Parkinson's disease treatment (resolved and unresolved issues). Diagnostics and treatment of parkinson's disease What pills help with parkinson's disease

14.07.2020 Sport

The cure for Parkinson's disease has been the topic of the most lively debate for many years. Treating this disease is not an easy task. The difficulty lies in the fact that a mechanism has not yet been established that can stop the progressive death of nerve cells that synthesize the neurotransmitter dopamine. Lat. The substantia nigra is one of the structures related to the extrapyramidal system, which is responsible for regulating the tone and motility of skeletal muscles. Today, it is only possible to slightly slow down this pathological process.

The situation is aggravated by the fact that the disease debuts only when almost half of the nerve cells have already been irreversibly lost.

The drug treatment of Parkinson's disease consists in the protection of dopamine-producing nerve cells that have not yet died. It is also required to increase the level of the dopamine mediator in the nervous tissue and to correct the biochemical and metabolic processes occurring in it.

One of the main areas of treatment for this progressive disease is substitution therapy. Medicines for Parkinson's disease that work in this direction contain substances that are biochemical precursors of the neurotransmitter dopamine, as well as active ingredients inhibiting the metabolism of this neurotransmitter.

To date, no specific medications have yet been created that can completely defeat Parkinson's disease once and for all. The drugs used today by specialists increase the dopamine content in the nervous tissue and are intended for long-term use. Although Parkinson's drugs affect different parts of the metabolism, they work for the same result.

Increasing dopamine synthesis by midbrain cells

This mechanism of action is inherent in the drug "Levodopa". This substance is a structural precursor of dopamine. Conversion to dopamine by cleavage of the carboxyl group occurs in the neurons of the substantia nigra. In order to avoid premature transformation of a substance under the influence of liver enzymes, agents have been developed that inhibit the decarboxylase enzyme:

  • "On whom";
  • "Stalevo";

Benserazide is also capable of protecting Levodopa from untimely destruction (it is used in the form of the drug Madopar). These drugs for Parkinson's disease should be used simultaneously with Levodopa.

Increase in dopamine release by the membrane of the presynaptic neuron

This effect is capable of providing "Amantadine", which, in addition to the specified action, stimulates the connection of dopamine with postsynaptic receptors.

"Amantadine" as active substance is part of the following drugs for the treatment of Parkinson's disease:

  • Midantan;
  • "Gludantan";
  • Viregit-K.

Stimulation of dopaminergic receptors

The following drugs for Parkinson's disease, also called dopaminomimetics, have this mechanism of action:

  • Bromocriptine (Abergin, Parlodel);
  • Piribedil (Pronoran);
  • Cabergolid (Agalates, Bergolak);
  • Rotigotine is one of the latest developments. Unlike most drugs produced in pill form, the medication is a transdermal therapeutic system (TTS). This is a special patch designed to be applied to the skin. Gluing is done once a day. Dosed intake of therapeutic doses of a medicinal substance is regulated by the electronic filling of the patch, which does not allow failures. This new form of release has undeniable advantages. In particular, a significantly lower effective dosage of the drug, compared with traditional forms, as well as a lower severity of undesirable adverse reactions.

By establishing a connection with postsynaptic receptors, these medicinal substances mimic the effect that dopamine normally has on them.

Slowing down dopamine reuptake by membranes of presynaptic neurons

Such an effect can be provided by drugs belonging to the group of tricyclic antidepressants:

  • "Amitriptillin";
  • Desipramine;
  • Lofepramine.

The result of treatment with these drugs is a significant increase in the content of dopamine in the synaptic cleft. Knowing the mechanism of action, it becomes clear how this group of agents improves dopaminergic transmission.

Inhibition of dopamine breakdown

  1. The use of monoamine oxidase inhibitors ("Selegilin", "Razagilin"). In addition to slowing down the metabolism of dopamine, these drugs for the treatment of Parkinson's disease may also have neuroprotective effects. This is because these compounds prevent neuronal cytolysis and stimulate the release of neuronal growth factor and antioxidants by glial cells.
  2. Use of catechol aminotransferase inhibitors. This action is possessed by the pharmaceutical agent Entokapon.

These medicines should be used in conjunction with decarboxylase inhibitors (Stalevo, Nakom).

Diet therapy also plays an important role in the treatment of Parkinson's disease. Of course, not as an independent therapeutic technique, but as an adjunct to improve the effectiveness of drug therapy. The inclusion in the daily diet of a number of foods that can increase the amount of dopamine in the body will improve general state the patient and can, in combination with the main treatment, slow the progression of the disease.

To stimulate the production of sufficient amounts of dopamine, the body needs the following substances:

  • amino acids - they are used by nerve cells as a building material for the synthesis of the dopamine molecule. A particularly important role is recognized for the amino acids betaine and tyrosine. In sufficient quantities, these useful substances are found in berries, dried fruits, bananas;
  • antioxidants - have a neuroprotective effect, minimizing the negative effect of free radicals on neurons. A source - fresh fruits and vegetables, green tea;
  • vitamins - vitamins B6 and PP play an especially important role in the biosynthesis reaction of the neurotransmitter dopamine, as well as folic acid). To create a sufficient supply of these substances in the body, it is necessary to include pistachios, sunflower seeds, fruits, spinach, asparagus in the diet;
  • trace elements - magnesium plays an especially important role: it not only participates in the synthesis of dopamine, but also helps to relax muscle fibers, preventing their spasms. Saturate the body with magnesium legumes, nuts, whole grains, fresh vegetables, especially dark-leaved;
  • macronutrients;
  • saturated fatty acid(called Omega-3).

The following herbs also regulate dopamine production:

  • ginseng;
  • dandelion;
  • peppermint.

After consulting with your doctor in advance, they can be used in the form of infusions.

