Posted by Aurora on Wed, 05/09/2012 - 2:10 PM
CHRONIC PAIN(1)
Chronic Pain is defined as a universal disorder that lasts for weeks, months, or even years and is often not responsive to regular pain medications(2). The International Association for the Study of Pain defines it as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage."(3) Pain is essential for life in that it warns us of danger. However, pain that persists past the purpose of warning us of danger decreases quality of life and taxes personal, familial, and communal resources. Dr. Albert Schweitzer in 1931 wrote that "Pain is a more terrible lord of mankind than even death itself."(4)
There are two basic types of pain: acute and chronic. Acute pain follows disease, inflammation, or injury to tissues and is confined to a given period of time and severity. Chronic pain persists over a longer period of time, is resistant to medical treatment, and may cause severe debilitation. "Hundreds of pain syndromes or disorders make up the spectrum of pain."(5)
Receptors in tissue trigger an electrical impulse that travels to the spinal cord, which in turn relays pain signals to the brain. Pain signals pass through the dorsal horn of vertebrae of the spinal cord to the brain. When pain reaches the brain, the most common destination is the thalamus.(6) From the thalamus, pain passes to the cortex. Neurotransmitters conduct nerve impulses on a cellular level. Neuroscientists have found that blocking glutamate in the brain reduces pain responses in mice. Opiod pain medications block pain by locking on to opioid receptors, inhibiting pain pathways or circuits.
Thin nerve fibers called nociceptors carry pain signals to the spinal cord and brain. The condition called allodynia develops when chemicals cause nociceptors to become inflamed, such as after a sunburn or infection, and to transmit a pain response even from a breeze or a caress. The brain may prompt the spinal column itself to release natural painkillers such as serotonin, norepinephrine, and opioid-like chemicals. The synthesis of these may lead to promising new pain killers.
Endorphins and enkephalins are other natural painkillers. Endorphins are released after exercise and are thought to be released after stimulation by TENS units. Endorphins, along with dopamine, contribute to the pleasurable sensation of smoking.
Peptides, compounds found in proteins in the body, may affect pain responses. Mice missing a gene for two peptides, tychykinins-neurokinin A and substance P, have a reduced response to severe pain, suggesting these peptides affect the production of pain responses.
Research involving receptors for acetylcholine, potentially using epibatidine found in the skin of an Ecuadorian frog, may help in the development of future pain killers. Epibatidine is highly toxic but an effective analgesic. Hopefully non-addictive blockers of the receptors of acetylcholine will be found.
Experiments are also being conducted on a tiny population of neurons in the spinal cord that carry persistent pain signals to the brain. Receptors for these neurons were neutralized after animals were injected with Substance P linked to saporin and other lethal chemicals. These animals responded to normal/acute pain but did not display exaggerated pain response or lingering pain response to injury.
Transplantation of chromaffin cells, which produce several of the body's pain-killing substances and are part of the adrenal medulla, into the spinal cords of rats appeared to contribute to recovery from pain-related cellular damage. There is hope this may be applied to severe pain in humans.
One mechanism of blocking pain is the inhibition of hormones called prostaglandins, which stimulate nerves at injury sites and cause inflammation and fever. Non-Steroidal Anti-Inflammatories (NSAIDs) block the cyclooxygenase-1 and cyclooxygenase-2 enzymes required for synthesis of prostaglandins. Newer COX-2 inhibitors block mainly cyclooxygenase-2 with fewer gastrointestinal side effects than NSAIDs. These help reduce the inflammation, fever, and pain of arthritis.
Serotonin levels fall before migraines. Migraine medications called triptans, known as serotonin agonists, mimic the action of natural serotonin and bind to some serotonin receptors, reducing migraine pain symptoms.
Cytokenes, proteins fround in the nervous system, can trigger pain by promoting inflammation even when there is no injury or damage. Cytokine levels rise in the brain and spinal cord and at the site of the injury in the peripheral nervous system. Future research may aim to block the action of cytokines.
Electrical stimulation for chronic pain may include Transcutaneous Electrical Stimulation (TENS), implanted electric nerve stimulation, peripheral nerve stimulation, spinal cord stimulation, and deep brain or intracerebral stimulation. Electrical stimulation may be invasive, expensive, and not suitable for all patients, although helpful to many.
Nerve blocks may be chemical or surgical, including neurectomy; spinal, dorsal, cranial, and trigeminal rhizotomy; and sympathectomy. New imaging technology may enable researchers to see what happens chemically in the brain and spinal cord as a result of injury and disease. This knowledge may help reduce or eliminate severe or chronic pain in the future. Research leads to hope for improvement in the quality of life for people in pain.
- Elizabeth S. York, M.Ed., LPC, LMFT