Saturday, January 29, 2005


Botulinum toxin (Botox®) is a medication that is mainly known for its cosmetic dermatology and plastic surgery usage. It can also be used to reduce the muscle tension and spasm in other conditions, for example chronic headaches, neck aches, back pain, even sciatica due to pelvic muscle spasm. It can assist in improved posturing and walking; and allow better range of motion and a more effective physical therapy. Botox® is a good alternative for patients who have had partial and short lived response to trigger point injections.

A diagnostic trigger point injection (TPI) using a local anesthetic must usually precede the Botox® injection. A significant relief from TPI (even short-term), is usually associated with a positive result from Botox® injection.

The actual procedure is very similar to trigger point injections except for the medication used. In this procedure, very small amounts of the diluted Botox® will be injected into the areas of significant spasm and/or trigger points. This will cause significant flaccidity of the target muscle.
The result is usually not immediate and takes a few weeks to set in. Duration of effect varies from a few weeks to several months. Physical therapy and life style plays an important role in therapy. Side effects are rare, although, some patients may experience flu like symptoms temporarily. The injection may be repeated if needed.

Wednesday, January 26, 2005

New Strategies for Managing Acute Pain Episodes in Patients With Chronic Pain

Daniel M. Gruener, MD

In the 18th century, the French philosopher Voltaire said, "Doctors are men who prescribe medicines of which they know little, to cure diseases of which they know less, in human beings of which they know nothing...." He also opined that " is dangerous to be right on matters on which established authorities are wrong." If he were alive today, writing a tome on pain medicine, it would be easy to imagine Voltaire describing physicians as people who withhold medications of which they know a great deal, to manage painful conditions of which they have learned even more, in human beings who perceive them as knowing nothing, amidst a regulatory climate that scares the hell out of them.

In the 21st century, it is ironic that although we have made significant advances in our understanding of how pain affects the nervous system and continue to develop innovative treatments, many pain sufferers, including dying cancer patients, receive little or no treatment. One possible explanation is the dizzying development of scientific theories of pain physiology, including the different subtypes of pain and the associated improvements in available treatment options, counterbalanced by increasing regulatory scrutiny and limited financial resources for some patients.

Breakthrough pain is a perfect example of the need to understand and treat all of the different pain subtypes. As is typical in pain medicine, breakthrough pain first came to the attention of clinicians in the cancer population. In 1990, Portenoy and Hagen[1] proposed that transient flares of pain in a cancer patient with stable persistent pain treated with opioids be defined as breakthrough pain. However, breakthrough pain is neither specific to cancer pain, nor is it purely an opioid-related phenomenon. Cancer pain often is the catalyst for improving the nomenclature used to describe the different types of pain, and advances in opioid pharmacology often help to define these changes.

The Pain Cascade in Brief

Acute pain follows some sort of injury to the body and generally dissipates when the injury heals. It serves a useful purpose in warning us that deferring treatment may result in life-threatening consequences. For example, a patient with acute appendicitis may complain of sudden, sharp, intense right lower quadrant abdominal pain. Without the pain, the diagnosis may be missed and the appendix could rupture, resulting in tragic consequences. By contrast, chronic pain serves no useful function, persisting beyond the time one would expect normal healing to occur.

Following an injury or other insult to the body, incoming pain signals trigger the release of glutamate, an excitatory neurotransmitter, into the synaptic cleft between nociceptors and dorsal horn cells. Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on the sodium and potassium channels are activated by acute pain. With prolonged activation, the magnesium plug in the calcium channel is removed, and N-methyl-D-aspartatic acid (NMDA) receptors in the channel are primed for glutamate activation. A cascade of neural events is triggered, leading to the facilitation of neural remodeling and hypersensitization. In other words, and admittedly, more research is needed to demonstrate this; it is possible that undertreatment of acute pain may facilitate the development of chronic pain and cause years of needless suffering by creating changes in the way the nervous system perceives painful impulses, ultimately confusing benign stimuli as being painful, such as in allodynia.[2] Breakthrough pain, which can be viewed as a type of acute pain, may also, in the opinion of this author, facilitate remodeling of the nervous system when not treated appropriately. At the very least, it can certainly cause needless suffering for patients when not identified and managed.

Breakthrough pain is defined as a transient increase in pain of moderate-to-severe intensity, which occurs against a background of persistent pain of mild-to-moderate intensity that has been controlled. It must be differentiated from uncontrolled persistent pain, acute episodic pain, and end-of-dose failure. If a patient has chronic low back pain and is in pain 24 hours per day despite taking a long-acting opioid and appropriate adjuvant analgesics, then adjusting the long-acting medication should be addressed before considering breakthrough pain. With acute episodic pain, there is no persistent pain between flare-ups. For example, a patient may have severe, debilitating migraine headaches 3 days a month, but be fine the rest of the time. In this case, long-acting medications would be unnecessary. End-of-dose failure occurs when a long-acting medication wears off sooner than one would expect, on the basis of the known duration of action of the medication. This can usually be solved by increasing the frequency of administration of the medication. For example, a patient receiving sustained-release morphine, which has a 12-hour duration of action, reports good pain relief for 8 hours, but then begins to decompensate. Adjusting the dose to every 8 hours should be tried before adding other medications.