Features of the use of antiparkinsonian drugs

  1. Parkinson's disease is progressive. In this regard, the initially selected dose of the drug may eventually turn out to be ineffective. This situation will require an increase in the dosage of the drug used or the appointment of a new treatment regimen.
  2. As a result of the progression of the disease, especially in its later stages, symptoms of dementia may develop, which will have to be corrected with anticholinesterase drugs (Galantamine) or anticholinergic agents of the central mechanism of action (Cyclodol).
  3. To avoid the cumulative effects of antiparkinsonian medicines, it is advisable to include in the therapeutic regimen several drugs with different mechanisms of action and different points of application, in small dosages.
  4. In order to avoid the development of undesirable side reactions, in no case should the recommended dosage of medicines be exceeded.
  5. Important! Despite the abundance in the public domain of information about the disease itself and about the means for its therapy, in no case should you try to diagnose yourself and select a treatment yourself. Anyone who has noticed symptoms that make him think about Parkinson's disease needs a consultation with a specialist neurologist and a detailed medical examination under his supervision.

Alternative treatments

Find their place in the therapy of Parkinson's disease and homeopathic methods of treatment, in particular, the following means:

  • Coenzyme Compositum;
  • Ubiquinone Compositum;
  • preparations of the Vitorgan series

other.

To obtain a convincing effect, a strictly individual approach is required in the diagnosis and selection of therapeutic agents, taking into account all the characteristics of the patient and the nuances of his condition. Almost everything matters:

  • the patient's condition at the time of examination;
  • what diseases it suffers from (including chronic diseases that are currently in remission);
  • what medications the patient is taking both for the treatment of Parkinson's disease and for concomitant diseases.

Most often, the course of therapy, which is prescribed to the patient according to the results of the examination, lasts from six months to two years. However, treatment can be continued for a longer time. The undoubted advantage of using homeopathic remedies is their almost complete absence of side effects.

At all stages, treatment with homeopathic remedies should proceed under the strict supervision of a treating specialist.

Homeopathy for Parkinson's disease not only improves the patient's emotional state, often completely relieving him of the depressive syndrome, but is also able, if properly selected and regularly taken, to reduce the amplitude and frequency of tremors, significantly improving the patient's quality of life. Such treatment allows the patient to refuse to take antidepressants, and, consequently, get rid of the side effects caused by this group of pharmaceuticals.

Shoshina Vera Nikolaevna

Therapist, education: Northern Medical University. Work experience 10 years.

Articles written

Parkinson's disease as a particular form of parkinsonism is still a mystery to a certain extent. She is the second most common after neurodegenerative disorders. Until now, the disease has not been completely cured, but surgical techniques and high-quality pills from Parkinson's make it possible to postpone the destructive effect of this most complex pathology in time.

Parkinson's disease treatment approaches

The disease has been known to mankind for many centuries, only it has not been studied and systematized. Characteristic signs ailment in the form of tremors, specific gait and muscle rigidity was described by many ancient authors, including Galen. The disease gets its name from James Parkinson, an English physician who wrote Essays on the Palsy Shaking in 1817. But full-fledged research began only at the end of the 19th - beginning of the 20th century.

In the middle of the last century, a role in the development of the disease of dysfunction of the neurotransmitter dopamine was revealed. The discovery influenced the methods of treatment. The first method was the use of belladonna alkaloids (atropine), which was used at the turn of the nineteenth and last centuries. At the end of the 30s of the twentieth century, they learned to perform operations to destroy the basal ganglia, which brought tangible results.

For several decades, surgical methods of treatment have developed and constantly improved, but they remained the only effective means of combating the disease, except for the use of anticholinergic drugs. Their work was aimed at blocking acetylcholine, a natural neurotransmitter.

At the very end of the 20th century, encouraging attempts were made to treat with electrical stimulation by impulses of deep brain structures. These techniques were found worthy of attention and further study for use.

But before the invention of a drug called Levodopa, treatment with drugs for Parkinson's disease was almost hopeless.

Preparations in the early stages of the disease

If a patient has Parkinson's disease, treatment should be started as early as possible. Although the disease is currently considered incurable, the early use of specialized drugs helps to delay the appearance of negative signs as much as possible.

The most common over the past years is considered "Levodopa". But this effective remedy has a fairly large number of side effects, in particular, with prolonged intake of significant doses, the patient develops intractable motor disorders.

Because of this, when deciding how to treat progressive Parkinson's disease, many doctors prefer to use modern alternative drugs, for example, dopamine antagonists - Ropinirole, Pergolid, Apomorphine, Pramipexole and others.

If the patient is given these funds at the first signs of tremor paralysis, then the use of "Levodopa" can be postponed to a later period, therefore, reduce the risk of developing motor disorders. However, dopamine agonist drugs themselves are capable of producing the same changes.

If the patient is over 70 years old, then the restriction on the use of "Levodopa" does not apply to him.

For use on early stages disease is more suitable for monotherapy, that is, the use of one specialized drug in order to avoid rapid development side effects.

Medication in the later stages

Drugs for progressive Parkinson's disease can also be used in monotherapy, but more often a combination is used:

  • Levodopa is the main drug at the moment.
  • "Amantadine", which has an effect against Parkinson's disease and stimulates the production of dopamine.
  • "Stalevo" and its analogues, which enhance the effectiveness of "Levodopa" and extend the duration of its action.
  • MAO-B inhibitors, for example, "Razagiline", which increases the concentration of dopamine and prevents its breakdown.
  • Dopamine receptor agonists.
  • Holinotropic drugs.

Drug treatment is complemented by physiotherapy procedures, exercise therapy, classes with a speech therapist aimed at correcting speech and swallowing disorders, psychotherapy for social rehabilitation.

In addition, symptomatic and supportive drugs are used to treat accompanying symptoms, for example, the essential amino acid phenylalanine. It is capable of converting in the patient's body into tyrosine, which is involved in the synthesis of dopamine.

