What are extrapyramidal disorders

Neuroleptic syndrome is a complication with varying symptoms and course that occurs due to the use of antipsychotic drugs, most often neuroleptics. The more common name is extrapyramidal disorders.

There is a risk of extrapyramidal disorders when taking any antipsychotic medications, but taking typical antipsychotics increases the likelihood of complications. The term extrapyramidal disorders was first used in 1960 by French doctors Delay and Deniker. ICD 10 code G20-G26.

Many researchers indicate the advantage of atypical antipsychotics. Typical antipsychotics have a higher degree of binding to dopamine D2 receptors and penetrate cells more easily. If the binding level is more than 75%, then the risk of developing extrapyramidal disorder reaches a critical level. Accordingly, the new generation of antipsychotics are atypical and have a much lower degree of binding to dopamine receptors.

Characteristic

The extrapyramidal system regulates motor activity, maintains a certain tone of skeletal muscles, and ensures the creation and maintenance of posture. The system is responsible for the formation of automatic movements that do not require conscious control, for example, maintaining balance when the center of gravity of the body shifts, avoiding a possible damaging factor - a flying stone, a tree branch moving due to the wind.

In clinical neurology, the extrapyramidal system is a department that controls such muscle parameters as strength, speed and duration of contraction, which normally ensures coordinated, harmonious work of the muscle group. Other functions of the system: formation of the motor component of emotions (facial expressions when crying, feeling angry, smiling, laughing), determining the initial pose for performing the planned movement, maintaining smoothness and uniformity of movements, ensuring that the posture corresponds to the intended action.

The pathways for transmission of nerve impulses within the system are formed by descending nerve branches. Extrapyramidal conductive fibers provide interaction between subcortical structures and distal parts of the nervous system. Extrapyramidal disorders occur due to damage to the structures that make up the system.

Extrapyramidal disorders are a disorder of motor activity that occurs in different forms, which determines the different nature of the manifestations. Movements can be excessive, obsessive, involuntary or impossible (in the case of a significant decrease in muscle tone - paresis of skeletal muscles).

The severity of manifestations varies depending on the nature and intensity of damage to the nervous system. Some patients experience short-term myoclonus (short-term, rapid contraction of a muscle group), while others experience constant tremor (shaking), hyperkinesis (involuntary pathological movements resulting from contraction of a muscle group, provoked by an erroneous brain command).

The pyramidal system provides fine motor coordination. With the help of its structures, technically complex, graceful, precise movements are carried out. The structures of the system are formed by special cells - giant pyramidal ones, also known as Betz cells. The pathways are formed by fibers descending from Betz cells to the spinal cord. In this gap there are collaterals with the pathways of the extrapyramidal system.

On each segment of the spinal cord there are synapses (the place of contact of two neurons) responsible for the motor activity of different parts of the body, for example, the neck, upper limbs, torso, lower limbs. Irritation of the motor cortical areas leads to the occurrence of seizures in the controlled part of the body. For example, irritation of the cortical structures in the area of ​​the upper third part of the anterior gyrus provokes muscle spasms located in the leg area.

Irritation of the middle segment of the same gyrus leads to the occurrence of muscle cramps in the arms, the lower segment - in the half of the face opposite the hemisphere in which the focus of pathological motor activity is located. We are talking about partial seizures, which are also known as Jacksonian (after the name of the neurologist of English origin D. Jackson).

Pyramidal insufficiency is a disorder of motor activity that in adults and children is manifested by paresis (muscle weakness), paralysis (inability to perform voluntary movements) and pathological reactions (reflexes) to an irritating factor, which indicates damage to a part of the pyramidal system. Damage to Betz cells in the cortex or their axons, manifested by paralysis or central paresis, is a sign of pyramidal insufficiency.

Pyramidal syndrome is manifested by increased muscle tone in the extremities (especially in the legs), which is a consequence of excess nerve impulses coming from Betz cells to the peripheral parts of the nervous system. As a result of increased muscle tone, pathological reflexes and resting tremor occur - constant trembling.

