Comparison of the effectiveness of Tizanidin-teva and Sirdalud
Sirdalud is more effective than Tizanidine-teva - this means that the ability of the drug substance to provide the maximum possible effect is different.
For example, if the therapeutic effect of Sirdalud is more pronounced, then it is impossible to achieve this effect with Tizanidin-teva even in large doses.
Also, the speed of therapy is an indicator of the speed of the therapeutic action; Sirdalud and Tizanidin-teva are also different, as is bioavailability - the amount of the drug reaching the site of its action in the body. The higher the bioavailability, the less it will be lost during absorption and use by the body.
Comparison of safety of Tizanidin-teva and Sirdalud
The safety of a drug includes many factors.
At the same time, in Tizanidin-teva it is quite similar to Sirdalud. It is important where the drug is metabolized: drugs are excreted from the body either unchanged or in the form of products of their biochemical transformations. Metabolism occurs spontaneously, but most often involves major organs such as the liver, kidneys, lungs, skin, brain and others. When assessing the metabolism of Tizanidin-teva, as well as Sirdalud, we look at which organ is the metabolizing organ and how critical the effect on it is.
The risk-benefit ratio is when the prescription of a drug is undesirable, but justified under certain conditions and circumstances, with the obligatory observance of caution in use. At the same time, Tizanidin-teva does not have any risks when used, just like Sirdalud.
Also, when calculating safety, it is taken into account whether only allergic reactions occur or possible dysfunction of the main organs. In other matters, as well as the reversibility of the consequences of using Tizanidin-teva and Sirdalud.
Sirdalud in complex therapy of chronic pain syndromes
About the article
1989
0
Regular issues of "RMZh" No. 4 dated February 23, 2006 p. 240
Category: General articles
Author: Shirokov E.A. 1 1 Branch of the Military Medical Academy named after S.M. Kirov, Moscow, Russia
For quotation:
Shirokov E.A. Sirdalud in complex therapy of chronic pain syndromes. RMJ. 2006;4:240.
Pain is an unpleasant sensation and emotional experience associated with actual or potential tissue damage [1]. There are somatogenic, neurogenic and psychogenic pain syndromes, acute and chronic pain. Pain syndromes are divided according to localization and etiological factors [2]. However, pain syndromes of various natures have some common pathophysiological mechanisms, knowledge of which makes treatment tactics more effective.
The pathophysiology of pain syndromes is complex and includes both pathobiochemical and neurophysiological aspects. In clinical practice, a significant place is occupied by prolonged pain syndromes, the correction of which is impossible with the help of analgesics. An important general mechanism for the chronicization of pain is the sensitization of nociceptive neurons in the dorsal horns of the spinal cord [1,3]. Sensitization is based on the phenomenon of “winding up” - a progressive increase in the frequency of action potentials of nociceptive neurons in response to repeated stimulation. Sensitization of nociceptive neurons can be reinforced by mechanisms of neuroplasticity and increased excitability of nociceptive neurons in the overlying parts of the nervous system, including the nuclei of the hypothalamus and cerebral cortex. Thus, peripheral damage can trigger a cascade of pathophysiological and dysregulatory processes affecting the entire nociceptive system - from tissue receptors to the cerebral cortex. Increased excitability of nociceptive neurons contributes to the generalization of local pathophysiological processes accompanying tissue damage. Irritation of tissue receptors leads to reflex activation of motor neurons in the corresponding segments of the spinal cord and muscle contraction. There is a decrease in the threshold for the occurrence of the nociceptive reflex and the appearance of spontaneous tonic activity. Muscle tension impairs microcirculation, hypoxia and acidosis occur, and arachidonic acid metabolites and biogenic amines accumulate in the tissues. Inflammatory mediators contribute to a further decrease in the sensitivity threshold of nociceptive neurons. This vicious circle plays an important role in the mechanisms of pain chronicity. Chronic pain syndromes accompany and form the basis of the clinical picture of diseases of the musculoskeletal system, diseases of the nervous system associated with changes in the spine, and chronic headaches [4]. The prevalence of chronic pain syndromes in the population is extremely high. Only spinal diseases and associated pain syndromes affect 30-80% of men and women of different age groups [3,5]. According to epidemiological studies, the prevalence of episodic and chronic tension-type headaches in the population reaches 20-38% [6]. The most common causes of chronic lumbodynia are considered to be pathological changes in the spine, muscles (myofascial syndrome) or pelvic and abdominal organs [7]. Painful impulses cause excitation of the segmental apparatus of the spinal cord, which leads to an increase in muscle tone, a change in body posture and increases pain. The most significant vertebrogenic causes of back pain are caused by root ischemia (discogenic radicular syndrome, discogenic radiculopathy) and various degenerative changes in the spine. Less commonly, back pain is associated with spondylolisthesis, spina bifida, and developmental anomalies of the lumbosacral spine (lumbarization and sacralization) [4,5]. Another