For drugs that have analgesic properties and are used in the treatment of pain syndromes of different localization, include means for stopping pain associated with a change in pain threshold, damage (or dysfunction) of the central and peripheral nervous system – this is flupirtine, drugs from the class of antidepressants, a group of anticonvulsants . Also regularly used drugs that have no analgesic effect, but reinforce the analgesic effect of other drugs. These include muscle relaxants and antispasmodic drugs.
The strict classification of painkillers is based on the principle of dividing drugs into opioid, non-opioid and combination drugs, including non-opioid and opioid drugs. The remaining drugs belong to the so-called adjuvant and symptomatic agents, allowing to achieve the desired effect with minimal side effects and in less time. Non-opioid drugs, all of which are non-narcotic, have received the maximum prevalence; non-prescription drugs usually provide free distribution in the pharmacy chain.
A feature of our country, in contrast to the countries of Europe and America, is the lesser spread of the use of paracetamol preparations and the unjustifiably high prescription of antispasmodics
Opioid drugs, most of which are related to narcotic drugs, are much less common, which is associated with significant difficulties in the procedure for prescribing and accounting for drug trafficking. However, despite the fact that in our country, accounting for narcotic drugs makes it difficult to assign them, in Europe and America, the appointment procedure is simpler, while accounting and expert assessment of the patient’s social and psychological characteristics fall on the prescriber’s doctor, including monitoring the level of the drug in blood plasma, accounting of prescribed drugs, counting used ampoules and so on. A special subclass of drugs from opioid drugs are potent drugs that do not possess narcotic properties due to their low narcotic potential (low ability to cause psychological dependence), which are easier to take into account, which allows them to be used more widely.
Pain is only a signal that informs us of the presence of current or possible tissue damage. Depending on the type and type of pain, the temporal characteristics of the pain mechanism of the so-called nociceptive transmission varies somewhat, which also changes the pharmacological types of drugs prescribed for the treatment of a specific pain syndrome.
If we dwell on some approaches to understanding pain as such, it is necessary to highlight the concepts of acute and chronic pain and the mechanisms of their formation. Acute pain is physiological: it is a signal of danger, reporting local damage. If the destruction of the tissue is not too great, then the development of pain is temporary. The mechanism of its formation is simple: activation of peripheral pain receptors (or nociceptors) develops in the area of damage, is transmitted along the nerves to the posterior horns of the spinal cord, switches to the ascending paths of the spinal cord and activates the structures of the central nervous system. The reflex response to the painful afferent (ascending impulse) is a muscular reaction (the study of the relationship between which is assessed by the nociceptive flexor reflex). As a result, a person involuntarily removes the damaged area from the danger zone where damage is caused.
Chronic pain is pain that lasts longer than the period of normal healing, often non-obvious damage
It is chronic pain that is currently a significant social, economic and, of course, medical problem.
In this case, the key role is played by the mechanisms of formation of a specific pathophysiological type of pain. This is the emergence or activation of the so-called inflammatory cascade, passing through the enzyme cyclooxygenase (COX), which has two isoforms (COX-1 and COX-2), the effect on which is associated both with the anesthetic effect of NSAIDs, which block COX, and with the development of reactions from the gastrointestinal tract (risks of exacerbations of a peptic ulcer or gastritis, mainly associated with isoform 1), as well as the possibility of increasing the risks of thrombosis, mainly associated with the isoform 2.
Changes in chronic pain also occur at the level of the central nervous system: superstrong and long stimulation of peripheral nociceptors leads to sensitization of central nociogenic structures, which then react to pronounced and persistent excitation even to a weak signal. Central sensitization is mediated by inflammatory mediators: in case of severe pain, such as tumor necrosis factor α (TNFα), interleukin (IL) 1 and 6, as well as PGE2. There is a change in the properties of the membranes of neurons; In this process, glutamate receptors (NMDA – N-methyl-D-aspartate receptors) and so-called slow calcium channels are of great importance.