IASP (International Association for the Study of Pain), pain is defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage."
From this definition can pull two conclusions. The first is that the perception of pain is an unpleasant sensation and emotional experience following the actual tissue damage. So the pain is due to actual tissue damage (pain with nociception). The second, the same feelings can also arise in the absence of actual tissue damage. So pain can occur without apparent tissue damage (pain without nociception). read more .... In other words, pain is generally the result of damage to the actual network, which is referred to as a state of acute pain such as post-surgical pain. But there is also a state where pain arises in the absence of actual tissue damage or pain occur after the healing process is over, which is referred to as a state of chronic pain such as post-herpetic pain, phantom pain or trigeminal pain.
From this definition can pull two conclusions. The first is that the perception of pain is an unpleasant sensation and emotional experience following the actual tissue damage. So the pain is due to actual tissue damage (pain with nociception). The second, the same feelings can also arise in the absence of actual tissue damage. So pain can occur without apparent tissue damage (pain without nociception). read more .... In other words, pain is generally the result of damage to the actual network, which is referred to as a state of acute pain such as post-surgical pain. But there is also a state where pain arises in the absence of actual tissue damage or pain occur after the healing process is over, which is referred to as a state of chronic pain such as post-herpetic pain, phantom pain or trigeminal pain.
Before discussing about this strange disease (disease that can not feel pain) then it's better if we first understand the cause of pain / pain mechanism.
Pain mechanism
pain mechanism in a simple starting transduction stimuli result in tissue damage to sensory nerves then transmitted through the electrical activity of nerve fibers bermielin A delta and C nerve bermielin not to the spinal cord dorsal horn, thalamus, and cerebral cortex. Electrical impulses are perceived and discriminated against as the quality and quantity of pain after a modulation along the peripheral nerves and the central nervous arranged. Stimuli that can evoke pain stimuli can be mechanical, temperature (hot or cold) and chemical agents that are released due to trauma / inflammation.
pain mechanism in a simple starting transduction stimuli result in tissue damage to sensory nerves then transmitted through the electrical activity of nerve fibers bermielin A delta and C nerve bermielin not to the spinal cord dorsal horn, thalamus, and cerebral cortex. Electrical impulses are perceived and discriminated against as the quality and quantity of pain after a modulation along the peripheral nerves and the central nervous arranged. Stimuli that can evoke pain stimuli can be mechanical, temperature (hot or cold) and chemical agents that are released due to trauma / inflammation.
The phenomenon of pain occurs due to the ability of the nervous system to change various mechanical stimuli, chemical, thermal, electrical action potential dijalarkan into the central nervous system.
Based on the pathophysiology of pain is divided into:
1. Nociceptive pain or inflammatory pain, which is pain that arises as a result of mechanical stimulus to nosiseptor.
2. Neuropathic pain, including pain resulting from a primary dysfunction in the nervous system (neliola, et at, 2000).
3. Idiopathic pain, pain where the pathological abnormalities could not be found.
4. Pain spikologik
1. Nociceptive pain or inflammatory pain, which is pain that arises as a result of mechanical stimulus to nosiseptor.
2. Neuropathic pain, including pain resulting from a primary dysfunction in the nervous system (neliola, et at, 2000).
3. Idiopathic pain, pain where the pathological abnormalities could not be found.
4. Pain spikologik
Based on the factors causing pain, there is frequently used in terms of pain osteoneuromuskuler, namely:
1. Nociceptor mechanism.
2. Nerve root compression or.
3. Trauma (deafferentation pain).
4. Inappropiate function in the control of muscle contraction.
5. Psychosomatic mechanism.
1. Nociceptor mechanism.
2. Nerve root compression or.
3. Trauma (deafferentation pain).
4. Inappropiate function in the control of muscle contraction.
5. Psychosomatic mechanism.
Journey pain (nociceptive pathway).
between tissue damage (as a source of pain stimuli) to be perceived as pain perception electrophysiologic there is a series of processes that are collectively referred to as nociception (nociception). There are four clear process that occurs in a nociception, namely;
between tissue damage (as a source of pain stimuli) to be perceived as pain perception electrophysiologic there is a series of processes that are collectively referred to as nociception (nociception). There are four clear process that occurs in a nociception, namely;
- Transduction Process (Transduction), is a process where a painful stimulus (noxious stimuli) was changed to be a power that will be accepted activity in nerve endings (nerve endings). Stimuli can be either physical stimuli (pressure), temperature (heat) or chemical (substance pain).
