Lidamitol 100 mg/ml + 2.5 mg/ml solution for intramuscular injection 1 ml ampoules 10 pcs.

- Symptomatic treatment of spasticity in adults caused by stroke.
- Treatment of painful muscle spasms associated with musculoskeletal disorders (spondylosis, spondyloarthritis, cervical and lumbar syndromes).

For adults, 1 ml twice daily by intramuscular injection.
Procedure for handling the polymer ampoule:
1. Take the ampoule and shake it while holding it by the neck.
2. Rotate and detach the cap from the ampoule using twisting motions.
3. Immediately connect the luer of the syringe to the ampoule through the opening formed.
4. Draw the contents of the ampoule into the syringe.
5. Attach the needle to the syringe.

1 ml of the preparation contains:
Active ingredients:
Tolperisone hydrochloride 100 mg
Lidocaine hydrochloride monohydrate (calculated as lidocaine hydrochloride) 2.5 mg
Excipients:
Methylparaben 0.6 mg
Propylene glycol 0.3 ml
1 M solution of hydrochloric acid to pH 3.0-4.5
Water for injections up to 1 ml.

A clear colorless or colored liquid with a specific odor.

Increased sensitivity to any of the components of the drug (including lidocaine), severe myasthenia, age under 18 years, pregnancy, lactation period (due to lack of data).
With caution:
The drug should be used with caution in patients with renal and hepatic insufficiency. Dose adjustment is not required.
Pregnancy and lactation:
The drug is contraindicated during pregnancy and breastfeeding (due to lack of data).

No data.
Impact on the ability to drive vehicles and operate other mechanisms:
Caution should be exercised when driving motor vehicles and engaging in other potentially hazardous activities that require increased attention and quick psychomotor reactions.

Classification of the frequency of side effects recommended by the World Health Organization (WHO): very common (≥1/10), common (≥1/100 and

Symptoms: ataxia, tonic and clonic seizures, dyspnea, and respiratory arrest.
Treatment: symptomatic and supportive therapy is recommended. There is no specific antidote.

There is no data on interactions with medications that limit the use of the drug. Although tolperisone affects the central nervous system, it does not cause a sedative effect and can therefore be used in combination with sedatives, sleeping aids, and medications containing ethanol. It does not enhance the effect of ethanol on the central nervous system.
It enhances the effect of non-steroidal anti-inflammatory drugs, so a reduction in the dosage of the latter may be required when administered simultaneously.

Tolperisone hydrochloride is a central muscle relaxant. The exact mechanism of action is unknown. As a result of its membrane-stabilizing effect, it prevents the conduction of excitation in primary afferent fibers, blocking mono- and polysynaptic reflexes of the spinal cord. A secondary mechanism of action likely involves the inhibition of neurotransmitter release by blocking the influx of calcium ions into the synapses.

It reduces reflex readiness in the reticulospinal pathways of the brainstem.

It enhances peripheral circulation. This effect is not related to the drug's action on the central nervous system and may be due to the weak spasmolytic and antiadrenergic effects of tolperisone.

Lidocaine hydrochloride has a local anesthetic effect and, when dosed according to the instructions for Lidocaine, does not exert systemic effects.

Tolperisone hydrochloride undergoes intensive metabolism in the liver and kidneys. It is excreted by the kidneys, almost exclusively (> 99%) as metabolites, the pharmacological activity of which is unknown. Following intravenous administration, the half-life is approximately 1.5 hours.

Lidocaine hydrochloride is completely absorbed (the absorption rate depends on the site of administration and dosage). The time to reach maximum concentration after intramuscular administration is 30-45 minutes. Plasma protein binding is 50-80%. It is rapidly distributed in tissues and organs. It crosses the blood-brain barrier and the placental barrier, and is secreted in breast milk (40% of the concentration in maternal plasma). It is metabolized in the liver (90-95%) involving microsomal enzymes through the dealkylation of the amino group and cleavage of the amide bond, resulting in the formation of active metabolites. It is excreted in bile (a portion of the dose is reabsorbed in the gastrointestinal tract) and by the kidneys (up to 10% in unchanged form).