Chronic Pain Information
Chronic Pain
Peripheral Neuropathy
Reflex Sympathetic Dystrophy or
Complex Regional Pain Syndrome
Central pain syndrome
Pain
Acute Pain
The body reacts with lightning speed to injury.
1. The stimulus: the body is lined with nerves that release chemical signals
when they sense tissue damage
2. The signal: pain impulses travel up the spinal cord, relayed from one nerve
cell to the next by chemical messengers
3. Response: when the brain receives a pain impulse, it locates the injury and
assesses its severity. Then it releases other messengers to calm or alert the
body
4. Resolution: once it has responded to a pain signal, the brain releases chemicals
that can interrupt it, stopping the message in the spinal cord
Chronic Pain
If an injury damages the pain system itself, patients may develop long-term
chronic pain
1. Damaged nerve: Injuries can alter pain-sensing nerves, causing them to send
out constant false-alarm signals
2. Sensitisation: the increased signals open up new chemical channels (receptors)
on spinal nerves, making them more susceptible to future pain signals
3. Mental overload: some chronic pain sufferers exhibit greater brain activity
than healthy people when subjected to pain. This may explain why they experience
pain more severely
4. Loss of control: some chronic pain sufferers may lose the ability to block
incoming pain messages, so signals fire unheeded, magnifying the pain of once
harmless sensations
Source of Information: S.G. Rao, Cypress Bioscience Inc. in Newsweek, May 2003
Neuropathic Pain
Neuropathic pain is very different from acute pain. It typically occurs when there has been damage to peripheral nerves, which extend from the spinal cord all the way to fingertips and toes and other body surfaces. That damage can lead to a "rewiring" of cells inside the spinal cord such that a light touch on the surface of the body ends up being transmitted to the brain as a pain signal. Or what may also occur is an amplification of the signal in the spinal cord, with the same result. In that situation the nervous system is abnormal and then the changes that occur can be very profound. Even the light touch of clothing can be intensely painful.
Such pain is also highly resistant to strong narcotics like morphine or heroin. There is no single drug that blocks just one receptor, although research is being done in this area of pain relief.
Source of Information: http://www.canada.com/health
Extract from NINDS Chronic Pain Information Page
While acute pain is a normal sensation triggered in the nervous system to alert you to possible injury and the need to take care of yourself, chronic pain is different. Chronic pain persists. Pain signals keep firing in the nervous system for weeks, months, even years. There may have been an initial mishap -- sprained back, serious infection, or there may be an ongoing cause of pain -- arthritis, cancer, ear infection, but some people suffer chronic pain in the absence of any past injury or evidence of body damage. Many chronic pain conditions affect older adults. Common chronic pain complaints include headache, low back pain, cancer pain, arthritis pain, neurogenic pain (pain resulting from damage to the peripheral nerves or to the central nervous system itself), psychogenic pain (pain not due to past disease or injury or any visible sign of damage inside or outside the nervous system).
Is there any treatment?
Medications, acupuncture, local electrical stimulation, and brain stimulation, as well as surgery, are some treatments for chronic pain. Some physicians use placebos, which in some cases has resulted in a lessening or elimination of pain. Psychotherapy, relaxation and medication therapies, biofeedback, and behavior modification may also be employed to treat chronic pain.
What is the prognosis?
Many people with chronic pain can be helped if they understand all the causes of pain and the many and varied steps that can be taken to undo what chronic pain has done. Scientists believe that advances in neuroscience will lead to more and better treatments for chronic pain in the years to come.
What research is being done?
Clinical investigators have tested chronic pain patients and found that they often have lower-than-normal levels of endorphins in their spinal fluid. Investigations of acupuncture include wiring the needles to stimulate nerve endings electrically (electroacupuncture), which some researchers believe activates endorphin systems. Other experiments with acupuncture have shown that there are higher levels of endorphins in cerebrospinal fluid following acupuncture. Investigators are studying the effect of stress on the experience of chronic pain. Chemists are synthesizing new analgesics and discovering painkilling virtues in drugs not normally prescribed for pain.
Study Links Chronic Pain to Signals in the Brain
Extract from NINDS Chronic Pain page
Overview
For centuries, doctors have tried to find effective ways to treat chronic pain, a devastating neurological disorder that affects almost 90 million Americans. A new study shows that two proteins in the brain trigger the neuronal changes that amplify and sustain this type of pain. The finding may lead to new ways of treating chronic pain.
