TOPIC: DISEASES OF THE EXTRAPYRAMIDAL NERVOUS SYSTEM. PARKINSONISM

Genuine parkinsonism and secondary parkinsonism (symptomatic) are a group of chronic progressive neurodegenerative diseases that are characterized by the predominant destruction of dopamine-containing neurons of the substantia nigra, leading to disruption of the basal ganglia of the brain. The disease is named after James Parkinson, who described the symptoms of the disease in his book An essay on the shaking palsy in 1817.

EPIDEMIOLOGY OF PARKINSONISM

Among degenerative diseases of the central nervous system, Parkinson's disease is the second most common after Alzheimer's disease. The lifetime risk of developing parkinsonism is 1:40, with a steady increase in incidence observed in recent decades. Parkinson's disease is much more common in Europe than in Asia and Africa. In the mid-latitudes of Europe, the incidence rate is 1% among adults under the age of 60, from 60 to 80 years - 5-10% and over 80 years - over 20%. However, currently there is a “rejuvenation” of the disease and the emergence of “early parkinsonism” with the onset of the disease at 40-50 years of age, as well as the presence of “juvenile parkinsonism” - up to 40 years of age.

Classification of parkinsonism

I. Primary (genuine or idiopathic)

Parkinson's disease

Juvenile parkinsonism

II. Secondary parkinsonism (symptomatic):

Vascular

In the presence of space-occupying brain formations.

Traumatic (for repeated traumatic brain injuries)

Drug

• beta1-adrenergic receptor blockers (reserpine)

  antidepressants (selective serotonin reuptake inhibitors)

  dopamine antagonists (metoclopramide, procloperazine)

  antitumor (vincristine)

  antipsychotics (buterophenones, phenothiazines)

  calcium channel blockers

  valproate

Toxic

• pesticides, herbicides,

  manganese compounds

  a narcotic drug containing the substance MPTP (1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine)

  carbon monoxide

• petroleum products.

Infectious

• postencephalitic

  Creutzfeldt-Jakob disease, etc.

Metabolic

• hypo- and hyperthyroidism,

  hypo- and hyperparathyroidism

III. Parkinsonism in combination with other neurodegenerative disorders - “plus parkinsonism”:

Alzheimer's disease

Corticobasal degeneration

Striato-nigral and pallido-nigral degeneration

Progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome)

Multiple system atrophy:

• Olivopontocerebellar atrophy

  Shy-Dredger syndrome

Etiology

The etiology of idiopathic parkinsonism is not completely known. Currently, the development of the disease is associated with both the presence of a genetic predisposition and the influence of environmental factors.

Risk factors include:

family history (10-24% of cases);

old age (less than 10 cases per 100,000 at age 50 and 200 per 100,000 at age 80);

gender (men are affected 1.5 times more often)

Genetic predisposition is determined by the presence of a number of genes and gene loci with dominant and recessive modes of inheritance and varying degrees of penetrance:

gene PRKN(parkin), PARK2 locus on chromosome 6q25.2-27;

gene LRRK2 (dardarin), PARK8 locus on chromosome 12p11.2;

gene SNCA(-synuclein), PARK1 locus on chromosome 4q21;

gene GBA(glucocerebrosidase) at locus 1q21.

Pathogenesis

The pathogenesis of the disease is associated with a deficiency of the dopaminergic system of the brain, its nigro-striatal bundle, the main mediator of which is dopamine. Damage to nigral dopaminergic neurons occurs, leading to a sharp decrease in the concentration of dopamine in the striatum and significant changes in its functional state. At the same time, the activity of the cholinergic system increases relatively or absolutely. It has been shown that inhibition processes are disrupted in the subthalamic nucleus (nSTh), which leads to pathological excitability of the internal segment of the globus pallidus (Gpi) and pars reticulata of the substantia nigra (SNpr). Disruption of normal interactions in the Gpi-nSTh-SNpr system leads to the development of the main symptoms of the disease. In the basal ganglia of patients with parkinsonism (in the caudate nucleus, putamen, globus pallidus), the content of not only dopamine, but also other biogenic amines: norepinephrine and serotonin, and tyrosine hydroxylase activity is reduced. Significant changes in noradrenergic, cholinergic, and serotonergic neurotransmission are observed. There is a death of dopamine receptors in the neostriatum (mainly type D-2 receptors). Other neuropeptides (acetylcholine, GABA, enkephalins) are also involved in the pathological process. Thus, in parkinsonism, an imbalance of one neurotransmitter (dopamine) leads to a pathological disturbance of many mediators and disorganization of the activity of the entire brain and the extrapyramidal system, primarily. Dysfunction of the dopaminergic system causes the development of motor, emotional and mental disorders, the noradrenergic system - autonomic, cognitive and postural, the cholinergic - cognitive and mental, the glutamatergic - dyskinesias, cognitive and mental, the serotonergic - emotional and mental. Factors of autoimmune aggression are important, and, as a consequence, the appearance of antibodies to one’s own catecholamines and especially to dopamine.

The key pathogenetic processes leading to the death of melanin-containing nigral neurons are oxidative stress, excitotoxicity and mitochondrial disorders.

