pain

from Wikipedia, the free encyclopedia
Headache ( The Head Ache , caricature by George Cruikshank )

Pain is a complex subjective sensory perception which, as an acute event, has the character of a warning and guide signal and can range in intensity from unpleasant to unbearable. As chronic pain, it has lost the character of a warning signal and is now seen and treated as an independent clinical picture ( chronic pain syndrome ) .

An animal's perception of pain cannot be determined directly, which is why it is controversial and was occasionally denied until the 1980s. It is always based on the transfer from humans to animals. In particular, it is hardly possible to compare or even quantify the subjective pain perception of different individual animals. In species that are more distantly related to humans, the structure of the nervous system differs considerably from that of vertebrates (as in molluscs , insects ), and the nervous systems of different animal phyla are not homologous .

The annual economic costs of pain conditions as the sum of medical treatments, lost productivity and compensation for incapacity for work amount to around one trillion US dollars in the developed and industrialized nations.

Etymology and synonyms

The term pain , even Weh called (from Middle High German  WE "Woe, pain, suffering, disease"; see also " woe "), comes over likewise Middle High German smërze of althochdeutsch  smërzo , and can be attributed to the Indo-European root (s) mer (d ) - (“rub, rub, grind”). Dutch smerte and West Frisian smart have the same meaning (the latter primarily means emotional pain, while physical pain is expressed as pîn "pain", formerly also known as Wehtag ). Related words are English smart ( Middle English smerte ) "pungent, bitter," ancient Greek σμερδαλέος, σμερδνός smerdaleos, smerdnos "terrible", Latin mordere "bite hurt," Slavic smrt (z. B. Russian смерть smert ) and Lithuanian smertis "Death ".

The outdated word Pein , like the adjective embarrassing , goes back to Middle High German. pīne, pīn and Old High German pīna . This comes as also English pain from the Latin poena (from Medieval Latin : pronunciation Pena , whose ē ī in Old High German to become). The literal translation of poena , “atonement, punishment, revenge”, refers to subjective interpretations of pain. In primary hyperparathyroidism , the three main symptoms are still summarized today as "stone, leg and stomach pain", for kidney stone disease, bone and stomach pain.

Medical terms are Dolor (from Latin dolor ) and from the Greek algesia ( noun : analgesia ), in compound words -algie , -algesia (all from ancient Greek ἄλγος algos "pain") or -odynia (from οδύνη odyne "pain").

definition

The International Association for the Study of Pain (IASP) defines pain as:

"Pain is an unpleasant sensory or emotional experience that is associated with actual or potential tissue damage or is described by affected persons as if such tissue damage were the cause."

The perception of pain is assumed to be complex interactions between biological, psychological and social factors (biopsychosocial pain concept). Pain is therefore a subjective perception that is not determined solely by neuronal signals from the nerve fibers , rather it is a perception that is strongly regulated by complex processes (see also pain modulation ). So pain is what the patient feels as such. Because this is a highly subjective perception, it can lead to communication difficulties between the patient and the treating person, especially with regard to the extent of the suffering.

Position within sensitivity

The pain feel is a sensory modality within the somatovisceral sensitivity . Further modalities are the sensation of mechanical and thermal stimuli as well as muscle tension and joint position . Sensitivity also includes the reception, transmission and processing of further proprioceptive and chemical stimuli, but due to the lack of sensation there are no sensory modalities. Within the pain modality , a distinction is made between sensory qualities such as stabbing, pressing, burning, and itching can also be classified here.

The sensations of the different modalities (and qualities) are based on stimulation of different fibers of the peripheral nervous system (a historical counter-draft to this specificity theory was the intensity theory , according to which pain arises from strong stimulation in the thermal or mechanical system). The sensors responsible for feeling pain are called nociceptors and are free nerve endings that express suitable receptor proteins ; their adequate stimulus is an existing or threatening tissue damage; such stimuli are called noxious . The irritation of itch fibers leads to the corresponding sensation only if nociceptors are not excited at the same time; in that case the itch fibers contribute to the sensation of pain, which explains the relief of itching from scratching. The objective basis of pain perception (i.e. the recording of noxious stimuli, the transmission of this information via the spinal cord into the brain and the processing of information including the triggering of reflexes ) is called nociception ; A sensation does not develop from this until it reaches the thalamus , a perception only through processing in the cerebral cortex .

