at the University of Tennessee College of Medicine in Memphis, Tennessee, where he maintains a private practice in family and palliative medicine. He is also the medical director of Comprehensive Primary Care, and of Methodist Hospice and Palliative Services. Dr. Jackson is the associate fellowship director of palliative medicine at the University of Tennessee College of Medicine. References 1. Noble M, Tregear SJ, Treadwell JR, Schoelles K. Long-term opioid therapy for chronic noncancer pain: a systematic review and meta-analysis of efficacy and safety. J Pain Symptom Manage. 2008;35:214-228. 2. Shah A, Hayes CJ, Martin BC. MMWR. Characteristics of initial prescription episodes and likelihood of long-term opiod use—United States, 2006-2015. March 17, 2017; 66(10):265-269.

Dr. Jackson will present a keynote address on Clinician Suicide at the AIPM 28th Annual Meeting in San Diego, California, on October 21, 2017.

ANNUAL MEETING/EDUCATION

AIPM Annual Meeting AIPM’s 28th Annual Meeting presents a broad-based program that includes the key stakeholders in the pain management arena: clinicians, researchers, patients, regulators/policy makers, payors, and industry. In today’s environment, where too often a discussion of pain management digresses into a discussion of the “opioid epidemic” and where the needs and the outcomes of the individual are often trumped by outdated insurance coverage models, inadequate education for clinicians, unrealistic expectations by patients, and lack of understanding among regulators, it is essential to operationalize the wise recommendations of the National Pain Strategy and engage all of the stakeholders in the discussion. AIPM’s 28th Annual Meeting is the only meeting dedicated to integrative pain management and our program includes a variety of evidence-based modalities to treat the most common pain conditions. Our program represents the newest thinking in team-based care, pharmacologic and non-pharmacologic treatments, behavioral interventions, patient self-management programs, clinician wellness, and regulatory responsibility and accountability.

MEETING KEYNOTES:

Colonel Gregory D. Gadson, USA (retired) will open the meeting with a discussion of the value of Integrative Pain Management, which he experienced first-hand after an improvised explosive device (IED) attack in Iraq cost him both legs above the knees and normal use of his right arm and hand. Despite this, Gadson remained on active duty in the Army and continued to inspire many with his message of courage, perseverance, determination, and teamwork. In 2007, Tom Coughlin, New York Giants head coach, asked Col. Gadson to meet with the thenstruggling team. Gadson talked to the players about service, teamwork, duty, perseverance, and adversity. His message resonated and the New York Giants defeated the 18-0 New England Patriots in Super Bowl XLII. Col. Gadson made his silver screen debut in 2012 in the movie “Battleship,” where he portrayed a war-injured veteran who helped save the world from an alien invasion. In 2015, he completed season one of “The Inspectors,” a family television series on CBS. Col. Gadson is an entrepreneur and managing partner of Patriot Strategies, LLC, a government services company. Vilayanur Subramanian Ramachandran, PhD, MBBS, is a neuroscientist known primarily for his work in the fields of behavioral neurology and visual psychophysics. He is currently a professor in the department of psychology and the graduate program in neurosciences at the University of California, San Diego. In 2011, Time magazine named Dr. Ramachandran one of 100 most influential people in the world. Thomas Insel said, “Once described as the Marco Polo of neuroscience, V.S. Ramachandran has mapped some of the most mysterious regions of the mind. He has studied visual perception and a range of conditions, from synesthesia (in which viewing black-

and-white figures evokes the perception of color) to autism. But Ramachandran, is best known for developing mirror-box therapy for phantom-limb pain. With his simple, creative and innovative ideas, V.S. Ramachandran is changing how our brains think about our minds.” Ramachandran is the author of several books: Phantoms in the Brain (1998), A Brief Tour of Human Consciousness (2004), and The Tell-Tale Brain (2010).

Beth Darnall, PhD, is a clinical associate professor in the department of anesthesiology, perioperative and pain medicine at Stanford University, and is on the faculty of the Stanford Systems Neuroscience and Pain Lab. A pain psychologist and scientist, she is a past president of the Pain Society of Oregon and co-chair of the Pain Psychology Task Force at the American Academy of Pain Medicine. Her NIH-funded research investigates mechanisms of pain catastrophizing, cognitive behavioral therapy for pain, and the effectiveness of a single-session pain catastrophizing treatment she developed. Additional projects are focused on preventing post-surgical chronic pain, and opioid reduction in outpatients with chronic pain. She is author of The Opioid-Free Pain Relief Kit (2016) and Less Pain, Fewer Pills: Avoid the dangers of prescription opioids and gain control over chronic pain (2014). W. Clay Jackson, MD, DipTh, Vice-President of the Board, is clinical assistant professor of family medicine and psychiatry at the University of Tennessee College of Medicine in Memphis, Tennessee, where he maintains a private practice in family and palliative medicine. He is also the medical director of Comprehensive Primary Care, and of Methodist Hospice and Palliative Services. Dr. Jackson is the associate fellowship director of palliative medicine at the University of Tennessee College of Medicine. He is board certified in family practice and hospice and palliative medicine. Dr. Jackson is a gifted storyteller and frequently presents at national conferences on the treatment of chronic pain. His work has been published in a number of leading academic journals and he is a recipient of numerous teaching honors.

For more information on the meeting, visit the AIPM website. Food for Thought: Special Programing on Nutrition >> Continued on Page 28

TH E PAIN PRACTITION ER

| VOLUME 27, NUMBER 2 |

ADVOCACY

State Policies Related to Demonstrations and Access to Non-pharmacological, Integrative Pain Care By Amy Goldstein, MSW, Director, State Pain Policy Advocacy Network One of SPPAN’s most important policy priorities is to ensure access to, and adequate insurance coverage for, integrative pain care. As part of this effort, we support demonstration projects that gather data about the effect of using integrative pain care treatments, and we advocate for non-discrimination against health care providers acting within their license and scope of practice. See the index below for current examples of state policy initiatives that relate to this policy priority. (Note: this list does not include specific scope of practice bills that passed, and is a living, breathing document as policies change.)

STATE

EVENT

DETAILS

Medicaid demonstration project (current)

Since 2012, Health First Colorado (Medicaid) has offered a waiver for persons with a spinal cord injury that provides participants with access to preventative acupuncture, massage, and chiropractic services, evaluating the consequential cost savings. On 3/21/16, the Department of Health & Human Services Region VIII approved the renewal of this waiver. In late 2016, an application was submitted to the Colorado Department of Health Care Policy & Financing to amend this waiver to add the Medicaid Buy-In Program for Working Adults with Disabilities—to be effective 3/1/17.

Medicaid demonstration project (past)

In 2003, Florida established the first demonstration through Medicaid for managing chronic pain with non-pharmacological therapies. It was called the Integrative Therapies Waiver Pilot Project and, after reviewing initial outcomes, the legislature renewed the program in 2007. The second phase evaluation from Florida Department of Health Services Research, Management and Policy can be seen here, and did not support the continuation of this program, despite some positive outcomes.

Pending legislation

House Bill 2009 was introduced in 2017 to appropriate funds for Johns Hopkins All Children’s Hospital-Mental Health Demonstration for Chronic Pain Patients.

Pending legislation

The bill LD 1030, “An Act to Require Nondiscrimination Policies in Providing Health Care Services,” was introduced in Maine in 2017. This bill would prohibit health insurance carriers, automobile insurers, and workers’ compensation insurers from discriminating against a health care provider who is licensed, registered, or certified by the State in providing covered services as long as the provider is acting within the scope of the provider’s license, registration, or certification.

Pending legislation

Minnesota Fair Care has introduced companion bills HF 886/SF 749 in 2017, “An Act Requiring Nondiscrimination Policies in Providing Health Care Services,” to support patient choice, access, and equitable insurance reimbursement. Read MN Fair Care white paper for more details.

Effective regulation

Related to New Mexico’s Managed Care Program and Home and Community Based Waiver program, definitions of various integrative therapies were included in 8.308.12.18. Newly-adopted language states “specialized therapies are non-experimental therapies or techniques that have been proven effective for certain conditions. A member may include specialized therapies in his or her care plan when the services enhance opportunities to achieve inclusion in community activities and avoid institutionalization.” Definitions for the following are included on pp. 13-14 under 8.308.12.18: acupuncture, biofeedback, chiropractic care, cognitive rehabilitation therapy, hippotherapy, massage therapy, naprapathy, and a Native American healer.

Effective statute

In 2015, House Bill 2468 passed, including measures that prohibit health insurers from discriminating with respect to participation in a health insurance plan against any health care provider who is acting within the scope of that provider’s license or certification. View the floor speech memorializing this event.

Medicaid

As of 7/1/16, the Oregon Health Plan (Medicaid) now covers acupuncture, chiropractic manipulation, cognitive behavioral therapy, osteopathic manipulation, physical and occupational therapy, medications (including short-term opiates, not long-term prescriptions), and surgery (for a limited number of conditions where evidence shows surgery is more effective than other treatment options) for all back conditions. In addition, yoga, intensive rehabilitation, massage, and/or supervised exercise therapy are recommended for inclusion in the comprehensive treatment plans. These treatments used to be limited to only those patients with muscle weakness or nerve damage.

Law passed

In 2015, Pennsylvania passed Senate Bill 487 to expand access to licensed physical therapists, chiropractors, and occupational therapists. This bill mandated that health insurers adhere to strict rules that ensure an insured is charged no more than one copayment amount per visit.

Law passed

In 2015, Rhode Island passed Senate Bill 168, prohibiting a group health plan and a health insurance issuer from discriminating with respect to participation under a health insurance plan or coverage against any health care provider who is acting within the scope of that provider’s license or certification under applicable state law.

Medicaid demonstration project (current)

Born out of increased emergency room visits, the Medicaid Community of Care model was made available to patients with 4+ ER visits annually. Key findings demonstrated a reduction in costs and ER use, and found a high incidence of chronic pain. Subsequently came the Rhode Island Medicaid Pain Management Program, making massage, acupuncture, and chiropractic services available to those willing to participate. Less than one quarter of patients referred to this program engaged in the services (2013-2015), with primary barriers being transportation and language. The latest evaluation shows that it’s difficult to keep participants engaged and that there is a need for additional interventions, but patient satisfaction is high. As a work in progress, they are determining how to target this program to the right people (1). Additionally, there has been a study evaluating this program since 2014, looking qualitatively at some of the participants and eligible participants in this Medicaid pain management program. The final recruitment ended in February 2017 and findings will be published at the end of 2017.

Law passed / includes future Medicaid pilot

In 2016, the state passed Senate Bill 243, “An act relating to combating opioid abuse in Vermont,” which includes $200,000 for a Medicaid pilot to use acupuncture as a non-opioid option for pain management.

References 1 Information accessed online on 3/3/17 from Governor’s Overdose Prevention and Intervention Task Force Meeting Minutes, dated 6/8/16

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FEATURES

Supplements and Botanicals for Arthritis By Rob Slater, MD, MPH, and Victor Sierpina, MD

tential toxicities. If medical management is unsuccessful, surgical joint repair may be recommended. However, joint replacement is traditionally limited to the large joints like the knee and hip, and is not a readily available option for patients with arthritis of the fingers or other small joints. This presents a quandary for many physicians: how can we appropriately manage this extremely common ailment when these options fail?