"This is the first [chronic pain] study to show clear molecular targets in the brain," says Min Zhuo, Ph.D., of Washington University in St. Louis, Missouri, senior author of the report. "Drugs that inhibit these two proteins may help to reduce chronic pain." The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) and appears in the November 14, 2002, issue of Neuron.1
Unlike the short-term, acute pain that people feel when they stub a toe or burn themselves, chronic pain is a disorder of the nervous system that persists for months or years and cannot be fully relieved by standard pain medications. It often includes burning, shooting, or shocking sensations. Chronic pain also may cause a problem called allodynia, in which people experience pain from stimuli that are not normally painful, such as a light touch or a breeze, or pain in places other than the area that is stimulated. There are many different kinds of chronic pain, including central pain, chronic regional pain syndrome (also called reflex sympathetic dystrophy), and peripheral neuropathy.
Most studies of chronic pain have focused on signals in the spinal cord and in the peripheral nerves, which carry pain messages from the limbs and other parts of the body to the spinal cord. However, recent studies have suggested that the brain not only receives pain signals from the spinal cord but also undergoes changes in neuronal connections that may permanently strengthen its reactions to those signals. Researchers believe these changes are key to the development of chronic pain.
In the new study, Dr. Zhuo and his team tested pain-related behavior in normal (control) mice and in mice missing the gene for two proteins called adenylyl cyclase 1 and 8 (AC1 and AC8). These two enzymes are found primarily in a part of the forebrain called the anterior cingulate cortex (ACC). Previous studies have shown that this region is important for feeling pain.
The two groups of mice reacted the same way to stimuli that cause acute pain. However, in tests of chronic pain, the mice without AC1 and AC8 had much smaller reactions than the control mice, suggesting that they did not feel as much pain. When the researchers gave these mice a substance that increases the amount of a chemical called cyclic AMP, which triggers changes in neuronal connections, they began to react to painful stimuli like the normal mice did. This showed that disabling the two genes blocked chronic pain by preventing pain-related changes in neuronal connections, rather than by permanently altering the brain during development.
The neuronal changes that underlie chronic pain are similar in many ways to those that occur when long-term memories are stored. Studies have found that animals with memory genes missing or "knocked out" often have reduced pain sensitivity, and that increasing the amount of cyclic AMP - which is crucial for long-term memory - increases animals' chronic pain sensitivity. Nature often uses proteins and systems in more than one way, Dr. Zhuo says. This is efficient from a biological standpoint, but it makes it difficult to design drugs without unwanted side effects.
"Hopefully, we can find a magic protein that is only involved in pain - not memory or other functions," Dr. Zhuo says. However, researchers have so far been unsuccessful at identifying pain drugs without potentially serious side effects, he adds.
Previous studies have shown that mice without AC1 and AC8 have impairments of several kinds of memory, including contextual memory (learning to avoid a specific situation when it is paired with an unpleasant stimulus). However, the mice can perform other kinds of memory tasks without difficulty, and the two proteins do not affect existing memories, Dr. Zhuo says. The potential memory impairment from drugs or gene therapy to inhibit these proteins may be acceptable to patients who otherwise have to live with intense pain, he suggests.
While the researchers do not know of any existing drugs that can inhibit AC1 and AC8, it might be possible to identify or design drugs for this purpose, Dr. Zhuo says. "Our study makes a good argument for drug companies to look at these proteins," he adds. He and his colleagues are now planning experiments to study the proteins and mechanisms that are triggered by AC1 and AC8. Those studies may lead to other potential targets for therapy.
The NINDS is a component of the National Institutes of Health in Bethesda, Maryland, and is the nation's primary supporter of biomedical research on the brain and nervous system.
Reference: 1Wei F, Chang-Shen Q, Kim SJ, Muglia L, Maas JW Jr., Pineda VV, Xu HM, Chen ZF, Storm DR, Muglia LJ, Zhuo M. "Genetic elimination of behavioral sensitization in mice lacking calmodulin-stimulated adenyl cyclases." Neuron, November 14, 2002, Vol. 36, pp. 713-726. -by Natalie Frazin Reviewed January 7, 2003
What is Peripheral Neuropathy?
Extract from Peripheral Neuropathy Information Page
Peripheral neuropathy is a common neurological disorder resulting from damage to the peripheral nerves. It may be caused by diseases of the nerves or as the result of systemic illnesses. Many neuropathies have well-defined causes such as diabetes, uremia, AIDs, or nutritional deficiencies. In fact, diabetes is one of the most common causes of peripheral neuropathy.
Other causes include mechanical pressure such as compression or entrapment, direct trauma, penetrating injuries, contusions, fracture or dislocated bones; pressure involving the superficial nerves (ulnar, radial, or peroneal) which can result from prolonged use of crutches or staying in one position for too long, or from a tumor; intraneural hemorrhage; exposure to cold or radiation or, rarely, certain medicines or toxic substances; and vascular or collagen disorders such as atherosclerosis, systemic lupus erythematosus, scleroderma, sarcoidosis, rheumatoid arthritis, and polyarteritis nodosa. A common example of entrapment neuropathy is carpal tunnel syndrome, which has become more common because of the increasing use of computers.
