Pain

Pain, according to the International Association for the Study of Pain (IASP), is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described as such damage (IASP Taxonomy Working Group, 2011). Pain is thus a conscious sensation that arises from the cognitive and emotional evaluation of information from the nociceptive system. The nociceptive system is a specialized part of the somatosensory system responsible for the detection and processing of noxious (harmful) stimuli through specific receptors (nociceptors). This process of detection and processing is called nociception.

Acutepain: Acute pain is a vital sensory perception that warns the body of danger and injury. The subjective severity of pain does not correlate with the extent of tissue damage, but with central processing. The sensors that perceive the pain stimulus (nociceptors) are free nerve endings and are located in almost every tissue of the body. They respond to noxious mechanical stimuli, noxious thermal stimuli, and chemical substances released during tissue injury and inflammation. There are also descending pathways for endogenous inhibition of pain (pain modulation).

Chronic pain: Often there is no longer any connection between the pain and the damage or disease that originally triggered it. The pain has then lost its actual warning function and has become an independent clinical picture.

The reaction to pain can be divided into 4 components:

• The sensory-discriminative component identifies the location and nature as well as the intensity and quality of the noxious stimulus.
• The cognitive component evaluates the pain and compares it to previous pain events.
• The affective-emotional component makes the assessment in terms of individual emotionality.
• The vegetative component records the reactive responses of the sympathetic nervous system to the noxious stimulus.

With regard to the quality of pain, a distinction is made between different forms of pain:

• Physiological nociceptive pain: takes a protective action to avoid tissue destruction.
• Inflammatory pain: occurs after inflammation and tissue damage due to sensitization of the (peripheral) nociceptive system.
• Neuropathic pain: occurs with dysfunction in the peripheral and central nervous systems. This leads to sensitization of the nociceptive system. Crucial to the development of neuropathic pain is previous damage to somatosensory nerve structures. This damage can affect both the peripheral and the central nervous system (brain and spinal cord). Peripheral nerves can be injured by a variety of mechanical, metabolic, toxic, or inflammatory noxious agents. When central neuropathic pain occurs, the cause must be sought in a primary damaging process of the CNS (lesions of the spinal cord, brainstem, thalamus, subcortical structures, or cortex). The plastic changes induced by the lesion in the peripheral and central nervous system may take on a life of their own and then become irreversible over time.
• Tumor pain: Here, on the one hand, intact nociceptors are excited by tumor products. On the other hand, the tumour itself can damage nerve tissue through direct infiltration. In these mixed forms, it is important to estimate the proportion of the neuropathic pain component in the total pain in order to plan therapy.

• Psychogenic pain: In this case, no demonstrable organic causes can be identified.

  
  

Nociceptors are freenerve endings that convert somatosensory, noxious stimuli into generator potentials and transmit them afferently as action potential sequences. These receptors have a polymodality with regard to chemical, thermal or mechanical stimuli. The nerve endings are equipped with a multitude of sensory receptors that convert noxious stimuli into depolarizing sensory potentials.

The prototypes of these receptors are the transient receptor potential (TRP) channels, which, depending on their type, respond to heat or cold as well as to chemical and mechanical stimulation.

Nociceptive nerve endings are found in skin, mucosa, parts of the musculoskeletal system, vessels, and viscera, and are either myelinated (A-δ fibers) or unmyelinated (C fibers). The conduction velocity of C-fibers is much lower than that of A-δ fibers, which are therefore important for fast reflex responses (e.g. for the pull-away reflex). In addition, these fibers can be further subdivided with regard to their conductive pain quality (mechanical, chemical, thermal).

Starting from the thalamus, the nociceptive fibers finally reach the cortical parts of the brain, mainly the primary or secondary somatosensory cortex (ssC), the insular cortex and the gyrus cinguli (GyC). Together with the thalamus and parts of the prefrontal cortex (pfC), they form a complex network that is regularly activated in response to nociceptive stimuli. Due to this complexity, this network is also referred to as the pain matrix.

The pain intensity is measured with an analogue scale from 0-10 (no pain), grade 1 (1-4 = mild to moderate), grade 2 (5-8 = strong to severe), grade 3 (8-10 = unbearable), adopted by the WHO, with the help of which the intensity of the pain can be indicated subjectively by the affected person.

1. Graefe KH et al. (2016) Nozieption. In: Graefe KH et al. (Eds) Pharmacology and Toxicology. Georg Thieme Verlag Stuttgart SS 2224-227