Chronic, Acute Pain And Its Modulation

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Chronic, acute pain and its modulation

Introduction.

Pain is defined as "an unpleasant sensory and emotional experience associated with a real or potential tissue lesion". Pain can be classified as acute or chronic. The difference between the two is not only a matter of temporality.

Developing.

Acute pain is the immediate consequence of the activation of nociceptive systems by a noxa. It has biological protection function (injured tissue level). Psychological symptoms are scarce and limited to slight anxiety. It is a pain of a nociceptive nature and appears due to the chemical, mechanical or thermal stimulation of specific nociceptors.

Chronic pain does not have a protective function, and more than a symptom is considered as a disease. It is a persistent pain that can self-perpetuate for a long time after an injury, and even in the absence of it. It is usually refractory to treatments and is associated with important psychological symptoms. Depending on the pathophysiological mechanisms, pain can be differentiated in nociceptive or neuropathic:

Nociceptive pain is the consequence of a somatic or visceral lesion. Neuropathic pain is the result of an injury and alteration of the transmission of nociceptive information at the level of the central or peripheral nervous system. One of its characteristics is the presence of allodynia, which is the appearance of pain against stimuli that are usually not painful.

Nociceptive pain and neuropathic pain represent the two extremes of a succession of events that are integrated at the nervous system level. In physiological conditions there is a balance between pain and injury. Before very intense, prolonged or repetitive painful stimuli, this balance can be lost, giving variations in the intensity and duration of the nociceptive responses. These changes are usually temporary;But if in some cases they become persistent, they alter the integration of painful information, losing any balanced relationship between injury and pain. (1)

Pain according to the International Association for the Study of Pain (IASP) is defined as an unpleasant sensory or emotional experience, associated with real or potential tissue damage, or described in terms of such damage. Pain is, therefore, subjective and there is whenever a patient says that something hurts.

The definition of the IASP emphasizes that the pain is associated with tissue damage or that is described as produced by it, but clearly avoids that the pain is produced by itself. This allows to consider that even in those forms of pain in which there is no tissue damage that causes them, generally as a consequence of neurological lesions, patients describe pain as if it were caused by a peripheral lesion.

The pain process begins with peripheral activation and sensitization where transduction takes place by which a nociceptive stimulus is transformed into electrical impulse. The stimulated nerve fiber begins a nerve impulse called action potential that is conducted to the second neuron located in the medulla dorsal horn, we are talking about the transmission. 

In the modulation process, the projections of peripheral fibers and descending fibers of higher centers are involved in the dorsal horn of the marrow. The transmission of impulses depends on the action of neurotransmitters. Finally, recognition from the higher centers of the CNS (central nervous system) or integration takes place. (two)

Acute pain and chronic pain

Acute pain is considered the immediate sensory consequence of the activation of the nociceptive system, an alarm signal fired by the organism’s protective systems. Acute pain is generally due to somatic or visceral tissue damage and develops with a temporary course that closely follows the process of repair and healing the causal lesion. If there are no complications, acute pain disappears with the injury that originated it. Chronic pain is that pain that persists beyond the injury that originated it and that remains once that injury disappears. Generally, chronic pain is a symptom of a persistent disease whose evolution, continues or outbreaks, entails the presence of pain even in the absence of peripheral injury.

Somatic pain and visceral pain

Somatic pain is one that affects the skin, muscles, joints, ligaments or bones. It is a well -located pain, circumscribed to the damaged area and characterized by clear and precise sensations. Visceral pain is produced by injuries that affect internal organs, so it is the form of pain that appears more frequently as a consequence of diseases and is a usual symptom in most acute and chronic painful syndromes of clinical interest.

Nociceptive pain and neuropathic pain

Nociceptive pain, normal or sensory pain. Is part of the repertoire of normal sensations, such as vision or touch. It is that form of pain that appears in all normal individuals as a result of the application of stimuli that produce damage or injury to somatic or visceral organs. Nociceptive pain is the consequence of the activation of the neurophysiological system constituted by peripheral nociceptors, central pathways of painful sensation and, finally, cerebral cortex. The intensity and duration of the sensations of nociceptive pain depends crucially on the modulation of the tissue lesion signals along the nociceptic pathway, but the nociceptive pain is always due to the activation of a specific sensory system in charge of its transmission. (3)

It is important to keep in mind that pain is, in principle, a defense mechanism, whose function is to detect and locate the processes that damage body structures, but it is also a subjective phenomenon that may or may not be linked to an organic injury or pathology. In addition, when this linking exists, the intensity of pain is not necessarily related to the seriousness of the alteration that produces it.