A special feature of pain perception (including the sensation of itching) is the unpleasant affect that almost always accompanies irritation in the nociceptive system. Pain is therefore more than information about the location, type, intensity and duration of an imminent or occurred tissue damage, pain is also the motivation to avoid injuries and protect injured body parts. As a negative reinforcer , pain helps learn to avoid harmful behavior through operant conditioning .

Neuroanatomically, as for the entire conscious sensitivity (without cranial nerves ), the first neuron with its cell body sits pseudounipolar in the spinal ganglion and is switched to a second neuron in the spinal cord that crosses to the opposite side and transmits the information to the thalamus, from where third neuron pulls to the cerebral cortex. Nociception is particularly similar to thermoception: in both cases, the stimuli are picked up by the C and Aδ fibers and switched to the second neuron in the posterior horn of the entry segment, which immediately switches to the contralateral side. There thermoceptive and nociceptive fibers move anatomically inseparable in the lateral spinothalamic tract towards the brain; Damage to the nociceptive tract in the spinal cord is therefore practically always accompanied by a limited sensation of warm cold in the same area. The dermatomes of the pain sensation overlap less than those of the touch sensation, so that damage to individual sensitive nerve roots can most likely be detected as hypalgesia in the neurological examination.

Nociception

Nociception and pain typically go hand in hand, but nociception is neither sufficient nor necessary for the sensation of pain. For example, nociceptive signals that reach the brain during sleep do not trigger pain, as the thalamus then does not transmit any sensory information to the cerebral cortex (sufficiently strong signals, however, lead to awakening). Conversely, the chronic pain disorder with somatic and psychological factors is characterized by a pronounced pain perception without corresponding noxious stimuli. Some stimuli that are picked up by the nociceptive system are usually not described as pain, including the sharp taste , pungent smell, the scratchiness of woolen fabrics and the sharp sensation.

Pain that actually arises through stimulation of nociceptors fulfills the important functions in the body described above and is therefore called physiological or (in the case of increased sensitivity to pain in the context of acute inflammation) pathophysiological nociceptor pain . If the nociceptive system is excited elsewhere than the nociceptors, for example by pressure on nerves, neuropathic pain results , which is felt in the area of ​​the nociceptors, although there is no damage there. A special case of neuropathic pain is central pain caused by direct stimulation in the central nervous system .

Recording of pain stimuli

Nociceptors are free endings of nerve fibers of classes C and Aδ , which guide the pain stimulus from the periphery to the spinal cord. Aδ fibers are thinly myelinated and reach a conduction velocity of 5–25 m / s. The evolutionarily older C-fibers are by far the most common afferent fibers, they are found almost everywhere in the body and, due to the lack of myelination, only reach 0.5–2 m / s. Local anesthetics completely interrupt the conduction of stimuli by blocking sodium channels, but are not specific for nociceptive fibers.

Nociceptors respond to different types of irritation:

  • thermal (heat, cold)
  • mechanical (e.g. severing, strong pressure)
  • chemical (e.g. ATP , protons , potassium ions)

As far as is known, these stimuli are detected via receptor proteins in the cell membrane. Nociceptors differ from normal mechano-, thermo- or chemosensitive nerve endings in that they have a higher stimulus threshold. They adapt slowly, i. . h, a continuing irritant leads after a relatively long time to decreased AP - frequency . Most nociceptors are polymodal; that is, they carry a multitude of receptors for different types of noxious stimuli in the same ending; such nociceptors are typically part of C-fibers and produce a dull sensation of pain. In addition, there are also monomodal nociceptors, especially among the Aδ fibers, e.g. B. high-threshold mechanosensors; Their excitement is responsible for the quick, easily localizable initial pain in the event of acute injury and plays a special role in protective and escape reflexes. Silent nociceptors are usually so high-threshold that they cannot be aroused at all.