Breakthrough Pain: Incident and Idiopathic

True breakthrough pain is either incident or idiopathic. Incident pain is predictable. A patient who has just had a total knee replacement may be stable except during physical therapy sessions, which cause a flare-up of pain. Administering short-acting medication preemptively may avoid the flare-ups and allow the patient to participate more fully in his/her therapy. Incident pain can occur with movement, coughing, and increased activity. Some patients tell me they avoid activity because they are afraid this will cause their pain to flare. Knowing they have options to treat these flare-ups can improve functioning.

Breakthrough pain can also be idiopathic, or spontaneous. It can occur randomly and unpredictably with little or no warning, and can be unrelated to activity level or adequacy of the persistent pain treatment. The intensity of breakthrough pain is generally moderate to severe. Onset tends to be rapid, with 43% of patients reporting an onset of 3 minutes or less.[1] The duration of idiopathic breakthrough pain tends to be short. Although variable, some patients report a duration of 20-30 minutes. The frequency averages 1-4 episodes per day. This represents an average, however, so a patient may have days free of breakthrough pain and other days marred by 8 episodes. Also, some patients may experience a more insidious onset and a longer duration of pain. This is why assessment is so important to individualize treatment.

Addressing Breakthrough Pain

After maximizing the treatment of background pain and ruling out end-of-dose failure, I ask my patients the following questions: (1) Do you have pain flare-ups; (2) if yes, how long does it take for you to feel the increase in pain; (3) how long does the increased pain last; (4) are the flare-ups associated with a specific activity, or do they occur randomly; (5) does the increased pain prevent you from doing any activities?

Why bother adding this to a pain evaluation? According to a study by Portenoy and associates,[3] patients with untreated breakthrough pain demonstrate reduced levels of functioning, have greater levels of anxiety and depression, and are less satisfied with their opioid therapy.

Not treating breakthrough pain can even add to economic burdens. Fortner and colleagues[4] studied patients with chronic cancer pain and found that those who had breakthrough pain incurred costs 5 times higher than patients without breakthrough pain. The greater costs were primarily related to hospitalizations for uncontrolled pain, emergency department visits, and unscheduled office visits. Although current economic data reflect the experience of patients with cancer, I recently participated as an investigator in a study examining the prevalence and impact of breakthrough pain in patients with noncancer pain. The data are still being analyzed, but this illustrates the point that breakthrough pain is not just a cancer-related phenomenon.

Managing Breakthrough Pain

The optimal treatment of pain should employ both pharmacologic and nonpharmacologic approaches, such as interventional pain management, cognitive behavioral therapy, and biofeedback. The World Health Organization analgesic ladder is still used to the pharmacologic treatment of pain. Nonopioids, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and acetominophen, are used to treat mild pain. The guidelines recommend opioids for moderate-to-severe pain. Thus, the pain intensity should drive the choice of medication when using the ladder. Some clinicians erroneously believe that they must begin with a nonopioid, even when the patient suffers severe pain.

Acute pain should be treated early and appropriately to avoid both needless suffering and to prevent possible remodeling of the central nervous system. Breakthrough pain should also be addressed on the basis of the results of the aforementioned evaluation. Some clinicians attend to breakthrough pain by increasing the dose of long-acting medication. This strategy may cause sedation and side effects, because the patient is now being exposed to a greater medication load. They are also receiving pain medication at times when they are not experiencing pain. Ideally, patients should be placed on long-acting medications to control their persistent pain and shorter-acting medications to control breakthrough pain.

Individualizing the Approach

The recommendation for dosing breakthrough medication at 10% to 15% of the daily long-acting dose does not seem to match clinical experience. Some patients may have more breakthrough pain relative to persistent pain. The treatment must therefore be individualized and based on proper evaluation. For a patient whose breakthrough pain comes on gradually and lasts 45 minutes to an hour, conventional, hydrophilic, shorter acting opioids (such as oxycodone, hydrocodone, morphine, or hydromorphone) may be fine. If a patient is taking sustained-release oxycodone for persistent pain and the characteristics of his/her breakthrough pain episodes match the pharmacologic profile of shorter acting oxycodone, then that would be a clinically feasible combination.

For the 43% of patients with an onset of breakthrough pain in less than 3 minutes and a duration of 20-30 minutes, the shorter acting, hydrophilic medications only begin to work when the pain has already dissipated. And we are, once again, subjecting the patient to unnecessary medication. In my practice, I've been able to dramatically reduce some patients' total opioid doses by properly addressing their previously untreated or mistreated breakthrough pain. The ideal breakthrough medication for this subset of patients should have a rapid onset, short duration of effect, minimal side effects, and be easy to use (noninvasive). Oral transmucosal fentanyl is the only medication that fits this profile without requiring patients to self-inject opioids at home, a practice I generally try to avoid. US Food and Drug Administration (FDA)-approved for management of breakthrough pain in non-opioid-naïve cancer patients, this short-acting formulation takes advantage of the oral transmucosal route of delivery. The oral mucosa is highly vascularized and very permeable, which, combined with the lipophilic nature of fentanyl, allows the agent to enter the bloodstream rapidly and directly without hepatic and intestinal first-pass metabolism. Rapid onset of action is achieved without invasive methods.

