|Systematic (IUPAC) name|
|Trade names||Mydocalm and others|
1st phase: 2 hrs
2nd phase: 12 hrs
|CAS Registry Number|
|ATC code||M02 M03|
|Molecular mass||245.36 g/mol|
- Clinical use 1
- Contraindications and cautions 2
- Side effects 3
- Overdose 4
- Interactions 5
- Mechanism of action 6
- Pharmacokinetics 7
- See also 8
- References 9
- External links 10
In Tolperisone is indicated for use in the treatment of pathologically increased tone of the cross-striated muscle caused by neurological diseases (damage of the pyramidal tract, multiple sclerosis, myelopathy, encephalomyelitis) and of spastic paralysis and other encephalopathies manifested with muscular dystonia.
Other possible uses include:
- Cervical and lumbar syndromes
- Arthrosis of the large joints
- Obliterating atherosclerosis of the extremity vessels
- Diabetic angiopathy
- Thromboangiitis obliterans
- Raynaud's syndrome
Contraindications and cautions
Manufacturers report that tolperisone should not be used in patients with myasthenia gravis. Only limited data are available regarding the safety in children, youths, during pregnancy and breastfeeding. It is not known whether tolperisone is excreted into mother's milk.
Adverse effects occur in fewer than 1% of patients and include muscle weakness, headache, arterial hypotension, nausea, vomiting, dyspepsia, and dry mouth. All effects are reversible. Allergic reactions occur in fewer than 0.1% of patient and include skin rash, hives, Quincke's edema, and in some cases anaphylactic shock.
Excitability has been noted after ingestion of high doses by children. In suicide studies of three isolated cases, it is believed that ingestion of tolperisone was the cause of death.
Tolperisone does not have a significant potential for interactions with other pharmaceutical drugs. It cannot be excluded that combination with other centrally acting muscle relaxants, benzodiazepines or non-steroidal anti-inflammatory drugs (NSAIDs) may make a dose reduction necessary in some patients.
Mechanism of action
Tolperisone is absorbed nearly completely from the gut and reaches its peak blood plasma concentration after 1.5 hours. It is extensively metabolised in the liver and kidneys. The substance is excreted via the kidneys in two phases; the first with a half-life of two hours, and the second with a half-life of 12 hours.