Peripheral sensitization

Due to tissue damage and the resulting immune reaction ( inflammation ), mediators are released in the pain area , which by binding to specific membrane receptors lower the stimulus threshold of the nociceptors:

The sensitization awakens silent nociceptors. Some nociceptors are sensitized to such an extent that the conditions in the tissue constantly excite them above the threshold. The person concerned experiences this as hyperalgesia (stronger pain in the case of noxious stimuli) and allodynia (sensation of pain in the case of normally non-painful stimuli) or as pain at rest. Painkillers from the class of non-steroidal anti-inflammatory drugs ( ASA , ibuprofen , diclofenac , ...) act as inhibitors of cyclooxygenase and thus reduce inflammation and sensitization; they cannot lower the sensitivity to pain below the level of non-inflamed tissue.

Switching in the spinal cord

In the spinal cord there are reflex interconnections that trigger escape movements and relieving postures; the primitive reactions at the level of the spinal cord are modulated to varying degrees by higher centers (in the brain). A largely spinally organized example is the flexion reflex , which pulls the affected extremity away from the noxious stimulus, as when pulling the leg when stepping on a pointed object (here with a crossed extension reflex, i.e. shifting force to the other leg, for which higher centers must be involved). Grasping an unexpectedly hot object actually causes the hand to be withdrawn before the pain is even recognized (even if, in retrospect, you may think you acted because of the pain). An example of motor responses to intestinal pain is the defense tension of the abdomen. In addition to motor stimuli, the pain stimuli also trigger vegetative reflexes (e.g. activation of the sympathetic nervous system); the higher-level control center here is the hypothalamus .

The switch to the second neurons, which transmit the information in the anterior branch of the spinal cord (lateral spinothalamic tract) to the ventrobasal core of the thalamus , takes place convergently, i.e. that is, several nociceptive fibers from the periphery excite a spinal cord neuron. Spinal cord neurons, which receive signals from internal organs, always receive signals from somatic areas of the respective spinal cord segment, which explains the poor localizability and sometimes paradoxical transmission of intestinal pain. At the synapses , the first neurons release glutamate as well as substance P and CGRP as excitatory neuropeptides . Among the glutamate receptors in the postsynaptic membrane of the second neurons are NMDA receptors , the opening of which strengthens the synapse in the long term (see long-term potentiation ). Together with the effect of the cotransmitter, central prostaglandins and glutamate on metabotropic receptors, there is a central sensitization that further increases pain sensitivity and can expand the pain-sensitive area to non-inflamed surrounding tissue (secondary hyperalgesia). The central sensitization is initially reversible, but in the long term it represents a mechanism for learning about chronic pain. Ketamine unfolds its analgesic effect primarily by blocking the NMDA receptor.

Pain inhibition through descending trajectories

The just described transmission of pain stimuli in the spinal cord is modulated by descending pathways from the brain, two pain-relieving pathways are to be deepened here: From the central cave gray opioidergic neurons project to the raphe nuclei , from where serotoninergic fibers descend in the spinal cord. Noradrenergic fibers, which have their starting point in the locus caeruleus , also lead to the switching points of pain transmission . The transmitters serotonin and noradrenaline stimulate spinal interneurons , which have an inhibitory effect on the first and second neurons of the pain pathway via GABA , glycine and the body's own opioids ( peptides with the characteristic N -terminal sequence Tyr - Gly - Gly - Phe - Met / Leu ).