- Transmission Process (Transmison), intended as the distribution of nerve impulses through the sensory transduction process followed. This impulse will be distributed by the nerve fibers A delta and C fibers as the first neuron, from the periphery to the spinal cord where the impulse is experiencing modulation before being forwarded to the thalamus by sphinotalamikus tract as a second neuron. From the thalamus further impulses channeled into the somato sensory neurons in the cerebral cortex through the third, in which the impulses are interpreted and perceived as pain perception.
- The process of modulation (Modulation), is the process by which the interaction between the endogenous analgesic system produced by our bodies with pain imput into spinal cord posterior horn. So it is a process that acendern controlled by the brain. Endogenous analgesic system include enkephalin, endorphins, serotonin, and noradrenaline have effects that can suppress pain impulses to the spinal cord posterior horn. Posterior horn can diiabaratkan as doors that can open doors tertetutup or pain is played by endogenous analgesic system mentioned above. Modulation process is what causes the pain becomes very subjective perception of individuals.
- Perception (perception), is the end result of a complex interaction process starting from the unique transduction, transmission and modulation which in turn results in a feeling known as subjective pain perception.
If electrotherapy intended to inhibit the activation mechanism nosiseptor at both the peripheral and supra spinal level.TENS as one way / effort in the application of electrotherapy for pain.
Nociceptor: sensor element that can send a signal to the CNS of the things that potentially harmful. Very much in our bodies, fibers afferentnya consists of: 1. A delta fibers, the nerve fibers with thin myelin membrane. 2. C fibers, nerve fibers without myelin.
Nociceptor: sensor element that can send a signal to the CNS of the things that potentially harmful. Very much in our bodies, fibers afferentnya consists of: 1. A delta fibers, the nerve fibers with thin myelin membrane. 2. C fibers, nerve fibers without myelin.
Not all fibers serves as nosiseptor, others react to stimuli heat or mechanical stimulation. Instead nosiseptor not found in large sensory fibers such as A Alpha, Beta A or group I, II. Fibers of the sensor is functioning at "propioception" and "motor control".
Nociceptor very sensitive tehadap chemical stimuli (chemical stimuli). In our body are "algesic chemical" substance such as: Bradykinine, potassium ions, sorotonin, prostaglandins and others.
substance P, a neuropeptide that is released and the ends of type C nociceptive peripheral nerves, resulting in increased local microcirculation, plasma extravasation. This phenomenon is referred to as "neurogenic inflammation" that the state lajut produce noxious / chemical stimuli, thus causing pain. Deregulation of the motor system
Nociceptor very sensitive tehadap chemical stimuli (chemical stimuli). In our body are "algesic chemical" substance such as: Bradykinine, potassium ions, sorotonin, prostaglandins and others.
substance P, a neuropeptide that is released and the ends of type C nociceptive peripheral nerves, resulting in increased local microcirculation, plasma extravasation. This phenomenon is referred to as "neurogenic inflammation" that the state lajut produce noxious / chemical stimuli, thus causing pain. Deregulation of the motor system
Pain Causes
We know hypertonus muscles can cause pain. In general, the muscles involved are "postural system". Nociceptive stimulus received by the afferent fibers to the spinal cord, resulting in muscle contraction due to some "motorcycle spinal reflexes". Nociceptive stimuli can be found in several places visceral organs such as skin, muscle and even himself. This reflex was actually beneficial to our bodies, such as "withdrawal reflex" is a survival mechanism of the organism.
We know hypertonus muscles can cause pain. In general, the muscles involved are "postural system". Nociceptive stimulus received by the afferent fibers to the spinal cord, resulting in muscle contraction due to some "motorcycle spinal reflexes". Nociceptive stimuli can be found in several places visceral organs such as skin, muscle and even himself. This reflex was actually beneficial to our bodies, such as "withdrawal reflex" is a survival mechanism of the organism.
Besides these functions, we also realize that the last contraction can increase the pain, through nosiseptor in muscles and tendons. The more frequent and stronger nosiseptor is stimulated, the stronger the reflex activity of these muscles. This will increase pain, causing a state of "vicious circle", this condition will be exacerbated by the presence of local ischemia, as a result of a strong muscle contraction and continuous or inadequate microcirculation as a result of dysregulation of the sympathetic system.
