A New Look at Heat Treatment for Pain Disorders, Part 1

A New Look at Heat Treatment for Pain Disorders, Part 1
Winter 2004
Bill McCarberg, MD FABPM, and Annie OÌConnor, PT OCS
American Pain Society

Evidence-based medicine should set the standard of care in all fields of medicine, yet many clinicians take common treatments for granted without subjecting these treatments to the critical assessment of randomized trials. Until recently, heat therapy only had empirical evidence. The first of this two-part series describes a new look at the use of heat as a frequent treatment for common pain disorders, including low back pain; neck pain from arthritis, trauma, and muscle strain; wrist pain; and menstrual-related pain. Information on the proposed mechanism of action of heat, measurements on depth of heating, a comparison of available products for heat treatment, randomized placebo-controlled trials using heat, and how to evaluate a patient for heat treatment will be presented. Part 2 will appear in the next issue of the APS Bulletin.

Heat and the Pathophysiology of Pain
Specialized nerve endings, called nociceptors, are activated in response to tissue injury. Nociceptors transmit nerve signals that travel through the spinal cord to the brain, where the sensation of pain is recognized. At the same time, neurotransmitters initiate a spinal reflex that increases muscle motor activity and tonicity at the site of the injury, leading to reflexive muscle contraction. If persistent, the increase in muscle tone can cause muscle spasms, which in turn lead to further damage to the surrounding tissues due to decreased blood flow and oxygen (i.e., hypoxia that leads to ischemia), thus increasing the pain. This injury process is called the pain-spasm-pain cycle. This cycle must be interpreted to prevent further tissue injury and to reduce the sensation of pain.

Low-level heat therapy affects pain by the thermo receptors, special temperature-sensitive nerve endings activated by changes in skin temperature. These receptors initiate nerve signals that block the nociception, the pain signal processing the results from a noxious stimulus within the spinal cord. Topical modalities applied with physical support activate another type of specialized nerve ending called a proprioceptor. Proprioceptors detect physical changes in tissue pressure and movement. Proprioceptor activity also inhibits the transmission of nociceptive signals to the brain. The activation of these receptors within the spinal cord reduces the muscle tone, relaxes painful muscles, and enhances tissue blood flow.

Heat and Common Usage
When confronted with painful disorders, patients frequently try a variety of over-the-counter remedies, including medications, topical agents, and wraps. They also use old family recipes. When all these fail, patients seek medical help and are often given prescriptions. Based on a telephone survey of a random sample of Americans 18 years old or older, Kaufman, Kelly, Rosenberg, Anderson, and Mitchel (2002) found that analgesics were the most frequently used FDA-regulated products (over-the-counter and prescription). Acetaminophen, ibuprofen, and aspirin were the three most commonly used drugs. Cost, side effects, the need for ongoing healthcare utilization for prescriptions, and the possibility of adverse events and risk are just a few of the reasons why medications may not be the best option for common pain complaints.

Alternative and complementary strategies for pain relief are becoming more popular. Thermal therapies ( e.g., heat and ice) have been used for thousands of years and are back in vogue. Heat and ice are often recommended for sports injuries and everyday strains and sprains. Physicians commonly recommend the rest, ice, compression, elevation therapy (RICE). Although heat therapy is widely accepted and practiced, until recently there were no clinical studies showing the efficacy of heat therapy for any pain disorder except for a few studies in migraine (Lance, 1988). The Agency for Healthcare Policy and Research (now the Agency for Healthcare Research and Quality [AHRQ]) stated that thermal therapy was unsupported by evidence. ÏThe panel found no evidence of benefit from the application of physical agents and modalities such as ice, heat, massage, traction, ultrasound, cutaneous laser treatment, transcutaneous electrical nerve stimulation (TENS), and biofeedback techniquesÓ (Bigos et al., 1994).

Heat: Mechanism of Action
The gate-control theory of pain inhibition is the basis for one hypothetical mechanism of action of heat (see Figure 1; Melzack & Wall, 1965). Heat applied externally increases the temperature of the skin and deep tissue-stimulating thermoreceptors (Cameron, 1999; DePace & Newton, 1996). This afferent thermal signal inhibits the transmission of nociceptive signals through the spinal cord to higher centers and the subsequent recognition of pain. Heat relaxes muscles by decreasing alpha-motor activity from the dorsal horn of the spinal cord, thus decreasing muscular tone (Lundeberg & Ekholm, 2002). Heat also has an effect on multiple pain generators, including inflammation, ischemia, and peripheral neuropathic generators. Physiological responses to heat therapy include increased local blood flow and metabolism, supporting the efficacy of this modality when pain results from ischemia, spasm, or the accumulation of chemical mediators of inflammation , such as prostaglandins (Ersala et al., 2001; Nanneman, 1991; Reid, Foley, Prior, Weingard, & Meyer, 1999).