During the catabolism of dopamine in the substantia nigra with the participation of MAO-B, excess hydrogen peroxide and free radicals are formed in brain tissue, which in turn cause lipid peroxidation, membrane damage and cell death.

Hyperactivity of the glutamatergic innervation of the striatum is accompanied by activation of NMDA receptors, excessive release of the neurotransmitter glutamate and an increase in intracellular Ca 2+ concentration, which initiates the generation of free radicals through the activation of neuronal NO synthase, which is involved in the formation of nitric oxide. The NO released as a result acts as a mediator of the neurotoxic effect of glutamate on the cell. Free radicals cause lipid peroxidation of the cell membrane and cause the development of mitochondrial dysfunction. However, nitric oxide also has a direct cytotoxic effect on the cell due to the formation of peroxynitrite ONOO -, as a product of the interaction of NO and the superoxide anion - O 2 -.

Numerous studies over the last decade have shown that one of the mechanisms of nerve cell death in degenerative diseases of the nervous system, and in particular Parkinson's disease, is apoptosis. Programmed cell death, observed during the physiological process of aging, can be enhanced under the influence of various exogenous and endogenous factors.

Rice. 3 Factors and processes leading to cell death.

A decrease in the number of melanin-containing dopaminergic neurons of the compact part of the substantia nigra, the presence of intracellular eosinophilic inclusions (Lewy bodies) in the remaining neurons is the most important sign of Parkinson's disease. Pathological studies reveal a significant decrease in the number of pigmented neurons in the substantia nigra of the midbrain compared to the norm (400,000). The severity of the clinical picture, as a rule, is directly proportional to the number of dopaminergic neurons in the substantia nigra. The smaller the number of neurons, the more severe the clinical manifestations of the disease and, first of all, the severity of bradykinesia.

In the deceased, the number of dopaminergic neurons is reduced by more than 90%, the first symptoms of the disease appear with the death of approximately 70%-80%, and an asymptomatic course is observed with the death of 50% of neurons.

Lewy bodies can be found in the substantia nigra, locus coeruleus, dorsal motor nucleus of the vagus, thalamus, hypothalamus, and in the cerebral cortex of predominantly elderly patients with a long history of Parkinson's disease who have developed symptoms of dementia. Lewy bodies contain a protein called alpha-synuclein, whose main function is to modulate synaptic plasticity. The appearance and role of alpha-synuclein in the death of neurons is explained from the standpoint of oxidative stress, as well as the presence of genetic mutations leading to damage and its intraneuronal accumulation.

Rice. 4. Factors affecting alpha-synuclein aggregation

Parkinsonism is a neurological syndrome characterized by a disorder of voluntary movements. This pathology accompanies a variety of diseases and always causes slowness of movements, trembling of the limbs, and muscle stiffness.

Medical history

Symptoms of the disease in neurology have been known for a long time. But they are most fully described in “An Essay on the Shaking Palsy” by James Parkinson.

Its publication took place in 1817. This work presented the distinctive signs of this disease. The doctor noted a strange condition, which was accompanied by impaired motor functions, resting tremor, and muscle stiffness.

In addition, the scientist was able to assess the dynamics of these signs as the pathology develops. After this, the question arose regarding the etiology of the disease.

Thus, Edouard Brissot put forward the hypothesis that the peduncles and subthalamic nucleus of the brain are responsible for the development of pathology. Frederick Levy managed to identify specific cellular inclusions, which were then called “Lewy bodies”. And the Russian neurologist K.N. Tretyakov. discovered that pathological disorders develop in the substantia nigra.

Forms

Experts distinguish two forms of parkinsonism:

Primary. This type is Parkinson's disease, which is directly related to the death of nerve cells. In this case, the following features are characteristic:

• old age;
• the presence of at least two main manifestations of pathology;
• asymmetry of signs or one-sided manifestation.

Secondary. Such parkinsonism is associated with exposure to external factors. These include infections, medication use, and injuries. This type of pathology is characterized by:

• vascular disorders;
• autonomic disorders;
• acute onset of the disease followed by stabilization;
• symmetry of features;
• a negative event before the onset of symptoms - trauma, contact with chemicals, overdose of antipsychotics, encephalitis.

Etiology

The development of the disease is associated with a variety of reasons that affect the subcortical ganglia. These include:

• insufficiency of enzyme structures;
• poisoning with toxic substances, including medications;
• encephalitis;
• brain tumor;
• brain injuries.

This condition is accompanied by a decrease in the level of catecholamines in the substantia nigra and caudate nucleus of the brain, which causes disturbances in the functioning of the extrapyramidal system.

Neurophysiological causes of parkinsonism

Control of movements occurs with the help of neurotransmitters, which are biologically active components that transmit impulses between cells. An imbalance between these substances leads to a disorder of the body's motor functions.

Parkinsonism is a consequence of such an imbalance. In patients suffering from this disorder, the level of excitatory neurotransmitters, namely glutamate, exceeds the level of inhibitory components - dopamine.

That is why the principle of treating the disease is to artificially maintain the correct balance of neurotransmitters.