Subcortical syndrome is a symptom complex for which hypomimia is typical, which is manifested by weakening or absence of facial expression (facial expressions). Subcortical syndrome is also manifested by other components, including oligobradykinesia (stiffness of movements), acheirokinesis (lack of friendly arm swings when walking), increased tone of skeletal muscles like parkinsonism, which is a reflection of extrapyramidal disorders.

Hyperkinesis, or damage to the neostriatum

We present the second, large group of subcortical or subcortical disorders, which are based on excessive motor activity. In addition to damage to the striatum, damage to the most ancient structure, the globus pallidus, is also possible. The result is pallidal syndrome, which is sometimes called striopallidal syndrome.

Morphologically, these diseases represent situations in which the influence of the striatum on “subordinate structures” is sharply weakened, and a wide variety of circulation of motor impulses occurs until spontaneous attenuation of the signal occurs. The main representatives of diseases of this group are :

• Athetosis.

This disease occurs when a network of small neurons in the striatum dies and is replaced by glial scars. As a result, the patient experiences bizarre, worm-like and extremely elaborate movements. There is a tendency to hyperextend and “wring” the fingers. In addition, grimaces of the tongue and facial muscles occur, laughter or crying may appear;

• Torsion spasm or torsion dystonia.

This is nothing more than athetosis of the trunk muscles. The movements are no less bizarre and resemble wriggling ones. Figuratively speaking, this is “a corkscrew entering a bottle.” As a result, such patients have very difficult gait. Dystonic motor activity is nothing more than rhythmic spasms of agonist-antagonist muscles .

Here we should make a digression, after which the very physical basis of all violent movements can become clear. Normally, after contraction, the muscle simply relaxes and goes into a resting state. But in this case, the inhibitory influences are blocked. The muscle cannot simply relax. And, in order to somehow replace complete relaxation, there is an alternating contraction of the agonist-antagonist muscles, “pulling” in opposite directions.

The second variant of hyperkinesis, which affects the putamen and the central medial thalamic nucleus, is spastic torticollis. The sternocleidomastoid and trapezius muscles are often affected. The result is movements, involuntary and slow, that pull and turn the head to the side and down. Often it needs to be supported by hand.

• Chorea.

This is an interesting subcortical syndrome, which manifests itself with fast, completely chaotic movements in the muscles, which are very reminiscent of voluntary ones. It is even difficult for a simple person to understand that he is not being played and is not being “made a fool” in front of him. With chorea, a dancing, bouncing gait and grimacing occurs. Huntington's chorea is of greatest importance as a serious, incurable and fatal disease. A separate article is dedicated to him.

In some cases, individual and involuntary contractions of individual muscles and entire groups occur, but without movement . Then we are talking about myoclonus. In its occurrence, a major role is played by the destruction of normal connections of the cerebellum with the red nuclei;

• Ballism, hemiballism.

Outwardly, it resembles a sports warm-up for a discus thrower, who, before throwing the disc, makes a series of fast, sweeping movements in which the large muscles of the pelvis and shoulders are involved. It often appears on one side of the body and is then called hemiballismus. In this case, the connections of the globus pallidus with one of the subthalamic nuclei (Lewis nucleus) are destroyed and hyperkinesis occurs on the side opposite to the lesion.

Instead of a conclusion

We have considered only a few, the most basic extrapyramidal disorders. Left aside were tics, drug-induced hyperkinesis, many types of tremors, facial spasms and blepharospasm, and Tourette's disease. In some cases, it is difficult even for professionals to identify an accurate diagnosis, and then it is possible to set “extrapyramidal and movement disorder, unspecified,” since this possibility is in the ICD-10.

Treatment of these diseases poses a serious challenge . Considering that many of the subcortical diseases are associated with dementia, doctors should have a wide variety of drugs in their arsenal. Unfortunately, it is very rarely possible to completely get rid of the clinical picture of extrapyramidal disorders, even with a combination of therapeutic and neurosurgical methods. But now new and promising means are emerging. In one of the following articles we will definitely talk about these drugs, which undoubtedly have a great future.

