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Противопаркинсоничес кие means
The groupThis фармакотерапевтическ ая Group unites medicines, as well as the ability to remove or alleviate the symptoms of Parkinson's disease ( наследственно-дегене��ативное chronic progressive disease) and parkinsonizma syndrome. The latter may be due to a variety of central nervous system injury (infection, intoxication, trauma, brain tumours receptacles, etc.) and the use of certain drugs, including Neuroleptics, calcium antagonists, etc.
AA Parkinson's disease and forms of sindromalnah remains unclear. It found that those with the degenerative nigrostriarnah dofaminergicakih neuronal and / or decreases in dopamine in striopallidarna system. The release resulted in the increased activity holinergicakih interneironov and as a consequence of the imbalance neiromediatornah systems. Violation balance between dofaminergicescoy and holinergicescoy neirotransmissiei is gipokineziei (rigidity movements) rigidity (expressed gipertonus skeletal muscle) and the rest tremorom (permanent involuntary shaking fingers, wrists, head, etc.). In addition, patients develop postural disorders, increased salivation, sweating and secretia sebaceous glands, a irritability and plaksivosti.
The drug Parkinson's disease and its sindromalnah forms is the restoration of balance between dofaminergicescoy and holinergicescoy neirotransmissiei, namely : increased dofaminergicakih functions or suppression holinergicescoy hyperactivity.
The medicines that can enhance dofaminergicescuu transfer to the central nervous system include levodopa, agonists dofamine receptors MAO inhibitors type B and �атехол-О-метилтрансф��разы (COMT), etc.
Levodopa eliminates deficit endogenous dopamine neuron in striopallidarna system. It is a physiological release predecessor, which did not have the capacity to penetrate the GEB. Levodopa permeates through GEB look for a mechanism under decarbauxilirovaniu with Dofa-decarboksilaza and effectively increases the level of dopamine striatume. However, the decarboxylation of levodopa happens in the peripheral tissues (where it is not necessary to raise the level of dopamine) making the unwanted effects, such as tachycardia, incredible, gipotenzia, vomiting etc. Ekstrazerebralnaya products prevent something besides Dofa-decarboksilaza (carbidopa, benserazid), which do not penetrate the GEB and no voice in the decarboxylation of levodopa in the central nervous system. The combinations of levodopa + Dofa-decarboksilaza inhibitor drugs are Madopar, Sinemet, etc. A significant increase in the level of dopamine in the central nervous system can lead to undesirable effects such as an involuntary movements (diskinesia), and mental disorders. Before taking swings in levodopa and some of its side effects to the use of drugs controlled release of substances (Madopar GSS, Sinemet SR). Such products provide stabilization plasma levels of levodopa, preserving them in a higher level for a few hours longer and the possibility of reducing the frequency reception.
Making the start in striopallidarna system is not only to increase its synthesis, but also by braking katabolizma. Thus, MAO-type destroys dofamin in polostom body. This izoferment selectively blocked selegilinom that soproprovozdaetsa oppression katabolizma release and stabilization of the level of the central nervous system. Furthermore, the effect antiparkinsoniceski selegilina from neiroprotectivei mechanisms, including oppression of free radicals. Degradation of levodopa and dopamine by Methylation inhibitors blocked another enzyme-COMT (entakapon, tolkapon).
Agonists dofamine receptors can also remove signs deficit dofaminergicescoy neirotransmission. Some of them (bromokriptin, lizurid, kabergolin, pergolid) are derived alkaloids LPV, others neergotaminovmi substances (ropinirol, pramipexol). The PP encourage D_1, D_2 and D_3 proved dofamine receptors and, as compared with levodopa is less clinical effectiveness.
To restore neiromediatonego balance in the central nervous system through oppression holinergicescoy hyperactivity may holinolitiki-antagonists m-holinoretseptorov (biperiden, benzatropin). Peripheric holinoliticaskie effects along with the violation of cognitive functions greatly restrict the use of this group of drugs. They are drugs of choice in parkinsonizme medication.
Derivative amantadina (hydrochloride, sulfate, glukuronid) interact with the receptor ion channel N-metil-d-aspartat (NMDA) receptors glutamatnah and reduce the release of acetylcholine holinergicakih neurons. Component антипаркинсоническог о effect of derivative amantadina is dofaminomimeticescoe indirect effect. They have the ability to increase the release of dopamine from presinapticakih endings hinder its reverse takeover and improve the sensitivity of receptors.
Therapeutic effect of antiparkinsonicakih develops gradually. Some of them are increasingly influencing the gipokineziu and postural disorders (levodopa, agonists dofamine receptors) others weaken tremor and lunch violation (holinolitiki). Perhaps as a mono or combination (drugs from different groups) antiparkinsonicescoy therapy. It should be borne in mind that the treatment of Parkinson's disease and its sindromalnah forms-symptomatic, the effects antiparkinsonicakih preparations are in the period of application and a short time after their lifting. Addition of these funds should be as ascertained. The appointment of a short-term breaks (1-2 per week) in admission to prevent tolerance. Not recommended long breaks in therapy антипаркинсоническим и drugs (possible serious or irreversible violations motion activity) but, if necessary, removal of the treatment is carried out gradually, in order to avoid aggravation of symptoms.