Symptoms

Typical movement disorders in parkinsonism will be:

• Trembling or . This is perhaps the most frequently mentioned symptom, although experts say that it does not always appear. Tremor occurs as a result of rhythmic muscle contraction. When performing directed movements, the tremor may disappear or become less pronounced.
• Muscle stiffness or stiffness. This symptom is associated with an increase in muscle tone in the limbs. Also, this symptom can manifest itself in a person’s stooped posture. Often, rigidity causes pain, which forces a person to see a doctor. If the doctor does not detect other manifestations, he may make an incorrect diagnosis - for example, rheumatism.
• Slowing down and reducing the number of movements. The patient may experience great difficulty in starting to move. In addition, others may notice the impoverishment of a person’s gestures and facial expressions. As the disease progresses, a person may experience difficulty changing the position of the body during sleep.
• Poor balance or postural instability. With this disease, postural reflexes may be completely absent or significantly weakened.
  

  It is not uncommon for people with Parkinson's to lose their balance and even fall. This symptom is considered one of the main ones in this pathology.

A patient with parkinsonism describes her feelings, symptoms and talks about what treatment was prescribed in a simple clinic:

Classification of types of parkinsonism

It is accompanied by disturbances in speech, coordination of movements, swallowing and other symptoms. In this case, there is no rest tremor.

The development of this condition may be based on cerebrovascular accident. The distinctive symptoms of this form of parkinsonism include:

• symmetry of symptoms;
• absence of tremor;
• the predominance of signs in the legs and axial sections;
• no worsening when dopaminergic drugs are discontinued;
• changes in gait at the onset of the disease.

This disease develops as a result of the appearance of cerebrovascular disorders. It could be:

1. Damage to small arteries of the brain.
2. Brain lesions of a cardiogenic nature.
3. Disruption of the large arteries of the brain.

For diagnostic purposes, perform. As a rule, this disease has characteristic clinical symptoms, and all changes can be easily identified through this type of study.

Neuroimaging may also be required to rule out the presence of a tumor. Modern treatment of vascular parkinsonism includes a set of measures aimed at preventing further damage to cerebral vessels.

The most commonly prescribed antiparkinsonian drugs are:

• dopamine receptor agonists;
• amantadine;
• levodopa drugs;
• MAO-B inhibitors.

Treatment of this type of parkinsonism is carried out in many clinics in Russia and other countries. Among domestic institutions we can highlight “Euromedprestige” and “Clinic of Restorative Neurology”.

As for other countries, it is worth paying attention to Israeli clinics - Sheba Medical Center, Hadassah Hospital, Assuta Clinic. The German clinic Friedrichshafen is quite successfully treating this pathology. And in the Czech Republic you can contact the Neurology Clinic.

It should be borne in mind that vascular parkinsonism usually has a progressive course. However, the forecast of the rate of its development directly depends on the dynamics of the vascular process and the timeliness of the assistance provided.

Toxic parkinsonism

Develops as a result of poisoning with toxic substances. Often, its appearance is caused by the ingestion of carbon monoxide, manganese, lead, carbon disulfide, ethyl or methyl alcohol.

Drug-induced parkinsonism

Its appearance is caused by the use of various medications - for example, antipsychotics.

Post-traumatic parkinsonism

This form of pathology develops as a result of damage to brain structures - very often it occurs in boxers. One type of the disease is Martland syndrome, which causes dystrophic changes in the brain.

Postencephalitic parkinsonism

This species is characterized by an infectious origin. Its development is associated with disorders in the upper brain stem in the case of epidemic encephalitis. Moreover, the distinctive symptom of such parkinsonism is oculomotor disorders.

Juvenile parkinsonism

This term refers to a special form of primary parkinsonism, which differs in hereditary origin. It occurs most often in women and has an autosomal recessive pattern of inheritance.

Manganese parkinsonism

This syndrome is associated with an increase in manganese content in the body. Most often, such intoxication is observed among workers employed in the mining industry and welders.

Atherosclerotic parkinsonism

Usually appears due to diffuse atherosclerotic brain lesions, which cause the development of lacunar strokes. This pathology is difficult to treat and in a short time becomes a cause of disability for the patient.

It is characterized by:

• rapid development;
• incomplete effect from the use of levodopa drugs;
• manifestations atypical for Parkinson's disease - cognitive dysfunction, postural disorders, pyramidal signs, autonomic dysfunction, cerebellar signs, etc.

Timely diagnosis of atypical forms of the disease is very important for choosing treatment tactics. In addition, making a correct diagnosis will help avoid not only ineffective, but even dangerous treatment.

Drugs that increase the risk of parkinsonism

The development of the disease can be provoked by the following drugs:

• Neuroleptics.
• Drugs that reduce the circulation of dopamine in synapses are alpha-methyldopa.
• Dopamine receptor antagonists – flunarizine and metoclopramide.
• Serotonergic agents that reduce neuronal activity are fluoxetine.
• Agents that reduce the sensitivity of the postsynaptic membrane to dopamine are lithium agents.
• Central sympatholytics that reduce dopamine reserves are rauwolfia drugs.