In Figure 1, visible input afferent fibers and visceral organs, skin, joints, tendons, or muscles and the brain impulses that can influence down to the spinal stimulation (exitability) and alpha and gamma motorneurons resulting in muscle contraction (muscle stiffness), for example increased nociceptive input from abdominal viscus will improve tone abdominal muscles. Or nociceptive input from the joint capsule can improve the "reflex excitability" and some antagonist muscles concerned with the movement of the joint so that it can block the joint, also known as "neurogenic block". The biggest influence comes from the brain, stress and emotions can lead to "descending excitatory pathways", thereby stimulating increased reflexes of postural muscles.
feeling pain depends on the activation of a series of nerve cells, including primary afferent pain receptors, cells nerve connections (inter neurons) in the spinal cord and brain stem, the cells in the ascending tract, nerve cells in the thalamus and the nerve cells in the cerebral cortex. Various primary pain receptors are found and provides innervation to the skin, joints, muscles and tools in the activation of different pain receptors produces a certain quantity of pain. Nerve cells in the dorsal horn of pain in the spinal cord contributes to pain reflexes or join regulate activation of ascending tract cells.The nerve cells of the tract mark spinothalamicus help feeling pain, while others are more tract contributes to the activation of the descending control system or the emergence of motivational-affective mechanisms.
Some studies show that the thalamus plays a role in pain sensation more than in the cerebral cortex (WD Willis, 1995).Yet other studies prove a significant role and the cerebral cortex in pain sensation. Diensepalik structure and telesepalik as the medial thalamus, hypothalamus, amygdala and limbic system thought to contribute to a variety of motivations and affective reactions of pain.
Pain is an individual experience that involves sensory and emotional sensation tidan fun. Pain can be divided by 2. First, the pain caused by the activation nosiseptf notion Ad and C receptor in response to noxious stimuli (thermal, mechanical, chemical). Second, neyri neuropathic pain arising from a damage / pathological changes in the peripheral or central nervous system. In the case of rheumatic pain inflicted pain is mixed, the combination of nociceptive and neuropathic pain.
Genes Cause Pain
London, two people with the same pains have different levels of pain. For example, both back pain but this one can still indulge while others could only lie down. Turns out this is caused by a different gene.
London, two people with the same pains have different levels of pain. For example, both back pain but this one can still indulge while others could only lie down. Turns out this is caused by a different gene.
Scientists are struggling to explain why some people are more sensitive and less able to withstand the pain. A gene called SCN9A is responsible for this. The findings are expected to be in the future of gene therapy as an alternative in patients with severe chronic pain.
"By finding genes that are responsible for pain, it can increase the ability to conquer and control it," said Dr Geoffrey Woods of the Cambridge University, as quoted from the Telegraph, Tuesday (9/3/2010). Dr Woods added during this biomedical researchers and doctors are looking for analgesics (pain relievers) are effective with acceptable side effects.Would require significant development of therapies and better.
Many people in the world suffer from chronic pain as a result of injury or arthritis that affects their lives and some even lead to depression. Scientists found the gene in a study involving 578 people with osteoarthritis, rheumatic pain, back pain and other pain problems.
Found a protein made by a mutated version of the gene known as SCN9A open longer than usual. This could increase the activation of nerves that produce pain or pain. "The pain serves as an adaptive mechanism that protects us from tissue damage and as a warning of the possibility of injury," said Dr. Woods. With the discovery of the genes of this pain, so the researchers can modify the function of SCN9A that could potentially treat conditions such as osteoarthitris. The results of this study have been published in the Proceedings of the National Academy of Sciences.
Stress Response (Stress Responds)
The response of the body to a surgery or pain will produce a reaction of the endocrine and immonologik, commonly referred to as the stress response. Stress response is very detrimental to the patient because in addition will reduce backup and endurance, increases the oxygen demand of the heart muscle, disrupting the function of respiration with all its consequences, will also invite the risk of thromboembolism, which in turn increases morbidity and mortality. Although a variety of pain management techniques have been developed, but postoperative pain control per se, is not always a guarantee for non-occurrence of stress responses that play a role in the prognosis of patients post-surgery.
The response of the body to a surgery or pain will produce a reaction of the endocrine and immonologik, commonly referred to as the stress response. Stress response is very detrimental to the patient because in addition will reduce backup and endurance, increases the oxygen demand of the heart muscle, disrupting the function of respiration with all its consequences, will also invite the risk of thromboembolism, which in turn increases morbidity and mortality. Although a variety of pain management techniques have been developed, but postoperative pain control per se, is not always a guarantee for non-occurrence of stress responses that play a role in the prognosis of patients post-surgery.
Hypersensitivity and CNS plasticity.
Laboratory studies show that after a trauma or surgery the pain of peripheral input to the central will change the threshold of pain receptors in both the peripheral and central (spinal cord posterior horn). Both pain receptors mentioned above will decrease the pain threshold, pain shortly after the input.
changes will result in a condition known as hypersensitivity either peripheral or central. These changes can be seen in the clinic, where the injury and the surrounding area will be turned into hyperalgesia. The area on the right will change to allodini injury, meaning a weak stimulation, which normally do not cause pain, can cause pain now, the area is also known as primary hyperalgesia. On the other hand, the area around the injury that still seems normal also turned into hyperalgesia, meaning that with a strong stimuli, to inflict enough pain, is now perceived as pain greater and lasted longer, the area is also referred to as secondary hyperalgesia.
