Pain is part of the conscious inventory of our lives. The experience of pain is immediately apparent to the perceiver through their perception of it

[1,2]. Every child, every sentient being, knows from their own experience what pain is. No explanation or definition is needed in the lived experience. However, those experiencing pain can and must actively intervene in their experience through behavior, emotions, cognitions, and evaluations in order to avoid, alleviate, resolve, interpret, and assess pain, to adapt their behavior, to motivate health and healing behaviors, to develop awareness, or to be able to live with chronic pain.

In medical practice and training, the mechanistic and purely physical concept of pain developed by the philosopher and natural scientist René Descartes [3] still largely guides the diagnosis and treatment of pain. It replaced the previously dominant view of pain as atonement for guilt: life, and especially dying, had to hurt. In contrast, according to Descartes, pain is the result of a purely mechanistic and neutral process; it arises as if "pulling on the end of a rope makes the bell hanging at the other end ring." Clinical experience and personal experience teach us that this purely mechanistic view of pain cannot encompass its diversity. For example, there are patients in whom even the most precise examination methods fail to reveal any pain-causing lesion, yet pain persists. Conversely, patients may exhibit pronounced lesions that are usually associated with pain, yet they do not experience any pain themselves. The purely neuronal, mechanistic view of pain as a one-sided, linear causal link between pain stimulus, pain transmission, and pain experience paradoxically led in the past to an almost hostile medical understanding of pain. The focus was on the supposed pain stimulus, which simply had to be identified and eliminated. Once this was done, pain was supposed to cease. If a pain stimulus could not be identified, then no pain was supposed to exist. If pain transmission was blocked, the pain had to stop. If the pain didn't comply, it was the patient's problem, not medicine's. Special attention for patients with chronic pain and specialized facilities for their treatment were deemed unnecessary. However, pain did not adhere to the prevailing medical and scientific establishment's understanding of pain at that time.

Only in recent decades has it become clear that pain originates and is modulated in a highly complex, specialized pain-processing sensory system [4-8]. This complex pain sensory system is modulated by exteroceptive and interoceptive stimulation. Cognitive, emotional, evaluative, motivational, and social factors vary the afferent and efferent processing of processes that ultimately enable pain perception and behavior. Knowledge, information, learning processes, reward, and avoidance behaviors protect against injury and illness and initiate protective and healing behaviors. The sensory, emotional, motivational, and cognitive components interact directly with the neuronal mechanisms. They influence current and anticipated healing and disease processes via descending systems and control the future course of the disease [5].

The mechanistic understanding of pain led to its marginalization in medicine for many years. It wasn't until 1974 that a dedicated international professional society – the International Society for the Study of Pain – was founded. A specially convened commission of 14 scientists from this society required three years of work to develop the following definition of pain [9]: “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage .” According to this definition, pain is more than just a sensory perception. Pain is also an unpleasant emotional experience. Pain can occur when tissue is damaged or threatened with damage. On the other hand, it is completely irrelevant to the experience of pain whether such tissue damage actually exists or whether a lesion can be detected.

To scientifically investigate pain or to diagnose and treat it clinically, one must define and systematically analyze its various properties or dimensions. It is not enough to identify the presumed pain stimulus or to quantify the resulting neuronal excitation. It is essential to determine and capture the different dimensions of pain in order to gain a comprehensive understanding of it. From a clinical perspective, seven main components of pain can be differentiated [10,1]:

  • The pain stimulus refers to the possible damage to tissue and cells as a result of external or internal influences that are seen as related to the pain experience.
  • The cognitive component : Pain has a location, a duration, and an intensity. These can be localized and quantified. For example, the location of the pain in square centimeters, the duration of the pain in hours, and the pain intensity can be quantitatively analyzed using a visual analog scale.
  • The affective component : Pain hurts, it changes mood and causes suffering.
  • The motor component : Pain leads to a change in facial expressions and gait; wiping, pulling away, and escape reflexes are activated.
  • The vegetative component : Pain leads to reactions of the autonomic nervous system and the organs controlled by it, e.g., sweating, changes in breathing, increased heart rate, increased blood pressure, etc.
  • The evaluative component : Well-being, moods, interests, expectations, and learning experiences influence sensory experiences, evaluating and judging them. These evaluations flow into the perception process before it is completed as a sensation and experience.
  • The social component : Social contextual factors within the family, professional sphere, and society influence pain perception and pain behavior. They interact directly with and modulate the content of the experience.

In clinical practice, therefore, there are very close interactions between biological, psychological, and social factors. These reflect the complex, interacting, systemic information processing within the pain-sensory system. Clinical examples show that the earlier unicentric, linear-causal model of pain overlooked the reality of experience and behavior. This deprived people with chronic pain of appropriate treatment. The complex interactions of cognitive, emotional, motivational, behavioral, and social conditions, as well as the systems-theoretical processing mechanisms within the pain-sensory system, were ignored.

literature

  1. Göbel H (1995) Definition and analysis of pain. Nervenheilkunde 14:216-221
  2. Göbel H (1992) Pain measurement: Theory – Methodology – Applications in headache G. Fischer, Stuttgart, Jena, New York
  3. Descartes R (1662) De homine figuris et latinatate donatus a Florentio P Leffen & F Moyardum, Leyden
  4. Rosenow D, Tronnier V, Göbel H (2006) Neurogenic Pain. Springer, Berlin, Heidelberg, New York, Barcelona, ​​Hong Kong, London, Milan, Paris, Tokyo
  5. Traue HC, Horn AB, Deighton RM, Kessler H (2005) Psychobiological influences on pain perception. An overview. Hypnosis
  6. Bromm B (2004) The involvement of the posterior cingulate gyrus in phasic pain processing of humans. Neurosci Lett 361(1-3):245-249. doi:10.1016/j.neulet.2004.01.018
  7. Bromm B (2001) Brain images of pain. News Physiol Sci 16:244-249
  8. Melzack RA, Wall PD (1965) Pain mechanisms: A new theory. Science (1560):3699-3709
  9. Taxonomy ISo (1979) Pain terms: a list with definitions and notes on usage. Recommended by the IASP Subcommittee on Taxonomy. Pain 6(3):249
  10. Göbel H (1995) Pain measurement and pain documentation. Neurology & Psychiatry 9:482-488