Also, drugs such as amoxapine, diprazine, and calcium antagonists can influence the development of the disease.

Parkinsonism is a serious pathology that leads to dangerous health consequences. Despite the fact that the reasons for its development are not fully understood, doctors have quite effective means in their arsenal that help stop the progression of this disease. Therefore, when the disease appears, you should immediately contact a specialist.

In the video, Alexander Misharin, he is 53 years old, 13 of them he has been diagnosed with parkinsonism, but he does not give up and looks quite healthy, which is facilitated by physical exercise:

A clinical term that unites all cases of parkinsonism syndrome caused by the influence of various factors affecting the central nervous system or the presence of a primary disease. Unlike Parkinson's disease, secondary parkinsonism has a more acute onset and is characterized by an initial symmetry of parkinsonian manifestations and the presence of other symptoms of central nervous system damage. Diagnosed on the basis of anamnestic and clinical data, taking into account the results of MRI of the brain. Treatment is aimed at stopping the main etiological factor and blocking the pathogenetic mechanisms of the development of parkinsonism.

ICD-10

G21

General information

Secondary parkinsonism is a general clinical concept that includes all cases of symptoms of Parkinson's disease associated with damage to the neurons of the basal ganglia of the brain under the influence of various exo- and endogenous factors. Unlike secondary parkinsonism, idiopathic Parkinson's disease occurs independently, without connection with any factor affecting the brain. Secondary parkinsonism accounts for about 30%; in the remaining cases, Parkinson's disease is diagnosed. In accordance with the etiology, drug-induced, post-traumatic, toxic, post-hypoxic, post-infectious, and vascular parkinsonism are distinguished. The most common is drug-induced parkinsonism. Most of its cases are due to neuroleptic malignant syndrome, which develops with prolonged or inadequate use of neuroleptics. The issue of differentiating Parkinson's disease and secondary parkinsonism is of fundamental importance for practitioners in the field of neurology, since the approaches to their treatment are significantly different.

Causes of secondary parkinsonism

Parkinsonian manifestations can occur in connection with severe TBI (contusion and compression of the brain) or frequent mild TBI (concussions). The causes of post-infectious parkinsonism are encephalitis and common infections (measles, HIV, mumps, herpes, etc.). Various poisonings (heavy metals, carbon monoxide, hydrocyanic acid, methanol), if timely detoxification is not carried out, can cause toxic parkinsonism. The occurrence of parkinsonism syndrome is possible due to manganese intoxication, which is observed in drug addiction with the use of synthetic drugs (synthetic heroin, ecstasy). Pharmaceuticals that carry a risk of developing secondary parkinsonism include antipsychotics (neuroleptics, some antidepressants), anticonvulsants, sympatholytics, and antiemetics (metoclopramide).

The etiofactors of vascular parkinsonism are extensive ischemic stroke, multiple lacunar cerebral infarctions, chronic cerebral ischemia in atherosclerosis. Parkinsonism can be observed after hypoxia, regardless of its genesis, including in patients who survived after resuscitation. The following can provoke the development of secondary parkinsonism: hydrocephalus, repeated episodes of hypoglycemia,. Parkinsonism syndrome can be observed in various degenerative diseases of the central nervous system: Wilson's disease, dementia with Lewy bodies, progressive supranuclear palsy, corticobasal degeneration, multiple sclerosis, etc. In relation to such cases, the term “parkinsonism plus” is used.

Symptoms of secondary parkinsonism

The main clinical manifestations of parkinsonism are bradykinesia, muscle rigidity and postural tremor. Bradykinesia is a decrease in the number and speed of movements; patients become slow, their gesticulation gradually disappears, their facial expressions become poorer, and walking is no longer accompanied by accompanying hand movements. Muscular rigidity is a constant muscle tension, which is first detected when attempting passive movements in the limb, and then becomes noticeable by the limbs constantly bent at the elbows and knees. Postural tremor is usually expressed in the hands and head, a fine trembling of which occurs at rest and disappears during motor acts. Over time, these symptoms lead to significant immobility of the patient and are accompanied by postural disorders (impaired coordination of movements, the ability to hold a certain position); characteristic personality changes occur, mnestic disturbances occur.

A distinctive feature of the clinic of secondary parkinsonism is the more rapid development of symptoms during the manifestation of the disease and their accelerated progression in the future. Symmetry of manifestations is typical, while in Parkinson's disease symptoms initially appear on one side and become bilateral only after some time. With the secondary nature of parkinsonism, its manifestations are combined with other symptoms of cerebral damage: pyramidal syndrome, cerebellar ataxia, early intellectual impairment, etc. In the patient's history, as a rule, there is an indication of the action of one or another etiofactor preceding the appearance of parkinsonian syndrome (TBI, stroke, drug use). neuroleptics, encephalitis, etc.). In treatment, dopaminergic drugs are insignificantly effective, and elimination of the etiofactor sometimes contributes to a significant regression of parkinsonian manifestations.