Nor should it be forgotten that it has a part of sensation, which is often described as a process that penetrates or destroys tissues (lancinating, oppressive), and another emotional (anxiety, excitement, fear) in which they include physical, psychological and psychological aspectssocial, which often complicates your therapeutic approach. Especially when it is chronic, it is common for concomitant disorders such as depression, sleep alterations and decrease in physical abilities.

Epidemiology

Pain is the most frequent cause of medical consultation and the most common reason for the request of medicines without recipe The most frequent is osteoarticular pain (mainly low back pain), followed by headaches and, at a greater distance, chest pain and abdominal pain. It is often chronic and greatly affects the quality of life and the ability to develop daily tasks. In addition to the direct costs involved in its treatment, it entails very high indirect costs in loss of working hours and reduction of performance.

Palliative care (CP) and pain treatment (TD) are essential elements to improve or maintain the quality of life of many patients affected by incurable, chronic or terminal processes. Its need is accentuated in countries with low and medium resources where the incidence of cancer and other diseases such as AIDS is increasing, with a high proportion of patients diagnosed in an advanced phase and with very difficult access to adequate CP or TD,Although they are the only realistic and human alternative to abandonment that most of these patients suffer. In addition, the epidemiological profile of many southern countries is changing with an increase in chronic diseases and access to higher antiretroviral coverage levels. To modify this situation,

Pain treatment (TD) prevents useless suffering, seeks relief and improves the quality of life of all chronic pain patients maintained for long periods and even all existence. These programs make several rights of the patients: to be relieved of their suffering reality;To have the greatest attainable well -being, and to live with the greatest possible dignity its last days. CP and TD, due to the important improvement of the quality of life they produce in cancer patients, increasing.

Modulation;It is the process by which the nociceptive signal in the dorsal horn of the medulla can be inhibited and modified for the higher pain centers. Endogenous and exogenous opiodes give rise to an indirect blockade of calcium channels and opening of potassium channels, with cell hyperpolarization and inhibition of the release of pain mediators. The activation of the descending neural system results in the release of b endorphins, encephalins, dinorphins;that relieve pain. 

The stimuli causing pain are called noxas and are detected by specific sensory receptors called nociceptors Nociceceptors are identified as f fibers and fibers A;They respond selectively to stimuli. These nociceptors are free nerve endings with cell bodies in the ganglia of the dorsal roots with termination in the dorsal horn of the spinal cord. The nociceptors are found throughout the body, but are more extensively located in: periosteum, arterial wall, teeth, articular surface, cranial vault.

The modulation represents the changes that occur in the nervous system in response to a nociceptive stimulus, it allows the nociceptive signal received in the medulhaspinal numbers to be selectively inhibited, so that the signal to the higher centers is modified. The Endogenous Pain Modulation system is made up of intermediate neurons within the superficial layer of the spinal cord and descending neural tracts;which can inhibit the pain signal. (6)

conclusion.

Pain is a sign of disease and a frequent reason for consultation;It is classified as acute or chronic, nociceptive or neuropathic, and according to fast or slow driving speed. The stimuli causing pain are detected by nociceptor receptors. The neural process of pain transmission includes: transduction;It is the process by which the nociceptive stimulus is converted into an electrical signal into the nociceptors. The broadcast;It is the process by which the nociceptive stimuli are referred to the dorsal horn of the spinal cord, where neurotransmitters of pain are released: glutamate, substance P, peptide related to the calcitonin gene. Then the stimulus crosses to the contralateral side of the spinal cord and travels in the spinothalamic beam to the thalamus and then to the cerebral cortex.

Bibliography.

  • Ferrandiz m. Pain Unit. In pathology of pain. Hospital de la Santa Creu I Sant Pau. Barcelona: Palo’s;2015.
  • Gomez, s. Clinic history of pain. In. Madrid: Gafos;2014. p. Chapter 71.
  • Espinoza, a. Pain and its treatment, guide of good clinical practice. In. Madrid: IM&C, SA;2016. p. 86.
  • Of the arc, J. Basic course on pain. Community Pharmacy. 2015 January – February;Vol. 29, no. 1.
  • 5. Astudillo, w. Palliative care and pain treatment in solidarity. Magazine of the Spanish Pain Society. 2008.
  • Zegarra, p. Pathophysiological bases of pain. Peruvian Medical Act. 2017 May/August;v.24 n.two.

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