The release of the exciting transmitters is inhibited via opioid receptors at the presynaptic endings of the pain fibers. The activation of postsynaptic receptors for GABA, glycine and endogenous opioids generates inhibitory potentials on the second neurons . Opioid receptors are found in many other places in the brain, including inhibiting the affective component of pain perception. Opioids used as pain relievers are highly effective because they also bind to opioid receptors despite their chemically very different structure. The analgesic effect of some antidepressants is attributed to the (originally intended in the brain) increase in the concentration of serotonin and noradrenaline in the synaptic cleft.

Processing in the brain

In the cerebral cortex, nociception turns into pain, which is now conscious and emotionally assessed in the limbic system . The conscious pain perception and precise localization of pain is a learning process. In the sensitive cortex , more precisely in the postcentral gyrus , there are representative and responsible areas for each skin area (so-called sensitive homunculus ); through experience, a prick in the little left finger is immediately made aware as such.

Pain modulation

Pain is a subjective perception that is not determined solely by the neuronal signals from the pain nerve fibers to the brain. Rather, z. B. Filter processes of our central nervous system to ensure that physical damage does not necessarily lead to pain ( stress analgesia ; e.g. injuries during a traffic accident, competition, in combat or during sexual intercourse are often not noticed) and, conversely, pain can persist even without physical damage ( e.g. phantom pain ). In addition, the subjective pain perception, especially in chronic pain conditions, is always characterized by cognitive and motivational influences.

Pain conditions are for the body to learn . Repeated pain leads to a more intense and prolonged feeling of pain, a so-called pain memory , as the pain threshold is lowered. That is why early and adequate pain relief with medication or other suitable methods is important. It could be shown that the nociceptive system in humans is subject to neuronal plasticity, which can be influenced by targeted electrical stimulation. Studies have shown that in Germany, compared to other countries, pain is often inadequately treated. This does not only apply to patients with cancer pain and after surgery. This probably stems from the ingrained and often unfounded fear of addiction to pain medication , v. a. when using opioids for non-tumor pain, back. Comprehensive, interdisciplinary pain management is crucial.

Description of pain

quality

The feeling of pain is always subjective. Pain descriptions can be divided into affective (expressing a feeling, e.g. tormenting, torturing, paralyzing, terrible, violent) and sensory (relating to the quality of the senses: stabbing, pulling, pinching, pressing, cramping, burning or gnawing) aspects. The affective aspect can be further divided into an immediate emotional component and a long-term emotional component. The doctor asks for this in the patient discussion and thus receives information on the type and cause of the pain.

According to localization theory, these three qualities are assigned to different brain areas of the so-called pain matrix:

In the case of chronic pain conditions in particular, structural changes in the CNS must also be taken into account, as well as changes in the so-called rest networks, e.g. B. the Default Mode Network .

Types of pain

The Pschyrembel (Medical Dictionary) divides pain into three forms according to its etiology : 1.  Nociceptor pain , 2.  Neuropathic pain , 3.  Pain as a result of functional disorders . Psychosomatic pain belongs to the third group. There are also various other classifications and subdivisions of pain.

Mixed Pain

Here, both nociceptor and neuropathic pain occur simultaneously in different forms.

Examples are:

  • Low back pain (pain in the lumbar spine)
  • Lumboischialgia (pain in the lumbar spine that radiates into one leg)
  • Pain after disc surgery
  • Tumor pain

Acute and chronic pain

Classification according to ICD-10
R52 Pain, not elsewhere classified Includes: pain that cannot be assigned to a specific organ or region
R52.0 Acute pain
R52.1 Chronic uncontrollable pain
R52.2 Other chronic pain
R52.9 Pain, unspecified
ICD-10 online (WHO version 2019)

In terms of duration, pain can generally be categorized into acute and chronic.

Acute pain is a pain that is limited in time and is perceived as a reaction to the development and transmission of pain explained above. It has the character of a warning and guidance signal, which can also point the way to diagnosing the cause. In addition to a generally effective analgesic therapy, the causal therapy that follows from the diagnosis is decisive both for the treatment of the triggering cause and for pain therapy.