Various etiological variants of parkinsonism are characterized by their own clinical features. Thus, parkinsonism after encephalitis is characterized by strong rigidity, the presence of pronounced vegetative manifestations and oculogyric crises; tremor is often absent. In posthypoxic parkinsonism, tremor, on the contrary, is pronounced. Vascular parkinsonism is accompanied by cognitive disorders and early formation of postural disorders; tremor is slightly expressed. Secondary parkinsonism in hydrocephalus is characterized by the dominance of the Hakim triad - dementia, ataxia, urinary incontinence; with corticobasal degeneration it is combined with cortical symptoms - apraxia, a disorder of complex types of sensitivity, “alien” limb syndrome; in dementia with Lewy bodies, along with parkinsonism, cognitive impairment and mental disorders - psychosis, hallucinatory syndrome.

Diagnosis of secondary parkinsonism

In the presence of a symptom complex of parkinsonism, identification of signs of its secondary nature is of significant diagnostic importance: the existence of an etiofactor in the anamnesis, rapid manifestation, and the presence of other neurological symptoms in the status. If psychopathological manifestations appear, consultation with a psychiatrist is necessary. An examination by an ophthalmologist can determine the presence of changes in the fundus characteristic of hydrocephalus or pigmentation along the periphery of the iris (Kayser-Fleischer ring) that is pathognomonic for Wilson's disease.

Identification of the probable causes of secondary parkinsonism syndrome is carried out using MRI of the brain, which is more informative in comparison with CT in visualizing degenerative lesions and differentiating intracerebral space-occupying formations. In case of hydrocephalus, MRI detects dilated ventricles of the brain, in post-stroke conditions - areas of infarction, etc. However, the detection of such changes in itself does not indicate the secondary nature of parkinsonism. It is necessary to interpret the results of tomography only by correlating them with clinical data, since it is impossible to exclude the presence of a combination of Parkinson’s disease with a number of other cerebral diseases or, for example, the existence of secondary non-vascular parkinsonism against the background of vascular disorders.

Treatment of secondary parkinsonism

The basis of therapy is the drugs used to treat Parkinson's disease. These include dopamine receptor agonists (piribedil, pramipexole, bromocriptine), levadopa pharmaceuticals, selective irreversible MAO inhibitors (moclobemide, pirlindole, befol). Treatment starts with monotherapy. The drug of choice, as a rule, is pronoran. Unlike Parkinson's disease, levadopa shows little effectiveness in secondary parkinsonism.

In parallel with antiparkinsonian treatment, therapy is carried out aimed at the cause of damage to the basal ganglia. For toxic parkinsonism, detoxification is carried out, for posthypoxic parkinsonism - oxygen therapy and neurometabolic treatment, for vascular parkinsonism - vascular therapy (vinpocetine, nicergoline, pentoxifylline). Drug-induced parkinsonism is an indication for discontinuation or replacement of the drug that caused it. For post-traumatic and post-infectious parkinsonism, courses of neurometabolic therapy (piracetam, pyritinol, B vitamins, lipoic acid) are indicated. aimed at slowing down the degenerative processes occurring in neurons. The main treatment is complemented by massage to reduce rigidity and exercise therapy to preserve the patient’s motor activity for as long as possible.

Parkinsonism refers to a group of disorders that have symptoms similar to those of Parkinson's disease, but differ from it in their origin. What are the features of this condition and what treatment options exist?

Parkinsonism concept

The term "parkinsonism" may be mistaken for many to be synonymous with Parkinson's disease, but it is not. Although these concepts are closely related, the differences are quite significant.

Parkinson's disease is a slowly progressive chronic neurological disease

Parkinson's disease (PD) is a brain disease mainly affecting older people, the essence of which is the death of groups of nerve cells from the structures of the extrapyramidal system responsible for controlling movement. At the same time, a gradual “dying away” of the corresponding parts of the brain occurs. The disease is characterized by slow, asymptomatic development over many years. So most patients are unaware of their illness for a long time until symptoms appear, expressed in a persistent loss of motor control. There are:

• involuntary trembling of the fingers (tremor) at rest;
• stiffness;
• retardation of movements;
• postural (static) instability.

The extrapyramidal system is a set of brain structures that are responsible for muscle movement, their tone and maintaining a certain posture by a person.

Initial symptoms of Parkinson's disease include: hand tremors, slowness of movement, shuffling gait

Parkinsonism is a syndrome of a collection of neurological disorders similar to the symptoms of Parkinson's disease. However, in this case, the clinical picture is not a consequence of PD, but of one of a number of disorders. Some of them are still not clearly marked.

Parkinsonism is a neurological syndrome, the symptoms of which are similar to the clinical picture of Parkinson's disease

In children and adolescents under 18 years of age, it is extremely rare, but so-called juvenile parkinsonism can also develop.