A neurostimulant is also used for the elderly when they are taking Levodopa, but the body responds poorly to treatment. In this case, stimulation of deep brain structures is used with the destruction of some subcortical nuclei. This causes a significant improvement in the patient's condition, a retreat of pronounced symptoms, an increase in a person's socialization. The doctor can reduce the dosage of Parkinson's drugs, which will reduce the negative manifestations and facilitate the patient's existence.

Using a stimulator is much easier and safer than using electrodes for classical forms of intervention. The operation takes less time, only one small hole is made in the skull. An antiseptic is used for treatment, and an antimicrobial drug is given to prevent infection. There is always a risk, but with this kind of jewelry surgery, it is minimal. The only obstacle is the high cost of the operation.

The use of a neurostimulator does not exclude the use of other methods of treatment, including medication, and the most advanced techniques under development - genetic engineering and stem cell therapy, the use of special viruses, impulse stimulation of neurons. The patient should be aware that an improvement in his condition does not mean complete recovery, that he still needs to be treated and take care of his health.

Side Effects of Treatment

Since the main remedies for Parkinson's disease are drugs that restore dopamine levels, side effects are mainly caused by the use of "Levodopa" and other drugs with similar effects.

The tablets have an excellent effect on strong tremors, muscle stiffness and limited mobility, which causes real euphoria in many patients at the beginning of use. However, this remedy has practically no effect on imbalance and stiffness in gait.

Moreover, prolonged use of "Levodopa" or its high doses lead to the development or intensification of dyskinesias - sharp involuntary and uncontrolled movements, twitching, twisting of the limbs. Anticonvulsants are useless or ineffective in such cases.

Levodopa can cause many negative symptoms. These include the following:

  • nausea;
  • vomit;
  • constipation;
  • hypotension;
  • high nervous irritability, irritability.

Because of this, doctors prefer not to prescribe "Levodopa" in the early stages of the disease, but to do with other drugs that raise the level of dopamine. The same is used if this particular medicine is contraindicated to the patient.

Possible reasons for the decrease in the effectiveness of therapy

As Parkinson's disease progresses, the prescribed pill treatment may weaken over time. The disease is increasingly affecting the body, less dopamine is produced, and the drugs used do not cope with the situation.

Due to the large number of side effects and a decrease in the effectiveness of treatment with one drug in recent years, "Levodopa" in its pure form is rarely used. Most often, its combination with dopadecarboxylase inhibitors is used for therapy. These are drugs such as Nakom, Madopar or their substitutes.

Also used is "Midantan" (amantadine) and its analogs: "Viregit", "Symmetrel", stimulants of dopamine receptors - "Parlodel", "Mirapex", "Apomorphine" and others.
In the treatment of Parkinson's disease, not only the use of pills and surgery is important, but also lifestyle changes. The patient needs to eat right in order to avoid the side effects of drugs, give preference to vitamin foods, and reduce protein intake in the morning.

An important role is played by helping to restore limb mobility and to strengthen muscles. There is also a free method - this is walking and a positive attitude, which depends on the support of the patient from family and friends.

Symptomatic therapy includes the use of painkillers for painful movements, sleeping pills - for sleep disorders, sedatives - with high excitability and aggressiveness, irritability, depression.

There are no trifles in the treatment of Parkinson's disease, since it affects the main organ - human brain... Maintaining good vascular health is important to improve health.

It has not yet been possible to cure the disease, but with the use of all the achievements of modern medicine and a complex effect, it is possible to prolong the patient's life and improve its quality.

Parkinson's disease is a slowly progressive neurodegenerative disease characterized by irreversible death of neurons that produce the neurotransmitter dopamine located in the compact part of the substantia nigra of the brain.

Parkinson's disease remains an incurable pathology to this day, but modern therapy regimens make it possible to improve the quality of work and life of patients with this pathology.

Given the pathogenesis of the disease (a decrease in the level of dopamine and inhibition of dopaminergic transmission in the circuit of the basal ganglia), the list of tablets from Parkinson's includes drugs that directly or indirectly increase its level in the substantia nigra.

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  • Provide an EXACT DIAGNOSIS you can only a DOCTOR!
  • We kindly ask you NOT to self-medicate, but make an appointment with a specialist!
  • Health to you and your loved ones!

Parkinson's disease treatment principles

All drugs used in Parkinson's disease affect various links in the synaptic transmission of the nerve cells of the substantia nigra, ultimately leading to an increase in the amount of dopamine in the synaptic cleft and an improvement in dopaminergic transmission.

In accordance with the principle of action of drugs, clinicians have established the following principles for the treatment of Parkinson's disease:

Increased dopamine production in the midbrain
  • This mechanism of action has levodopa - the structural precursor of dopamine, DOPA. Dopamine cannot penetrate from the blood into the substance of the brain and cannot be used in therapy.
  • Levodopa, penetrating into the cells of the substantia nigra, loses its carboxyl group and is converted into dopamine.
  • When taken orally, levodopa undergoes premature decarboxylation in the liver to dopamine by the DOPA-decarboxylase enzyme, and therefore it is usually used in combination with inhibitors of this enzyme - carbidopa (Nakom, Stalevo preparations) or benserazide (Parkinson's Madopar tablets).
Increased dopamine release from the presynaptic terminal
  • This principle of action is possessed by the antagonist of glutamate NMDA receptors amantadine (Viregit-K, Gludantan, Midantan), also used against influenza.
  • In addition to stimulating the release of dopamine from the depot, it sensitizes postsynaptic receptors for communication with dopamine.
Stimulation of dopamine sensitive receptors
  • This principle underlies the action of dopamine receptor agonists (dopaminomimetics) - bromocriptine (Abergin, Parlodel), piribedil (tablets from Parkinson Pronoran), cabergolide (Agalates, Bergolak) and others.
  • These substances, acting on postsynaptic receptors, mimic the effects of binding to these dopamine receptors.
Inhibition of the process of re-uptake (reuptake) of dopamine by presynaptic endings
  • This principle is provided by tricyclic antidepressants (TCAs) - amitriptyline, desipramine, lofepramine and others.
  • These drugs slow down the reuptake of dopamine by the presynaptic terminals, increasing its amount in the synaptic cleft and, therefore, improving dopaminergic transmission.
Inhibition of dopamine breakdown
  • Dopamine is catabolized by one of two enzymes: monoamine oxidase type B (MAO-B) or catecholamitotransferase (COMT).
  • MAO-B inhibitors (selegiline, rasagiline), in addition to inhibiting the breakdown of dopamine, prevent the death of gray matter cells, induce the synthesis and release of glial cells of neuronal growth factor, trigger the synthesis of antioxidant enzymes by neurons, thereby exerting a neuroprotective effect.
  • The only COMT inhibitor available on the market is entokapone. As with levodopa, the blood-brain barrier is not impenetrable for him.
  • These two compounds are used in combination (for example, the drug Stalevo): this accelerates the achievement of the maximum concentration of levodopa in the blood plasma and prolongs its action.

To control symptoms, especially in the later periods of the disease, drugs that do not modulate dopaminergic transmission can be used: central anticholinergics (cyclodol, aprofen, tropacin) for severe movement disorders, cholinesterase inhibitors (galantamine, rivastigmine) for dementia, modafinil for daytime sleepiness.

Parkinson's disease progresses steadily, and as it progresses, the originally prescribed dose may become ineffective.

Due to the availability of a large number of drugs with different points of application, it will be advisable not to increase the dose of the original drug, but to write in the treatment plan a drug from another group with a different mechanism of action.

This is one of the main concepts of Parkinson's disease therapy to avoid the cumulative side effects of drug use.

Pills at the initial stage of Parkinson's

Manifestations initial stage Parkinson's disease is mild and can be controlled without levodopa in patients under 70 years of age.

Patients are forced to take drugs for the rest of their lives, so younger people will certainly face fluctuations that irreversibly occur when taking levodopa for several years, in which periods of hyperkinesis (pronounced tremor, excessive movements) are replaced by periods of immobility (akinesias).

The drugs of choice in this case are dopaminomimetics, for example, pills from Parkinson's Pronoran or Bromergon. These medications effectively control the progression of symptoms for 2-4 years. The high cost of drugs in this group inhibits their use.

Lower cost and, at the same time, no less efficiency have selective inhibitors MAO-B (selegiline) and the NMDA receptor antagonist midantan (amantadine).

The effect of using drugs of both groups develops after about a month after the start of administration; their therapeutic effect is 15-20 times less than that of levodopa, but the initially selected dose remains effective for 1.5-5 years.

All drugs that are used in the initial stage of Parkinson's fit well into the combination therapy with levodopa when the symptoms of the disease worsen.

Medicines in a pronounced form

With an increase in symptoms, the dose of the initially prescribed drugs should be gradually increased to the maximum therapeutic dose.

The amount of the drug is titrated for each patient, starting with the lowest therapeutic dose (125 mg for Madopar and Nakoma). The combination of DOPA-containing drugs with drugs of other groups, for example, with dopaminomimetics, can reduce the amount of levodopa taken daily by a quarter or more.

The dosage of DOPA-containing agents is adjusted when the worsening of the patient's symptoms significantly reduces the quality of his household and social activities. On average, a good therapeutic response to levodopa medications begins to decline after 3-4 years of use.

Side effects of therapy

The side effects (ADEs) of antiparkinsonian therapy are classified as early and late.

Early PEs appear shortly after starting a particular drug and are usually a consequence of the mechanism of action.

Such problems are eliminated by lowering the dose, establishing a "drug vacation" (breaks in admission for several days) or replacing the drug with a drug from another group.

Late PE occurs many years after starting treatment. These AEs are difficult to correct by dose selection and require additional pharmacological intervention. Among them, the most serious are psychoses and dyskinesias (involuntary movements).

The psychoses arising from the treatment of Parkinson's disease have a very dramatic effect on the lives of patients, taking into account the steadily increasing dementia.

The situation is aggravated by the fact that most neuroleptics (antipsychotic drugs) have a mechanism of action that is diametrically opposite to that of antiparkinsonian drugs: they block dopamine receptors, thereby accelerating the development of Parkinson's disease.

Fortunately, the pharmaceutical arsenal today has atypical antipsychotics lacking antidopaminergic effects. Some patients with mild psychosis also respond to the use of anxiolytics (tranquilizers) and antidepressants.

Fluctuation of motor manifestations (“on-off” -phenomenon) is due to fluctuations in the concentration of levodopa in the blood; the frequency and amplitude of these fluctuations increases over time, forcing the patient to shorten the intervals between doses to equalize the concentration of the drug in the blood, and then to increase the dose.

Levodopa-induced dyskinesia is divided into 3 types depending on clinical picture developing after oral administration DOPA-containing preparation:

Dystonia Akinesia (impossibility of voluntary movements) associated with a low concentration of levodopa in the blood plasma. It most often occurs after a night's sleep and initially manifests itself as painful spasms and inability to move one of the feet. Disappears after taking the next dose of the drug.
On-period dyskinesia (peak dose dyskinesia) The most common type of dyskinesia that occurs when taking levodopa. Associated with the maximum concentration of levodopa in the blood. It is manifested by chorea-like movements of the head, trunk and limbs, sometimes of the respiratory muscles. For correction, it is necessary to reduce the dose of the drug and maintain the concentration below the peak.
Biphasic dyskinesia (D-I-D-dyskinesia) It occurs when the concentration of levodopa increases and decreases; does not manifest itself at a constant concentration of levodopa in the blood and manifests itself only with significant shifts in one direction. By its nature, this is atonic dyskinesia, however, a picture of chorea or a mixture of these states can be observed.