PATHOPHYSIOLOGY To better understand the mechanisms of action of treatments for arthritis, it may be helpful to review the underlying pathophysiology of the disease. The inciting event in osteoarthritis (OA) appears to be overuse or injury of a joint, whereas rheumatoid arthritis (RA) is likely caused by a pathologic immune response in a genetically predisposed person following a viral or bacterial infection. These stressful stimuli initiate the inflammatory cascade, beginning with activation of nuclear factor kappa beta (NF-kB), which then activates inflammatory genes. This leads to the production of inflammatory mediators, including enzymes, cytokines, and adhesion molecules. Inflammatory enzymes include cyclooxygenase and lipoxygenase, which produce signalling molecules known as eicosanoids, and nitric oxide synthase (NOS), which produces nitric oxide. Inflammatory cytokines include tumor necrosis factor alpha (TNF-Îą); interferons; and interleukins, such as IL-1, which induces the production of collagenase and matrix metalloproteinases, both of which destroy connective tissue. In arthritis, the inflammatory cascade is perpetuated beyond the acute response, and results in progressive deterioration of affected joints.

ANTIINFLAMMATORY DIET

Arthritis is the most commonly reported condition in older adults, and involves inflammation and gradual degeneration of joints throughout the body. Non-steroidal antiinflammatory drugs (NSAIDs) have become a standard arthritis treatment, but can prove problematic for many patients. Arthritis increases in prevalence with age, as do contraindications to NSAID therapy. For example, about 20,000 people a year die from gastrointestinal bleeding due to NSAIDs. Other contraindications include advanced kidney disease or concomitant anticoagulant therapy. Finally, NSAIDs may not prove strong enough to control pain in patients with advanced arthritis. Steroid injections into the joint may reduce inflammation more than NSAIDs, but have significant metabolic impacts, and are generally not recommended more often than every three months. When NSAIDs and steroid injections prove inadequate, the next treatment option is often opioid medications, which carry many risks of their own. For rheumatoid arthritis, immunosuppressive disease-modifying antirheumatic drugs (DMARDs) are the mainstay of therapy, but have other po-

Although the inciting stimulus for arthritis may not be easily avoided or prevented, the subsequent inflammatory response can be mitigated through a variety of modalities, which act at different points along the inflammation pathway. NSAIDs reduce inflammation by inhibiting cyclooxygenase; steroids suppress inflammatory genes; DMARDs inhibit inflammatory cytokines. Botanical treatments for arthritis likewise disrupt the inflammatory pathway, but interestingly, many foods also exert antiinflammatory effects! Because of this, all patients with arthritis should be encouraged to follow an antiinflammatory diet, which is a whole foods, plantbased diet rich in antioxidants and polyphenols from vegetables, fruits, whole grains, legumes, nuts, seeds, and tea. This diet excludes processed and fast foods, as well as foods with a high glycemic load. The antiinflammatory diet also involves a more balanced ratio of omega-6 and omega-3 polyunsaturated fatty acids. Cyclooxygenase and lipoxygenase are traditionally considered to be inflammatory enzymes due to their products, the eicosanoids. Cyclooxygenase (COX-1/COX-2) transforms fatty acids into thromboxanes and prostaglandins, and 5-lipoxygenase (5-LOX) produces leukotrienes. However, the inflammatory eicosanoids are primarily derived from omega-6 fatty acids, whereas omega-3s have an overall antiinflammatory effect. Some of these

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SUPPLEMENTS AND BOTANICALS FOR ARTHRITIS

over-the-counter products only contain about 300 mg of these omega-3s per capsule. More concentrated omega-3 supplements are available, and are recommended for inflammatory conditions such as arthritis. Gamma-linolenic acid (GLA) is not ordinarily found through dietary sources. And although GLA is an omega-6 fatty acid that can be a precursor to arachidonic acid and inflammatory eicosanoids, it appears that supplementation with GLA favors the production of antiinflammatory prostaglandins. GLA is found in high amounts in borage, evening primrose, and black currant oils. Large doses of 6 to 11 grams daily of borage oil have been shown to be helpful for RA, although the effects may take several weeks (1). Glucosamine is a prominent precursor for the formation of proteoglycans in the structural matrix of joints, and chondroitins are Omega 3 Fatty Acids Omega 6 Fatty Acids the main glycosaminoglycans in joints and (Alpha-Linolenic Acid / ALA) (Linoleic Acid) connective tissue. Glucosamine sulfate Δ6-Desaturase increases IkBα, inhibits NF-kB activity in a dose-dependent manner, inhibits the gene Gamma-linolenic acid expression and protein synthesis of COX-2 (GLA) Δ5-Desaturase induced by IL-1beta, and inhibits the release Evening Primrose Oil Borage Oil Eicosapentaenoic Acid of PGE2, although it does not appear to Black Currant Oil (EPA) affect COX-1 synthesis. Chondroitin sulfate decreases NF-kB nuclear translocation Δ5-Desaturase COX Lipoxygenase and consequently, reduces the formation Arachidonic Acid of proinflammatory cytokines (including Prostaglandins Less Inflammatory PGE1, PGE3 IL-1beta and TNF-alpha) and proinflammaLeukotrienes (Favorable) Cyclo-oxgenase Lipoxygenase tory enzymes, such as COX-2, NOS-2, and (COX) phospholipase A2. Beyond their antiinflammatory properties, glucosamine and Docosahexaenoic acid Prostaglandins (PGE2) Leukotrienes (DHA) chondroitin enhance the production of cartilage matrix, (Inflammatory) (Inflammatory) increase hyaluronic acid production, and prevent collagen degeneration in chondrocytes. These disease-modifying Figure 1. Omega-6 and Omega-3 Eicosanoid Pathways (1) effects are particularly attractive for slowing the progression of arthritis. Early studies of glucosamine and chondroitin showed impresfeatures as many as 10 to 25 times more omega-6s than omegasive results, with no radiographic evidence of joint space narrowing 3s. This omega imbalance may help to explain the predominance after three years of supplementation with crystalline glucosamine of chronic inflammatory diseases in modern society (2). sulfate in two pivotal studies, and a two-year study of chondroitin Alpha-linolenic acid (ALA) is a plant-based omega-3, and is sulfate appeared to retard radiographic progression of disease. found in high amounts in flax, hemp, and chia seeds, canola oil, Subsequently, glucosamine and chondroitin did not meet statistical nuts (especially walnuts), leafy vegetables, and grass-fed animal significance for reduction of pain in mild OA (but did for moderate fat. Our bodies use ALA mostly for energy, but can convert a small to severe OA pain) in a large NIH-funded randomized controlled amount into the other two omega-3s, eicosapentaenoic acid (EPA) trial (RCT), the Glucosamine/Chondroitin Arthritis Intervention Trial and docosahexaenoic acid (DHA). EPA and DHA are found almost (GAIT). However, the relevance of the GAIT results is questionable, exclusively in seafood, particularly in the fat of cold water fish such as it utilized glucosamine hydrochloride instead of sulfate, and the as salmon, mackerel, anchovies, sardines, herring, and trout. placebo response rate was much higher than usual (60% for mild In contrast to grain-fed meat and dairy products high in linoleic pain, and 54% for moderate to severe pain) (6). acid, grass-fed meat and dairy products contain much higher Following the publication of GAIT, multiple literature reviews levels of conjugated linoleic acid (CLA), which may interfere with reaffirmed the efficacy of glucosamine sulfate and chondroitin the formation of inflammatory eicosanoids (3). This appears to be sulfate for OA treatment. In particular, crystalline glucosamine clinically significant for rheumatoid arthritis, with improvements sulfate has shown significant improvement of pain and functional in activity level, morning stiffness, and erythrocyte sedimentation limitation, and multiple reviews (including a review of four metarate after three months of CLA supplementation (4). analyses) have generally concluded that chondroitin sulfate is Olive oil (and cooked vegetables) may have independent protechelpful for pain reduction and improved function in OA. Additiontive effects for rheumatoid arthritis. Olive oil is rich in monounsaturatally, long-term follow-up of patients in the two three-year trials ed (omega-9) oleic acid and appears to confer many health benefits, of crystalline glucosamine sulfate who had received treatment despite the fact that oleic acid can be synthesized de novo in the for at least 12 months revealed a 57% reduction in risk of total body, unlike the essential omega-3 and omega-6 fatty acids (5). joint replacement. A more recent meta-analysis (of three RCTs of Healthy fats are a vital component of the antiinflammatory diet, two-year duration) examining the structure-modifying effects of but can also be taken in the form of fatty acid supplements. chondroitin sulfate demonstrated a small but significant reduction Omega-3s are readily available commercially as fish oil, krill oil, in the rate of decline in joint space width (7,8). and most recently as algae oil. However, antiinflammatory doses Glucosamine and chondroitin have minimal side effects. Recuse 3,000 to 4,000 mg of combined EPA/DHA a day, and most effects stem from an alternate, less inflammatory omega-3 eicosanoid pathway that competes with the omega-6 pathway, and other effects appear to be mediated through intracellular signalling pathways, transcription factor activity, and gene expression. Many nutrition experts believe that before processed foods became common, humans ate roughly the same amount of omega-3s and omega-6s. Linoleic acid is the primary omega-6 fatty acid in the diet. With the advent of modern agriculture and food processing, linoleic acid became abundant in grain-fed beef, pork, and poultry, as well as in the refined vegetable oils (such as soybean oil) that are used in most fast foods, snack foods, cookies, crackers, and sweets. The standard American diet now