Classification

Extrapyramidal hyperkinesis is classified according to the system of the Russian neurologist L. Petelin. Taking into account the anatomical and pathophysiological features, Petelin systematized hyperkinesis taking into account the level of damage to the structures that form the brain. There are types of hyperkinesis as a result of damage to the departments:

1. Brain stem. Organic tremor, rest tremor of the parkinsonian type, myoclonus (short-term, rapid, rhythmic contraction of a muscle group), stereotypy (persistent aimless repetition of the same type of movements).
2. Subcortical layer. Athetosis (slow tonic-type convulsions in the area of ​​the limbs, face, body), chorea, torsion spasm, ballism.
3. Subcortical-cortical layer. Myoclonus, manifested in various forms.

Extrapyramidal and movement disorders of sporadic and hereditary origin, unspecified and identified etiology in modern clinical practice are considered as movement disorders. In this case, there are 2 main forms - hypokinesia (deficit of motor activity) and hyperkinesia (pathological excess of motor activity). Hypokinetic disorders include Parkinson's disease, hyperkinetic disorders include tremor, myoclonus, chorea, and dystonia.

Classification and symptoms

Distinguishing symptoms of disorders of the extrapyramidal system makes it possible to diagnose various extrapyramidal syndromes.

Extrapyramidal disorders are divided according to the severity of motor activity resulting from impaired muscle tone. As a result:

• hypokinesis, characterized by lack of movement (immobility);
• hyperkinesis, characterized by an excess of violent, uncontrollable movements (twitching).

The most common extrapyramidal syndromes of a hyperkinetic nature include:

• akathisia;
• ballism;
• chorea;
• tremor;
• dystonia;
• tics;
• myoclonus.

Akathisia

This extrapyramidal syndrome causes patients serious discomfort, expressed in an irresistible desire to move all the time and change body position. Due to internal anxiety, the patient cannot sit still, twitches his lower limbs, touches and rubs his face, walks, and fidgets with his fingers. There is a serious problem with falling asleep, but the syndrome does not manifest itself during sleep.

Ballism

The pathological condition is characterized by sweeping movements produced by the forearms and pelvis with the help of large muscles. They resemble the warm-up of an athlete, a discus thrower, just as sharp, with a wide amplitude and a rotational component.

Chorea

The syndrome is hereditary in nature, which manifests itself after the age of thirty. Jerky movements are made in disarray and lack regularity. Outwardly similar to normal ones, the difference is in the increased amplitude and sharp execution. This peculiar “dance” is called the “Dance of St. Vitus.”

Tremor

The movements of extrapyramidal tremor are similar to trembling, produced in a constant rhythm with a small amplitude. Tremor is noticeable when the patient extends his arms forward or tries to touch his nose with a finger.

Dystonia

Prolonged contraction of different muscle groups throughout the body forms twisting. The fingers of the upper limbs take on an abnormal position due to the professional activities of writers and musicians. Contraction of the eyelid muscles in adults leads to blindness. The freedom of repetitive movements is disrupted by severe muscle spasms, often painful and life-threatening.

Tiki

They manifest themselves as twitching of individual muscle groups, most often affecting the head, face (tick eyelids, lips, chin, forehead), neck, shoulders. Tics appear under severe nervous tension and stress.

Myoclonus

This syndrome is characterized by short twitching of muscle groups that occur synchronously, but not regularly. The result is a sudden shudder in the form of a jolt.

Parkinsonism

Hypokinetic movement disorders include Parkinson's syndrome.

This is a chronic disease with a gradual deterioration of the condition, characterized by the following symptoms:

• muscle hardness and inflexibility;
• twitching of the muscles of the face, upper limbs;
• decreased clarity and intelligibility of speech;
• changes in posture and gait;
• disturbance of mental activity.

Parkinsonism is diagnosed as a separate pathology - Parkinson's disease. But it can develop after an injury, an infectious disease, or as a result of neurological pathologies. Every third case of the disease is of neuroleptic origin.

The progression of extrapyramidal disorders leads to patient disability.