Although the causes of peripheral neuropathy are diverse, they produce common symptoms including weakness, numbness, paresthesia (abnormal sensations such as burning, tickling, pricking or tingling) and pain in the arms, hands, legs and/or feet. A large number of cases are of unknown cause.
Is there any treatment?
Therapy for peripheral neuropathy differs depending on the cause. For example, therapy for peripheral neuropathy caused by diabetes involves control of the diabetes. In cases where a tumor or ruptured disc is the cause, therapy may involve surgery to remove the tumor or to repair the ruptured disc. In entrapment or compression neuropathy treatment may consist of splinting or surgical decompression of the ulnar or median nerves. Peroneal and radial compression neuropathies may require avoidance of pressure. Physical therapy and/or splints may be useful in preventing contractures (a condition in which shortened muscles around joints cause abnormal and sometimes painful positioning of the joints). Avoidance of provocative situations (such as heat and immobility in my case) is another way to avoid setting off an episode of peripheral neuropathy.
What is the prognosis?
Recovery from peripheral neuropathy is usually slow. Depending on the type of peripheral neuropathy, the patient may fully recover without residual effects or may partially recover and have sensory, motor, and vasomotor (blood vessel) deficits. If severely affected, the patient may develop chronic muscular atrophy.
Reflex Sympathetic Dystrophy or Complex Regional Pain Syndrome
Information from RSD Information page
What is Reflex Sympathetic Dystrophy or Complex Regional Pain Syndrome
RSD/CRPS is a chronic condition characterized by severe burning pain, pathological changes in bone and skin, excessive sweating, tissue swelling, and extreme sensitivity to touch. The syndrome is a nerve disorder that occurs at the site of an injury (most often to the arms or legs). It occurs especially after injuries from high-velocity impacts such as those from bullets or shrapnel. However, it may occur without apparent injury.
The condition called "causalgia" was first documented in the 19th century by physicians concerned about pain that Civil War veterans continued to experience after their wounds had healed. Doctors often called it "hot pain," after its primary symptom. Over the years, the syndrome was classified as one of the peripheral neuropathies, and later, as a chronic pain syndrome. Currently, there are two types of CRPS that are differentiated-type I and type II. Both types share the same basic set of symptoms, but have one distinct difference: type I (previously referred to as RSD) describes cases in which there is no nerve injury, while type II (formerly called causalgia) refers to cases in which a distinct nerve injury, for example from a gunshot wound, has occurred
What are the symptoms of RSD/CRPS?
The symptoms of RSD/CRPS usually occur near the site of an injury, either major or minor, and include: burning pain, muscle spasms, local swelling, increased sweating, softening of bones, joint tenderness or stiffness, restricted or painful movement, and changes in the nails and skin. One visible sign of RSD/CRPS near the site of injury is warm, shiny red skin that later becomes cool and bluish.
The pain that patients report is out of proportion to the severity of the injury and gets worse, rather than better, over time. It is frequently characterized as a burning, aching, searing pain, which may initially be localized to the site of injury or the area covered by an injured nerve but spreads over time, often involving an entire limb. It can sometimes even involve the opposite extremity. Pain is continuous and may be heightened by emotional stress. Moving or touching the limb is often intolerable. Eventually the joints become stiff from disuse, and the skin, muscles, and bone atrophy.
The symptoms of RSD/CRPS vary in severity and duration. However, there are usually three stages associated with RSD/CRPS, and each stage is marked by progressive changes in the skin, nails, muscles, joints, ligaments, and bones. Stage one lasts from 1 to 3 months and is characterized by severe, burning pain at the site of the injury. Muscle spasm, joint stiffness, restricted mobility, rapid hair and nail growth, and vasospasm (a constriction of the blood vessels) that affects color and temperature of the skin can also occur.
In stage two, which lasts from 3 to 6 months, the pain intensifies. Swelling spreads, hair growth diminishes, nails become cracked, brittle, grooved, and spotty, osteoporosis becomes severe and diffuse, joints thicken, and muscles atrophy.
As the patient reaches stage three, changes in the skin and bones become irreversible, and pain becomes unyielding and may now involve the entire limb. There is marked muscle atrophy, severely limited mobility of the affected area, and flexor tendon contractions (contractions of the muscles and tendons that flex the joints). Occasionally the limb is displaced from its normal position, and marked bone softening is more dispersed.
What causes RSD/CRPS?
RSD/CRPS was originally thought to be the result of malfunctioning nerves of the sympathetic nervous system-the part of the nervous system responsible, for example, for controlling the diameter of blood vessels. This idea has been called into question and the mechanism remains controversial.