Some patients say that they feel "empowered" to have a tool that can give them rapid relief that in the past could only be achieved by a trip to the emergency department for an injection. It is also the only way to use fentanyl for breakthrough pain when patients are using the fentanyl transdermal patch. Some clinicians, including myself, believe that if persistent pain is responsive to fentanyl, then the likelihood is that the same will hold true for breakthrough pain. This of course entails off-label use at times, a practice not uncommon in pain medicine. Concerns about abuse, diversion, and addiction are certainly valid; however, any controlled substance can potentially be abused. Proper patient selection, monitoring, use-of-treatment agreements, and toxicology screens can help to reduce these risks. This medication provides the opportunity to ask patients to bring in the used sticks, which can be counted to help determine that the medication is not being diverted.

Some patients may be able to use nonopioids, such as NSAIDs, for breakthrough episodes or tramadol, a centrally acting analgesic with weak mu-receptor affinity that also inhibits the reuptake of norepinephrine and serotonin. However, because breakthrough pain is at least moderate in intensity by definition, opioids are the most likely pharmacologic intervention.

Other strategies that can be helpful for breakthrough pain episodes include relaxation training, hypnosis, and cognitive behavioral therapy, although scientifically controlled studies have not validated these techniques in breakthrough pain. Patient education and family involvement are critical and should be addressed early in treatment.

In summary, acute pain should be managed early and effectively both for proper medical care and to help prevent remodeling of the central nervous system, which may facilitate the development of persistent pain. Breakthrough pain is a valid type of acute pain that occurs commonly in patients with persistent pain, and it has to be managed. Increasing the dose of long-acting opioids often exposes the patient to needlessly high doses of medication and can result in sedation, constipation, and other side effects. Some physicians believe that prescribing only long-acting opioids will reduce their liability; however, addicts can crush, liquify, inject, and snort long-acting opioids, essentially converting them to rapid-acting agents. Treatment should therefore be individualized on the basis of the nature of an individual's breakthrough pain. Optimally, however, medication should be noninvasive, have a rapid onset, and have a relatively short duration of effect.


  1. Portenoy RK, Hagen NA. Breakthrough pain: definition, prevalence and characteristics. Pain. 1990;41:273-281. Abstract
  2. Burstein R, Yamamura H, Malick A, Strassman AM. Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons. J Neurophysiol. 1998;79:964-82. Abstract
  3. Portenoy RK, Payne D, Jacobsen P. Breakthrough pain: characteristics and impact in patients with cancer pain. Pain. 1999;81:129-134. Abstract
  4. Fortner BV, Okon TA, Portenoy RK. A survey of pain-related hospitalizations, emergency department visits, and physician office visits reported by cancer patients with and without history of breakthrough pain. J Pain. 2002;3:38-44. Abstract
Daniel M. Gruener, MD, Clinical Assistant Professor, Jefferson Medical College, Philadelphia, Pennsylvania
Disclosure: Daniel M. Gruener, MD, has disclosed that he has received grants for educational activities and has served as an advisor or consultant for Cephalon, Pfizer, and Janssen.

Medscape Neurology & Neurosurgery 6(2), 2004. © 2004 Medscape

Botulinum Toxin A Relieves Pain of Trigeminal Neuralgia

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NEW YORK (Reuters Health) Oct 24 - Injections of botulinum toxin A substantially reduce the pain associated with trigeminal neuralgia, physicians report in the October 25th issue of Neurology, with pain relief lasting at least 60 days.

Dr. Elcio J. Piovesan, from Hospital de Clinicas da Universidade Federal do Parana in Curitiba, Brazil, and colleagues administered subcutaneous injections to four men and nine women who had trigeminal neuralgia for an average of 10.25 years and 8.22 years, respectively. Depending on the nerve branch, patients were treated with 6.45 to 9.11 units of botulinum toxin A.

Patients assessed the pain in the three branches of the trigeminal nerve with a 10-point visual analog scale (VAS), which ranged from 9.82 to 10 points at baseline. At day 10, VAS scores averaged 3.78 to 5.83. Maximal pain relief was noted at day 20 (average VAS 0.00 to 0.82).

Pain had increased slightly by day 60 (average VAS 1.82 to 3.17).

Prior to botulinum treatment, patients had used carbamazepine, gabapentin, codeine, Lioresal, and oxacarbamazepine as prophylactic treatment. "Most of our patients reduced their preventive medication by more than 50%," Dr. Piovesan's group notes, while "others stopped them completely, and some taking multiple medications converted to monotherapy."

Neurology 2005;65:1306-1308.

Advanced Pain Management Techniques: An Overview of Neurostimulation

Posted 04/19/2004
Philip Kim, MD

Neurostimulation is the application of precise targeted electrical stimulation on nociceptive pathways. Electric stimulation has a long history in medicine for treating various ailments. Beyond the application of electrodes on the skin such as in transcutaneous electrical nerve stimulation (TENS), electrodes have been applied directly to nociceptive pathways.