For optimal biophysical effects (i.e., muscle lengthening), the intramuscular temperature should reach at least 40?C, which requires at least a 3Ò4?C increase in surface temperature (Kankaanpaa, Taimela, Airaksinen, & Hanninen, 1999). A 1?C increase in tissue temperature is associated with a 10%Ò15% increase in tissue metabolism (Smith, 2002). Recent research has shown that heat applied directly to the skin at 40?C increases muscle tissue temperature at least 1?C at depths ranging from 2.0 to 3.8 cm below the surface of the skin (Mulkern et al., 1999). In addition, heat applied on the skin of the upper back (Kankaanpaa, Taimela, Airaksinen, & Hanninen, 1999) and knee (Reid et al., 1999) increases blood flow in the trapezius muscle and popliteal artery, respectively.

This research also shows that only low levels of continuous topical heat (approximately 40?C or 104?F) are needed to increase deep tissue temperature and blood flow. Heat transfer is directly related to the temperature gradient, the surface area covered, and the duration of application. Low-level heat from nonelectric heating pads appears to provide better safety than electric heating pads.

The traditional approach of short-term treatment (i.e., 20 minutes) multiple times during the day may require rethinking. Continuous, long-term heat therapy (i.e., eight hours or more) represents a new treatment option that has proven to be practical, safe, and effective. As an example of long-term therapy, consider the Lidoderm? patch, the only topically applied product approved by the FDA for the treatment of one specific type of painÛpostherpetic neuralgia (Physicians Desk Reference, 2003). The manufacturer recommends 12 hours of constant application, not short duration intermittent therapy, which is the rule with some heat treatments.

Another example of long-term cutaneous therapy is the use of the TENS unit, which is also applied continuously over many hours to impart an enduring benefit. Heat has a known mechanism of action that includes increased blood flow, decreased motor neuron activity, and enhanced pain modulation. Not only does continuous application of low-level heat provide immediate pain relief in some cases, but it also may produce an ongoing analgesia over several days. All of these mechanisms suggest that long-term continuous heat therapy is a well-reasoned approach for pain control, but this will need to be studied more formally.

Musculoskeletal pain from the central nervous system (CNS), however, does not have the local properties discussed above as the primary peripheral input to the pain system. CNS-mediated pain syndromes are considered a neurological disease processes because the inputs to the pain experience appear to be central and are perhaps dominated by the personÌs cognitive thoughts and beliefs about pain (cortical and limbic input). These affective emotional responses to the pain (i.e., fear, anxiety, blame, and so on) appear to involve psychological processes that are greater than the local physical tissue restrictions (strictly peripheral, bio-medical response [Janssen, 2002]).

Low-level heat therapy can be an adjunct treatment with persons with CNS-mediated pain syndromes. Heat therapy will certainly continue to produce the physiological effects at the local, painful, deconditioned tissue. Education, explanation, and demonstration will be the most effective therapy, however, to reset the circuitries of pain, address maladaptive thoughts and beliefs, address fears, establish trust, and expose patients gradually to new activities so they can regain control of their lives.

Heat and Musculoskeletal Pain Types
Musculoskeletal pain can be divided into two types: (1) peripheral nervous system (PNS) and (2) CNS (Lundeberg & Ekholm, 2002). Within PNS we see pain as a result of neuronal irritation, either directly or from inflammatory and ischemic properties in target tissues of ligaments, muscles, tendons, cartilage, and peripheral nerves (Hagen et al., 2002). PatientsÌ subjective histories show patterns in 24-hour pain behavior, location, description, frequency, and onset. PatientsÌ objective histories display patterns toward movements and positions when they are dealing with qualities of inflammation or ischemia in target tissues. Continuous low-level heat therapy is usually effective when the patients are dealing with irritation because of ischemic qualities (from sustained spasm ÏbracingÓ) or when they have reached stages in healing and repair of connective tissue that require blood flow and movement to continue.

When a person is suffering from inflammatory pain as a result of peripheral inflammatory mediators, they often complain of constant pain that has happened acutely (i.e., within 2 weeks) or acute exacerbation of a chronic problem. The pain will be localized to an anatomical structure, which they usually describe as swollen, hot, red, and so on. They typically state that over a 24-hour period the symptoms are worse in the morning, improve as the day progresses, and worsen again in the evening (Gifford, 1995). They usually tell you that ice and over-the-counter ibuprofen lessen the intensity of the pain but never eliminate it. In the objective part of the examination, patients will display pain in every direction, and as a result of repetitive movements in each direction the pain will increase with no identified preferred direction or position.

Inflammatory pain as a result of mechanical irritation to target tissues typically has the same presentation as that caused by a chemical process with respect to location, 24-hour behavior, and even descriptorÛwith a few extra descriptive terms like crackling and stiffness. The differences are the pain caused by mechanical irritation is intermittent and responds to ice when irritated. Anti-inflammatory meds are usually not helpful, and in the objective examination there is a close relationship between stimulus-response and identified preferred direction with a repeated movement examination. Heat therapy is generally, not prescribed for inflammatory pains from chemical and mechanical processes until the healing tissue moves into stages where blood flow is required to finish remodeling in the reparative process.