Classification and causes of the disease

Initially, it can be quite difficult to distinguish idiopathic (of unclear origin) Parkinson's disease of a primary nature from a syndrome that mimics it. Secondary parkinsonism always occurs on the basis of another reason, according to which it is classified as one or another subtype:

1. Drug-induced is the most common form of secondary parkinsonism (up to 10% of cases), usually a side effect of antipsychotic drugs (antipsychotics), calcium channel blockers and narcotic stimulants such as amphetamine and cocaine, which affect dopamine levels in the brain. Hence the second name - neuroleptic parkinsonism. As a rule, it is characteristic of patients in psychiatric institutions. Symptoms are difficult to distinguish from Parkinson's disease, although tremors and postural (static) instability may be less severe. If the patient stops taking the medications, the symptoms subside over time, sometimes it takes up to a year and a half.
2. Vascular - usually caused by thrombus formation in the brain due to a series of micro-strokes, especially in the area of ​​the substantia nigra or other components of the extrapyramidal system. The cause of chronic vascular parkinsonism can also be encephalopathy - damage to the white matter of the brain. People diagnosed with this form have significant problems with gait and with the lower body in general. The disorder progresses very slowly compared to other types of parkinsonism. Patients often report sudden onset of symptoms or gradual worsening followed by a plateau effect (normalization of the condition).
3. Metabolic - provoked by systemic metabolic disorders in the body, manifested, in particular, by dysphagia (swallowing disorder), leading to weight loss and lack of nutrients.
4. Toxic - caused by poisoning with chemicals: methyl alcohol, mercury, lead, cyanide, etc. The substantia nigra, striatum and pallidum (globus pallidus) - components of the extrapyramidal system - most often suffer from toxic damage. Specific signs: polyneuritis, speech disorders, convulsive syndromes, etc.
5. Traumatic - develops as a result of trauma to the skull.
6. Oncological - occurs when a tumor affects the structures of the extrapyramidal system.
7. Encephalic - is one of the possible consequences of past inflammation of the brain.
8. Hemiparkinsonism is unilateral tissue atrophy (hemiatrophy), accompanied by symptoms of parkinsonism.
9. Juvenile parkinsonism - observed in childhood, develops as a result of other diseases, such as:
   • whooping cough;
   • viral encephalitis (inflammation of the brain);
   • dystonia (involuntary muscle contractions throughout the body);
   • neurological conditions (nervous tics) due to gene mutations, etc.

The clinical picture of secondary parkinsonism is difficult to distinguish from the symptoms of Parkinson's disease

There is also a type of parkinsonism with additional neuropsychiatric pathology known as atypical parkinsonism, or parkinsonism-plus. It accounts for about 10% of all diagnosed cases of parkinsonism (100,000 people) and is distinguished by the fact that it is not affected by therapy with the drug Levodopa. The following forms are distinguished:

1. Progressive supranuclear palsy (PSP) - Symptoms begin around 60–65 years of age. Typical early manifestations include forgetfulness, personality changes, and loss of balance when walking, leading to unexplained falls. Vision problems associated with PSP usually occur three to five years after the onset of difficulty walking and are associated with an inability to focus correctly due to weakness or paralysis of the muscles that control the eyeballs.
2. Multiple system atrophy (MSA) refers to a group of disorders in which one or more systems in the body stop working. In MSA, the autonomic nervous system is often severely affected early in the disease. Symptoms include bladder problems (urgency, incontinence) and orthostatic hypotension, where blood pressure drops when standing up, which can lead to fainting. In this case, in a supine position, a person’s blood pressure can be quite high. Loss of erectile function is often an early sign in men. Speech disturbances, difficulty breathing and swallowing, and an inability to sweat are also common. MSA is characterized by a lack of response to drug treatment against Parkinson's disease.
3. Dementia with Lewy bodies (DLB) is second only to Alzheimer's disease in the list of the most common causes of dementia in older people. Causes progressive intellectual and functional impairment. In addition to the signs and symptoms of Parkinson's disease, people with DLB tend to experience impaired thinking, decreased levels of attention and vigilance, and visual hallucinations. They usually have little or no tremor. Treatment with Levodopa can be either effective or unsuccessful.
4. Corticobasal degeneration (CBD) is the least common atypical parkinsonism. Develops after 60 years. Symptoms include loss of function on one side of the body, involuntary and jerky movements of the limbs, and speech problems. It may be difficult or impossible to control the affected limb, although there is no weakness or loss of sensation. There is currently no specific treatment for CBD.

It is important to understand that the symptomatic nuances of different types of disorders are difficult to determine. Often the diagnosis is simply referred to as the general term “parkinsonism.”

General symptoms

Symptoms of Parkinsonism include:

• tremor that occurs in one hand when its muscles are relaxed (involuntary trembling of the fingers at rest);
• muscle stiffness;
• slow movements;
• difficulty maintaining balance when walking, etc.

Anemia may also indicate secondary parkinsonism. One of the signs of toxic (lead) parkinsonism is anemia.

Disorders that cause parkinsonism often cause other manifestations or variations of parkinsonian features. Some of them indicate no connection with Parkinson's disease, for example:

• memory loss in the first year of the disease (indicates dementia);
• Parkinsonian symptoms that appear on only one side of the body (often due to certain neoplasms or corticobasal ganglion degeneration);
• hypotension, swallowing reflex disorders, difficulties with urination and defecation (including due to MSA);
• falls and confinement in a wheelchair from the first months or years of the disorder;
• abnormalities in eye movement;
• problems with orientation in space, vision (for example, the patient may get lost in the layout of the rooms of his own house), which develop at the early stage of the disorder;
• symptoms that do not improve in response to treatment with Levodopa;
• inability to express or understand spoken or written language (aphasia);
• difficulty performing simple skills (apraxia);
• inability to associate objects with their usual role or function (agnosia).