Causes

Extrapyramidal disorders are motor dysfunction that occurs against the background of damage to the extrapyramidal system, which is associated with damage to brain structures such as the red and basal ganglia, the substantia nigra, the cerebellum, and the reticular formation. A common cause of extrapyramidal pathologies is an imbalance of neurotransmitters.

Other causes of these diseases are associated with traumatic, damaging factors, such as previous neuroinfections, mechanical head injuries, cerebrovascular accidents, hemorrhage, abnormalities in the development of brain structures in children, and hypoxic-ischemic processes occurring in the brain tissue.

Extrapyramidal diseases often develop as a result of long-term use of antipsychotics - drugs that suppress mental nervous activity. These medications are used to eliminate symptoms of mental illness, such as hallucinations, delusions, emotional lability, and inappropriate behavior. Neuroleptics do not affect the state of consciousness (do not depress it), but they inhibit psychomotor agitation - the transmission of nerve impulses by motor neurons.

An example is dopamine receptor blockers (Haloperidol, Fluphenazine). Extrapyramidal neuroleptic syndrome is often called secondary parkinsonism. Signs of parkinsonism are more often detected after 2-12 weeks of taking antipsychotics. More often, Parkinson's syndrome is diagnosed in women over 40 years of age, less often in men of the same age group. Features of the development of the syndrome:

1. Subacute, non-progressive course.
2. Symmetrical manifestation of symptoms.
3. Combination with dyskinesia (involuntary movements caused by contraction of a muscle group).
4. Combination with endocrine pathologies (for example, with hyperprolactinemia - increased concentration of the hormone prolactin).

In the secondary form of parkinsonism, provoked by taking antipsychotics, an important sign of the primary form is absent - postural instability (inability to maintain balance). Extrapyramidal syndrome may occur as a side effect after single or long-term use of other pharmaceutical drugs:

• Antidepressants (used to eliminate symptoms of depression). Regulate the concentration of neurotransmitters - serotonin, dopamine, norepinephrine.
• Calcium antagonists (calcium channel blockers, inhibit the movement of calcium ions into the smooth muscle cells of the heart and blood vessels from the intercellular space). Regulate (increase or decrease) heart rate.
• Medicines used in complex therapy of Parkinson's disease.
• Antiarrhythmic drugs (sodium and potassium channel blockers, β-blockers).

Late extrapyramidal disorders can occur after discontinuation of these drugs and are often irreversible and not amenable to therapeutic correction. Acute dystonic extrapyramidal reactions occur in 5% of patients in the first days after taking the drug Metoclopramide (antiemetic, antimigraine effect).

Side effects in the form of movement disorders appear less frequently if therapy begins with small or very large doses of Metoclopramide. Pyramidal syndrome can develop as a consequence of etiological factors:

1. Previous infectious disease of the central nervous system (meningitis, encephalitis).
2. An acute disorder of cerebral blood flow (stroke).
3. A tumor localized in the brain tissue.
4. Injury in the head area.
5. Disturbance of metabolic processes.
6. Infection with prion agents.
7. Chronic and acute intoxication.
8. Genetic mutations.

When the pathological focus is localized in the cortical motor areas, central paralysis is more often observed. A sign of damage to the pyramidal structures in the area of ​​the internal capsule is hemiplegia (paralysis of the arms and legs in one half of the body) on the side opposite to the location of the pathological focus. Damage to the system in the area of ​​the brain stem is accompanied by an alternating syndrome (hemiplegia, signs of damage to the cranial nerves).

Extrapyramidal side effects

Extrapyramidal side effects (EPS), usually drug-induced movement disorders, are among the most common side effects that patients have from dopamine receptor blocking drugs. These symptoms were first described in 1952 during treatment with chlorpromazine, and these symptoms resembled the clinical manifestations of Parkinson's disease. Since then, various movement disorders have been described across the spectrum of extrapyramidal symptoms, including dystonia, akathisia and parkinsonism, which occur acutely or take a chronic course, as manifestations of tardive akathisia and tardive dyskinesia. Extrapyramidal symptoms are often associated with poor quality of life and patient refusal of treatment, which can lead to relapse of mental illness and readmission to hospital, especially in patients with schizophrenia who have stopped pharmacological therapy.