The nociceptive pathways are made up of tracts in the central and peripheral nervous systems. The central nervous system includes nociceptive pathways in the spinal cord and brain, specifically the dorsal roots, dorsal ganglion, spinothalamic tracts, and all ascending neural tracts to the cerebrum. The peripheral nervous system includes pathways outside the spinal cord, specifically various plexuses and peripheral nerves.

Components of the System

Spinal cord stimulation involves the placement of an electrical system to block nociception. The system comprises the surgical placement of epidural electrodes, cables, and radiofrequency transmitter or battery. Much of this method has evolved from cardiac pacemaker technology. The minimal invasiveness and trialing has led to the success of this approach. Neurostimulation can be placed during an outpatient procedure, with local anesthesia and sedation. The patient experiences minimal discomfort when the system is placed and during the postoperative period.

Before the system is placed, a simple trial of percutaneous lead placement can be performed. In this case, the patient goes home with the lead connected to a screener box. No incision is necessary and the procedure is performed using only local anesthesia. The purpose of the trial is to determine the effectiveness of the stimulation for relieving pain and improving the patient's quality of life. If this temporary method allows the patient to sleep better, use less pain medication, and sit and stand longer, then it becomes more convincing to place an internalized spinal cord stimulation system.

Mechanism of Action

The mechanism of action of spinal cord stimulation is based on the placement of epidural electrodes along the dorsal columns. Originally, spinal cord stimulation was called dorsal column stimulation. It is thought that spinal cord stimulation works through the gate-control theory of Wall and Melzack, which theorizes that stimulating large nerve fibers (A beta fibers) can inhibit or modulate smaller nerve fibers (A delta or C fibers), transmitting nociceptive input possibly at the dorsal root or horn of the spinal cord. Strategically placed epidural electrodes stimulate the dorsal columns (A beta fibers) to inhibit or modulate incoming nociceptive input through the A delta or C fibers. Ongoing research suggests that spinal cord stimulation may inhibit transmission in the spinothalamic tract, activation of central inhibitory mechanisms influencing sympathetic efferent neurons, and release of various inhibitory neurotransmitters.

Pain Conditions

Spinal cord stimulation can be applied to treat neuropathic pain conditions, including arachnoiditis, complex regional pain syndrome (formerly called reflex sympathetic dystrophy), neuropathies, brachial and lumbosacral plexopathies, radiculopathies, deafferentation syndromes, phantom limb pain, and postherpetic neuralgia. Clinical studies and 30 years of clinical experience have continued to show efficacy in these conditions. Visceral syndromes such as interstitial cystitis, chronic abdominal pain, and chronic pancreatitis have been treated with limited success.

Intractable pain caused by peripheral vascular disease and angina can be treated with spinal cord stimulation. Indeed, in Europe, the primary indication for spinal cord stimulation once was peripheral vascular disease. The success of stimulating the lower extremities may be based on microvascular blood flow changes via alterations in sympathetic outflow. It could also be that one is treating a concurrent ischemic neuropathy in the lower extremities.

Limited success of spinal cord stimulation may depend on the extent of peripheral vascular disease. Based on one study,[1] spinal cord stimulation does not reduce the incidence of amputation in the lower extremities. The same rationale for using spinal cord stimulation for treating peripheral vascular disease is now being applied in clinical trials of patients with intractable angina, including those with patent coronary vessels who continue to have intractable angina and patients who are not candidates for coronary bypass and stent procedures. It is theorized that these patients have a neuropathic condition and microvascular blood flow deficiency.

Some painful conditions cannot be stimulated along the spinal cord and therefore are not responsive to spinal cord stimulation. Thus, peripheral nerve and plexus stimulation has evolved as a complementary neurostimulation approach. The mechanism of peripheral nerve and plexus stimulation is unclear since the electrodes are not stimulating the dorsal columns. Some postulate that a variation of the gate-control theory is involved at the peripheral nervous system level. Moreover, peripheral nerve stimulation may activate central structures leading to inhibition of various nociceptive pathways, similar to the way acupuncture results in somatosensory cortex activation.

Clinical Trials

Current clinical trials and experience have involved 3 different patient groups. First, intractable headaches caused by neuropathies of the trigeminal and occipital nerves may benefit from neurostimulation. Trigeminal neuralgia is a painful constant condition for which neurodestructive neurolysis may not work. Neurostimulation of the actual trigeminal ganglia has been performed. Stimulation of various branches of the trigeminal ganglia, such as supraorbital and auriculotemporal nerve, has been performed with limited success. Ongoing clinical research is under way on occipital nerve stimulation; electrodes are placed percutaneously and surgically along these nerves at the subcutaneous occiput level. The peripheral nerve stimulation system is placed in a manner similar to the spinal cord stimulation system.