Dyskinesias of this nature are stereotyped in terms of time of onset and signs, and therefore predictable. There are also unpredictable variants of dyskinesias. They have a reliable connection with the intake of levodopa, but cannot be compared either with the level in the blood, or with the time between doses (so-called yo-yo-dyskinesias).

Described and non-motor fluctuations associated with the amount of levodopa in the blood. They consist in the appearance of neuro-emotional, gastrointestinal, vascular-cardiac and other changes and disorders.

The main condition for reducing fluctuations is maintaining a constant concentration of levodopa in the blood. For this, prolonged DOPA-containing formulas are introduced into treatment - for example, Nakom R, Sinemet SR, Madopar HBS. Relief of biphasic dyskinesias can be achieved by increasing the dose of drugs.

Atypical antipsychotics (thiopride, clonazepam) and GABA-ergic antiepileptic drugs (valproate) are used as secondary means of combating movement disorders.

Vitamin B6, being a decarboxylase cofactor, can be used for peak dose dyskinesias. Any effect will be observed only under the condition of ultra-high dosages, which is fraught with overdose and the occurrence of side effects of B6 hypervitaminosis.

The reasons for the decrease in the effectiveness of treatment

The key reasons for the decrease in the effect of antiparkinsonian drugs are as follows:

  • death of dopaminergic nerve cells;
  • decreased expression of dopamine receptors at the postsynaptic terminal;
  • desensitization of dopamine receptors;
  • depletion of the ability of the remaining neurons of the substantia nigra to synthesize dopamine;
  • competition of dopamine for receptors with false mediators;
  • decrease in intestinal absorption of levodopa due to competition with other amino acids.

Together, they lead to first a relative, and then, as neurons die, an absolute insufficiency of the dopaminergic system.

Thus, given the variety of Parkinson's products and pills on the market, it becomes increasingly difficult to plan a treatment. The original treatment regimen, taking into account the inevitable side effects, is doomed to dynamic changes throughout the rest of the patient's life.

Parkinson's syndrome - complex chronic illness, disturbing nervous system and motor function. All over the world, there are about 1% of patients with parkinsonism, in 90% of cases they are people after 60 years. Pathology is progressive in nature, therefore it requires early diagnosis and timely started treatment. Therapy, which is started at the initial stage, allows you to delay clinical manifestations as much as possible and allow the patient to continue to live fully.

Types of drug therapy

As with any disease, Parkinson's syndrome requires systematic drug treatment. The selection of drugs should be carried out individually based on the stage of the disease, the severity, the patient's age and clinical manifestations. The main tasks of the upcoming treatment are to relieve the symptoms of the pathological process and restore dopamine synthesis to prevent the death of still healthy neurons. The problem with all drugs in the fight against this syndrome is addiction to drugs, which leads to an increase in the dose and power of the drug. For this reason, in the early stages, the doctor tries to prescribe the minimum dosage, which is more gentle. drugs, combine them with each other to achieve maximum effect and minimum harm.

Groups of medicines

Antiparkinsonian drugs:


At the beginning of treatment, preference is given to dopamine receptor agonists, the dose is selected experimentally, starting with a minimum, gradually increasing until the desired result is achieved. Typically, drugs in this group are available in pill form, such as:

  • piribedil (pronoran);
  • pramipexole;
  • bromocriptine.

Levodopa

The antiparkinsonian medication, which is considered the best available today, effectively fights such clinical manifestations as:

  • muscle stiffness;
  • salivation;
  • tremor;
  • hypokinesia;
  • dysphagia.

Patients notice an improvement in their well-being 6-8 days after the start of taking levodopa, the maximum effect is observed after 25 days. Most often, drugs are combined with medications such as carbidopa, benserazide, which allows you to reduce the required dose of levodopa, thereby reducing possible side effects. Levodopa tablets are taken with meals, 2-3 times a day, the drug is canceled only gradually.

It is undesirable to accept funds from this group in the following cases:

  • glaucoma;
  • chronic liver and kidney failure;
  • psychosis;
  • melanoma;
  • stomach ulcer;
  • bronchial asthma;
  • history of heart attack.

The drug has many side effects, the main ones are:

When taking levodopa, it is important to stick to a certain type of diet with a reduced amount of protein, as it interferes with the absorption of dopamine.

Pronoran

The active substance of the drug is piribedil, it is used in the treatment of early and late stages of parkinsonism. Pronoran improves motor function and alertness. Pronoran is shown both in monotherapy and in combination with levodopa medications, take pills after meals, drinking plenty of water, three times a day.

Pronoran is contraindicated in the acute phase of a heart attack, individual intolerance to the components and in combination with neuroleptics. Pronoran, like levodopa, has many side effects:

  • nausea;
  • flatulence;
  • hallucinations;
  • confusion of consciousness;
  • drowsiness;
  • dizziness;
  • arterial hypotension;
  • instability of blood pressure.

Pronoran practically cannot cause an overdose, since in this case vomiting occurs, and the substance is not absorbed into the blood. Initially, pronoran is prescribed at a dose of 50 mg. per day, gradually increasing the amount if necessary.

Amantadine

Another drug in the fight against Parkinson's syndrome is not effective only for dosage form pathology. Actively fights against movement disorders in particular with tremors.

Has contraindications:

  • glaucoma;
  • epilepsy;
  • thyrotoxicosis;
  • stomach ulcer;
  • pregnancy;
  • pathology of the kidneys and liver.