Since RSD/CRPS is most often caused by trauma to the extremities, other conditions that can bring about RSD/CRPS include sprains, fractures, surgery, damage to blood vessels or nerves, and cerebral lesions. The disorder is unique in that it simultaneously affects the nerves, skin, muscles, blood vessels, and bones.
Who gets it?
RSD/CRPS can strike at any age, but has usually been more common between the ages of 40 and 60. Recent reports show that the number of RSD/CRPS cases among adolescents and young adults is increasing. It affects both men and women, but is most frequently seen in women.
Investigators estimate that two to five percent of those with peripheral nerve injury and 12 to 21 percent of those with hemiplegia (paralysis of one side of the body) will suffer from RSD/CRPS.
How is RSD/CRPS diagnosed?
RSD/CRPS is often misdiagnosed because it remains poorly understood. Diagnosis is complicated by the fact that some patients improve without treatment. A delay in diagnosis and/or treatment for this syndrome can result in severe physical and psychological problems. Early recognition and prompt treatment provide the greatest opportunity for recovery.
RSD/CRPS is diagnosed primarily through observation of the symptoms. However, some physicians use thermography — a diagnostic technique for measuring blood flow by determining the variations in heat emitted from the body — to detect changes in body temperature that are common in RSD/CRPS. A color-coded "thermogram" of a person in pain often shows an altered blood supply to the painful area, appearing as a different shade (abnormally pale or violet) than the surrounding areas of the corresponding part on the other side of the body. An abnormal thermogram in a patient who complains of pain may lead to a diagnosis of RSD/CRPS. X-rays may also show changes in the bone.
What is the prognosis?
Good progress can be made in treating RSD/CRPS if treatment is begun early, ideally within 3 months of the first symptoms. Early treatment often results in remission. If treatment is delayed, however, the disorder can quickly spread to the entire limb and changes in bone and muscle may become irreversible. In 50 percent of RSD/CRPS cases, pain persists longer than 6 months and sometimes for years.
What is the treatment?
Physical therapy is the mainstay of therapy. Physicians use a variety of drugs to treat RSD/CRPS, including corticosteroids, vasodilators, and alpha- or beta-adrenergic-blocking compounds. Elevation of the extremity may be helpful. Injection of a local anesthetic, such as lidocaine, is sometimes used. Injections are repeated as needed. TENS (transcutaneous electrical stimulation), a procedure in which brief pulses of electricity are applied to nerve endings under the skin, has helped some patients in relieving chronic pain.
In some cases, surgical or chemical sympathectomy-interruption of the affected portion of the sympathetic nervous system-has been used to relieve pain. Surgical sympathectomy involves cutting the nerve or nerves, destroying the pain almost instantly. But surgery is controversial and may also destroy other sensations.
Are there any other disorders like RSD/CRPS?
RSD/CRPS has characteristics similar to those of other disorders, such as shoulder-hand syndrome, which sometimes occurs after a heart attack and is marked by pain and stiffness in the arm and shoulder; Sudeck's syndrome, which is prevalent in older people and in women and is characterized by bone changes and muscular atrophy, but is not always associated with trauma; and Steinbrocker's syndrome, which affects both sexes but is slightly more prevalent in women, and includes such symptoms as gradual stiffness, discomfort, and weakness in the shoulder and hand.
Information from Central Pain Syndrome page
What is Central pain syndrome?
Central pain syndrome is a neurological condition caused by damage specifically to the central nervous system (CNS) — brain, brainstem, or spinal cord. The pain is steady and is usually described as a burning, aching, or cutting sensation. Occasionally there may be brief, intolerable bursts of sharp pain. Central pain is characterized by a mixture of pain sensations, the most prominent being constant burning. Mingled with the burning are sensations of cold, "pins and needles" tingling, and nerve proximity (like that of a dental probe on an exposed nerve). The steady burning sensation is increased significantly by any light touch. Patients are somewhat numb in the areas affected by this burning pain. The burning and loss of touch appreciation are usually most severe on the distant parts of the body, such as the feet or hands. Pain may be moderate to severe in intensity and is often exacerbated by movement and temperature changes, usually cold temperatures. Central pain syndrome may develop months or even years after injury or damage to the CNS. The disorder occurs in patients who have, or have had, strokes, multiple sclerosis, limb amputations, or brain or spinal cord injuries.
Is there any treatment?
Pain medications often provide little or no relief for those affected by central pain syndrome. Tricyclic antidepressants, such as nortriptyline, or anticonvulsants such as gabapentin can be useful in this condition. Patients should be sedated and the nervous system should be kept quiet and as free from stress as possible.
What is the prognosis?
Central pain syndrome is not a fatal disorder. But for the majority of patients, the syndrome causes intractable pain and much suffering.