One form of acute pain is the so-called breakthrough pain , an increase in pain that occurs within minutes in patients who are otherwise adequately controlled (for example by long-term medication or basic medication with opioids) (chronic) persistent pain.

Chronic pain is pain that lasts longer in time, the exact time frame being defined differently, typically three to twelve months. Long-lasting pain can develop into a chronic pain disorder (own disease value). The pain then lost its guiding and warning function. This pain disorder is defined not only by the organic but also by the resulting psychosocial changes that must be incorporated into the integrative pain treatment .

In contrast to acute pain, chronic pain almost never has a single triggering or entertaining cause; it is multi-causal. The pain therapy treatment concept is logically based on the bio-psycho-social model , which alone makes it clear that one-sided treatment with analgesics alone does not do justice to chronic pain patients.

Examples include certain head and back pain (even after several operations ), stump and phantom pain , post- zoster neuralgia , trigeminal neuralgia , cancer pain, sympathetically entertaining, post-operative and post-traumatic pain. From a psychosomatic and neurobiological point of view, chronic non-malignant pain can also be an expression of psychological disorders or certain life or childhood experiences, which are also reflected on a neurobiological level.

Primary chronic pain is, for example, migraine , cluster headache , trigeminal neuralgia, stump and phantom pain, thalamic pain and cancer pain. In the case of such pain and acute pain that cannot be eliminated after the expected time, treatment measures must be taken that have a preventive effect, i.e. can counteract the development of the pain disorder.

Emotional / psychological / social pain

Various studies show that strong emotions (e.g. in grief, relationship crises or separation from a partner) activate brain areas similar to physical pain.

Social pain , e.g. B. as a result of experiences of loss or rejection, shows more neural overlaps with physical pain than differences with regard to its affective processing. Similar findings can be made on the basis of more recent imaging examinations if we - without feeling pain ourselves - perceive the pain of others in pain-inducing situations, e.g. B. hear (human) pain sounds or get them presented visually (so-called pain empathy).

Assessment of chronic pain

On May 31, 2012 and November 7, 2017, the guidelines of the AWMF for the medical assessment of people with chronic pain were updated. The assessment of pain is an interdisciplinary medical task. It serves to standardize and ensure the quality of the assessment for applicants for a pension or compensation who complain of pain as a key symptom .

In the expert situation, three categories of pain can be distinguished in simplified form:

  • Pain as an accompanying symptom of a physical disorder with the subgroups
    • "Usual pain" as an accompanying symptom of a physically perceptible illness or nerve damage.
    • "Exceptional pain" z. B. for stump and phantom pain or
    • as part of a “ complex regional pain syndrome ” (CRPS).
  • Physically partly explainable pain with psychological comorbidity as numerically the largest group to be assessed.
  • Pain as an expression of a primary mental illness, especially in the context of depressive disorders

The expert assessment is essentially based on answering two questions:

  • Can the complained of pain and the associated functional disorders be proven “without reasonable doubt” (“consistency check”)?
  • Can the proven malfunctions be overcome at least in part by “reasonable tension of will” (“examination of the willful controllability”)?

If pain-related functional disorders are proven, the expert generally has to quantify them. According to the categories of chronic pain syndromes, the following differences arise:

  • Pain as an accompanying symptom of tissue damage or disease.
  • Pain in tissue damage / disease with psychological comorbidities.
  • Pain as a key symptom of a mental illness.

See also the Tübinger sheet for recording pain behavior

Pain production

By torture pain or other ailments targeted and inflicted violently torture victims. Torture is outlawed worldwide, but it is practiced. Torture can cause chronic pain.

Pain theories

Historical theories of pain

In ancient times, Aristotle saw the center of the senses in the heart and accordingly localized the center of pain perception there. This theory remained effective through the reception of Aristotle in the Middle Ages beyond antiquity. With Hippocrates of Kos, however, according to the humoral pathology, an imbalance of “body fluids” (e.g. blood, lymph, black and yellow bile, water) was the cause of pain. There were also findings derived from anatomical examinations of prisoners.