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SUPPLEMENTS AND BOTANICALS FOR ARTHRITIS

ommended doses are 1500 mg once daily of crystalline glucosamine sulfate, and 800 mg-1,200 mg once daily of chondroitin sulfate. These once-daily dosing regimens increase ease of patient adherence and appear to be more effective when compared to thrice daily dosing in other studies. For unknown reasons, not all patients respond to glucosamine and chondroitin sulfate, but these supplements should be taken for a minimum of six weeks (manufacturers recommend three months) before deeming a patient a non-responder. S-Adenosylmethionine (SAM-e) is a physiologic molecule formed from the essential amino acid methionine, and functions in a wide variety of reactions throughout the body. The mechanism of action of SAM-e in the treatment of OA is still being studied, but current theories include stimulation of proteoglycan synthesis in cartilage, reduction of inflammatory mediators, increasing levels of glutathione, and/or maintenance of DNA methylation. Although the underlying mechanism is incompletely understood, a meta-analysis of 11 studies concluded that SAM-e appears to be as effective as NSAIDs in reducing pain and improving function in OA, although with a slower onset of action (one month), but without the adverse effects of NSAIDs (9). Dosing of SAM-e for osteoarthritis in most studies has ranged from 600 to 1,200 mg per day. SAM-e appears to be more effective with adequate intake of vitamin B12 and folate, either through increased consumption of leafy green vegetables or supplementation. Possible side effects include nausea/GI upset and insomnia (particularly when taken near bedtime). Methylsulfonylmethane (MSM) and its metabolite, dimethyl sulfoxide (DMSO), are dietary supplements with preliminary data for an analgesic and antiinflammatory effect in osteoarthritis. A single RCT showed that the combination of MSM with glucosamine sulfate may improve pain reduction and functional ability, with a more rapid onset of action (10). A pilot clinical trial used a dose of 3,000 mg of MSM twice a day for a 12-week period (11). Avocado/soybean unsaponifiables (ASUs) are derived from the oily fractions of avocado and soybean, and contain phytosterols, beta-sterols, sitasterol, and campesterol. ASUs may stimulate the synthesis of collagen by inhibiting inflammatory cytokines (such as IL-1, IL-6, IL-8, and TNF), and modulation of NF-kB and MMPs (MMP-2 and MMP-3). When combined with epigallocatechin gallate (EGCG, a major component of green tea catechins), ASUs may have additional impacts by reducing the expression of COX-2. Clinically, ASUs have been shown to reduce pain and stiffness and improve joint function in multiple studies, and studies are ongoing to determine if ASUs may reduce joint degeneration (12). Doses of 300-600 mg per day reduced pain and swelling in hip and knee OA over three to six months in four RCTs, although ASUs have not been appreciably studied for the treatment of RA. ASUs appear to have a slow onset of action over four to six weeks (prior to tapering other drugs), but have minimal side effects. Turmeric (Curcuma longa) is an herbaceous plant in the ginger family that is harvested for its rhizome (rootstalk), which can then be prepared fresh or in dried powdered form for cooking. The health effects of turmeric are numerous, with antiinflammatory and antineoplastic effects that appear to be mediated by inhibition of NF-kB, COX-2, 5-LOX, TNF-alpha, IL-1 beta, IL-6, IL-8, MMPs (matrix metalloproteinases), and AMs (adhesion molecules). A meta-analysis of eight RCTs supported turmeric extract (~1000 mg per day of curcumin) for arthritis; and curcumin exhibited superior efficacy to NSAIDs for RA in an open trial (13,14). Typical doses of turmeric range from 500 to 1,000 mg two to three times a day. Curcumin phytosome is a complex of turmeric extract with phosphatidylcholine that increases bio-availability 29-

fold. Interestingly, black pepper (piperine) naturally increases the absorption of turmeric (15). Ginger (Zingiber officinale) is a flowering plant that is also harvested for its rhizome, and used fresh or powdered for cooking. Aside from ginger and turmeric, other spices in the ginger family (Zingiberaceae) include cardamom, galangal (Thai ginger), and grains of paradise (melegueta pepper). Ginger may have efficacy in RA via inhibition of inflammatory prostaglandins (via modulation of IkBα, which inhibits NF-kB, with effects on COX-2, PGE-2, and TNF-Alpha). A small number of studies for the use of ginger in OA have shown conflicting results; a systematic review in 2011 concluded that “available data provide tentative support,” and suggested that further rigorous trials are warranted (16). Ginger is also recommended as an anti-emetic in nausea and vomiting during pregnancy, but high doses may cause GI side effects. Ginger may have an interaction with anticoagulants, although a systematic review of the literature in 2015 was equivocal regarding the effect of ginger on reduction of platelet aggregation (17). The dosing range of ginger is flexible. As the dried root, 1 gram two or three times per day is a typical antiinflammatory dose, and may be increased up to 4 grams daily. As a tea, a common dose is one cup up to four times daily made of 1 gram of dried root steeped in 150 mL, or a 1-inch cube of grated fresh ginger in two cups, of boiling water for 5 to 10 minutes. Devil’s claw (Harpagophytum procumbens) is a traditional South African herbal remedy used for rheumatic conditions named for its peculiar appearing hooked fruit. Devil’s claw appears to inhibit cytokine production (TNF-alpha and IL-6), and COX-1 and COX-2 expression, possibly via suppression of NF-kB. A review of devil’s claw for treatment of OA concluded that higher quality studies suggest efficacy for pain reduction. Other studies have shown short-term pain improvement with devil’s claw in other inflammatory conditions, such as low back pain (18,19). The dose is a minimum of 50 mg per day of harpagoside, generally well tolerated, although gastrointestinal upset has been reported. Boswellia serrata (Indian frankincense) has been used for centuries as an Ayurvedic (traditional Indian) medicine for arthritis. Boswellia extracts and boswellic acids inhibit activation of NF-kB, with a consequent down-regulation of TNF-alpha and decrease of IL-1, IL-2, IL-4, IL-6 and IFN-gamma. A Cochrane review of Boswellia included high-quality evidence from two studies showing that 90 days of treatment with 100 mg of enriched Boswellia serrata extract improved OA symptoms, with additional benefit suggested from moderate-quality evidence from two studies and low-quality evidence from a small single study of other Boswellia extracts. There is preliminary evidence for the use of Boswellia in rheumatoid arthritis, pending clinical studies of the individual herb (20,21). The dose for Boswellia depends of the formulation used, and is often found in combination with other herbs/botanicals. GI irritation is the most commonly reported side effect of Boswellia, and it is not recommended in pregnancy. Ashwagandha (Withania somnifera) is derived from the root of an herb in the nightshade family, although all parts of the plant have been used in Ayurvedic medicine. Ashwagandha inhibits NFkB activation and gene expression, as well as COX-2, MMP-9, and TH E PAIN PRACTITION ER

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SUPPLEMENTS AND BOTANICALS FOR ARTHRITIS ICAM-1, which may confer chondroprotective activity. Preliminary studies in animal models suggest potential utility in the treatment of arthritis, and polyherbal formulas with ginger, Boswellia, curcumin, and other Ayurvedic herbs have shown positive results, although clinical studies of the individual plant are needed (22,23). Ashwagandha is considered an adaptogen, a substance that enhances the adaptive response to stress and exerts a normalizing effect upon bodily processes, and is also used in the treatment of anxiety and depression for stress reduction. High doses can cause drowsiness or even respiratory depression, and ashwagandha is not recommended during pregnancy. A typical dose of ashwagandha is 2 to 3 grams per day of powdered root or equivalent in tincture, and standardized extracts come in doses of 500 mg taken two to three times per day. A variety of other supplements and botanicals may have utility in the treatment of arthritis. Antioxidants such as Vitamin E (800 units daily as mixed tocopherols may have analgesic effects), Vitamin C 250 mg twice a day), and selenium (via Increased dietary intake of nuts, or 100 mcg daily, not to exceed 400 mcg daily) may have utility in both OA and RA (24). Botanicals with preliminary evidence for arthritis treatment include topical capsaicin, bromelain, rosemary, rosehips, stinging nettle, cat’s claw, sage, and oleaster (19). ❏ Victor S. Sierpina, MD, is associate professor of family medicine with tenure at the University of Texas Medical Branch (UTMB) in Galveston, Texas. He recently became the first designated W.D. and Laura Nell Nicholson Family Professor of Integrative Medicine. He was recently recognized as one of the Best Doctors in the US in Family Medicine. Dr. Sierpina is board certified by the American Board of Family Practice and the American Board of Holistic Medicine. Rob Slater, MD, MPH, is a physician trained in family medicine and public health, and is the current Integrative and Behavioral Medicine Fellow at the University of Texas Medical Branch in Galveston, Texas.

FO R FREE BERS MEM

References 1. Kohatsu W. The Antiinflammatory Diet. In: Rakel D, ed. Integrative Medicine. 3rd ed. Philadelphia: Elsevier Inc.; 2012:797 (Fig. 86-2). 2. Ernst E, and Chrubasik S. Phyto-anti-inflammatories: a systemic review of randomized, placebo-controlled, double-blind trials. Rheum Dis Clin North Am. 2000;26:13-27. 3. Banni S. Conjugated linoleic acid metabolism. Curr Opin Lipidol. 2002 Jun;13(3):261-6. 4. Arylaeian N, Shahram F, Djalali M, et al. Effect of conjugated linoleic acids, vitamin E and their combinations on the clinical outcome of Iranian adults with active rheumatoid arthritis. Int J Rheum Dis. 2009;1220-28. 5. Linos A, Kaklamani VG, Kaklamani E, et al. Dietary factors in relation to rheumatoid arthritis: a role for olive oil and cooked vegetables? Am J Clin Nutr. 1999;70:1077-1082 6. National Center for Complementary and Alternative Medicine. The NIH Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT). J Pain Palliat Care Pharmacother. 2008;22(1):39-43. 7. Rovati C, Girolami F, Persiani S. Crystalline glucosamine sulfate in the management of knee osteoarthritis: efficacy, safety, and pharmacokinetic properties. Ther Adv Musculoskelet Dis. 2012 Jun;4(3):167–180. 8. Hochberg MC. Structure-modifying effects of chondroitin sulfate in knee osteoarthritis: an updated meta-analysis of randomized placebo-controlled trials of 2-year duration. Osteoarthritis Cartilage. 2010 Jun;18 Suppl 1:S28-31. 9. Soeken K, Lee WL, Bausell RB, Agelli M, Berman BM. Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis: A meta-analysis. J Fam Pract. 51.5 (2002):425-30. 10. Usha PR, Naidu MU. Randomised, Double-Blind, Parallel, Placebo-Controlled Study of Oral Glucosamine, Methylsulfonylmethane and their Combination in Osteoarthritis. Clin Drug Investig. 2004;24(6):353-63. 11. Kim LS, Axelrod LJ, Howard P, Buratovich N, Waters RF. Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial. Osteoarthritis Cartilage. 2006 Mar;14(3):286-94. 12. Christiansen BA, Bhatti S, Goudarzi R, Emami S. Management of Osteoarthritis with Avocado/Soybean Unsaponifiables. Cartilage. 2015;6(1):30-44. 13. Daily JW, Yang M, Park S. Efficacy of Turmeric Extracts and Curcumin for Alleviating the Symptoms of Joint Arthritis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. J Med Food. 2016;19(8):717-729. 14. Chandran B, Goel A. A randomized, pilot study to assess the efficacy and safety of curcumin in patients with active rheumatoid arthritis. Phytother Res. 2012 Nov;26(11):1719-25. 15. Gupta SC, Patchva S, Aggarwal BB. Therapeutic Roles of Curcumin: Lessons Learned from Clinical Trials. AAPS J. 2013;15(1):195-218. 16. Sirivastava KC, Mustafa T. Ginger. Med Hypotheses. 1989;29:25-28. 17. Marx W, McKavanagh D, McCarthy AL, et al. The Effect of Ginger (Zingiber officinale) on Platelet Aggregation: A Systematic Literature Review. Freson K, ed. PLoS ONE. 2015;10(10):e0141119. 18. Brien S, Lewith GT, McGregor G. Devil’s Claw (Harpagophytum procumbens) as a treatment for osteoarthritis: a review of efficacy and safety. J Altern Complement Med. 2006 Dec;12(10):981-93. 19. Ghasemian M, Owlia S, Owlia MB. Review of Antiinflammatory Herbal Medicines. Adv Pharmacol Sci. 2016; 2016:9130979. 20. Cameron M, Chrubasik S. Oral herbal therapies for treating osteoarthritis. Cochrane Database Syst Rev. 2014 May 22;(5):CD002947. 21. Ammon HP. Modulation of the immune system by Boswellia serrata extracts and boswellic acids. Phytomed. 2010 Sep;17(11):862-7. 22. Khan MA, Subramaneyaan M, Arora VK, Banerjee BD, Ahmed RS. Effect of Withania somnifera (Ashwagandha) root extract on amelioration of oxidative stress and autoantibodies production in collagen-induced arthritic rats. J Complement Integr Med. 2015 Jun;12(2):117-25. 23. Chopra A, Lavin P, Patwardhan B, Chitre D. A 32-week randomized, placebo-controlled clinical evaluation of RA-11, an Ayurvedic drug, on osteoarthritis of the knees. J Clin Rheumatol. 2004 Oct;10(5):236-45. 24. Muller D. Rheumatoid Arthritis. In: Rakel D, ed. Integrative Medicine. 3rd ed. Philadelphia: Elsevier Inc.; 2012:456-463.