Laboratory studies show that after a trauma or surgery the pain of peripheral input to the central will change the threshold of pain receptors in both the peripheral and central (spinal cord posterior horn). Both pain receptors mentioned above will decrease the pain threshold, pain shortly after the input.
changes will result in a condition known as hypersensitivity either peripheral or central. These changes can be seen in the clinic, where the injury and the surrounding area will be turned into hyperalgesia. The area on the right will change to allodini injury, meaning a weak stimulation, which normally do not cause pain, can cause pain now, the area is also known as primary hyperalgesia. On the other hand, the area around the injury that still seems normal also turned into hyperalgesia, meaning that with a strong stimuli, to inflict enough pain, is now perceived as pain greater and lasted longer, the area is also referred to as secondary hyperalgesia.
Both of the changes mentioned above, both primary hyperalgesia and secondary hyperalgesia is a consequence of the occurrence of hypersensitivity following peripheral and central pain due to an input of a trauma or surgery. This means that our nervous system, both the peripheral nervous system and central nervous system can change its input follows a continuous pain. In other words, we can be likened to the nervous system as a rigid cables (rigid wire), but was able to change according to its function as a means of protection.
Sususnan ability to change our nerves like plastic called as our nervous system plasticity (plasticity of the nervous system). Preemptive analgesia (Preemptive analgesia) Once the nervous system undergo plasticity, meaning will become hypersensitive to some stimuli and the patient will complain with more severe pain that required high doses of analgesic drugs to control it. On this basis, to reduce postoperative pain, efforts to prevent the occurrence of neural plasticity. One way to reduce the plasticity of a elective surgery is to use a nerve block (epidural / spinal), because then the pain of peripheral input will be blocked to enter the posterior horn of spinal cord. On the other hand if the trauma occurred prior to surgery, the administration of systemic opioids can restore neural plasticity changes back to normal. Efforts to prevent the occurrence of plasticity is called preemptive analgesia (preemptive analgesia), it means treating pain before it occurs (to treat pain before it Occurs). In this way the pain will be greatly decreased postoperative pain compared with postoperative patients operated on with general anesthesia facility. This has been proven by many clinical studies.Analgesia Balans (Balanced Analgesia) As explained earlier the concept of balance is an attempt to intervene analgesia pain in the way that the process of transduction, transmission and modulation. So it is a pain interventions that are integrated and sustainable, inspired by the concept of preemptive analgesia plasticity and as mentioned in atas.Pengalaman show that by using preemptive analgesia, initially will obtain good results, but this method has a limited time. No preemptive analgesia may be maintained until a few days after the healing process. In addition to continuous epidural iti using local anesthesia, also have limitations as mentioned earlier.
therefore concluded that preemptive analgesia, although the results are very good, especially in preventing the occurrence of plasticity in the posterior horn, but has limitations, namely the difficulty maintained during postoperative healing process. Where the benefits of balance in which the intervention of pain analgesia done multimodal and sustainable.Multimodal, meant that the interventions made on the third trip the pain that is in the process of transduction using NSAIDs, the transmission process with a local anesthetic, and the process of modulation by opioids.
therefore concluded that preemptive analgesia, although the results are very good, especially in preventing the occurrence of plasticity in the posterior horn, but has limitations, namely the difficulty maintained during postoperative healing process. Where the benefits of balance in which the intervention of pain analgesia done multimodal and sustainable.Multimodal, meant that the interventions made on the third trip the pain that is in the process of transduction using NSAIDs, the transmission process with a local anesthetic, and the process of modulation by opioids.
With an emphasis on how this happened transduction processes and process improvement modulation, in order to prevent the occurrence of hypersensitivity in both peripheral and central. In other words, balance can produce analgesia in addition to pain free responses also stress free. With this balance analgesia regimen will result in a postoperative analgesia who rationally will produce optimal analgesia is not only a break, but also in a state of mobilization.
DISEASE CAN NOT FEEL SICK???
Normally, the human body will feel pain when injured or certain disorders. But it will never be felt by a girl who had mutations in the gene since birth.
This is experienced by Ashlyn, 10-year-old girl from Florida. He was born with congenital insensitivity to pain congenital (inborn), which is a rare condition caused by a genetic mutation and can not feel pain.