The main positions of the ancient theories of pain are found gathered in Cicero 's Tusculanae disputationes . There Cicero defines pain as "rough movement in the body that is rejected by the senses" ( motus asper in corpore, alienus a sensoribus ; Tusc. Disp. II, 35), according to which the pain is not a mental state. In Books III and IV, Cicero criticizes the Epicurus theory of pleasure and pain, as well as the pain theory of the Stoics , in particular, according to his subdivision of physical pain (dolor) and the specific emotion of sorrow (aegritudo) , because both schools of philosophy only recommend cognitive awareness techniques and therefore choose the wrong starting point. Cicero's catalog (Tusc. Disp. II, 34–41) of people who, in his opinion, actually succeeds in bearing pain: Spartans , Roman soldiers, hunters, athletes, gladiators is noteworthy in terms of cultural history .

Illustration to Descartes' De homine

In the 17th and 18th centuries, mechanistic explanations determined the understanding of pain. In his essay De homine , Descartes explained the conduction of pain by comparing the nerves with a rope on which a bell hangs. The pain stimulus (A) causes a pull at the nerve end (B), which is conducted via the nerve cable pull (C) into the brain (F), where the pull is registered as a pain signal. For the first time he gave a physiological explanation for the occurrence of phantom pain. According to him, these arise when the nerves ending at the amputation stump continue to function as if the limbs were still intact. Despite such at least scientific approaches, quackalberic methods remained in the swing of the concrete treatment of pain, such as the "pulling out" of pain with the so-called "Perkins tractors" invented and patented by the American doctor Elisha Perkins .

In the 19th century, new theories about the origin of pain were formulated in research. In 1856 , Moritz Schiff put forward the so-called “specificity theory”. Accordingly, pain is a specific sensory experience that is passed on via specific nerve pathways. In 1858 he demonstrated that the sense of touch and pain run on different paths in the spinal cord. As a counter-theory to this, Wilhelm Heinrich Erb developed the “summation theory” (intensity theory) in 1874, which states that every stimulus can be perceived as pain, provided it is correspondingly intense. In 1794 he had a forerunner in Erasmus Darwin . The summation theory was supported in 1889 by experiments by Bernhard Naunyn , which also caused Alfred Goldscheider to switch from the specificity theory to the summation theory. At the beginning of the 1890s, physiologists such as Maximilian von Frey and clinical doctors advocated the theory of specificity - von Frey believed in 1896 that he had found specific pain points in the skin (which he identified as free nerve endings), independent of sensors for heat, cold or the sense of touch. The intensity theory was mainly advocated by psychologists. After the experiments of Max von Frey and Henry Head , the theory of specificity became dominant at the end of the 19th century, even if the theory of summation continued to be represented in theoretical work in the 20th century, for example in the pattern theory. A synthesis of both points of view took place in the Gate Control Theory (1965), which caused a revolution in the theoretical field, even if it was corrected in details.

The relationship to pain is subject to the social understanding of roles. Pain is endured differently in different situations and depending on the membership in certain social groups. A cultural conception declares pain suffered voluntarily to be a pain that brings redemption. Depending on the mythological background, z. B. cited the lossy exodus of the original clan into the promised land, which saved the cultural or physical survival of the people and has a role model function.

In initiation , a ritual of acceptance in traditional societies, bearing the pain inflicted is indispensable and has something liberating about it, as it accepts the initiate into the group of initiates. The Hamar in southern Ethiopia are a people who assure themselves of their cultural identity by collective infliction of pain.

In addition to physical pain, there is also emotional pain. The Jewish culture knows z. B. the term of Tzar Gidul Banim , which describes the pain and tension that parents who raise children are accompanied on a daily basis, for example through illnesses, death or the insubordination of these children.