EARN 1 CME CREDIT! An Evidence-Based Review of Dietary Supplements Used To Treat Pain by David Kiefer, MD This 1-hour program reviews the most well-studied dietary supplements used for several pain conditions, using an integrative medicine approach to development a treatment plan. For more information, go to: goo.gl/rwbeRN

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MASSAGE THERAPY FOR ARTHRITIS

Massage Therapy for Arthritis By Dolly Wallace

Massage therapy is becoming increasingly recognized as a valuable component in integrative care, especially for various types of pain. This is the result of both an increasing body of research on its efficacy and the experience of people who suffer with acute or chronic pain. In a 2016 national poll of individuals who had a massage from a massage therapist in the previous 12 months, 35% said they sought their last massage for acute pain relief, chronic pain management, soreness, or spasms. Those who had a massage from a massage therapist in the previous five years reported similar reasons (1). A recently published review of research on massage therapy for pain management conducted through the Samueli Institute indicates that massage therapy can improve pain, anxiety, and health-related quality of life (2). In addition, since 2014 The Joint Commission has stated in its Standard PC.01.02.07 that massage therapy plays a significant “role in the management of pain” (3). Can massage therapy be a significant part of integrative care for those with arthritis?

WHAT THE RESEARCH SAYS Massage therapy is the manual manipulation of soft tissue intended to promote health and wellbeing. The effects of massage therapy on arthritis are therefore related to the soft tissue around the joint, impacting levels of pain and flexibility. Studies indicate that weak muscles around the knee are often associated with the development of osteoarthritis (OA) (4). Massage therapy can impact those muscles, decrease pain, increase flexibility, and improve quality of life for those with OA. While research on massage therapy for all forms of arthritis is still evolving, research indicates it can be an effective approach for pain from OA of the knee and other joints (4), as well as for rheumatoid arthritis of the wrist and upper arm (5). In a study supported by the National Center for Complementary and Alternative Medicine (NCCAM), 60-minute sessions of Swedish massage for those with osteoarthritis of the knee significantly reduced their pain (4). The study involved a group of 68 subjects divided into two equal groups. One group received 60-minute massages over a period of eight weeks, while the other group received less massage or usual care without massage. The massage group received twice-weekly sessions of standard Swedish massage in weeks 1-4 and once-weekly sessions in weeks 5-8. Each massage therapy session followed a specific protocol, including the nature of the massage strokes. These results were similar to those reported in previous investigations on massage for the pain of OA of the knee that included fewer patients. Another study examined the benefits of weekly massage in 42 adults with rheumatoid arthritis of the upper limbs over a period of four weeks (5). Researchers found that moderate-pressure massage vs. light-pressure massage reduced participants’ pain, increased grip strength, and improved range of motion in the wrist, elbows, and shoulders after one month of treatment. Several smaller previous studies have shown promise, demonstrating positive results of massage therapy and a need for further research. My own experience as a massage therapist reflects similar results. I have been working with clients with arthritis for more than 25 years and have seen definite improvements in mobility and pain. Most of the arthritis clients I see have OA.

It is the position of the American Massage Therapy Association (AMTA) that massage can aid in pain relief. A summary of general research on massage therapy for pain to support this position is available (6). More extensive research citations on massage therapy for pain are found at the Samueli Institute Research Archives website (7). AMTA also provides an online course on massage therapy for OA (8).

FIND THE RIGHT MASSAGE THERAPIST Massage therapists work in a variety of settings and environments from spas to health clubs, from independent practices to hospitals. How to best find a massage therapist who can work with those who have arthritis? First, patients and other health care providers who want to refer their patients need to find massage therapists with experience in arthritis. Obviously, the severity of the patient’s arthritis will determine the necessary level of experience of the massage therapist and the extent of the involvement of other members of the integrative health care team. As is standard professional practice, the massage therapist should do a thorough intake interview to fully understand the extent of the patient’s arthritis and any other health issues. The American Massage Therapy Association provides a free online service to locate professional massage therapists throughout the country (9). The provider or the patient can search by zip code and select a local massage therapist based on his or her credentials and areas of expertise. It may be helpful to call several massage therapists and discuss the nature of the patient’s arthritis to determine their level of experience. The patient/client should also talk to the massage therapist about their health and wellness goals to customize a treatment plan that addresses their arthritis condition. Starting with a trusted resource will ensure that patients get the most out of massage therapy. ❏ Dolly Wallace is the President of the American Massage Therapy Association. A native of Muskegon, Michigan, she has had a local massage therapy practice for more than 25 years and works in collaboration with her husband at his chiropractic practice. References 1. 2. 3. 4. 5. 6. 7. 8. 9.

AMTA Consumer Surveys 2003-2016. American Massage Therapy Association 2016. Boyd C, Crawford C, Paat C, Price A, et al. The impact of massage therapy on function in pain populations: Part I. Pain Med. 2016;17:1353-1375. The Joint Commission. Clarification of the Pain Management Standard PC.01.02.07. Joint Commission Perspectives, 2014;34(11):11. https://www.jointcommission.org/assets/1/18/Clarification_of_the_Pain_Management__Standard.pdf. Accessed March 6, 2017. Perlman AI, Sabina A, Williams AL, Njike VY, Katz DL. Massage therapy for osteoarthritis of the knee. Arch Intern Med. 2006;166(22):2533-2538. Field T, Diego M, Delgado J, Garcia D, Funk CG. Rheumatoid arthritis in upper limbs benefits from moderate pressure massage therapy. Complement Ther Clin Pract. 2013 May;19(2):101-103. American Massage Therapy Association. Massage can aid in pain relief. https://www.amtamassage.org/statement6.html. Accessed March 6, 2017. Samueli Institute. Research archives. http://www.samueliinstitute.org/research-areas/researcharchives-page.html. Accessed March 6, 2017. American Massage Therapy Association. Massage Therapy for Osteoarthritis. amtamassage.org/ learn. Accessed March 6, 2017. American Massage Therapy Association. Find a Massage Therapist. findamassagetherapist.org. Accessed March 6, 2017.

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| VOLUME 27, NUMBER 2 |

VISIBLE/INVISIBLE TRAUMAS AND CHRONIC PAIN

Visible/invisible Traumas and Chronic Pain By Robert J. Gatchel, PhD, ABPP, and Nancy D. Kishino, OTR/L, CVE

The focus of PTSD has broadened to include medical-related traumas, such as chronic pain sufferers and traumatic brain injury patients.

“The rate at which post-traumatic stress disorder (PTSD) and chronic pain co-occur is alarming; moreover, co-occurrence of these conditions is associated with a poor prognosis, increased work and social impairment, poor treatment prognosis, overuse of opioid medications, and considerable personal and societal cost …” (1). Ever since the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) by the American Psychiatric Association introduced PTSD as a distinct diagnostic disorder, empirical evidence has accumulated demonstrating the high number of victims affected by physical and psychological traumas (2). PTSD is now included as a new distinct category in the DSM-V and includes the exposure to actual (or threatened) events, such as death, serious injury, or a sexual violation (3). This exposure must cause clinically significant emotional distress or impairment, and must result from one or more of the following: directly experiencing the traumatic event; personally witnessing a traumatic event; “first-hand” experience of repeated or extreme exposure to the aversive details of the event; and/or knowledge that a close family member or friend experienced a traumatic event. Our initial focus on PTSD was primarily on veterans of the Vietnam War who experienced military trauma. Subsequent versions of the DSM also focused on the returning wounded warriors from the conflicts in Iraq and Afghanistan. This focus has become even much broader and appropriate for other groups: survivors

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of motor vehicle accidents; sexual assault victims, including adult survivors of childhood sexual and physical abuse; medical-related traumas (such as chronic pain sufferers and traumatic brain injury patients); and survivors of natural disasters. Another area is “invisible trauma,” which includes not knowing the long-term health consequences of technological disasters, such as exposure to radiation, chemicals, and other “invisible” contaminants in the environment (4). The nuclear power plant accident in 1979 at Three Mile Island (TMI), with its resulting radiation leakage into the environment, is an example of emotionally stressful concerns leading to an invisible trauma for those living around the plant, as well as around other nuclear plants. In fact, a study found that, even one year after the TMI nuclear accident, the residents of the area exhibited more symptoms of stress than individuals living near undamaged power plants or more than 20 miles from any power plant (5). Other types of large-scale disasters may increase pain on a community-wide level (6), especially when the media constantly replay the incident and, thus, unintentionally produces PTSD-like aftereffects. Another new area of clinical research is the critical role that a second unpredictable traumatic experience can play in substantially increasing the stressful memory of an initial trauma, and making it more resistant to extinction-based treatments (7). PTSD is associated with regional changes in brain structures and functions that appear to contribute to various characteristic symptoms and cognitive deficits (8). Many individuals who are suffering from chronic pain sustained their injuries as a consequence of some trauma (9). Of course, chronic pain does not simply represent discomfort in some specific body part. Rather, it occurs as part of a holistic or “whole person,” with a unique phenotype, previous learning experiences and adaptive resources, as well as premorbid coping skills. Thus, the biopsychosocial model of chronic pain has been proven to be the most heuristic approach developed during the past decade for better understanding chronic illnesses (especially chronic pain), and the complex interaction among biological (e.g., neurophysiological underpinnings), psychological (e.g., anxiety and depression), and social (e.g., interpersonal distress and conflicts) factors (10,11).

PTSD FROM WAR TRAUMA The current increased public awareness of PTSD has been due to our country’s sustained involvement in the ongoing military conflicts in Iraq and Afghanistan, and now throughout the Middle East. Besides the major physical wounds and trauma experienced

VISIBLE/INVISIBLE TRAUMAS AND CHRONIC PAIN

Figure 1. The Diathesis-Stress Biopsychosocial Model of Trauma and Chronic Pain (24)

SEXUAL ASSAULT

by soldiers in these conflicts, PTSD symptoms are also significant factors that need to be treated. Our experience in the two World Wars, as well as in the Korean War, convinced psychiatrists, psychologists, and others that traumatic stress, regardless of what it was called, could inflict serious, long-term mental health consequences. Autopsy data have suggested the presence of chronic traumatic encephalopathy (CTE) in returning veterans, and CTE has been suspected in some cases of PTSD (12). CTE is a progressive degenerative brain disorder in which an abnormal accumulation of μ protein in the brain eventually destroys cells in areas of the brain that are crucial for decision-making, judgement, memory, and impulse control (mostly in the frontal and temporal lobes; [12,13]). CTE is receiving even more attention today because of the realization of the toll that multiple concussions and concomitant pain are having on the brain health of athletes participating in popular contact sports such as football.