common cause of back pain is myofascial pain, caused by the formation of so-called trigger points in the muscles and/or associated fascia. The occurrence of trigger zones is also associated with muscular dystonia. Vertebrogenic reflex-muscular syndromes occur during the life of almost every person; compression syndromes develop much less frequently and in most cases are associated with damage to the intervertebral discs. Psychogenic factors occupy a significant place among the causes of chronic pain. The pathogenetic essence of such syndromes is due to the stable connection of emotional stress with the mechanism of its implementation - the muscular system [8,9,10]. A decrease in the sensitivity threshold of the nociceptive apparatus contributes to the occurrence and maintenance of pain. Long-term muscle dystonia is observed with depression and chronic stress. The most striking example of emotion-related pain is tension-type headache (TTH). TTH is usually of moderate intensity, pressing or squeezing in nature. Chronicity is very often observed with tension-type headache - almost constant feelings of heaviness and tension can persist for weeks, which leads to a significant decrease in working capacity. Treatment of chronic pain syndromes associated with the muscular-tonic component involves the development of three main directions: the use of analgesics, psychotropic drugs and muscle relaxants (Fig. 1). Of course, the best results are achieved through complex therapy using the capabilities of psychotherapy, physiotherapy and other treatment methods. However, pharmacotherapy takes a leading place in the treatment of chronic pain syndromes. The purpose of drug exposure can be sources of pain stimulation (for example, pathological processes of the musculo-ligamentous apparatus), functional or structural changes in the nervous system (for example, the segmental apparatus of the spinal cord), or muscles. In some cases, the use of psychotropic drugs (antidepressants, antipsychotics) allows one to obtain a stable therapeutic effect in psychogenic reflex-muscular syndromes. Muscle relaxants have extremely wide indications in the treatment of chronic pain syndromes [4,11]. One of the most effective modern muscle relaxants, widely used in the treatment of all types of muscle-tonic and pain syndromes, is Sirdalud. The drug reduces increased muscle tone in both the a- and g-motor systems, and has a direct and indirect analgesic effect. Direct - due to the antinociceptive effect through the non-opioid neuronal system; indirect - due to the antispasmodic effect. A fairly wide range of effective doses (from 2 to 36 mg per day) allows the drug to be used for short and long courses of treatment, alone or in combination with other drugs. In some cases, large doses of the drug may be used. The only side effect that may limit the use of Sirdalud is related to its sedative effect. The sedative effect when taking the drug manifests itself quite individually and quite rarely, but its possibility must be taken into account. At the beginning of treatment, you can prescribe 2-4 mg of the drug at bedtime and, if well tolerated, increase the dose to the required value. The optimal daily dose, as a rule, does not exceed 4-8 mg (only in some cases larger dosages are required). Severe pain syndromes, characteristic of damage to large nerve trunks, require large doses of Sirdalud and combination therapy. In these cases, the dose of the drug is increased to 8-12 mg per day and combined with non-steroidal anti-inflammatory drugs (NSAIDs). It has been established that Sirdalud reduces the side effects of NSAIDs and enhances their analgesic effect. In some cases, chronic pain syndromes require the inclusion of antidepressants in the treatment regimen. Thus, chronic pain syndromes with complex pathogenesis, as a rule, require complex therapy including muscle relaxants. The combination of Sirdalud with analgesics and psychotropic drugs in most cases allows one to obtain a sufficient clinical effect. Literature 1. Kukushkin M.A., Khitrov N.K. General pathology of pain (Guide for doctors). M.: Medicine, 2004. – 140 p. 2. Mashford M.L., Cohen M.L. et al. Pain and analgesia: A practitioner's handbook. M.: Littera, 2004. 488 pp.. 3. Coward DM Pharmacology and mechanisms of action of tizanidine (Sirdalud). /In: Spasticity: The current status of research and treatment. Ed. by M. Emre, R. Benecke. -Carnforth etc.: The Parthenon Publishing Group, 1989. -P.131-140 4. Kamchatnov P.R., Chugunov A.V., Umarova Kh.Ya., Volovets S.A. Therapy of acute vertebrogenic pain syndrome//Consilium medicum. 2005. –T. 7. –S. 125-132. 5. Berry H., Hutchinson DR Tizanidine and ibuprofen in acute low-back pain: Results of a double-blind multicentre study in general practice. //J. Intern. Med. Res. -1988. -Vol.16. –R.83-91. 6. Filatova E.G., Solovyova A.D., Danilov A.B Treatment of tension headaches // Journal of Neurology. and a psychiatrist. 1996, 4, 21-25. 7. Coward DM Tizanidine: Neuropharmacology and mechanism of action. //Neurology. -1994. -Vol.44., N.11 (Suppl.9). -P.S6-S11 8. Bokonjic R. Headache. M., 1984; 312. 9. Vein A.M., Kolosova O.A., Yakovlev N.A., Karimov T.K. Headache. M., 1984, p. 285. 10. Solovyova A.D., Filatova E.G., Voznesenskaya T.G., Kanavets E.V. Clinic, diagnosis and therapy of headaches in patients with hypothalamic syndrome. Travel JG, Simons DG. Myofascial pain. M., “Medicine”, 1989. 11. Davies J. et al Selectiv inhibition of responses of feline dorsal horn neurones to noxious cutaneus stimuli by tizianidine (DS 103-282) and noradrenaline: involvement of &2-adrenoreceptors. Neuroscience (1986) 673–682.