When a person is suffering from ischemia-related pain, again consistencies in the patients subjective and objective reactions are observed. The patient will describe the location of symptoms as localized to the target tissue and of intermittent nature; and they will mention fatigue, weakness, or tightness. The onset of symptoms will either be several weeks from the injury or have no apparent reason, which usually means the symptons were caused by a positional or cumulative mechanical situation not yet recognized (Kincaid, 1997). The 24-hour behavior is very different from inflammatory because the morning is the best time of day. There are no further problems during the day unless the patients have resumed the positional or cumulative stress for greater than one to three hours: in that case, they will feel worse as the day progresses. In the objective examination, if there has been an actual injury that is healing and in the remodeling stage, the movement examination will reveal restrictions of movement and end-range pain that does not get worse as a result of repetition. If this tissue is not injured but is utilizing positions too long or repeating movements too often, then you will not find restriction or pain in any range. Nor will you reproduce symptoms on the movement and static loading examination unless you repeat movement enough times or sustain the position long enough to reproduce the painful situation. Generally this type of painÛpain from ischemic propertiesÛusually responds to heat therapy, especially when the heat therapy has been used for prolonged periods of time and is portable, thus allowing movement to occur simultaneously to encourage blood flow and remodeling of tissue.

Summary
Evidence-based medicine suggests heat therapy, behavioral, and movement-based approaches as the keys to treating musculoskeletal pain.

After reviewing clinical features related to the different types of pain, pain professionals can discuss with patients why they may need heat therapy, movement therapy, or discussion (i.e., talk) therapy. Individualized care plans may be developed to help patients develop coping strategies for different aspects of their lives, as needed.

References
Bigos, S., Bowyer, O., Braen, G., Brown, K., Deyo, R., Haldeman, S., et al. (1994, December). Acute low back problems in adults. Clinical Practice Guideline, No. 14. Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services.

Cameron, M.H. (1999). Heat-thermotherapy. In Physical agents in rehabilitation (pp.149Ò175). Philadelphia: Saunders.

DePace, D.M., & Newton, R. (1996). Anatomic and functional aspects of pain-evaluation and management with thermal agents. In S.L. Michlovitz (Ed.), Thermal agents in rehabilitation (3rd ed.) (pp. 30Ò57). Philadelphia: F.A. Davis Co.

Erasala, G.N., Rubin, J.M., Tuthill, T.A., Fowlkes, J.B., de Drue, S.E., Hengehold, D.A., et al. (2001). The effect of topical heat treatment on trapezius muscle blood flow using power Doppler ultrasound. Physical Therapy, 81, A5.

Gifford, L.S. (1995). Fluid movement may partially account for the behavior of symptoms associated with nociception in disc injury and disease. In M.O. Shacklock (Ed.), Moving in on pain (pp. 32Ò39). Chatswood, Australia: Butterworth-Heinemann.

Hagen, K.B. , Bjorndal, A., Uhlig, T., & Kvien, T.K. (2000). A population study of factors associated with general practitioner consultation for non-inflammatory musculoskeletal pain. Annals of the Rheumatic Diseases, 59, 788Ò793.

Janssen, S.A: (2002). Negative affect and sensitization to pain. Scandinavian Journal of Psychology, 43, 131Ò37.

Kankaanpaa, M., Taimela, S., Airaksinen, O., & Hanninen, O. (1999). The efficacy of active rehabilitation in chronic low back pain. Effect on pain intensity, self-experienced disability, and lumbar fatigability. Spine, 249 (10),1034Ò1042.

Kaufman, D.W., Kelly, J.P., Rosenberg, L., Anderson, T.E., & Mitchel, A.A. (2002). Recent patterns of medication use in the ambulatory adult population of the United States: The Slone Survey. JAMA: The Journal of the American Medical Association, 287, 337Ò344.

Kincaid, J.C. (1997). Muscle pain, fatigue, and fasciculationÌs. Neurologic Clinics, 15, 697Ò709.

Lance, J.W. (1988, August). The controlled application of cold and heat by a new device (Migra-lief apparatus) in the treatment of headache. Headache, 7, 458Ò61.

Lundeberg, T., & Ekholm, J. (2002). Pain from periphery to brain. Disability and Rehabilitation, 24, 402Ò406.

Melzack, R., & Wall, P.D. (1965). Pain mechanisms: A new theory. Science, 150, 971.

Mulkern, R.V., McDannold, N., Hynynen, K., Fielding, J., Panych, L., Jolesz, F.A., et al. (1999, May 22Ò28). Temperature distribution changes in low back muscles during applied topical heat: A magnetic resonance thermometry study. Proceedings of the Seventeenth Annual Meeting of the International Society of Magnetic Resonance in Medicine (p. 1054), Philadelphia.

Nanneman, D. (1991). Thermal modalities: heat and cold. A review of physiological effects with clinical applications. AAOHN Journal: Official Journal of the American Association of Occupational Health Nurses, 39, 70Ò75.

Physicians Desk Reference (57th ed.) (p. 1298). (2003). Clifton Park, NY: Thomson-Delmar.

Reid, R.W., Foley, J.M., Prior, B.M., Weingand, K.W., & Meyer, R.A. (1999). Mild topical heat increases popliteal blood flow as measured by MRI. Medicine and Science in Sports and Exercise, 31(5), S208.

Smith, R.P. (2002). Heat therapy: The next hot topic. The Female Patient, 27, 25Ò31.