This is experienced by Ashlyn, 10-year-old girl from Florida. He was born with congenital insensitivity to pain congenital (inborn), which is a rare condition caused by a genetic mutation and can not feel pain.
Congenital insensitivity to pain can not be cured and there is no treatment to cure it. There are only 45 to 50 cases have been reported. Gene mutation experienced Ashlyn shaped wrench, so he had a decreased sensitivity of pain but it is still possible to feel the warmth and touch someone. Ashlyn did not cry when she was born, when teething, when they're hungry or when the diaper is wet. The only condition that makes her cry was ruptured eardrum when he was 3 years old."Ear drum ruptured and she was bleeding from the ear, she felt the pressure for the first time," says Tara Blocker, Ashlyn's mother, as quoted by FoxNews, Thursday (26/08/2010).
According to Tara, without having the ability to feel pain, Ashlyn often chewed his lower lip when he fell asleep. These conditions have made experience severe swelling. In addition, patients with congenital insensitivity to pain are also frequently injured, such as biting the tip of the tongue, eye damage or even burn themselves on hot surfaces like stove. In this case, Ashlyn had experienced severe burns when his hand put in the washing machine is on, when he was 2 years old. Although it did not bother him, but Tara is very anxious and could only cry.
Years toughest was when he was a toddler Ashlyn. But though he often suffered bumps, bruises and burns, and his parents did not understand why Ashlyn never cried.
Families Blocker began experiencing a long way after Ashlyn was diagnosed congenital insensitivity to pain by a geneticist in 2004. Tara never heard of it before and she and her husband happy, because they finally know the reason why Ashlyn never cried. In 2004, Dr. Roland Staud invited Ashlyn and her family to come to the University of Florida in order to study and learn more about the rare cases in Ashlyn.
Families Blocker began experiencing a long way after Ashlyn was diagnosed congenital insensitivity to pain by a geneticist in 2004. Tara never heard of it before and she and her husband happy, because they finally know the reason why Ashlyn never cried. In 2004, Dr. Roland Staud invited Ashlyn and her family to come to the University of Florida in order to study and learn more about the rare cases in Ashlyn.
The research team conducted preliminary tests, namely by taking blood Ashlyn and her family to get a DNA sample.Five years later in 2009, a team of Florida University determines that Ashlyn had two mutations in the gene SCN9A, which closes a molecule involved in the direction of nerve impulses to the brain. SCN9A gene is a gene that sends pain messages to the brain and nerve impulses. Mutations of this gene can cut both functions, thus causing pain insensitivity.And if this gene becomes overactive, it can cause hypersensitivity.
Finally Dr. Staud and the family decided not to deter Ashlyn gene therapy in order to avoid potential triggers the gene becomes overactive. "I would never want to risk messing with genes that could eventually make Ashlyn extreme pain," explains Tara.
Among the many physical tests, psychological, genetic and neurological disorders that have been conducted by Dr. Staud on Ashlyn, he found that Ashlyn sensitive to touch, temperature and vibration, but not sensitive to pain and bad pain.
In 2009, a broken ankle in the crash Ashlyn bike. It is known to his parents after showing symptoms of swollen Ashlyn body two days later.
Though injuries are not so great because he did not feel anything, Ashlyn's parents remain concerned and aware of the danger of infection. Finally, the family asked him to use a wheelchair to prevent the development of infection and reduce the pressure.
In 2009, a broken ankle in the crash Ashlyn bike. It is known to his parents after showing symptoms of swollen Ashlyn body two days later.
Though injuries are not so great because he did not feel anything, Ashlyn's parents remain concerned and aware of the danger of infection. Finally, the family asked him to use a wheelchair to prevent the development of infection and reduce the pressure.
Regards, Dwi Hartoyo, SP
REFERENCES
1. http://www.painspecialist.com.sg/ind/neuropathicpain.htm
2. http://goodhaladon.blogspot.com/2012/01/ashlyn-gadis-kecil-yang-tak-punya-rasa.html
3. http://berita-apa-aja.blogspot.com/2010/08/gadis-kecil-yang-tak-punya-rasa-sakit.html
4. http://hidayat2.wordpress.com/2009/03/24/mekanisme-nyeri/
1. http://www.painspecialist.com.sg/ind/neuropathicpain.htm
2. http://goodhaladon.blogspot.com/2012/01/ashlyn-gadis-kecil-yang-tak-punya-rasa.html
3. http://berita-apa-aja.blogspot.com/2010/08/gadis-kecil-yang-tak-punya-rasa-sakit.html
4. http://hidayat2.wordpress.com/2009/03/24/mekanisme-nyeri/
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