Dystonia is also one of the possible symptoms of parkinsonism. This is a condition defined as a contraction of a muscle or group of muscles resulting in an abnormal position of the involved body part. Muscle spasms can be continuous or intermittent.

Akinetic-rigid syndrome - inhibition of active movements against the background of specifically increased muscle tone - is the main manifestation of parkinsonism.

Atypical parkinsonism tends to progress more quickly and with additional symptoms, such as falls early in the disease, dementia, or hallucinations.

Diagnostics

The diagnosis is carried out by a neurologist, assessing the patient’s condition through a detailed survey of the patient regarding complaints, as well as his family and friends regarding possible behavioral changes (if necessary). The specialist finds out whether there has been drug therapy or exposure to other toxic substances that can cause parkinsonism.

Imaging diagnostic methods carried out to assess structural changes in the brain include:

When the diagnosis is controversial, the doctor prescribes Levodopa to the person to rule out Parkinson's disease. If the medicine does not lead to a clear improvement, then with a high degree of probability the cause of the disorders is parkinsonism.

Treatment

Treatment of parkinsonism begins with eliminating the cause that caused it. If it is a pharmacological drug, then stopping it can cure the disorder or significantly reduce the symptoms. For any type of pathology, therapy is aimed at minimizing symptoms that affect a person’s quality of life.

Medicines

Drugs used to treat Parkinson's disease, such as Levodopa, L-dopa, Kaldopa, Doparkin, Dopaflex, are not effective in people with atypical parkinsonism, but can lead to moderate improvement in other cases.

Antiparkinsonian medications are based on a substance that precedes the synthesis of dopamine in the body. The drugs replenish dopamine deficiency and eliminate negative symptoms.

To neutralize side effects from therapy with such drugs (nausea, vomiting, depression, insomnia, etc.), doctors recommend combining Levodopa and analogues with peripheral dopa decarboxylase inhibitors (Carbidopa, Benserazide). The therapeutic effect of antiparkinsonian drugs appears after a week, and the maximum effect is achieved after about a month.

If an antipsychotic drug causes annoying symptoms of parkinsonism, and it must be taken for a long time, then the neurologist replaces it with another antipsychotic drug. However, if it is impossible to find an analogue, then medications are prescribed to relieve symptoms - dopaminomimetics - stimulants of dopamine receptors in the brain and at the same time stimulators of dopamine release. This is Amantadine and its analogues:

• VK-Merz;
• Midantan;
• Gludantan;
• Wiregit-K.

Anticholinergic drugs (anticholinergics) are used to eliminate the symptoms of neuroleptic parkinsonism. In Western countries this is the drug Benzatropine (Cogentin), but the drug is not registered in the Russian Federation. Instead, analogues are used - trihexyphenidyl (Cyclodol) or biperiden (Akineton). Their action is based on blocking and replacing the natural neurotransmitter acetylcholine.

Nootropic and gamkergic drugs improve the functions of nerve cell membranes, stabilize them, forming new phospholipids. Medicines in this group improve cognitive functions and mental activity, reduce neurological deficits. Usually prescribed:

• Piracetam;
• Nootropil;
• Phezam.

Medicines that improve cerebral circulation work as antioxidants, preventing lipid peroxidation of cell membranes. Increases tissue resistance to oxygen deficiency and oxygen-dependent disorders. Group representatives:

• Vinpocetine;
• Cavinton;
• Cinnarizine;
• Xanthinol nicotinate.

Additionally, biological additives are used, for example Lecithin, which is part of the myelin sheath of nerve fibers and is actively involved in the transmission of nerve impulses. Reduces rapid fatigue, irritability, and the risk of nervous exhaustion inherent in patients with parkinsonism.

Drug treatment of parkinsonism: gallery

Levodopa is a biogenic substance, a precursor of dopamine Amantadine is an antiparkinsonian dopaminergic drug Mexidol prevents peroxidation of cell membranes Ceraxon improves cognitive function
Lecithin - a biological additive to improve the transmission of nerve impulses

Modern methods of therapy

Scientists have long been developing methods for eliminating painful sensations in dystonia, from which patients suffer in the morning before taking the necessary symptomatic medications or throughout the day. The solution was botulinum toxin.

Botulinum toxin has found its use not only in cosmetology, but also in medicine, in particular in the treatment of symptoms of parkinsonism

Botulinum toxin blocks the release of acetylcholine at the neuromuscular junction, thereby effectively cutting off the “messages” coming from the brain and carried by the nerves (impulses) to the muscles.

Most often, Botox is used and injected into contracting muscles, which are precisely identified in advance using electromyography. By blocking the exchange of impulses with these muscles, the drug effectively weakens them, thereby allowing the muscles to return to a healthier state. The medication must be re-introduced every 3-4 months.