A growing body of literature on the negative biopsychosocial consequences of sexual assault indicates, for example, an increase in cortisol levels of victims of rape when they are later confronted with trauma reminders, as compared to trauma victims who did not experience rape (17). In addition, a co-occurrence of PTSD and depression symptoms has been reported after sexual assault (18). In another study of acute PTSD symptoms that could predict the course of PTSD over time, the presence of re-experiencing the trauma and emotional numbing, but not strategic avoidance and hyperarousal, within one month of an assault predicted the presence of PTSD symptoms at the fourthmonth (19). Programs are now being developed to help reduce sexual victimization among adolescent females (20) and in the military (21). In the military, 41% of women and 4% of men reported experiences of military sexual trauma (22). Such sexual trauma has been shown to be a risk factor for suicidal mortality (23).

MOTOR VEHICLE ACCIDENTS

DIATHESIS-STRESS BIOPSYCHOSOCIAL MODEL

Motor vehicle accidents (MVAs) may be seen as equivalent to war-time traumas, albeit in a civilian population. Approximately 1.3 million individuals worldwide are killed by road traffic injuries each year (12), and automobile and motorcycle accidents are one of the largest causes of accidental death in the US. (14). One important cause of increased stress and emotional disturbance is not being at-fault for causing the accident (15). Relatedly, the authors of a systematic review concluded that individuals involved in motor vehicle accidents who were most likely to develop PTSD were characterized as having prior anxiety disorders, persistent rumination about the accident trauma, a higher perceived threat to life, and lack of social support (16).

We have now extended the biopsychosocial model of chronic pain to introduce a diathesis-stress component, which emphasizes that predispositional factors interact with an acute

Chronic exposure to stress, chronic pain, or trauma negatively affects neuroendocrine-immune mechanisms, for example, and results in greater ‘wear and tear of the body’

TH E PAIN PRACTITION ER

| VOLUME 27, NUMBER 2 |

VISIBLE/INVISIBLE TRAUMAS AND CHRONIC PAIN stressor, such as pain or trauma (24). Once pain or trauma is established, they become stressors in their own right. For example, as illustrated in Figure 1, individuals “bring with them” certain diatheses or predispositions, such as certain candidate genes. Environmental influences, such as stress, can alter their phenotypic expression and result in long-lasting effects on health and behavior (25). Research has shown that epigenetic modifications play a role in PTSD (26). Additional potential biological, psychological, and social vulnerabilities may affect a person’s ultimate experience of comorbid trauma and chronic pain. The probability of this comorbidity becoming even more chronic and intransient may be lessened by the presence of potential mediators/moderators, such as social support and coping skills. If they are absent, they cannot “buffer” the individual from the full impact of the trauma-related event. This may then lead to central sensitization, as well as a significant increase in the allostatic load of the individual (27). Chronic exposure to stress, chronic pain, or trauma negatively affects neuroendocrine-immune mechanisms, for example, and results in greater “wear and tear of the body,” thus accelerating the development of illnesses such as cardiovascular disorders, as well as psychoneuroendocrinology disorders.

CENTRAL SENSITIZATION Central sensitization (CS) has received increasing attention in recent years because many common and prevalent somatic symptoms, such as fibromyalgia, widespread pain, TMJ disorders, and irritable bowel syndrome, often appear to overlap but have no known specific organic pathophysiology or basis. Yunus originally suggested that CS, which involves an abnormal and intensified experience of pain by mechanisms such as excitability in the central nervous system, may be a common link underlying these symptoms/disorders (28). Thus, many somatic symptoms

Help your patients find a trusted massage therapist for their pain relief.

that had earlier been assumed to be separate are now viewed as various forms of central sensitization syndrome (CSS), with CS as the root cause (29). Dysregulation in both the descending and ascending pathways of the central nervous system (due to physical trauma injuries and emotional distress) has been implicated in the development and maintenance of CSS (30). Even psychosocial constructs, such as catastrophizing, appear to increase the pain experience as the result of centrally mediated noxious inhibitory control (31). Thus, both afferent and efferent pathways are involved. Finally, genetic factors are thought to play an important role in certain subgroups of these patients (32). These factors affect the resulting configuration of the patient’s biopsychosocial response, and how complex the assessmenttreatment process will need to be for each patient. PTSD can be associated with regional alterations in brain structure and functioning that, in turn, may contribute to symptoms and cognitive deficits. Neuropsychological functioning (involved in attention, memory and speed of information processing) may need to be addressed for the successful treatment of PTSD patients (8).

CONCLUSION The diathesis-stress biopsychosocial model argues that the degrees/complexities of the interaction among biological, psychological, and social factors may serve as diatheses or vulnerabilities that victims “bring with them” when exposed to stressors such as pain or trauma, and then can affect the ultimate symptoms they display. Potential mediators/moderators, as well as the potential role of epigenetics in central sensitization, are also included in this model because of the confluence of their effects. A comprehensive interdisciplinary assessment-treatment approach will need to be administered to the traumatized and chronic pain victim in order to more effectively assess and treat the complexity of the factors often seen in trauma and chronic pain patients. ❏

Search AMTA’s Find a Massage Therapist National Locator Service® to find one near you. FindaMassageTherapist.org

The most trusted name in massage therapy.

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VISIBLE/INVISIBLE TRAUMAS AND CHRONIC PAIN

Robert J. Gatchel, PhD, ABPP, is currently a distinguished professor of the department of psychology, college of science, as well as the Nancy P. and John G. Penson Endowed Professor of Clinical Health Psychology at The University of Texas at Arlington. He is also the director of the Center of Excellence for the Study of Health & Chronic Illnesses. Dr. Gatchel has conducted extensive evidence-based clinical research in the area of pain, published more than 410 journal articles and 140 book chapters, and has authored or edited 28 books. He was also the recipient of a prestigious Senior Scientist Award from NIH, and the 2017 recipient of the American Psychological Foundation’s Gold Medal Award for Life Achievement in the Application of Psychology. Nancy D. Kishino, OTR/L, CVE, is a licensed and registered occupational therapist. She has specialized in the management of spinal dysfunction for over 34 years, and has worked for more than 37 years in the areas of physical disability and psychosocial dysfunction. She is the director and owner of the West Coast Spine Restoration Center and the West Coast Spine and Sports Therapy Center in Riverside, California. She has enhanced and perfected the team approach by effectively managing spinal dysfunction and physical disabilities between the physical therapist, occupational therapist, speech therapist and physician through all different insurance types. She also is the proud recipient of the Volvo Award won by the PRIDE team in 1985 for outstanding research on back and neck injured patients.

20. Rowe LS, Jouriles EN, McDonald R. Reducing sexual victimization among adolescent girls: a randomized controlled pilot trial of My Voice, My Choice. Behav Ther. 2015;46(3), 315-327. 21. Katz LS. Treating Military Sexual Trauma. New York: Springer;2015. 22. Barth SK, Kimerling RE, Pavao J, et al. Military sexual trauma among recent veterans: correlates of sexual assault and sexual harassment. Am J Prev Med. 2016;50(1), 77-86. 23. Kimerling R, Makin-Byrd K, Louzon S, Ignacio RV, McCarthy JF. Military sexual trauma and suicide mortality. Am J Prev Med. 2016;50(6);684-691. 24. Bevers K, Watts L, Kishino ND, Gatchel RJ. The biopsychosocial model of the assessment, prevention, and treatment of chronic pain. US Neurol. 2016;12(2):98-104. 25. Hunter RG. Epigenetic effects of stress and corticosteroids in the brain. Front Cellular Neurosci. 2012;6:18. 26. Yehuda R, Bierer, LM. The relevance of epigenetics to PTSD: implications for the DSM-V. J Trauma Stress. 2009;22(5):427-434. 27. McEwen BS. Allostasis and allostatic load: implications for neuropsychopharmacology. Neuropsychopharmacol. 2000;22:108-124. 28. Yunus MB. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Sem Arthritis Rheum. 2007;36:339-356. 29. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152:2-15. 30. van Wijk G, Veldhuijzen DS. Perspective on diffuse noxious inhibitory controls as a model of endogenous pain modulation in clinical pain syndromes. J Pain. 2010; 11(5):408-419. 31. Weissman-Fogel I, Sprecher E, Pud D. Effects of catastrophizing on pain perception and pain modulation. Exp Brain Res. 2008;186(1):79-85. 32. Adams LM, Turk DC. Psychosocial factors and central sensitivity syndromes. Curr Rheumatol Reviews. 2015;11(2);96-108.

References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Asmundson GJG. The emotional and physical pains of trauma: contemporary and innovative approaches for treating co-occurring PTSD and chronic pain. Depression Anxiety. 2014;31(9), 717-720. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: APA; 1980. American Psychiatric Association. Diangostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC. APA;2013. Vyner HM. Invisible Trauma: The Psychosocial Effects of the Invisible Environmental Contaminants. Lexington, Massachusetts: Lexington Books; 1988. Baum A, Gatchel RJ, Schaeffer M.A. Emotional, behavioral, and physiological effects of chronic stress at Three Mile Island. J Consult Clin Psychol. 1983;51(4):565-572. Polatin PB, Young M, Mayer M, Gatchel R. (2005). Bioterrorism, stress, and pain: The importance of an anticipatory community preparedness intervention. J Psychosomatic Res. 2005;58(4):311-316. Finsterwald C, Steinmetz AB, Travaglia A, Alberini CM. From memory impairment to posttraumatic stress disorder-like phenotypes: the critical role of an unpredictable second traumatic experience. J Neurosci. 2015:35(48):15903-15915. Scott JC, Matt GE, Wrocklage KM, et al. (2015). A quantitative meta-analysis of neurocognitive functioning in posttraumatic stress disorder. Psychol Bull. 2015:141(1):105-140. Schatman M, Gatchel, R. Introduction to special issue on traumatically induced pain: assessing and addressing controversies. Psychol Injury Law. 2010;3(3):165-168. Gatchel RJ, McGeary DD, McGeary C A, Lippe B. Interdisciplinary chronic pain management: past, present and future. Am Psychol. 2014;69(2), 119-130. Gatchel RJ, Peng Y, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psycho Bull. 2007;133, 581-624. Taylor SE. Health Psychology. 9th ed. New York, New York: McGraw Hill; 2015. Goldstein LE, Fisher AM, Tagge C A, et al. Chronic traumatic encephalopathy in blastexposed military veterans and a blast neurotrauma mouse model. Sci Transl Med. 2012; 4(134):134ra160. Centers for Disease Control and Prevention. Ten leading causes of death and injury. https://www.cdc.gov/injury/wisqars/leadingcauses.html. Accessed March 14, 2017. Littleton SM, Hughes DC, Poustie SJ, et al. The influence of fault on health in the immediate post-crash period following road traffic crashes. Injury. 2012;43(9):1586-1592. Heron-Delaney M, Kenardy J, Charlton E, Matsuoka Y. A systematic review of predictors of posttraumatic stress disorder (PTSD) for adult road traffic crash survivors. Injury. 2013;44(11), 1413-1422. Gola H, Engler H, Schauer, M, et al. Victims of rape show increased cortisol responses to trauma reminders: A study in individuals with war- and torture-related PTSD. Psychoneuroendocrinol. 2012;37(2):213-220. Au TM, Dickstein BD, Comer JS, Salters-Pedneault K, Litz BT. Co-occurring posttraumatic stress and depression symptoms after sexual assault: A latent profile analysis. J Affect Dis. 2013;149(1–3):209-216. Carper TL, Mills, MA, Steenkamp, MM, Nickerson, A, Salters-Pedneault, K, Litz, BT. Early PTSD symptom sub-clusters predicting chronic posttraumatic stress following sexual assault. Psychol Trauma. 2015;7(5):442-447.