Modern theories of pain

  • Pattern theory (DC Sinclair, G. Weddell 1955, precursor JP Nafe 1929), a variant of the intensity theory. According to this, all sensory nerve endings in the skin (except on the hair cells) are capable of producing pain if the stimulus is intense enough. The theory ignored much of the evidence previously gathered for specificity theory. The type of sensory impression and intensity and thus also pain is represented by the type of spatio-temporal pattern of the “firing” of the nerve fibers.
  • Neuro theory (Hedway, 1961)
  • Gate control theory ( Ronald Melzack , Patrick David Wall , 1965, forerunner Willem Noordenbos ). It revolutionized the theory of pain and combined the apparently contradicting knowledge of specificity theory and intensity theory (pattern theory).
  • Primary theory ( Arthur Janov deals with both neurological and psychological aspects of pain processing in his complete works.)

Pain and suffering in religion

Within Christian traditions, pain is related to sin and guilt, since God's original plan of creation did not provide a place for pain. According to the teaching of Christian theology, people in Paradise possessed supernatural gifts of full integrity and health ( dona integritatis , specifically the donum immortalitatis, impassibilitatis, scientiae, perfecti dominii ), e.g. B. also freedom from suffering of the body and from external unhappiness ( donum impassibilitatis ; cf. Augustine , De civitate dei XIV 10.26; Thomas Aquinas , Summa theologiae  I, qu. 97, art. 2). Only through the fall of man does pain or the sensitivity to pain enter the world of man. In Christianity one refers to the suffering of Christ , the suffering of the Mother of God Mary (see especially the sequence Stabat mater dolorosa ), to biblical models (especially Job ) to understand and cope with the pain, which is always attached to a moment of the incomprehensible . and on the example of saints and martyrs. A special Christian form is the mysticism of suffering .

The Roman Catholic Pope John Paul II , who himself became seriously ill at the end of his life, wrote the Apostolic Letter “ Salvifici doloris . On the Christian meaning of human suffering “as theological meditation, explaining the salvific power of suffering.

See also

literature

  • Ralf Baron: Diagnosis and therapy of neuropathic pain. In: Deutsches Ärzteblatt. 103, issue 41 of October 13, 2006, p. A-2720 ( aerzteblatt.de ).
  • Thomas Flöter (Ed.): Basics of pain therapy. In: Medicine & Knowledge. Munich 1998.
  • Thomas Flöter, Manfred Zimmermann (Ed.): The multimorbid pain patient. Thieme, Stuttgart 2003, ISBN 3-13-133071-6 .
  • Uwe Junker, Thomas Nolte (Hrsg.): Basics of special pain therapy. Curriculum Special Pain Therapy of the German Society for Pain Therapy e. V. according to the course book of the German Medical Association . Urban & Vogel, Munich 2005, ISBN 3-89935-218-1 .
  • Birgit Kröner-Herwig, Regine Klinger, Jule Fretlöh, Paul Nilges (eds.): Pain Psychotherapy . Basics - diagnostics - clinical pictures - treatment. 7th, completely updated and revised edition. Springer, Berlin 2011, ISBN 978-3-642-12782-3 .
  • Robert F. Schmidt: The Physiology of Pain. In: Pharmazie in our time , Volume 31, No. 1, 2002, pp. 23-30, ISSN  0048-3664 .
  • H.-P. Schmiedebach: The pain - cultural phenomenon and illness. In: Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz , Volume 45, No. 5, 2002, pp. 419-424, ISSN  1436-9990 .
  • Ministry of Labor, Health, Family and Social Affairs Baden-Württemberg, Stuttgart and State Medical Association BW (ed.): Pain therapy for tumor patients. A guide. Common recommendation of the tumor centers, Kassenärztl. Vereinig., State Medical Association. In: Health Policy. 13. 3., unchanged. Edition.