Side effects may include:

  • delay in urination;
  • nausea;
  • arrhythmia;
  • dry mouth;
  • swelling;
  • deterioration of vision;
  • hallucinations;
  • deterioration in attention.

Amantadine tablets should not be used in conjunction with alcohol, and abrupt withdrawal of the drug should also be avoided.

Bromocriptine

This medication stimulates dopamine receptors and suppresses prolactin secretion. Also, like Amantadine, it is effective in all forms of the disease, except for drug parkinsonism. Contraindicated in persons with mental disorders, pregnant women, people with serious gastrointestinal disorders and children.

Side effects are similar to those of the medication pronoran. It is taken both independently and in combination with levodopa, the dose of the latter with a combination can be reduced.

Cabergoline

The action of the drug is similar to Bromocriptine, but has a longer effect and fewer side effects. The average daily dose of the drug is 2-6 mg, treatment of the syndrome begins with 1 mg, gradually increasing the amount of the drug. side effects allocate:

  • cardiopalmus;
  • nosebleeds;
  • depression;
  • dyspeptic symptoms;
  • swelling.

Pramipexole

As an independent remedy, effective in the early stages of the disease, at later stages it is recommended to take it in combination with levodopa. Contraindications other than pregnancy, breastfeeding and has no personal intolerance.

Side effects are noted:

  • constipation;
  • dry mouth;
  • vomiting;
  • dyskinesia;
  • mental disorders;
  • drowsiness;
  • swelling.

It is well tolerated with many types of drugs, including medications levodopa and pronoran, in addition to dopamine antagonists, the latter reduce the effectiveness of pramipexole. The dose is increased gradually, taken three times a day, the drug is gradually canceled.

Selegiline

The main indication for the use of Parkinson's syndrome and its different shapes, except for medicinal. Able to delay the start of taking levodopa, but there is no information about the possibility of delaying the progress of the disease. Should be used with caution when peptic ulcer stomach and duodenum, angina pectoris and mental disorders. It is strictly prohibited for glaucoma, hyperplasia prostate and arrhythmias.

May cause:

  • skin rash;
  • increased activity of liver enzymes;
  • retention of urine;
  • agitation;
  • dry mouth;
  • loss of appetite;
  • nausea and vomiting.

You should be careful when taking it together with levodopa, as selegiline can increase side effects the latter, and also increases the risk of death. The drug should be canceled gradually, abrupt discontinuation of the drug contributes to an increase in the clinical picture. It should be taken twice a day, in the morning and at lunchtime.

Tolcapon

Increases the therapeutic effect of levodopa, is rapidly absorbed and begins to take effect within a few hours.

Indications:

  • Parkinson's syndrome.

Side effects:

  • diarrhea;
  • insomnia;
  • anorexia;
  • dyskinesia;
  • nausea.

It is canceled gradually, otherwise neuroleptic syndrome may occur. The minimum dosage is 100 mg. three times a day, later, an increase in a single dose to 200 mg is possible.

Entacapon

Indications: Parkinson's syndrome, with the ineffectiveness of therapy with other medicines.

Contraindications:

  • heart failure;
  • pregnancy, breastfeeding;
  • children under 18;
  • liver failure;
  • hypersensitivity to the components of the drug.
  • Of the frequent side effects, they describe:
  • headache;
  • an increased sense of anxiety;
  • hallucinations;
  • excessive sweating;
  • falling;
  • insomnia;
  • asthenia.

It should not be taken simultaneously with MAO-A and MAO-B inhibitors, and the production of liver enzymes should also be monitored.

Central anticholinergics

The main indications for use are Parkinson's syndrome. This group is less effective than levodopa, but in the early stages with minor symptoms, therapy can be started with anticholinergics. There is a moderate effect in relieving symptoms such as tremors and muscle stiffness. Have no effect on bradykinesia. With extreme caution, drugs should be taken in old age, as they can enhance cognitive manifestations. One of the main drugs in this group is Trihexyphenidil, it effectively affects the syndrome, including drug parkinsonism. Contraindicated in dementia, pregnancy, intestinal obstruction and glaucoma.

Side effects:

  • attention disorders;
  • tachycardia;
  • dizziness and headache;
  • dry mouth;
  • decreased visual acuity;
  • increased irritability.

Attention! With prolonged use, you may experience drug addiction from the drug.

Biperiden according to its indications and side effects similar to Trihexyphenidil, the only difference is that it can cause drowsiness and reduce arterial pressure... In patients with epilepsy, it can provoke new seizures. It is taken twice a day.

The modern pharmaceutical industry offers a wide range of drugs in the fight against parkinsonism. Unfortunately, none of them is able to completely eliminate the pathology. The syndrome is progressing in any case, the task of medicines in this case is to make this process as slow as possible. And also to help the patient to continue to lead the usual way of life as long as possible. Drug therapy in combination with auxiliary procedures, faith in the patient's recovery and support of loved ones, pledge successful treatment and long life!

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Parkinson's disease

One of the common organic diseases central nervous system, which occurs most often in people of older age groups. According to statistics, parkinsonism is observed in 1% of the population, and in age groups over 60 years of age, the incidence increases to 5%.

The disease is named after the English physician James Parkinson, who in 1817 described its clinical manifestations in detail. The disease is polyetiological. The etiological factors of parkinsonism are usually divided into 2 groups: Parkinson's disease (or primary idiopathic parkinsonism), which is a slowly progressive systemic degeneration of the extrapyramidal parts of the nervous system, and symptomatic (secondary) parkinsonism, including vascular (including atherosclerotic), postencephalic, toxic and other forms.

With parkinsonism, there is a lesion of the substantia nigra (degeneration of neurons, disappearance of melanin pigment) and subcortical nodes (globus pallidus and, to a lesser extent, striatum).