5 REASONS

To Apply for AIPM’s Advanced Pain Management Practitioner (APMP) Certificate – Prescriber Edition ➊ ➋ ➌ ➍ ➎

Document your knowledge and use of best practices in pain care. Demonstrate your extensive experience treating people with pain. Show your patients and peers you’ve gone above and beyond to provide safe and effective pharmacologic pain care. Gain visibility in AIPM’s online directory as an APMP certificate-holder. Conveniently schedule your exam when and where you want it.

Plus, when you bundle this certificate with our optional Curriculum Overview Course, you’ll receive $500 off! TH E PAIN PRACTITION ER

| VOLUME 27, NUMBER 2 |

THE INTERIOR WORLD OF THE PAIN PATIENT

The Interior World of the Pain Patient By Rachel B. Aarons, MSW, PhD

The primary goal of pain practitioners is to help pain patients.We want our help to be as effective, immediate, and long-lasting as possible. Sadly, what may sometimes get in the way of fully achieving this goal is our limited understanding of what it is like to be a person in pain. I offer the following portrait of what is going on under the surface in our patients’ lives in the hope of expanding comprehension and deepening compassion toward the people we serve.

PAIN CHANGES THE WORLD YOU EXPERIENCE. However you lived before, once you are in pain you can be sure things will be different. This is because pain sets limits. Sometimes gradually, sometimes suddenly, a wall comes up. You can’t move in the same way you did before—now it hurts. Perhaps a little, perhaps a lot. There seem to be a million details you can be busy obsessing about. How far do you need to go and are there hills or slopes or stairs? Do you have everything you might need? Your umbrella? Jacket? Mitts? Sunglasses? Sunscreen? Hat? Cane? And all the necessary medications? How close is the parking? How close are the restrooms? Is there an elevator? Wheelchair access? Are the chairs comfortable or will you be squirming in your seat the whole time and then be unable to get up at the end? Will you disturb other people with your grunts and groans? What if you get tired and just want to go home? As a person in pain, you are now absorbed in a negative, downright boring, and seemingly endless train of anxious thoughts. And if it is negative and boring for you to think this way, just imagine how negative and boring it is to listen to! Now you can top it off with a load of guilt. You are miserable and you are making others miserable too. At bottom, pain constitutes an assault on your freedom of choice in the world. Others get to do so many exciting things while you are walled in by can’ts. As the world shrinks and sours, it will inevitably affect the person you are.

PAIN CHANGES THE PERSON YOU ARE. Along with the limits and walls, go the losses. It is not so easy letting go of those hopes and dreams you have cherished. There is less pleasure in the present; there is less to look forward to in the future. You may be worrying about whether this is a temporary or permanent state. Or you may see it not only as not getting better but as inevitably getting worse. People in chronic or extended acute pain will likely be depressed. How devastating to be caught up in a nightmare that has become your life while you were busy planning other things.

PAIN GENERATES ANGER. People in pain get cranky and cantankerous. Just tolerating the pain itself takes effort and a force of will. It is an effort to keep your spirits up and this effort is tiring. Your tone of voice may register strain and this may be perceived as anger and criticism. Sometimes that perception is correct. You really are angry at the situation you are in.

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Some people give themselves permission to express their anger at anyone or everyone who is around. A person like this on a hospital ward gets known pretty quickly. This is no accident. This sort of person wants to make their presence known. It must feel better on some level to make your protest heard and not just take it quietly “lying down.” Most of us are more inhibited. We try to hold back and contain our anger. Perhaps we have moral compunctions about being offensive to others. Perhaps we are sheltering others from knowing about our pain. Or perhaps we are exercising self-protection in not wanting to alienate the people we depend on in our support system. We don’t want them to turn against us and walk away. So we put on a brave front and keep up appearances. Our inner suffering selves are hidden from view.

PAIN FRAGMENTS THE SELF. We can see how a split may develop between the way we act on the surface and the way we feel inside. This distance between appearance and reality creates a sense of isolation and loneliness. We can’t let others into our inner experience. Who we really are underneath is invisible. As a result, people in pain are likely to feel alone and disconnected. Even if you wanted to communicate your inner experience, it is difficult to find the language to do so. There is a stigma attached to being in pain that makes it shameful. It is as if there is an unspoken assumption that if you had it “together,” you would not be in pain. You would be in a sound body, healthy, and vibrant. So there must be something wrong with you psychologically if you are going through so much bodily pain. Now, you not only have to put up with the pain in your body. You also have to feel bad about yourself for having it. Somehow— although you may have no idea how—you are to blame for your suffering. So you pull back from making contact with people and exposing your imperfections. Although you want and need connection, there is a powerful tendency to isolate. You feel judged by others and you judge yourself. You are embarrassed to be seen in the world. You retreat and isolate.

PAIN FOSTERS SELF-HATRED. At the same time as you are turning away from others, you may also be turning away from yourself. The experience of being in unceasing and intolerable pain feels very much like being tormented. Who is the tormenter that treats you this way? It is your own body. The despot who subjects you to this torture is an intimate part of yourself. You are not free to check out of your body, although you can make efforts to dissociate. To the degree that it is possible, not feeling your body’s pain may be the best way to live with it. Dissociation is a method of removing oneself from that which is intolerable. When we are physically unable to run away from a situation, our only escape route may be in our minds. When the perpetrator of the intolerable is not outside but inside us, we may try to stop feeling connected to our body. At this point, we will find ourselves genuinely turning against ourselves. It is almost certainly one of the deepest forms of

THE INTERIOR WORLD OF THE PAIN PATIENT

betrayal when it is your own body that is the enemy. How can we come to terms with being locked inside a body that abuses us in this way? It may seem that we are condemned, without reprieve, to live in a body that seems to hate us. And we may come to hate our body in return. Is there a way out then? Do we humbly submit to our fate or decide to take action?

PAIN IS IN

PAIN FORCES US TO CONFRONT LIFE AND DEATH. Suspended over the cliff, staring into the abyss, we are face to face with one of the wrenching and highly controversial issues of our time—the issue of suicide. When people experience pain that is extreme and overwhelming for a long time—long enough to have had numerous experiences of finding it unbearable—I think it fair to conjecture that their thoughts may turn to wanting it to end. It is like being asked to live the unlivable. Without doubt, intense pain can take us to the brink. In the end, facing death is like a gritty values clarification exercise. You find out what really matters to you after, as the saying goes, “all is said and done.” However, the difference is: this is no exercise. This is the real thing. As practitioners, we are bound by the Hippocratic Oath that requires us to protect and sustain life. The assumption underlying this oath is that sustaining life is always in the best interests of the patient. But is this always true? In support of this position, it is argued that the patient may act out of a state of despair that is temporary and would pass if a sufficient period of time were provided. In fact, there is evidence that people who attempt suicide but fail are often grateful later that they were unsuccessful. Further, one may act out of a conviction that their condition is untreatable and that intense pain will be their inescapable companion every moment in the future. However, medical science is advancing all the time. There is always the possibility of some new discovery or unforeseen methodology that makes a fundamental change in the patient’s situation. Does this mean that we should never give up—either as practitioners or as patients—regardless of how hopeless the situation may appear to be? In my opinion, we cannot dictate an answer—either pro or con—to this question. I believe it may only be answerable by each patient for him or herself. Do we have the right to override another person’s right to be the author of his or her own life and death? Would you want to surrender that right yourself? Would you want to let the person you care about suffer indefinitely—even if that person is yourself?

CONCLUDING NOTE: TO PAIN PRACTITIONERS If you let yourself absorb the information presented here on a heart and gut level and are beginning to understand the internal world of a person in pain, this will make a dramatic difference in your practice. You will notice a deeper connection with your patients. And your patients will experience a deeper connection with you. Genuine empathy is felt in the room. It is a spirit of loving kindness that reaches into the hearts of those who suffer and lets them feel seen. It allows you to go below the surface to the interior of the person before you and opens up the possibility of a new and profound level of healing. Dr. Rachel Aarons is a licensed clinical social worker who has been working with individuals, couples, and families for over 40 years. This article is a condensed and revised excerpt from Dr. Aarons’ book About Pain: For Those Who Suffer and Their Caregivers, Journey Press, 2015.

THE BRAIN A New View of Pain No matter where it is felt in the body, all pain is ultimately registered in the brain. Research is revealing that stubborn, chronic pain is largely a problem of maladaptive plasticity.Through repeated stimulation, pain circuits in the brain become sensitized and fire at high volume, even when no physical injury or disease is present. Chronic pain then becomes a self-perpetuating disease process in itself. Targeted Plasticity Since chronic pain is a problem of plasticity gone wrong, it makes sense to use therapies that help restore normal brain function.The BAUD, or Bio-Acoustical Utilization Device, is a novel device that uses acoustical stimulation to inhibit the reconsolidation of pain circuits.This results in rapid relief for the patient.Typical results reported are a 50%-70% reduction in pain after just one session. The BAUD • a safe, FDA-approved, Class II device • clinically proven in over 500,000 clinical uses in 22 countries • effective for most people – over 75% success rate reported by pain professionals • simple to learn and administer, with no major negative side effects Effective even in stubborn cases “In 2005 I was hit by a roadside bomb in Iraq and the shrapnel cut the ulnar and medial nerves. I suffered a burning pain sensation for the next 5 years until I used the BAUD…just 3 times in one week…and the pain disappeared. It hasn’t returned in over 6 years.” — Jeremy Lee, PHD For more Information and Ordering:

www.BAUDtherapy.com Questions? Contact Richard Bruursema at: rich@BAUDtherapy.com 913-217-5319

TH E PAIN PRACTITION ER

| VOLUME 27, NUMBER 2 |

MINDFUL AWARENESS ACOUSTICAL NEUROMODULATION TRAINING FOR CHRONIC PAIN MANAGEMENT

Acoustical Neuromodulation for Chronic Pain Management By John E. Garzione, PT, DPT, DAAPM, and L. Richard Bruursema

For health professionals of every specialty, chronic pain is one of the most pervasive and difficult problems to treat—especially when central sensitization (CS) has occurred. With repeated stimulation of pain circuits, central sensitization becomes part of the development and maintenance of chronic pain. CS maintains pain even after an injury heals by causing the pain circuit to remain in a hyperaroused state, making chronic pain a self-perpetuating illness in itself. Poorly managed CS worsens with anxiety and lack of sleep, which often accompany the stress of chronic pain. (1,2).