Centrally acting drugs that block dopamine receptors, namely the first-generation antipsychotics haloperidol and phenothiazine antipsychotics, are the most common drugs that relieve extrapyramidal symptoms. First-generation antipsychotics were associated with EPS in 62% of patients in a study of patients with schizophrenia.

Although EPS is less common with atypical antipsychotics, the risk of extrapyramidal symptoms increases with increasing antipsychotic dose. At the same time, clozapine has the lowest risk, and risperidone has the highest risk of extrapyramidal symptoms.

Other drugs that block central dopaminergic receptors, including antiemetics (metoclopramide, droperidol, and prochlorperazine), lithium, serotonin reuptake inhibitors (SSRIs), stimulants, and tricyclic antidepressants (TCAs) can also cause extrapyramidal symptoms. In rare cases, it is also caused by antiviral, antiarrhythmic drugs and valproic acid drugs. For antiemetics with dopamine D2 receptor antagonist effects, the incidence of extrapyramidal symptoms is reported to range from 4% to 25% with metoclopramide and 25% to 67% with prochlorperazine.

Risk factors include a history of episodes of extrapyramidal symptoms and a high dose of medication.

Older women are more susceptible to drug-induced parkinsonism and tardive dyskinesia, while young men are more likely to exhibit dystonic reactions.

Pathogenesis

It is assumed that the mechanism of extrapyramidal symptoms is due to antagonistic binding of dopaminergic D2 receptors in the mesolimbic and mesocortical tracts of the brain. However, antidopaminergic effects in the caudate nucleus and other basal ganglia may also contribute significantly to extrapyramidal symptoms. Some investigators have hypothesized that the faster dissociation of atypical antipsychotics from the dopamine receptor compared with typical antipsychotics explains the reduced incidence of EPS. However, a recent study by Sykes, using a new time-resolved fluorescence energy transfer assay, demonstrated that binding kinetics and association rates, rather than dissociation, are more correlated with extrapyramidal symptoms.

Clinical picture

Dystonia most often occurs within 48 hours of exposure in 50% of cases and within 5 days in 90% of cases. Dystonia is characterized by involuntary muscle contractions leading to abnormal posture or repetitive movements. It can affect muscles in different parts of the body, including the back and limbs (opisthotonus), neck, jaw (trismus), eyes (oculogyric crisis), muscles of the abdominal wall and pelvis (tortipelvic crisis), and muscles of the face and tongue (buccolingual crisis). . It is important to assess patients for pain, difficulty breathing, swallowing and speaking.

Akathisia is characterized by a subjective feeling of inner restlessness and an irresistible urge to move, resulting in repetitive movements that include crossing the legs, or moving from one leg to the other. The first manifestations of akathisia usually occur within 4 weeks after starting or increasing the dose of the medication that causes this movement disorder. Because of its often vague and nonspecific presentation of nervousness and discomfort, akathisia is often misdiagnosed as anxiety, restless legs syndrome, or agitation. The doctor may mistakenly increase the amount of antipsychotic drugs or SSRI drugs, which will further worsen the symptoms of akathisia. This can have detrimental consequences as the severity of akathisia is associated with suicidal ideation, aggression and violence. Relief of akathisia occurs when the dose of antipsychotic drugs is stopped or reduced and, as a rule, goes away on its own within 6 weeks.

Drug-induced parkinsonism manifests itself as tremors, rigidity, and slow motor function. The classic appearance of such a person is manifested by a mask-like face, stooped posture and a slow shuffling gait. There are gait disturbances and difficulty rising from a sitting position. Finally, tardive dyskinesia manifests itself in the form of involuntary choreoathetoid movements, most often affecting the muscles of the mouth and tongue and less often the limbs. These symptoms are not usually painful, but they can interfere with social communication and cause difficulty chewing, swallowing and speaking.