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Comparison of habituation in Tizanidin-teva and Sirdalud
Like safety, addiction also involves many factors that must be considered when evaluating a drug.
Thus, the totality of the values of such parameters as “o syndrome” in Tizanidin-teva is quite similar to the similar values in Sirdalud. Withdrawal syndrome is a pathological condition that occurs after the cessation of intake of addictive or dependent substances into the body. And resistance is understood as initial immunity to a drug; in this it differs from addiction, when immunity to a drug develops over a certain period of time. The presence of resistance can only be stated if an attempt has been made to increase the dose of the drug to the maximum possible. At the same time, in Tizanidin-teva the meaning of the “syndrome” is quite small, however, the same as in Sirdalud.
Drug interactions
Simultaneous use with inhibitors is permissible only if treatment is carried out at low doses of Sirdalud. Once in the blood, CYP1A2 increases the amount of the main substance in human plasma, which can cause symptoms of overdose. In turn, CYP1A2 inducers, entering the blood with Sirdalud, on the contrary, reduce the amount of tizanidine in the body, which makes the expected therapeutic effect insignificant even at high doses of consumption.
Concomitant use with antibiotics leads to a sharp decrease in blood pressure, the development of dizziness and drowsiness, which can cause loss of consciousness.
Rifampin, entering the blood, displaces tizanidine, which means it reduces the therapeutic effect. Treatment with Sirdalud should not be combined with alcohol intake. The drug significantly enhances the effect of alcohols on the central nervous system, leading to a pronounced change in consciousness.
Comparison of side effects of Tizanidin-teva and Sirdalud
Side effects or adverse events are any adverse medical event that occurs in a subject after administration of a drug.
Tizanidin-teva's state of adverse events is almost the same as Sirdalud's. They both have few side effects. This implies that the frequency of their occurrence is low, that is, the indicator of how many cases of an undesirable effect of treatment are possible and registered is low. The undesirable effect on the body, the strength of influence and the toxic effect of Tizanidin-teva are similar to Sirdalud: how quickly the body recovers after taking it and whether it recovers at all.
Sirdalud
To figure out whether Mydocalm or Sirdalud is better, let’s look at the last drug on our list. It is used for muscle spasticity and produces a central muscle relaxant analgesic effect.
This remedy is usually used for painful muscle spasms, during rehabilitation after spinal surgery, for skeletal muscle spasms and other conditions. Sirdalud is prohibited if the body is highly sensitive to tizanidine or other active ingredients or if liver function is severely impaired.
Side effects include drowsiness, increased fatigue, nausea, dizziness, disruption of the gastrointestinal tract, muscle weakness and some other abnormalities. Follow the dosage and do not stop taking the drug abruptly, and then the listed effects will be avoided.
Comparison of drugs
Sirdalud is the most modern muscle relaxant, suitable for combating skeletal muscle spasticity in diseases of a neuralgic nature:
- chronic myelopathy;
- multiple sclerosis;
- degenerative pathologies of the spinal cord;
- circulatory disorders in the brain.
The drug Sirdalud MR is available in a special form that creates a prolonged release of the active component tizanidine. Thus, the drug can be taken in the morning, and the side effects are less pronounced.
If you don’t know what to choose Sirdalud or Baclofen, it’s better to choose the first one if it suits you for the price.
Mydocalm is an older medicine that needs to be taken several times during the day. The drug has been well studied and has many indications, and the side effects are similar to those described above. Sirdalud, Mydocalm and analogues of these drugs have clear indications and contraindications, so only doctors should prescribe them.
Comparison of ease of use of Tizanidin-teva and Sirdalud
This includes dose selection taking into account various conditions and frequency of doses. At the same time, it is important not to forget about the release form of the drug; it is also important to take it into account when making an assessment.
The ease of use of Tizanidin-teva is approximately the same as Sirdalud. However, they are not convenient enough to use.
The drug ratings were compiled by experienced pharmacists who studied international research. The report is generated automatically.
Last update date: 2020-12-04 13:48:04