Second, stimulation of the sacral nerves or lumbosacral plexuses can be beneficial for painful conditions resulting from chronic abdominal, pelvic, genital, and anal pain syndromes. Specific conditions that have been treated include interstitial cystitis, coccydynia, pyelonephritis, pancreatitis, rectal fugax, and vulvodynia. These perplexing syndromes are difficult to treat in significant part because we lack a complete understanding of what perpetuates them. Procedures allowing access to sacral and lumbosacral nerves include a retrograde epidural approach and a sacral transforaminal approach.

Third, some peripheral neuropathies, neuromas, and plexopathies are difficult to stimulate along the spinal cord and may not respond to spinal cord stimulation. Surgically or percutaneously placed electrodes along nociceptive pathways have been performed with success. The most common sites are along the ulnar, median, common peroneal, and saphenous nerves.


Neurostimulation of the central and peripheral nervous systems is playing a vital role in the treatment of various intractable pain conditions, including conditions for which we have limited pathophysiologic understanding, such as complex regional pain syndrome. Until we develop treatments that truly eliminate pain, neurostimulation can play a major role in improving the quality of life for pain patients. These systems do not damage neural pathways and could be removed when curative therapy becomes available.

As patients and their physicians become aware of the benefits of these techniques for managing intractable and difficult-to-treat pain syndromes, more people may be interested in undergoing this kind of treatment and will achieve improvements in the quality of their lives. The comedian Jerry Lewis lives with intractable low back pain and has attributed his spinal cord stimulation system with giving him his life back. Hopefully, he will continue to talk about his life and persuade others that they don't have "to live with it [pain]."


  1. Horsch S, Schulte S, Hess S. Spinal cord stimulation in the treatment of peripheral vascular disease: results of a single-center study of 258 patients. Angiology. 2004;55:111-118.

Suggested Reading

Albutaihi IA, Hautvast RW, DeJongste MJ, et al. Cardiac nociception in rats: neuronal pathways and the influence of dermal neurostimulation on conveyance to the central nervous system. J Mol Neurosci. 2003;20:43-52.

Augustinsson LE. Spinal cord stimulation in peripheral vascular disease and angina pectoris. J Neurosurg Sci. 2003;47(1 suppl 1):37-40.

Buschmann D, Oppel F. Peripheral nerve stimulation for pain relief in CRPS II and phantom-limb pain. Schmerz. 1999;13:113-120.

Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year literature review. J Neurosurg. 2004;100(3 suppl):254-267.

Erdek MA, Staats PS. Spinal cord stimulation for angina pectoris and peripheral vascular disease. Anesthesiol Clin North Am. 2003;21:797-804.

Jessurun GA, Hautvast RW, Tio RA, DeJongste MJ. Electrical neuromodulation improves myocardial perfusion and ameliorates refractory angina pectoris in patients with syndrome X: fad or future? Eur J Pain. 2003;7:507-512.

Murray S, Collins PD, James MA. Neurostimulation treatment for angina pectoris. Heart. 2000;83:217-220.

Rushton DN. Electrical stimulation in the treatment of pain. Disabil Rehabil. 2002;24:407-415.

Weiner RL. Peripheral nerve neurostimulation. Neurosurg Clin North Am. 2003;14:401-408.

Zamotrinsky AV, Kondratiev B, de Jong JW. Vagal neurostimulation in patients with coronary artery disease. Auton Neurosci. 2001;88:109-116.

Philip Kim, MD, Medical Director, Center for Pain Medicine, P.C., St. Francis Pain Center, Wilmington, Delaware
Disclosure: Philip Kim, MD, has disclosed that he has served as a consultant for Medtronic.
Medscape Neurology & Neurosurgery 6(1), 2004. © 2004 Medscape

Tuesday, January 25, 2005

Chronic Pain and Its Management in Primary Care

from Southern Medical Journal

Hani Raoul Khouzam, MD, MPH, Department of Psychiatry, VA Medical Center, Manchester, NH

Abstract and Introduction


Background. Chronic pain is commonly encountered in primary care, but it can be difficult to manage.
Methods. The purpose of this article was to review the definition of chronic pain, general guidelines of management, pharmacologic and nonpharmacologic treatment, the role of pain clinics, and rehabilitation goals.
Conclusions. Effective management of chronic pain is usually achieved by an interdisciplinary team, with involvement of both patients and their families, and integrates pharmacologic and nonpharmacologic treatment with needed surgical interventions, psychotherapy, and rehabilitation.


Chronic pain (ie, pain lasting more than 3 to 6 months) is one of the most common conditions for which people seek medical attention.[1] Although chronic pain is less common than acute pain, it may affect at least one of every three Americans at some point in their lives.[1] It is estimated that every year 40 million American adults will have debilitating headaches, 90 million will complain of joint pain, and about 100 million will report episodes of back pain.[2] By the turn of the 20th century, the medical treatment of chronic pain in combination with the loss of productivity and financial compensation reached an estimated yearly cost of $100 billion.[3]

Despite its prevalence, chronic pain remains one of the most poorly understood and untreated conditions in primary care.[4] This article focuses on the management of chronic nonmalignant pain.