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Stress plays a key role in the development of CS, as it generates hyperalgesia and chronic pain through both peripheral and central mechanisms. CS causes spinal neuroinflammation, decreases in the mechanical nociceptor threshold, increases in sensory hypersensitivity, and long-lasting anxiety-induced hyperalgesia (3-5). CS encompasses muscle pain, dysesthesia, hyperpathia, allodynia, shooting pain, circulatory pain that mimics circulatory insufficiency, and peristaltic pain in the visceral organs (6,7). Many people with CS are sensitive to bright lights, loud noises, medications, temperature, touch, and mechanical pressure (8). It is well established that trauma creates potentiated or sensitized neural circuits in the limbic system, especially the amygdala, that perpetuate problematic emotions (9,10). The amygdala also receives sensory input of all types, including nociceptive information in the latero-capsular portion of the central nucleus (11). In the amygdala, perceptions of threat or helplessness are integrated with nociceptive pain sensations. This establishes neural memories of fear and pain that can progress to the development of chronic pain (12). The subconscious helplessness helps promote maladaptive plasticity and an aberration of memory that changes the patient’s entire perception of reality (13,14), such that the pain memory circuits fire and the patient feels pain as if the injury were still there, much like the amputee with phantom pain. Limbically augmented pain syndrome (LAPS) describes the condition in which a patient experiences more pain and pain behaviors than would be attributed to purely physical causes. LAPS provides an integrated model of how limbic kindling can produce cross-sensitization and account for both the primary pain and secondary non-pain symptoms that present with chronic pain. This experimental model describes how patients’ histories of trauma literally reconfigure their neuronal responses to increase their susceptibility to an overamplified pain response at a later time (15). Fortunately, new treatments are on the horizon, as research is rapidly driving the development of therapies focused on brain plasticity, with the more promising ones based on modulating activity in the limbic system. Since it is maladaptive brain plasticity that creates chronic pain in the first place, it makes sense to treat this process therapeutically. The Bio-Acoustical Utilization Device (BAUD; Insight NeuroSystems, Olathe, Kansas) is a sound-based treatment that was originally developed to improve brain function for treatment of attention deficit disorder/attention deficit hyperactivity disorder (ADD/ADHD) and later discovered to be useful in the treatment of stress and negative emotional symptoms (16). Initial fMRI research suggests it works by disrupting the reorganization of long-term processing memory circuits in the limbic system (17). Since BAUD has been successful in reducing negative emotional perceptions, it could be a safe and effective adjunct treatment for chronic pain because of the close relationship of those circuits in the amygdala (17). BAUD is an FDA-cleared, Class II biofeedback device that emits two adjustable frequency tones that intersect to create a third

ACOUSTICAL NEUROMODULATION FOR MINDFUL CHRONIC AWARENESS PAIN MANAGEMENT TRAINING

Figure 1. BAUD binaural beat which then produces the acoustical neuromodulation (Figure 1). This stimulation appears to affect the amygdala and the hippocampus of the limbic system by theta wave stimulation. Theta activity has been established as essential to both the consolidation and reconsolidation of all memories including pain memories (18,19). The BAUD instrument produces a square wave that is perceived by the patient as an unpleasant sound resembling a swarm of angry bees. Kumar, et al., (20) postulated that adverse sound has an arousal effect on the amygdala through the medial geniculate nucleus via the thalamus (Figure 2). This therapy creates both a stimulation and a temporary disruption of a sensitized circuit, while not imposing a potentially negative neural state based on external measures. This stimulates a neural “reset” based on the brain’s innate ability to self-regulate. Research has shown that once a memory circuit is activated, it can be modified (21).

The treatment protocol requires that the patient focuses his or her attention on the area(s) of pain throughout the treatment, which increases the neural activity of pain circuits and aids in the reset process (22). The earphones are placed on the patient, who initially sets the left and right volume controls to a comfortable, moderately loud level in each ear. The pitch of the sound is then adjusted to the point at which the person feels the sound connect to the body’s location of their pain. This is the most challenging part of the treatment, as many people who have chronic pain also have cognitive difficulties (23). In our case studies we used lower pitch frequencies for pain in the lower body and low back and high pitch frequencies for upper body areas. The disruptor knob is then slowly advanced, producing a pulse or beat, to where the sound is felt to reduce the pain that the person is focusing on. The disruptor creates a binaural pulse that, when properly set in the 4-8 Hz theta range, has the effect of weakening or reducing the target symptom. Research showing that fear memories are reconsolidated during synchronous theta wave activity (24) lends support to the theory of disruption. The unit is left on for 15 to 20 minutes while the patient focuses on the areas of pain to maintain the activation level necessary for acoustical neutralization.

CASE STUDY 1 A 67-year-old male runner was struck by a motor vehicle in 1989 and sustained a fracture in his left femur, a fracture in his right humerus requiring ORIF, and an L4-5 vertebral fracture with right drop foot. He underwent an L5-S1 discectomy in 2002 and developed bilateral lower extremity peripheral neuropathies. Nevertheless, he was running six miles a day prior to his current pain flare-up one month ago. Lumbar MRI showed multiple-level degenerative disc disease at L1 through S1 with moderate central canal stenosis, L5 pseudo-slip posteriorly on S1, L1-2 anterior disc bulge, and Schmorl’s node at L2, as well as an old posterior vertebral fracture at L4 and L5. He was referred for physical therapy because of left > right shin pain, increasing bilateral foot paresthesias, and difficulty sleeping more than two hours at a time. He admitted to being depressed because of mounting stress over his long-term love interest, his brother’s alcoholism, and financial difficulties. The patient’s lower extremity range of motion was within functional limits throughout. His lower extremity strength was 5/5 throughout, except the right anterior tibialis was 4-/5 and the left lower extremity was 4-/5 throughout. There was left > right foot pronation and flexed left > right knee during standing and walking, and he walked with bilateral functional hallux limitus (FHL) and a slight slapping of the right foot, which were not corrected with his current orthotics. The treatment plan included a revision of the patient’s foot orthotics to decrease his FHL and foot pronation, and iontophoresis with iodine and methyl salicylate to bilateral pretibial areas to decongest the compartment pressure and soften the pretibial fascia scar tissue. Soft tissue and joint mobilization was also employed

Figure 2. TH E PAIN PRACTITION ER

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ACOUSTICAL NEUROMODULATION FOR CHRONIC PAIN MANAGEMENT

as well as strengthening exercises. He continued to be depressed and his pain levels remained unchanged for three treatments. BAUD was added to his treatment plan to help decrease his stress and depression. The patient noticed an immediate reduction of pain, stress, and depression after the BAUD treatment. He was able to sleep for seven hours without interruption and returned to running two miles a day after three further treatments. His lower extremity strength returned to 5/5 throughout except for his right ankle tibialis anterior, which remained at 4/5. He subsequently progressed to running six miles a day.

CASE STUDY 2 A 60-year-old woman with a history of childhood sexual abuse was involved in a work-related altercation 20 years ago with a mentally challenged client, which resulted in injuries to her lower back, knees, and right ankle. She underwent extensive physical therapy for 10 years following her injury with little symptom improvement. She was referred to physical therapy because of constant spinal and left > right knee pain with paresthesias in her left knee and both feet. She had difficulty sleeping at night, walking, standing, and driving, and she had constant headaches. Her range of motion was within functional limits. Sensation was normal throughout except decreased for touch, vibration, and pain on the left knee. Her strength was 3-/5 for the left lower extremity, 4-/5 for the right lower extremity, and 3+/5 for the bilateral upper extremities. She stood with a 10 degree forward flexed posture and walked in a step-to gait pattern with a rolling walker. She wore a left knee support because of pain. Her Neck Disability Index was 76%, Back Disability Index was 78%, and her Pain Sensitivity Questionnaire score was 62%, which indicated CNS hypersensitivity (25), and her lower extremity functional scale was 6/80. Her treatment plan consisted of spinal mobilization and core strengthening exercises with electrical stimulation to the cervical through lumbar spine for pain control, upper and lower extremity isometric and rhythmic stabilization exercises, and postural training. After four visits with little symptomatic improvement, BAUD was added to her treatment, and she noticed an immediate improvement. She was seen for a total of eight visits in physical therapy and was able to sleep six to seven hours at a time and walk for two blocks with a cane on level surfaces. She still used her rolling walker on uneven surfaces, and she was able to drive for two to three hours at a time with only intermittent headaches. Her Back Disability Index was 45%, lower extremity functional scale was 20/80, Neck Disability Index was 50%, and Pain Sensitivity Questionnaire score was 45%.

CASE STUDY 3 A 63-year-old woman injured her lumbar and cervical spine while taking care of her disabled paraplegic husband five years ago. She initially underwent physical therapy for pain control, including electrical stimulation, ultrasound, and extensive core strengthening. She was discharged with a home exercise

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program, which she did consistently. Six weeks before returning to physical therapy, she developed neck and back pain again without injury. She tried chiropractic and had some symptomatic improvement, but her pain and stiffness persisted, especially when she was under the stress of managing her husband and elderly parentâ&#x20AC;&#x2122;s care. Her spinal assessment was normal, except her lateral cervical flexion was 30 degrees to the right and 38 degrees to the left. There was hypertonus of the lumbar paraspinals and left > right scalene with left shoulder elevation. X-ray results included multi-level degenerative changes throughout the cervical through lumbar spine, mild levoscoliosis of the lumbar spine, and C7-T1 spondylosis. Her Pain Sensitivity Questionnaire score was 65%, Back Disability Index was 36%, and Neck Disability Index was 32%. She initially received six treatments, including soft tissue mobilization, positional release techniques, and passive and active stretching exercises. When progress was minimal, BAUD was added to her treatment plan because of her high pain sensitivity score. After three treatments with the addition of BAUD, her pain and stiffness decreased by 50%. Her Pain Sensitivity Questionnaire score decreased to 35% and she was discharged to PRN care, which she required one year later after she fell and fractured her right wrist.

CONCLUSION Treatment for people with chronic pain and central sensitization needs to address both physical and central nervous system dysfunction. These patients are excellent candidates for BAUD therapy providing they are not overly sensitive to loud, noxious noises. Those who have this auditory sensitivity are more prone to agitation and a worsening of their symptoms. Theoretically, this treatment would be the nonpharmaceutical treatment of choice in people who are hypersensitive to touch, such as those with known tactile autism.

John E. Garzione, PT, DPT, is a founding member and pastpresident of the Pain Management Special Interest Group of the Orthopaedic Section of the American Physical Therapy Association. He is a diplomate of the Academy of Integrative Pain Management and serves on the Academyâ&#x20AC;&#x2122;s Board of Directors. L. Richard Bruursema is the founder and CEO of Insight NeuroSystems, which provides research and support for health professionals using the BAUD, a unique acoustical neuromodulation device.