Treatment

If a patient experiences an acute attack of extrapyramidal symptoms, especially dystonia, the physician should evaluate the need for emergency airway intervention, as dystonic reactions of the larynx and pharynx may increase the risk of imminent respiratory arrest. Dystonic reactions are rarely life-threatening, and the physician should discontinue the drug that caused the dystonic reaction and relieve pain if it occurs. Administration of an antimuscarinic (benztropine, trihexyphenidyl) or diphenhydramine may relieve dystonia within minutes. In cases of tardive dystonia, additional therapeutic strategies include benzodiazepine administration, botulinum toxin injection to relieve facial dystonia, a muscle relaxant (eg, baclofen), dopamine-depleting agents (eg, tetrabenazine), and consideration of deep brain stimulation or pallidotomy for treatment-resistant cases. Treatment of akathisia uses strategies similar to those for dystonia, including stopping or reducing the dose of offending medications, switching to an atypical antipsychotic if the offending drug is the typical first-generation antipsychotic, and administering antimuscarinics.

Symptoms

Extrapyramidal symptoms appear in Parkinson's disease, which is caused by damage and death of neurons producing the neurotransmitter dopamine; these destructive and degenerative processes occur mainly in the area of ​​the substantia nigra. Main signs: postural instability, muscle rigidity, limitation of motor activity, trembling of individual parts of the body.

Other extrapyramidal disorders are represented by hypokinetic-hypertensive or hyperkinetic-hypotonic syndrome, which manifest themselves in the following: shaking paralysis, parkinsonism, hyperkinesis (dystonia, chorea). Symptoms of extrapyramidal disorders that occur during treatment with antipsychotics are represented by all forms of hyperkinesis. Extrapyramidal insufficiency is manifested by types of motor disorders:

1. Chorea. A symptom complex characterized by irregular, jerky, erratic, uncontrolled movements. The movements produced resemble normal ones, but differ from them in amplitude, frequency, and intensity.
2. Torsion spasm (torsion dystonia). Changes in muscle tone, expressed in hypotension (decreased tone, muscle weakness) or extrapyramidal rigidity (hardness, inflexibility of the muscles). Leads to the development of hyperkinesis (pathological, uncontrolled movements) or the formation of fixed postures.
3. Tic (a form of hyperkinesis). An elementary movement manifested by rapid, short-term, uncontrolled muscle twitching. Spontaneous movements arise or increase under the influence of stress factors.
4. Ballism, hemiballism. Irrhythmic, sharp movements of large amplitude in the proximal (located closer to the center or median plane) parts of the body, often with a rotational component. Hemiballismus reflects similar disorders in one half of the body.
5. Tremor. Uncontrolled, oscillatory movements of a rhythmic nature, provoked by contraction of antagonist muscle groups (during contraction, they pull in opposite directions). Contraction of agonist muscles (perform the main task) leads to movement directed against the movement caused by contraction of antagonist muscles. Tremor affects the muscles of the limbs, head, face, and torso.
6. Facial hemispasm (hemifacial spasm). Involuntary, unilateral contraction of the facial muscles of the tonic or clonic type in the area of ​​innervation of the facial nerve. During tonic contraction, muscle fibers function asynchronously - areas of tension and relaxation alternate. Clonic contraction occurs as a consequence of stretching of certain muscles, which is accompanied by reflex activity of antagonist muscles. As a result, a contraction of the antagonist muscles occurs, which provokes another contraction of the agonist muscles.

The listed symptoms of damage to the extrapyramidal system are combined with each other in different variations. Extrapyramidal and other movement disorders are often accompanied by psychopathological symptoms:

• Anxiety, unreasonable, unreasonable fear.
• Increased irritability.
• Deterioration of cognitive abilities (memory, mental activity).
• Closedness, feelings of inferiority.
• Apathy, loss of interest in events in the outside world.

Steele-Richardson-Olszewski syndrome, also known as progressive supranuclear palsy, is characterized by damage to the tissues of the central nervous system, accompanied by impaired voluntary movements of the visual organs and bradykinesia (slowing of active movements). Extrapyramidal rigidity with progressive dystonia (pathological change in tone) of the axial muscles, dementia and pseudobulbar syndrome are other signs of supranuclear palsy.