Guidelines

Types of pain

  • H. W. Striebel: Therapy of Chronic Pain - A Practical Guide. Schattauer, Stuttgart 2002, ISBN 3-7945-2146-3 , pp. 9-11 ( online in the Google book search).
  • Franz-Josef Kretz, Jürgen Schäffer a. a .: anesthesia, intensive care medicine, emergency medicine, pain therapy. 4th edition. Springer Medizin Verlag, Heidelberg 2006, ISBN 3-540-25698-9 , p. 398 ( limited preview in the Google book search).

Cultural history

  • Eugen Blume, Annemarie Hürlimann, Thomas Schnalke, Daniel Tyradellis (eds.): Pain. Art + science. Book accompanying the exhibition Pain, April 5 - August 5, 2007 in the National Gallery Hamburg Central Station and the Medical History Museum of the Charieté. Dumont, Cologne 2007, ISBN 978-3-8321-7766-9 .
  • Johannes Flügge, Matthias Kroß, Nikola Grahek: Pain. I. Antiquity to early modern times; II. Modern times; III. Science and medicine. In: Historical Dictionary of Philosophy . Vol. 8 (1992), Sp. 1314f., 1315-1323, 1323-1330.
  • Iris Hermann: Types of Pain. Prolegomena of an Aesthetics of Pain in Literature, Music and Psychoanalysis. Carl Winter, Heidelberg 2006, ISBN 3-8253-5255-2 (literary studies).
  • Bernhard Koch: Philosophy as medicine for the soul. Investigations on Ciceros Tusculanae Disputationes (= Palingenesia. 90). Steiner, Stuttgart 2006, ISBN 3-515-08951-9 , pp. 151-164.
  • Franz-Josef Kuhlen: History on the subject of pain and pain therapy. In: Pharmazie in our time , 31 (1) (2002), pp. 13-22, ISSN  0048-3664 .
  • Matthias Laarmann: Pain. In: Lexicon of the Middle Ages . 7 (1995), col. 1502 f. (on medicine, philosophy and theology of the Middle Ages).
  • David Le Breton: Pain - A Cultural History. Diaphanes Verlag, Zurich / Berlin 2003, ISBN 3-935300-20-4 .
  • David B. Morris: History of Pain. Insel-Verlag, Frankfurt am Main 1994, ISBN 3-458-16615-7 (cultural-historical).
  • Hans-Jochen Schiewer u. a. (Ed.): Pain in the literature of the Middle Ages and the early modern period. Vandenhoeck & Ruprecht, Göttingen 2010, ISBN 978-3-89971-771-6 .
  • Monika Specht-Tomann , Andreas Sandner-Kiesling: Pain. How can we react to that? Düsseldorf 2005, ISBN 3-530-40171-4 .

Web links

Commons : Pain  - Collection of pictures, videos and audio files
Wiktionary: pain  - explanations of meanings, origins of words, synonyms, translations
Wikiquote: Pain  - Quotes

Individual evidence

  1. ^ Bernard Rollin: The Unheeded Cry: Animal Consciousness, Animal Pain, and Science. Oxford University Press, 1989, xii, pp. 117-118.
  2. ^ KMD Rutherford: Assessing pain in animals. In: Animal Welfare. Volume 11, No. 1, 2002, pp. 31-53.
  3. ↑ GT Whiteside, A. Adedoyin, L. Leventhal: Predictive validity of animal pain models? A comparison of the pharmacokinetic-pharmacodynamic relationship for pain drugs in rats and humans. In: Neuropharmacology. Volume 54, Number 5, April 2008, pp. 767-775, ISSN  0028-3908 , doi: 10.1016 / j.neuropharm.2008.01.001 , PMID 18289614 (review).
  4. ^ Q. Hogan: Animal pain models. In: Regional anesthesia and pain medicine. Volume 27, Number 4, 2002 Jul-Aug, pp. 385-401, ISSN  1098-7339 , PMID 12132063 (review).
  5. ↑ SM Schappert: National Ambulatory Medical Care Survey: 1992 summary. In: Adv. Data. Volume 235, 1994, pp. 1-20, PMID 10172117 .
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