why chronic pain hurts
Chronic pain is estimated to affect 50-70 million Americans directly and countless other spouses, family members and caregivers indirectly. To help us understand why we experience pain and how chronic pain can impact our lives, we must first explore what causes the feeling of pain.
There are two broad categories for pain: nociceptive (arising from sensory neurons in damaged tissue) and neuropathic (arising from damage to the nervous system itself). Nociceptive pain can be further divided into somatic pain and visceral pain, depending on the type of tissue that is damaged. The viscera are the organs of the body; therefore, visceral pain refers to pain originating in an organ or hollow structure, such as the stomach or the gall bladder. These organs have a very low density of nociceptive fibers (when compared to the skin), meaning that pain from the viscera is very hard to localize and is often vague. Visceral pain may be described as gnawing or aching, and may also include feelings of nausea. Referred pain has the potential to occur in this setting. It originally comes from one organ or part of the body, but is felt in a different place or refers to another location. For example, anginal chest pain (heart attack) typically causes referred pain down the arm. Somatic pain, on the other hand, refers to pain from structures other than the internal organs and includes bones, ligaments and tendons. This type of pain is more common and tends to be more localized than visceral pain. It is often sharp in nature and worsens with activity.
Every tissue in your body is supplied by nerve receptors called nociceptors. These are nerves that are specially designed to detect painful stimuli. For example, extreme heat, mechanical pressure, or irritating chemicals can stimulate these receptors. When the nociceptors detect a painful stimulus, the nerve will fire off an impulse, which travels back, or ascends, to the spinal cord. From there, the pain message is relayed to the brain by traveling through a part of the brain called the thalamus and ending in many different areas of the brain's cortex.
These parts of the brain are important because they affect the way we perceive pain. For example, some of the nerve fibers end in parts of the frontal lobe, which normally handles behavior and decision-making. Other pain fibers may enter the limbic system and will cause us to perceive pain as an unpleasant emotional sensation and may produce fear and anxiety. Once the brain receives the pain signals, nerve impulses will descend and are modulated along the way to the periphery. The descending pathway is responsible for inhibiting pain sensations in the acute pain state, however in chronic pain it may act as a promoter and increase pain.
Amplification and propagation of pain signals occur in both the ascending and descending system through an everlasting barrage of neuronal information that eventually becomes chronic pain. As the chronic state of pain ensues, long-term changes occur at every level in the pain system, including the spinal cord and brain. Eventually, the constant pain alters how we think, interact, behave and interpret pain. Somewhere in this process, the acute pain that was once felt becomes chronic and the nociceptive pain that initiated the discomfort becomes neuropathic and serves as a major contributor to chronic pain.
Neuropathic pain is defined by the International Association for the Study of Pain (IASP) as pain caused by a lesion or dysfunction of the nervous system. It is a pathologic process that serves no useful purpose and is a great source of suffering and disability. Neuropathic pain is typically described as shooting, stabbing, burning or searing. It is not relieved by anti-inflamatories, but typically responds to anti-convulsants, anti-depressants or opioid type drugs. Neuropathic pain is a different type of pain compared to nociceptive pain in that it is not associated with true tissue damage. In essence, the pain signal is maintained by the erratic firing of nerves, which are repeatedly stimulated. When this pain pathway misfires, one will experience pain even in the absence of any real injury.
Neuropathic pain can best be illustrated by the disease herpes zoster, commonly known as shingles. Herpes zoster is an infection that establishes itself in the central nervous system during childhood when the chickenpox (Varicella Zoster) infection occurs. The virus waits dormant for forty or fifty years until reactivation occurs in the form of acute herpes zoster. The acute pain associated with this disease is horrendous; however, there is a vaccine that can help prevent this condition. The lesions and rash tend to heal after several weeks as the pain also subsides. However, ten out of a hundred people who have herpes zoster may develop a dreaded painful condition called post-herpetic neuralgia. This neuropathic pain disorder is caused by damaged nociceptive nerve fibers in the skin that send pain signals up to the brain even when no tissue damage is occurring. Chronic pain is fueled by this signal of "potential tissue damage."
The model of diabetic neuropathy is another example of this kind of pain. With diabetic neuropathy, a constant burning pain occurs in the feet or hands. People often describe a feeling that their feet are on fire. In this disease, nerve endings are being stimulated to send amplified pain signals in the absence of traumatic injury (the hallmark of neuropathic pain). This is quite different from a sprained ankle, which may also create a burning sensation in the foot. The acute pain of a sprained ankle causes discomfort by stimulating nociceptors that transmit information via nerves that is processed as pain when it reaches the central nervous system.
Chronic pain may begin as acute pain (as with a sprained ankle), but lasts longer than would normally be expected for the type of injury that has occurred. When the connection between tissue damage and pain is lost, acute pain may become chronic. The interval for this change to occur is generally three months; however some physicians may use six months as the dividing line. To help clarify and define the term, the International Association for the Study of Pain (IASP) published a statement saying that pain is "an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage". In 1994, this definition was reaffirmed and pain was further recognized to occur in the absence of tissue damage and to be impacted by psychological factors.
We must stress that pain is not only a physical sensation, but is also tied to emotion, by definition. Pain often waxes or wanes depending on emotional factors, level of optimism, degree of hopelessness, positive reinforced behaviors and mood, to mention a few. Pain and emotion are strongly connected because pain signals are sent to areas of the brain that also control how we feel, think and behave. Emotions and pain are intricately intertwined and inseparable, which leads to pain being a personal and subjective experience. Everyone experiences and expresses pain differently. As a result, chronic pain can be very difficult to treat and is often frustrating for both the patient and medical professional. The optimal treatment approach should involve looking for the source of the pain and other physical factors, while also taking into consideration the environmental and psychological factors that may be contributing to the pain syndrome.
Treatments for chronic pain include pharmacotherapy (medication management),
interventional approach (injections), psychological support, lifestyle changes,
complementary and alternative medicine, physical medicine and rehabilitation.
Sleep improvements, anxiety/depression control, nutritional support, and a strong
social support system are imperative to the management of chronic pain. Cognitive-behavioral
therapy is particularly important for the treatment of chronic pain, as it lays
a sturdy foundation to build towards a goal of chronic pain management.
References
Bonica JJ. The Management of Pain. 2nd ed. Philadelphia: Lea & Febiger; 1990: 234-246.
National Institute of Health – www.nih.gov NIH Manual: Management of Chronic Pain; 2001.
Woolf, CJ Pain: moving from symptom control toward mechanism specific pharmacological management. Add Intern Med 2004:441-445.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. American: American Psychiatric Pub, 2000: 623-625.
Food and Drug Administration - www.fda.gov Managing Chronic Pain; 2004.
International Association for the study of Pain – www.Isap-pain.org
Posted August 2008
Disclaimer: The Content is not intended as a guide to self-medication or as a substitute for proper medical advice, diagnosis or treatment. This healthcare content is for reference only and should not be used to determine treatment for specific medical conditions. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.
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