Definition of Pain

The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in term of such damage."[5] This definition highlights the complexity and multidimensional aspect of pain and suggests that pain is not just a reflection of the amount of physical injury but is a process that may be influenced by age, sex, culture, and environment, as well as unique individual makeup.[6]

General Guidelines in Management

First, managing chronic pain requires an interdisciplinary team and involvement of both patients and their families.[3] Such a team can be part of primary care setting or a specialty care clinic.[4] The interdisciplinary team approach is multimodal and includes pharmacologic management, physical rehabilitation, psychologic intervention, behavior modification, and familial and spiritual support.

Second, any patient who has chronic pain needs comprehensive initial assessment, including detailed history, physical examination, diagnostic evaluation, and psychiatric assessment to identify the presence of comorbid psychiatric disorders. When these disorders are treated and the psychosocial stressors that trigger pain exacerbations are addressed, chronic pain levels can substantially decrease.[8] Patients need to be supported and encouraged to maintain and improve their mobility and daily functioning. They need to be fully engaged in an active, productive life with normal interpersonal and social interactions.[7]

Third, because the perception of pain is an individualized subjective experience, the most reliable indication of its existence is the patient's report rather than visible clinical signs, radiographic findings, abnormal vital signs, or behavioral disturbances.[4] The absence of known physical, medical, or surgical causes of pain does not negate the presence of chronic pain.[3,4]

Fourth, narcotics can alleviate pain when integrated within a rehabilitative model of treatment. The fears of drug dependence and addiction should not deter their usage in patients who respond to their effects and do not show signs of abuse.[6] Surgical procedures should be used only when there is clear evidence of a reversible problem.

Monday, January 24, 2005

Adaptation to Stress and Natural Therapies

Homeopathic & Natural Remedies Products

In our modern society we are barraged with various forms of stress throughout each day. We are readily able to adapt to some of those stresses, yet others are or become seemingly
insurmountable. Stress and stress-related disorders have been considered a significant cause of disease and may contribute to perhaps 75 % of all illnesses.

A Canadian professor, Hans Selye, MD, is responsible for pioneering the field of stress research and is commonly known as, "the father of stress." His writings on the subject date back to the 1930 s, and he is credited with writing over 1700 papers and 39 books on the subject. As the undisputed expert on the subject, he observed as early as 1925 that common symptoms were present in many diseases. He explained this as the syndrome of “ just being sick.” A triad of physical changes was always present in this syndrome. After exposing rats to various types of stress they were dissected. The dissection revealed: 1) adrenal cortex enlargement; 2) atrophy of the thymus, spleen, lymph nodes and all other lympatic structures and; 3) deep bleeding ulcers in the stomach and duodenum.

Selye classified the progression of stress on the body and it’s influence on the adrenal glands. The classification is called the “ General Adaption Syndrome” (GAS) (Selye, 1956; Ward, 1998). The three stages which are described include alarm, resistance and finally exhaustion. The " Alarm Reaction" is characterized by surprise and anxiety and is considered to be a general call to arms. The adrenal glands secrete hormones, i.e epinephrine, norepinephrine and hydrocortisone. This phase occurs quickly and accounts for a phenomenon such as a petite mother lifting a car to free her child. "Resistance" represents the second phase of stress, when the body prepares to continue and adapt to the prolonged fight ahead. Adrenal hypertrophy and other factors of the triad of stress are found in this stage. An individual can respond and meet the demands of the stress as long as this stage continues. If the adaptive stress is resolved, a rapid return to the resting state can be achieved. “ Exhaustion” occurs when the adrenal glands can no longer meet the demands placed on them due to the prolonged stress. Dilman and Dean (1992), who are responsible for the neuroendocrine theory of aging, refer to this phase as adrenal maladaptation or hyperadaptosis. Hyperadaptosis is considered by some to be a precursor to Cushing’s Syndrome, and is characterized by prolonged exposure to excess cortisol levels and is caused by the loss of hypothalamic sensitivity to the inhibitory effect of cortisol
(Dilman, 1981). It is the chronically hyperactive Hypothalamus- Pituitary-Adrenal (HPA) Axis that causes these symptoms. These same high levels of stress have been shown by Selye to lead to many of the diseases of aging (Selye, 1976). Robert Sapolsky, the author of Why Zebras Don’t Get Ulcers, also recognizes the role of these hormones in disease (Sapolsky,1987). Additionally, chronic health problems, long-term nutritional deficiencies, and long-term emotional problems can all lead to the state of adrenal exhaustion.

Researchers have identified eight physical indicators of an individual’s stress load (McEwen, 1998). Stressful life events such as divorce, job loss, family arguments and even traffic jams, in addition to daily maladaptation all add to stress. Among the stress indicators are: increased blood pressure; suppressed immunity to disease; increased fat around the 10 The Pain Practitioner In modern society, the long-term, never-ending emotional stress creates tired or exhausted adrenal glands, primarily because the adrenal glands do not have an opportunity to rebuild. abdomen; weak muscles; bone loss; increases in blood sugar; increases in cholesterol levels and; increases in steroid hormones, i.e. cortisol.

How our bodies react by producing stress hormones is ostensibly even more important than how we feel about the events. When an episode of acute stress is experienced, cortisol is secreted to protect us by activating, through a complex chain of events, the body’s defenses. Acute stress (in the sense of "fight or flight" or major life events) and chronic stress (the cumulative load of minor day-to-day stresses) can both have long-term consequences (, 1998).