ACOUSTICAL NEUROMODULATION FOR CHRONIC PAIN MANAGEMENT

References 1. Baliki MN, Geha PY, Apkarian AV, Chialvo DR. Beyond feeling: chronic pain hurts the brain, disrupting the default-mode network dynamics. J Neuroscience.2008; 28(6):1398-1403. 2. Ready, M. Medication overuse headache: Just following doctor’s orders? Pain Practitioner. 2015;25(2):23-27. 3. Omoigui S. The biochemical origin of pain–proposing a new law of pain: the origin of all pain is inflammation and the inflammatory response. Part 1 of 3–a unifying law of pain. Med Hypotheses. 2007;69(1):70–82. 4. Handwerker HO, Reeh PW. Pain and inflammation. In: Bond MR, Charlton IE, Woolf CJ (eds). Proceedings of the VIth Word Congress on Pain, Pain Research and Clinical Management. Amsterdam: Elsevier; 1991:59-70. 5. Tennant F. Microglial modulators: a new therapeutic class. Pract Pain Manage. 201;15(5):11-128. 6. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895-926. 7. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2-S15. 8. Nijs J, Van Houdenhove B, Oostendorp RA. Recognition of central sensitization in patients with musculoskeletal pain: application of pain neurophysiology in manual therapy practice. Manual Ther. 2010;15(2)(:135-141. 9. Seidenbecher T, Laxmi TR, Stork O, Pape HC. Amygdalar and hippocampal theta rhythm synchronization during fear memory retrieval. Science. 2003;301(5634):846-850. 10. Francati V, Vermetten E, Bremner JD. Functional neuroimaging studies in posttraumatic stress disorder: review of current methods and findings. Depress Anxiety. 2007;24(3):200-218. 11. Veinante P, Yalcin I, Barrot M. The amygdala between sensation and affect: a role in pain. J Mol Psychiatry. 2013;1(1):9. 12. Scaer R. The Trauma Spectrum. New York, NY: WW Norton and Company; 2005. 13. Green PG, Chen X, Alvarez LP, Ferrari LF, Levine JD. Early life stress produces muscle hyperalgesia and nociceptor sensitization in the adult rat. Pain. 2011;152(11):2549-2556. 14. Lawlis F. A study of the BAUD activation for emotional and chronic pain issues. Presented at: International Society for Neurofeedback and Research. September 30-October 3, 2010, Broomfield, Co. 15. Rome HP Jr, Rome HD. Limbically augmented pain syndrome (LAPS): kindling, corticolimbic sensitization, and convergence of affective and sensory symptoms in chronic pain disorders. Pain Med. 2000;1(1):7-23. 16. Bruursema R, Martin L. BAUD Intervention effect on spider phobia: an exploratory fMRI study. Unpublished raw data, 2013. University of Kansas, Hoglund Imaging Center. 17. Schreiber KL, Martel MO, Shnol H, et al. Persistent pain in post mastectomy patients: Comparison of psychophysical, medical, surgical, and psychosocial characteristics between patients with and without pain. Pain. 2013;154(5):660-668. 18. Paré D, Collins DR, Pelletier JG, et al. Amygdala oscillations and the consolidation of emotional memories. Trends Cogn Sci. 2002;6(7)306-314. 19. Narayanan RT, Seidenbecher T, Sangha S, Stork O, Pape HC. Theta resynchronization during reconsolidation of remote contextual fear memory. Neuroreport. 2007;18(11):1107-1111. 20. Kumar S, von Kriegstein K, Friston K, Griffiths TD. Features versus feelings: dissociable representations of the acoustic features and valence of aversive sounds. J Neurosci. 2012;32(41):14184-14192 21. Schiller D, Monfils MH, Raio CM, Johnson DC, Ledoux JE, Phelps EA. Preventing the return of fear in humans using reconsolidation update mechanisms. Nature. 2010 Jan 7;463(7277):49-53. 22. Bantick SJ, Wise RG, Ploghaus A, Clare S, Smith SM, Tracey I. Imaging how attention modulates pain in humans using functional MRI. Brain; 2002;125(Pt 2):310-319. 23. Jones T. The 5 coping skills every chronic pain patient needs. Pract Pain Manage. 2014;14(1):64-69. 24. Ruscheweyh R, Verneuer B, Dany K, et al. Validation of the pain sensitivity questionnaire in chronic pain patients. Pain. 2012;153(6):1210-1218.

Thank you to our Corporate Council Members!

Academy of Integrative Pain Management CORPORATE COUNCIL MEMBERSHIP

Contact Leslie Ringe, (209) 288-2207, leringe@verizon. net to become a Corporate Council Member today!

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AIPM Annual Meeting (continued from page 11)

Food for Thought:

Special Programming on Nutrition The AIPM Annual Meeting will have special focus on food as medicine. Although many cultures view food as a healing therapy, Western medicine has been slow in coming to the table. In addition to regular meeting programing on elimination diets and other food-based therapies, we are delighted to offer two special programs.

NUTRITIONAL PAIN MANAGEMENT WORKSHOP This year we will present a pre-conference certificate program on Nutritional Pain Management (CNPM), a practical clinical workshop covering the importance of food as a pain management intervention. This program, chaired by Robert A. Bonakdar, MD, and Nancy Cotter, MD, will include a discussion of where to start the conversation with patients about using diet and supplements to treat pain. It will also include the five components necessary in a diet for those in pain. Evidence and case studies will show participants how to incorporate this vital intervention into their practices. Other interventions include: • Initiating a specialized diet in specific pain conditions • Antiinflammatory diet • Elimination Diet: When and How: FODMAPs, specific carbohydrate diet, etc • Role of omega-3 in pain management • Role of herbal supplements in pain management Nutrition and supplements for: • Fibromyalgia

• Chronic low back pain

• Migraine/headache

• Obesity

The course will be presented Thursday, October 19, from 9:00 am until 4:30 pm, and will cost $399. For more information, please visit the AIPM website.

Robert A. Bonakdar, MD

Nancy Cotter, MD

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Cooking Demo and Lunch Saturday, October 22 U.S. Pain Foundation President/ Founder Paul Gileno (pictured here) and Academy Board Member and expert on food as a therapy to manage pain Robert A. Bonakdar MD, will present a lively, informative, and delicious program that combines the evidence for an antinflammatory diet with a cooking demonstration. Gileno, a former chef and caterer, will be joined by his colleague Sharon Weiner, who will demonstrate tools and techniques to help make food preparation easy. This program, open to both patients and clinicians, should be informative, lively, and delicious!

The education you need, when you want it.

• AIPM’s Pain Care Learning Center offers comprehensive, on-demand, integrative pain management education with CME/CEU provided for physicians, nurses and psychologists and documentation of attendance for other disciplines. • Basic content offered free for AIPM members. New programs are offered monthly. • 14-hour Curriculum Overview Course for those taking the APMP. To get started, go to: education.aapainmanage.org OR FOR MORE INFORMATION: CONTACT CATHLEEN CONEGHEN AT CCONEGHEN@AAPAINMANAGE.ORG

Earn 5 CME Credits for FREE! CHRONIC PAIN AND OPIOID USE: BEST PRACTICES IN THE CURRENT ENVIRONMENT For a limited time, this 5-hour online program is available FREE to all clinicians who treat people with pain.

YOU WILL LEARN: •

Strategies for assessing a patient’s risk for opioid misuse, abuse, and addiction.

•

How to select an opioid and alternative treatment options.

•

Safe prescribing and ongoing monitoring such as urine drug testing and prescription databases

•

Legal and regulatory perspectives on opioid prescribing

•

… and more!

Led by our distinguished faculty, including Paul Christo, MD (chair), Brett Badgley Snodgrass, FNP-C, CPE, FACPP, Gary Reisfield, MD, and Jennifer Bolen, JD. FOR MORE INFORMATION, GO TO GOO.GL/CCLSIB

TH E PAIN PRACTITION ER

| VOLUME 27, NUMBER 2 |

ADVERTISING DIRECTORY TO ADVERTISE LESLIE RINGE (209)288-2207, LERINGE@VERIZON.NET

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PRACTICES WANTED: PAIN MANAGEMENT, PM&R, & PT Considering Selling your Practice? We are seeking practices on behalf of qualified buyers. Flexible deal structure, all-cash, with favorable terms. Option for sellers to remain post-sale as employed providers. Contact: Mo Majdi 800-416-2055 http://TransitionConsultants.com

JOIN AIPM NOW! WHY JOIN? For more information, go to http://www.aapainmanage.org/membership/.

The only professional organization dedicated to Integrative Pain Management. • We are the FUTURE in integrative pain management • We are a multidisciplinary pain organization: Acupuncturists, Chiropractors, MDs and DOs, Nurses, Physical Therapists, Behavioral Health specialists, and the list goes on! For more information, go to www.aapainmanage.org/membership

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LET NOTHING STOP THEM.™

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Through rigorous testing, the Alpha-Stim® M has been proven to effectively reduce acute, chronic, and post-traumatic pain by providing Microcurrent Electrical Therapy (MET). Additionally, the unique Cranial Electrotherapy Stimulation (CES) feature of the Alpha-Stim treats anxiety, depression, and insomnia in pain patients. Alpha-Stim is: t Cumulative in effectiveness, with most patients showing improvement after the first treatment t Safe, with no serious adverse events in over 35 years

In a study of severe pain patients, Alpha-Stim reduced pain by an average of 71% after only 5 treatment sessions1

Chronic pain patients using Alpha-Stim reported significantly improved functionality compared to the usual care and sham groups2

t Used as a first-line therapy, or as an adjunct to pharmacotherapy (without polypharmacy effects)

HELP FOR YOUR PATIENTS IS HERE. To get started and to see more clinical data, visit www.Alpha-Stim.com or call 1-800-FOR-PAIN (in USA) or +940-328-0788 (Outside USA). REFERENCES 1. Holubec JT. Cumulative response from Cranial Electrotherapy Stimulation (CES) for chronic pain. Practical Pain Management. 2009; 9(9):80-83. 2. Taylor AG, Anderson JG, Riedel SL, et al. Cranial Electrotherapy Stimulation improves symptoms and functional status in individuals with fibromyalgia. Pain Management Nursing. 2013 Dec; 14(4):327-335. Alpha-Stim and the Alpha-Stim logo are registered trademarks, and LET NOTHING STOP THEM is a trademark of Electromedical Products International, Inc. ©2017 Electromedical Products International, Inc. All rights reserved. Read a full disclosure of the minor and self-limiting risks here: alpha-stim.com/risk.

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THE 28TH ANNUAL MEETING

The ONLY Clinical Meeting Dedicated to Integrative Pain Management

San Diego, California October 19-22, 2017 Hilton San Diego Bayfront Over 3+ days, you’ll earn up to 25 hours of CEU/CME – plus you will:

Immerse yourself in the latest techniques for pain management at the year’s largest meeting for all members of the pain care team!

•

Learn about the newest, evidence-based, integrative approaches to pain management.

•

Get best practices of team-based care for the most commonly encountered and challenging painful conditions.

•

Participate in interactive discussions about case studies and lessons learned from other members of the pain care team and experts in the field.

•

Be at the forefront of the biggest policy and advocacy issues affecting access and reimbursement for integrative pain care.

Join the largest network of pain care professionals at this once-a-year opportunity! Secure your spot now at the lowest rates all year: aipm28.eventbrite.com

Program Chairs

Robert A. Bonakdar, MD, FAAP

Michael Kurisu, DO

Roger Mignosa, DO