The action of botulinum toxin is discrete, that is, it affects exclusively those muscles where it was injected, in contrast to oral (taken by swallowing) drugs, which are absorbed through the gastrointestinal tract and excreted by the kidneys or liver, which is accompanied by a corresponding negative effect on these organs.

Treatment prospects: telomerase activation

Scientists suggest that neurodegenerative diseases, which are one of the causes of parkinsonian syndrome, are associated with a decrease in telomeres - the end sections of chromosomes. An enzyme called telomerase can slow, stop, or even prevent the shortening of telomeres that occurs with aging. The amount of telomerase in the human body decreases as we grow older.

In 2009, the Nobel Prize in Physiology or Medicine was awarded to three scientists who discovered the importance of telomerase's influence on telomere length.

The effect of telomerase on human cells slows down their aging and allows them to begin dividing again. Enzyme activation can:

• prevent telomere shortening and cellular aging;
• help cells live longer and continue to function properly;
• making older cells function the same way they did when they were younger.

Homeopathy

An alternative treatment method is homeopathy, the goal of which in the case of parkinsonism is to reduce symptoms with the help of safe drugs that do not cause addiction or side effects.

Before using any drug from the arsenal of homeopathic remedies, you must consult with your treating neurologist.

Folk remedies

Folk remedies for parkinsonism are not considered as a treatment, but can be used to reduce the symptoms of the disease. The following recipes are used:

1. Nettle infusion helps calm trembling hands. Preparation:
   • take 1 tbsp. a spoonful of crushed leaves and pour 250 ml of boiling water;
   • leave covered for about an hour;
   • cool, strain and take 50 ml before meals.
2. Alfalfa compresses are also intended to reduce tremors. Preparation:
   • take a fresh bunch of fresh fruit and hold it over steam or put it in hot water;
   • Apply the steamed herb to your hands for half an hour, covering it with a warm blanket.
3. An infusion of oregano, lavender, purslane and snakehead - relieves stiffness and numbness of the limbs. Preparation:
   • grind equal parts of dry plants into powder;
   • pour the finished mixture in the amount of 120 g with a liter of boiling water and leave under the lid in a warm place for 2–3 hours;
   • take 50 ml three times a day before meals.

Exercise therapy and massage

People suffering from Parkinsonism should remain as active as possible for as long as possible. If necessary in everyday life, they should use auxiliary devices, but they should perform everyday tasks independently, even if in a simplified form (for example, choosing clothes with snaps rather than buttons).

Exercises for parkinsonism should be simple, aimed primarily at stretching muscles

Stretching and gentle exercise can be helpful to prevent muscle stiffness from progressing. They are designed to help patients cope with everyday tasks by reducing muscle soreness and spasms. An example of a simple warm-up that is recommended to be done daily:

1. Stand 20 cm from the wall and raise your arms up. Lean against a wall for balance and feel the muscles in your arms and back stretch.
2. Then turn around and lean against the wall for balance. Walk smoothly in place, raising your knees as high as possible.
3. Sitting on a chair, stretch your arms behind the back, bringing your shoulders together. Raise your head toward the ceiling as you stretch.
4. Without getting up from the chair, lift your feet off the floor and put them back in place, while moving your clasped hands behind your head, then returning them to the position in front of you.

Acupuncture and acupuncture massage can relieve symptoms of Parkinsonism by triggering a neural response in areas of the brain that are particularly affected by inflammation.

Acupuncture is thought to help slow cell death and mitigate oxidative stress, which causes damage to dopaminergic neurons in the substantia nigra.

Acupuncture may relieve parkinsonism symptoms

Drug therapy for parkinsonism: video

Forecast and consequences

Parkinsonism caused by antipsychotic drugs, toxic poisoning or narcotics is cured or significantly reduced within 12-18 months after discontinuation of the underlying drug. The remaining types of the disease are considered irreversible with a tendency to progress over time.

Possible complications of the syndrome:

• progressive symptoms up to the inability to perform daily activities, and sometimes even eat;
• injuries after falls;
• results of side effects of antiparkinsonian drugs (dystonia, gastrointestinal, liver and kidney diseases);
• malnutrition and exhaustion (due to swallowing and drooling disorders).

Life expectancy with parkinsonism syndrome depends on many factors, including:

• cause of the disease;
• age;
• general condition;
• presence of complications.

A quarter of patients experience disability or death in the first 5 years of the disease. With adequate therapy and initially good health, a person (taking into account the fact that patients are predominantly elderly) can live on average up to 10–15 years with this pathology.

Prevention

Since the cause of the syndrome cannot be foreseen, there are no ways to prevent the development of the disease. There is also no vaccine against Parkinsonism, such as the one recently developed for Parkinson's disease and currently undergoing clinical trials. Vaccination is possible only against certain causes of pathology, for example, viral encephalitis.

The best prevention of disease progression is a timely visit to a neurologist, competent diagnosis and determination of the cause of the pathology.

Parkinsonism: video

Parkinsonism can be caused by medications, exposure to toxins, neurodegenerative diseases, and other disorders that affect the brain. If possible, it is necessary to eliminate the cause of the syndrome, while simultaneously taking physical measures to maintain physical activity.