The pathogenetic basis of parkinsonism is a violation of catecholamine metabolism in the brain - in patients, the level of dopamine in the subcortical nodes decreases sharply, the synthesis of melanin in the substantia nigra decreases, the complex balance of cholinergic, dopaminergic, serotonin- and histaminergic mediator systems is disturbed.

From different types secondary parkinsonism most often occurs the so-called vascular parkinsonism, which can be caused by atherosclerosis of the cerebral vessels, hypertension and age-related changes in the vessels. These reasons are usually closely intertwined. It is often difficult to single out the leading role of one of them; therefore, it is more correct to speak of vascular parkinsonism in the collective sense of this term.

In recent years, the proportion of vascular parkinsonism (including atherosclerotic) has increased and, according to our data, is 40% among other major etiological forms of the disease. This is due to the “aging” of the population in different countries as a result of an increase in life expectancy and the proportion of cerebrovascular disease in general. Vascular parkinsonism is more common among men (69.3%). The onset of the disease refers to old age (60-74 years), in contrast to idiopathic and postencephalitic parkinsonism, when the disease begins, as a rule, earlier (45-59 years for idiopathic, up to 45 years for postencephalitic parkinsonism). In families of patients with vascular parkinsonism, there is a clear predisposition to cardiovascular disease and very rarely (in contrast to Parkinson's disease) such cases of the disease occur.

The disease begins most often gradually, without visible external cause, sometimes (34.72%) immediately after mental trauma. Even Charcot spoke out in favor of the etiological significance of "moral shock" in tremulous paralysis. It is now known that a severe affective reaction is accompanied by vascular and humoral changes. In 20% of the cases of vascular parkinsonism observed by us, its direct cause was acute cerebral circulation disorders, more often in the basin of the middle cerebral artery, proceeding according to the ischemic type.

The main clinical manifestations of vascular parkinsonism include stiffness and trembling. Stiffness includes plastic muscle rigidity (increased muscle tone) and bradykinesia or akinesia (slowness of the pace of movement), which is the most severe symptom of vascular parkinsonism. When the patient is in the supine position, muscle rigidity decreases. Vascular parkinsonism is characterized by the greatest increase in muscle tone in the legs, and this symptom is often the first manifestation of the disease, and stiffness occurs in both legs at once.

Bradykinesia is manifested by a sharp slowdown, depletion of active movements. The patient develops hypomimia; characteristic "mask-like, icy" facial expression that does not change in connection with the experienced emotions. Mimic emotional reactions are prone to "tonic fixation", and the patient, for example, continues to smile, although the reason for joy has long passed. Patients lose their individual characteristics of gait gestures, they are likened to a “wooden doll”. Sometimes, under the influence of superstrong emotions, “paradoxical kinesia” appears; the ability to perform "motor feats", to talk animatedly, to run.

The slowness of movements is not accompanied by a noticeable violation of muscle strength; its peculiar dissociation is revealed: the force is great when the patient is asked to hold the limb in a given position, and is insignificant when actively overcoming resistance. One of the early symptoms of bradykinesia is a peculiar change in handwriting in the form of micrographs. Posture, posture and gait are also impaired. A patient with parkinsonism often stands, hunched over, bent forward, with lowered shoulders, bent at the elbow joints and arms pressed to the torso, slightly bent knees and head lowered to the chest. It is difficult for the patient to start moving. He treads in place before taking a step forward, walks slowly, in small steps, shuffling his feet. In vascular parkinsonism, extrapyramidal gait disturbances are often combined with cerebellar ataxia and spastic disorders associated with spinal circulatory failure (vascular myelopathy).

Tremor (tremor) is not an obligatory symptom of vascular parkinsonism. The most common tremor is "rest" (static tremor). Trembling is most often localized in distal parts limbs, mainly hands. The amplitude of the jitter is unstable; in vascular parkinsonism, the "pill roll-off" or "coin-counting" symptom characteristic of Parkinson's disease is rare. Head tremors can occur in the horizontal plane ("no-no"), less often in the vertical ("yes-yes").

Vegetative disorders (increased salivation, hyperhidrosis, greasiness of the skin of the face and head) with vascular parkinsonism are unsharp and more characteristic of postencephalitic parkinsonism.

In 44.19% of cases, vascular parkinsonism is combined with arterial hypertension... Hypertension can be the leading cause of vascular parkinsonism, regardless of whether it occurs with atherosclerosis or not. More often it is diagnosed long before the onset of parkinsonism, and the latter develops in these cases as a result of chronic hypertensive encephalopathy.

Rehabilitation measures for vascular parkinsonism should include a rational regimen, diet food(as in any vascular pathology), physical methods of treatment, rational psychotherapy and autogenous training aimed at reducing tremors, muscle rigidity and bradykinesia, reducing cerebral and neurotic disorders, improving cerebral circulation and cardiac activity.

The patient should strive to maintain the habitual life stereotype as long as possible (stay in the work collective, continuation professional activity). If this is not possible, feasible physical labor, sufficient physical activity are recommended. Patient self-care should be encouraged. Excessive care is harmful and contributes to faster disability. Thus, activity slows down, and inactivity accelerates the progression of the disease.

In the complex of therapeutic measures for parkinsonism, drug treatment remains the main one. Given the complex pathophysiological mechanisms of the main symptoms of parkinsonism, the occurrence of which depends on damage to various levels of the nervous system: (cortex, subcortex, reticular formation of the brain stem, spinal cord and, possibly, the peripheral parts of the nervous system), it is natural to conclude that any one pharmacological drug does not have a multifaceted corrective effect. Only the use of a complex of drugs that affect various links of the pathological process can be most effective.