Tardive dyskinesia

Tardive dyskinesia (TD) is a persistent motor disorder that can be not only severe, but also irreversible. It is believed that the risk of developing PD and the likelihood of its persistence increase with the duration of treatment and the total dose of antipsychotic.

In addition, PD can develop, although quite rarely, after a relatively short period of treatment at low doses or after discontinuation of the drug.

Tardive dyskinesia usually begins with abnormal movements of the lips and tongue, but can progress to involve other parts of the body and also manifest with a wide range of involuntary movements.

PD is a stigmatizing phenomenon. In its severe form, severe maladjustment is observed, associated with difficulties in eating, articulation, movement and breathing [8].

The development of PD is facilitated by many risk factors, including long-term use of antipsychotics and advanced age [8–11], as well as female gender in the elderly, comorbid affective disorders, acute EPS, race, and diabetes mellitus [8, 12–15].

The mechanism presumably underlying tardive dyskinesia is caused by prolonged blockade of postsynaptic dopamine receptors, dopamine hypersensitivity, and damage during neuroleptic therapy to striatal interneurons, the mediator of which is gamma-aminobutyric acid or acetylcholine.

One meta-analysis found that patients treated with atypicals had a lower risk of PD compared with patients treated with haloperidol [10].

It is assumed that this is due to less pronounced blockade of D2 receptors in the basal ganglia, as well as a low likelihood of postsynaptic dopaminergic hypersensitivity [16]. However, it remains unknown whether atypical antipsychotics differ from each other in their ability to cause PD.

Diagnostics

Determination of the presence and severity of extrapyramidal disorders occurs in the office of a neurologist during a visual examination and testing. The diagnosis is made based on medical history and the results of instrumental examination. Basic diagnostic methods:

1. Neuroimaging (CT, MRI).
2. Electroencephalography (study of bioelectrical activity of the brain).
3. Electroneuromyography (study of the conduction of nerve impulses in muscles).

In Parkinson's disease, an ultrasound scan of the substantia nigra area is performed. Diagnosis is often based on clinical data. A blood test can determine the concentration of glucose, hormones, tyrosine hydroxylase and dopamine. In Parkinson's disease, a blood test shows a disturbance in the activity of the mitochondrial complex.

Treatment

Treatment is prescribed taking into account the reasons that provoked the impairment of motor function. If movement disorders are associated with the use of pharmaceutical drugs, the therapy program is adjusted. In cases of progressive supranuclear palsy, palliative treatment is carried out aimed at reducing the severity of symptoms.

Treatment for Parkinson's disease includes taking neuroprotectors and drugs that eliminate the symptoms of the disease. Psychotherapeutic treatment is indicated. At the same time, rehabilitation is carried out, during which motor skills are restored. Rehabilitation activities include classes on special simulators, gymnastics, massage, water treatments, and physiotherapy.

Extrapyramidal disorders reflect damage to the structures of the corresponding system responsible for the tone of skeletal muscles, reflex and voluntary motor activity in general.

Diagnosis and treatment principles

Due to the fact that extrapyramidal disorders include many different diseases and syndromes, the diagnosis for each specific case can be completely different. Most often the patient is prescribed:

• blood and urine testing (toxicological);
• ophthalmological examination;
• cerebrospinal fluid examination;
• genetic;
• electrophysiological;
• neuropsychological testing;
• stabilography;
• biopsy of muscles, mucous membranes, skin, nerve and brain tissue.

Treatment of extrapyramidal disorders is primarily aimed at getting rid of the underlying disease. But, in most cases, symptomatic therapy is used. Treatment is with anticholinergic drugs, antioxidants, nootropic and restorative drugs, and adrenergic blockers. Often specialists resort to neurosurgery.

In cases with local dystonia, subcutaneous injections of neurotoxin are used. The course of treatment is 3-4 procedures. The result lasts 3 months.