Back pain treatment

Back pain: Causes, symptoms, and treatments

In the complex treatment of various clinical options for back pain, an important place is occupied by the use of drugs. Among them, the leading place is taken by NSAIDs.

Currently, in the field of sports traumatology a large range of these drugs is used. They have two basic requirements:

  • efficiency, which means rapid regression and the elimination of pain and early functional (sports) rehabilitation;
  • safety, which means the absence of undesirable side effects, allergic reactions and effects that are in conflict with the rules of the international anti-doping committee.

Despite the large variety of NSAIDs, all standard preparations of this class of drugs have common positive and negative properties. This is due to the universal molecular mechanism of their pharmacological activity, namely the inhibition of the enzyme cyclooxygenase (COX), which regulates the synthesis of prostaglandins (PG). There are two isoforms of COX: a structural enzyme (COX-1) that regulates the production of PG, providing normal (physiological) activity of cells, and an inducible isoenzyme (COX-2), which participates in the synthesis of PG in the area of inflammation. It is believed that the analgesic effects of NSAIDs determine inhibition of COX-2, and the most common side effects (gastrointestinal lesions, impaired renal function and platelet aggregation) – inhibition of COX-1.

In recent years, new facts have been obtained on the role of COX-1 and COX-2 in normal and pathological conditions, as well as on COX-independent mechanisms of the effectiveness of NSAIDs action: inhibition of pro-inflammatory cytokines; the formation of superoxide radicals of nitric oxide, phospholipase C, transcription factor NF-kB, which is involved in the regulation of the synthesis of pro-inflammatory cytokines and adhesion molecules, which serves as an additional (albeit at the experimental level) justification for the use of NSAIDs. It is reasonable to assume that drugs with a balanced inhibitory activity against COX-1 and COX-2 may have an advantage over specific COX-2 inhibitors (coxibs), since there is evidence that not only COX-2 is involved in the development of inflammation and pain, but also COX-1, and the physiological role of COX-2-dependent PG synthesis in the healing of ulcers of the upper GI tract, ovulation, and the formation of prostacyclin (PG-2) by vascular endothelium cells (reduction of the antithrombotic effect) has been established. The deepening of knowledge and the accumulation of clinical data on the mechanisms of action of NSAIDs made it possible to form a working classification and divide all existing NSAIDs into four groups:

  • selective COX-1 inhibitors (low doses of acetylsalicylic acid);
  • nonselective COX inhibitors (most standard NSAIDs are diclofenac, ibuprofen, lornoxicam, etc.);
  • predominantly selective COX-2 inhibitors (aceclofenac, meloxicam, nimesulide);
  • specific (highly selective) COX-2 inhibitors (celecoxib, rofecoxib).

Regulation and suppression of nociceptive impulses in the central nervous system and enhancing the activity of the antinociceptive system are achieved by using centrally acting analgesics. The main drug of this group is tramadol.

Tramadol, a racemic mixture of two enantiomers, has a dual mechanism of action. Its programing enantiomer binds to -opiate receptors and inhibits serotonin reuptake, and the levorotating enantiomer inhibits norepinephrine reuptake. As a result of the activation of the noradrenergic and serotonergic systems, tramadol inhibits the transmission of pain impulses at the spinal level. In normal doses, it does not cause depression of respiration and blood circulation, impaired motility of the gastrointestinal tract and urinary tract, with prolonged use does not lead to the development of drug dependence. Its important advantage is the minimum narcotic potential. Tramadol is not listed in the Drugs Convention under international control and is not subject to special registration as a drug. According to a study of tramadol hydrochloride using controlled (including double-blind) randomized studies, it was shown that it relieves severe and moderate pain in the treatment of osteoarthritis of large joints to the same extent as diclofenac and meloxicam, without causing side effects inherent in NSAIDs. Tramadol is rapidly and 90% absorbed with a maximum concentration in the blood 2 h after administration. Of particular interest are the results of the successful combined use of tramadol and NSAIDs, allowing not only to achieve an adequate analgesic effect with minimal adverse reactions, but also to reduce the dose of NSAIDs. The drug has no side effects characteristic of NSAIDs, and can be used in patients with drug gastropathy, gastric ulcer, as well as liver, heart and kidney failure. It should be noted that in oncological practice the drug is used for a long time, for 2-3 years, without the development of addiction.

Tramadol  is the Pain Reliever for Back Pain

  • intolerance to NSAIDs;
  • contraindications to the use of NSAIDs;
  • insufficient effect of NSAID therapy, when an increase in their dose is undesirable;
  • exacerbation of pain in patients receiving NSAIDs;
  • the appointment of glucocorticoids, since the use of tramadol does not increase the risk of gastrointestinal disorders.

Side effects: sedation, dizziness, nausea and vomiting, loss of appetite, dry mouth, constipation. Slow, for 2-3 days, increasing the dose at the beginning of therapy helps to avoid unpleasant consequences when taking this drug. Often, the side effects of tramadol gradually disappear during the first days of therapy. All this allows us to consider tramadol as a promising tool in the treatment of PCBS. Tramadol is usually prescribed in 50 mg (with severe pain in 100 mg) up to 2 times a day.

In the acute period of lumbar pain syndrome (discoradicular conflict, facet syndrome), both NSAIDs and a wide range of analgesic drugs may be ineffective, as they do not eliminate reflex muscle spasm, whose role in the development and progression of CCPD is now considered proven. In this regard, in the complex therapy they use muscle relaxants, which contribute to the interruption of the above described vicious circle of pain and muscular spasm-pain. This is tolperisone and tizanidine. Tolperisone blocks mono-and polysynaptic spinal reflexes, selectively reduces the activity of the caudal part of the reticular formation of the brain, reducing spasticity. It has a central n-anticholinergic effect, also leading to muscle relaxation. Due to its chemical affinity with lidocaine, it reduces pain sensitivity in the peripheral nerve pathways and has a local anesthetic effect. Its vasodilating effect is explained by a blocking effect on the -adrenoreceptors localized in the vessels. It is prescribed 1 tablet (0.05 mg) 3 times a day during the entire acute period, but not more than 3-4 weeks. The drug tizanidine also has antispasmodic and analgesic effects. It reduces the release of excitatory amino acids from the intermediate neurons of the spinal cord, thereby providing a reduction in increased muscle tone, while not altering the contractility of the muscles. It is essential that tizanidine protects the mucous membrane of the stomach from the action of NSAIDs, and with their simultaneous appointment, the effectiveness of treatment is greatly increased. The drug is prescribed during the entire acute period, usually within 5-10 days at a dose of 6-8 mg per day.