One of Selye’s first observations regarding the general adaptation syndrome was that animals under prolonged stress developed sexual derangements. Intense stress caused young animals to cease growing and caused lactating females to produce no milk. Prolonged stress may be partially or totally responsible for amenorrhea in female athletes who are under intense training (Brooks-Gunn, Warren & Hamilton, 1987). Recent research in Ohio reports that wounds heal slower when patients are under psychological stress (Kiecolt-Glaser & Glaser, 2000). With constant sympathetic activation, the immune system becomes depressed.

In modern society, the long-term, never-ending emotional stress creates tired or exhausted adrenal glands, primarily because the adrenal glands do not have an opportunity to rebuild. Because stress is cumulative, the stresses to which the body must react over time can cause mild to moderate adrenal insufficiency, the most common clinically observed entity. In this condition the individual can still react to stress, however, it will be less efficient and take more time.

The goal of health is to maintain homeostasis. When the HPA Axis is disturbed homeostasis is lost. A DHEA/cortisol balance (two hormones secreted by the adrenals) is considered to be a critical marker of overall hormonal health. These adrenal hormones can be tested utilizing saliva samples. A natural approach using hormonal and herbal therapies may be utilized to adjust the DHEA/cortisol balance. Current literature is recommending that DHEA at 12.5 to 50 mg. taken daily in the morning and Pregnenolone at 10 to 100 mg. taken daily in the morning (Hornsby, 1997).

Adaptogens, a group of substances that help the body adapt to stress, have been shown to reduce the damage of the stress response, maintain homeostasis during chronic stress, reduce most evidence of the alarm stage and help delay the exhaustion phase. Royal bee jelly , one of the world’s richest sources of pantothenic acid need for the adrenal glands, is an adaptogen. The most widely researched adaptogens are Siberian ginseng (Eleutherococcus Senticosus) and licorice (Glycyrrhiza) (Ritchason, 1995). Licorice is a natural way to supplement the body’s endogenous cortisol production, giving the adrenals a well needed rest. Studies have been performed to investigate a licorice daily dosage of 25-100mg and its affect on anxiety (Chen & Hsieh, 1985). Precautions are to use licorice for no more than several weeks at a time to prevent
potentiation of glucocorticoids and mineralcorticoids.

Other herbs that have been shown to be of benefit to the adrenal glands include astragalas, bayberry, borage, burdock, kava, kelp, parsley and rose hips (Chen & Hsieh, 1985). Vitamin C also reduces the effects of chronic stress by decreasing cortisol production (American Chemical Society, 1999). Acupuncture, chiropractic manipulation, biofeedback, deep breathing, massage, meditation, avoidance of food allergies and hypersensitivities, proper diet and changed attitudes are just some of the positive things that can be used in the mind/body/spirit realm.

No article on the adrenal glands would be complete without mentioning the positive affect exercise plays in reducing daily stress (Carmack, 1999).

In summary, stress is everywhere we turn, it is essentially pandemic. Our inability to handle these stresses well, leads to adrenal gland overutilization, and ultimately exhaustion. This condition can and does have a negative impact on pain and anti-aging. Through lab testing, lifestyle changes and nutritional and/or herbal supplementation doctors can begin restoring homeostasis and well being in their patients.

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The Pain Practitioner 11

Acupuncture May Be Helpful for Chronic Daily Headache CME

Medscape Medical News

News Author: Laurie Barclay, MD

CME Author: Désirée Lie, MD, MSEd


Oct. 24, 2005 — Acupuncture may be helpful for chronic daily headache (CDH), according to the results of a randomized trial published in the October issue of Headache.

"Approximately 4% of adults experience headaches nearly every day," write Remy R. Coeytaux, MD, PhD, from the University of North Carolina at Chapel Hill, and colleagues. "Nonpharmacologic interventions for frequent headaches may be appropriate because medical management alone is often ineffective."

In 74 patients with CDH, the investigators compared medical management provided by neurologists to medical management plus 10 acupuncture treatments. The main endpoints were daily pain severity and headache-related quality of life (QoL).

Patients who received only medical management did not show improvement in any of the standardized measures. Although daily pain severity scores trended downward, they were not different between treatment groups (P = .60). Compared with medical management only, medical management plus acupuncture was associated with an improvement of 3.0 points (95% confidence interval [CI], 1.0 - 4.9) on the Headache Impact Test (HIT) and an increase of at least 8 points on the role limitations caused by physical problems, social functioning, and general mental health domains of the Short Form 36 Health Survey (SF-36). Patients in the acupuncture group were 3.7 times more likely (95% CI, 1.7 - 8.1) to report less pain from headaches at six weeks (absolute risk reduction, 46%; number needed to treat, 2).

"Headache-specialty medical management alone was not associated with improved clinical outcomes among our study population," the authors write. "Supplementing medical management with acupuncture, however, resulted in improvements in health-related QoL and the perception by patients that they suffered less from headaches."