To influence the main symptoms of parkinsonism (tremor, stiffness, bradykinesia), 3 main groups of drugs are currently used:

  1. central anticholinergics, i.e. drugs with the ability to reduce the sensitivity of organs and tissues to acetylcholine. These include tropacin, cyclodol (synonyms: artan, parkinzan, parkopan, romparkin), ridinol, norakin, bellazon, amedin, etc.
  2. adamantans - midantan, viregit, symmetrel;
  3. drugs from the L-DOPA group, compensating for the lack of dopamine in the subcortical nuclei: levopa, levodopa, dopaflex, dopar, as well as drugs synthesized on the basis of L-DOPA: madopar, nakom, cinemet.

Anticholinergic agents of central action in elderly and senile people are usually effective in doses 2-3 times lower than in young or middle-aged patients with parkinsonism. Treatment should be started with minimal doses (1 mg per dose, 1-2 times a day). The dose is gradually increased until a satisfactory therapeutic effect appears, continuing the treatment with the lowest effective doses for many months. The maximum daily dose of anticholinergics (otherwise, anticholinergic drugs) in the elderly, and therefore in patients with vascular parkinsonism, should not exceed 7.5 mg (2.5 mg 3 times a day). Large doses of anticholinergics are not only ineffective, but are also directly contraindicated due to pronounced side effects (dizziness, accommodation disturbances, intestinal paresis, etc.). Atropine-like drugs (anticholinergics) should be taken after meals. Of central anticholinergics, it gives fewer side effects and is better tolerated by patients with vascular parkinsonism Ridinol. In terms of chemical structure, it is close to cyclodol. Available in tablets of 1, 2 and 5 mg. The use of ridinol significantly reduces muscle tone, increases range of motion, reduces hypersalivation, improves sleep and pelvic organ function. Ridinol has a weaker effect on hyperkinesis.

Central anticholinergics are undesirable in glaucoma. In these cases, they are replaced with drugs of the phenothiazine series - dinesin (latibon, deparkin), parsidol (diparkol, antiparkin). These drugs, unlike atropine-like drugs, do not cause accommodation disturbances and are acceptable in patients with glaucoma.

With vascular parkinsonism, caused by widespread atherosclerosis with atherosclerotic endarteritis of the extremities, mydocalm is useful. In terms of its properties, it is close to central muscle relaxants. There is evidence of the n-anticholinergic action of the drug. In addition, mydocalm has a beneficial effect on venous and arterial circulation in the extremities, has an antispasmodic effect. It is indicated in patients of any age. With parkinsonism, treatment should be started with a daily dose of 0.15 grams (0.05 grams 3 times a day), increasing it by 0.05 grams every 3 days. The maximum daily dose is 0.45 grams (0.15 grams every 8 hours). The maintenance dose usually does not exceed 0.05 grams 3 times a day. The course of treatment is 5-6 weeks. In especially severe cases in a hospital, intramuscular injections are advisable: 1 ml of a 10% solution 1-2 times a day.

Midantan (amantadine hydrochloride) belongs to the new, most effective antiparkinsonian drugs. It was proposed in the USA (Symmetrel) for the treatment of Asian influenza (A-2 virus). Its positive effect on parkinsonism was discovered by chance: several patients with parkinsonism got the flu and took amantadine-HCl, and there was a significant reduction in akinesia, stiffness and tremors. The domestic drug midantan has a positive effect on all the main symptoms of the disease: to a greater extent on rigidity and bradykinesia, to a lesser extent - on tremors. The drug is usually prescribed in a dose of 100 mg (0.1 gram) 2 times a day. The treatment takes several months. The best effect is provided by complex therapy with midantan in combination with central anticholinergics. Mindantan and other drugs from the adamantane group expressed side effect do not possess, however, with prolonged use of them, increased irritability, insomnia are possible, therefore, it is undesirable to prescribe them at night. When side effects appear, it is possible to recommend combined treatment with minor tranquilizers (tazepam, nozepam, relanium, trioxazine, etc.).

The study of dopamine imbalance in parkinsonism led to the discovery of a fundamentally new effective treatment - L-DOPA. It should be remembered that the results of treatment with drugs from the L-DOPA group (L-DOPA, levopa, levodopa, dopaflex, dopar) become noticeable most often 2 months after the start of treatment. Most of all, the technique of careful slow increase of doses in accordance with the individual characteristics of the patient has justified itself. It is the only one possible with vascular parkinsonism. Drug treatmentL-DOPA, prescribing and changing dosages are carried out only under the supervision of a neuropathologist. In case of overdose and individual intolerance, pronounced side effects occur in the form of gastrointestinal disorders, cardiovascular disorders, and with prolonged use (as a rule, 2 years after the start of treatment) hyperkinesis of the extremities and oral muscles may occur, resembling choreiform, as well as psychotic disturbances in the form of hypnagogic hallucinations, delusional statements.

New possibilities for the treatment of parkinsonism have opened up after the appearance of drugs that are a combination of L-DOPA and DOPA-decarboxylase inhibitors, which promote the rapid penetration of L-DOPA through the blood-brain barrier (Nakom, Madopar, Sinemet). These drugs allowed to reduce the daily dose of L-DOPA by 75-80%, significantly reduce the frequency and severity of its side effects. The effect when using nakoma and madopar occurs in most cases on the 7-15th day with daily dose 2-2.5 tablets. It is expressed in a significant decrease in muscle rigidity, a decrease in bradykinesia; the circle of self-care of patients expands, they begin to carry out subtle movements of the fingers. The best effect in vascular parkinsonism is provided by complex drug therapy, which includes, along with antiparkinsonian drugs, agents that directly affect the atherosclerotic process (diosponin, cetamifen, parmidin, miscleron, vitamin complexes, stugeron, cavinton), as well as drugs that improve cerebral circulation, lowering blood pressure with arterial hypertension.

A caring attitude, sensitivity to old, sick people, understanding of their interests create a positive emotional background for them, contribute to the desire to remain useful to the family and society, and favor the best effect of drugs.