Study limitations include unblinded study design, use of subjective outcomes introducing potential bias, failure to isolate acupuncture as the single causal variable, lack of a sham control, bias inherent in the study design, and inability to evaluate the efficacy of medical care provided by the three study neurologists.

"Additional research is needed to elucidate the extent to which placebo effects associated with acupuncture contribute to clinical benefit, to identify clinical characteristics that predict favorable response to acupuncture, to explore which acupuncture traditions and protocols are most effective for treating the various causes and manifestations of CDH, and to determine whether acupuncture is a cost-effective approach to the treatment of frequent headaches," the authors write.

The National Institutes of Health have disclosed that they funded this study, and the Verne S. Caviness General Clinical Research Center at University of North Carolina School of Medicine also disclosed that they supported it. The Robert Wood Johnson Clinical Scholars Program have disclosed that they supported Dr. Coeytaux during the design phase of the study.

Headache. 2005;45:1113-1123

Learning Objectives for This Educational Activity

Upon completion of this activity, participants will be able to:
  • Describe clinical features of CDH.
  • Compare the outcomes of usual care vs usual care plus acupuncture for six weeks for CDH.

Clinical Context

CDH is a clinical syndrome characterized by the occurrence of headache 15 or more days per month. According to the current authors, it affects 3% to 5% of the general population and is responsible for up to 80% of new presentations to headache specialty clinics. Headache type may consist of migraine, tension, or other headaches by the International Headache Society classification system. Medications commonly used for this condition include acetaminophen, aspirin, nonsteroidal anti-inflammatory drugs, triptans, narcotics, and barbiturates, but all are associated with adverse effects and may paradoxically convert episodic to chronic headaches. Acupuncture has been described as a promising treatment of CDH, and according to the current authors, a systematic review identified 23 studies in which acupuncture was considered positive for various types of headache.

This is a randomized, open clinical trial conducted on patients with CDH at a neurology clinic to examine the effect of adjunctive acupuncture on CDH outcomes for six weeks.

Study Highlights

  • Inclusion criteria were headache 15 or more times in the previous month, older than 18 years, and English proficiency.
  • Exclusion criteria were intracranial surgery, head or neck surgery, or treatment with acupuncture within 6 weeks.
  • Patients were paid $80 for completion of headache diaries and follow-up assessments.
  • 39 patients were randomized to usual care by the treating neurologist and 35 to usual care and 10 sessions of acupuncture by one provider.
  • There was no sham acupuncture group. Patient expectations of acupuncture was not described.
  • At baseline health-related QoL was assessed by the HIT using a 6-item questionnaire to assess headache burden from the patient perspective in the past month.
  • Health status was also measured using the SF-36, a scale for pain severity from 0 to 10, with 10 being the most severe; and the Beck Depression Inventory (BDI).
  • Primary outcomes were change in HIT scores from baseline to the 6-week follow-up visit and daily ratings of pain severity during the 6-week intervention period.
  • Patients completed the HIT and BDI at 6 and 12 weeks.
  • Adverse effects of acupuncture were elicited from patients.
  • Acupuncture was delivered by an experienced physician and acupuncturist trained in Traditional Chinese Medicine (TCM) in the People's Republic of China and who was a diplomate of the National Certification Commission for Acupuncture and Oriental Medicine.
  • The acupuncturist interviewed and examined each patient prior to randomization.
  • The acupuncturist needled points according to TCM pattern diagnoses and tender points at or near the site of maximal headache pain when indicated for a maximum of 30 needles left in place for up to 30 minutes.
  • A total of 10 acupuncture sessions was delivered for 6 weeks.
  • Mean age was 44 to 47 years, 77% to 85% were female. 50% were employed full-time, and most had migraine-type headache.
  • Average duration of CDH was 1 to 5 years, with more than 80% experiencing near daily headache for at least one year.
  • Daily pain severity scores tended downwards for 6 weeks and was not different between the 2 groups.
  • Usual medical care plus acupuncture was associated with a 3-point decrease in HIT score for 6 weeks vs usual medical care.
  • Medical care plus acupuncture was associated with an improvement of 8 or more points in the role limitations due to physical, social, and general mental health domains of the SF-36, and a decrease of 3.5 points in the BDI relative to usual medical care only.
  • At the 12-week follow-up, the acupuncture group experienced an improvement of 7 or more points for the role limitations in the SF-36 due to physical problems, vitality, and social functioning.
  • Patients who did not receive acupuncture did not demonstrate improvements in the SF-36 or other outcomes at the 6- or 12-week follow-up.
  • In the acupuncture group, 62% reported having less pain from headaches at 6 weeks vs 16% in the usual care group (P < .001), corresponding to an absolute risk reduction of 46% and number needed to treat of 2.
  • Adverse events related to acupuncture were reported in 34 (97%) of 35 patients in the acupuncture group. These included headaches, neck soreness, and difficulty sleeping.

Pearls for Practice

  • CDH is a clinical syndrome characterized by the occurrence of headache 15 or more days per month and may include any headache type.
  • The use of 10 sessions of acupuncture as an adjunct to usual care is associated with improvements in perceived pain, BDI score, and physical and social functioning in patients with CDH.