Movement in Parkinson's disease. Why exercise is beneficial for Parkinson's disease

For parkinsonism caused by taking medications (neuroleptics, etc.), stop them and look at the result. Also confirmed is the positive effect and disappearance of symptoms when prescribing Cyclodol.

Signs of parkinsonism are not always noticeable to the person affected, but with careful attention, relatives may be the first to spot warning signs.

In such cases, you should immediately contact a neurologist for a full diagnosis.

When making a diagnosis, you should constantly take medications; their dosage is selected carefully and individually for each patient, usually in a hospital setting.

And acheirokinesis, as one of its main symptoms, is far from a rare phenomenon in the world of modern people who never know what rest is. Modern man is constantly in blissful ignorance of his fate, not having the habit of calculating every step throughout his more or less long life.

But if at the beginning of life’s journey this has a purely rhetorical meaning, then closer to its end the time comes to save energy and literally think through each of your movements: a step, a gesture, a turn of the head. As the famous satirist said, old age is the time to bend down to tie your shoelaces and think about what you can do along the way.

A person reaches a point when some structures of his brain are either almost completely unusable, or their resources are extremely depleted.

This is what's happening to me

But becoming deliberate both in your desires and in your movements can be forced not only by reaching old age, but also by Parkinson’s disease, which is possible at an age that is far from ancient.

Parkinson's disease (idiopathic parkinsonism) is a degeneration of the extrapyramidal system due to an acute lack of dopamine due to the death of its producing neurons, primarily in the substantia nigra, as well as activation of the influence of the basal ganglia on the cerebral cortex. Changes occur in the subthalamic nucleus, parts of the midbrain and brain stem, leading to the formation of Lewy bodies in the cells of the latter.

In other diseases that make up the concept of “”, changes in the nervous system differ in some details, but this is always a degenerative process in the extrapyramidal (striopallidal) system, leading to a characteristic clinical picture of the disease. Including acheirokinesis.

Features of “parkinsonian” movements

The term "acheirokinesis" literally means: absence of movement in the hand. But in neurology this is the name given to the absence of marching, waving arm movements accompanying walking. Or their extremely weak expression.

The position of the arms when walking in a person suffering from Parkinsonism is very indicative: half-bent at the elbows with frozen tension and some elevation of the shoulders, they are adjacent to the body in the wrist area, the hands are half-bent and turned inward. And they are motionless or almost motionless when walking, justifying the term: oligokinesia of the limbs.

The gait itself is also significantly different from the gait of a healthy person.

These are the characteristic changes:

• walking pace;
• step width;
• position of the body and legs.

Against the background of general stiffness of the body with the body moving forward and motionless arms, the patient begins to move with a slow “start” reflex”, trying to move his legs as if stuck to the floor. After a series of foot actions in the form of quick and shallow stomping in one place, he manages to initiate walking, most often having the character of a slow shuffle with a small step width (a symptom of microbasia). In the case of hemiparkinsonism, only one leg shuffles.

Marking time is repeated if it is necessary to go through the door or in the presence of outside observers. The patient seems to hesitate in choosing the leg with which to begin performing the important maneuver. At the moment of a hitch, the body continues to move forward, but the legs lag behind, and due to a shift in the center of gravity, a fall forward occurs (a symptom of propulsion).

The need to turn while moving leads to the same result - falling backward (retropulsion) or to the side (lateropulsion).

It is possible to move both naturally and parallel to each other with feet, or it is pseudo-stepping walking.

An increase in step width (symptom of macrobasia), like climbing stairs, for patients “catching up” with their own forward-shifted center of gravity, is a less severe test than walking on a flat surface.

Mobilization of attention at the command of the researcher leads to a short-term improvement in the situation, but it does not persist for long due to the increase in muscle tension in the patient’s body and usually ends with his fall.

As a result

In addition to the manifestation in Parkinson's disease, the symptom of acheirokinesis accompanies the course of pathologies designated by the concept of “Parkinson-plus” - multisystem degeneration with:

• Steele-Richardson and Shy-Dreiger syndromes;
• degenerations of striato-nigral, olivo-ponto-cerebral, cortico-basal;
• combination of parkinsonism phenomena with and.

Acheirokinesis, which appeared long before the full development of the parkinsonism clinic, is one of the most important signs of the disease precisely because of its early appearance.

Clinical manifestations of Parkinson's disease
Tremor. Parkinson's disease is characterized by resting tremors of the "pill-rolling" or "coin-counting" type. Most often, tremors initially appear in the arm, but may begin in the leg, face, jaw, or tongue. In most cases, as the disease progresses, the term progressively involves parts of the body in the following order: 1-arm, 2-arm and leg on the same side, 3-opposite half of the body. With voluntary movement of the involved limb, the tremor disappears or is significantly weakened. When performing repeated movements with the opposite limb, the tremor, on the contrary, intensifies. In addition, resting tremor in the hands increases with walking.
Postural-kinetic tremor. In a significant proportion of patients with Parkinson's disease, in addition to rest tremor, there is also a postural-kinetic thermore, which occurs or intensifies when holding a pose or moving. In some cases, such a tremor is a kind of “continuation” of a resting tremor and has the same frequency. In other patients, this is an independent type of tremor that limits hand movements to a greater extent than resting tremor. It can make it difficult to eat, get dressed, and do other activities that involve fine movements or maintaining a certain posture.
Hypokinesia is one of the most disabling manifestations of Parkinson's disease. It is characterized by slowness of movements and delayed initiation, impoverishment of the pattern, and exhaustion of movements. The patient may describe hypokinesia as fatigue or clumsiness, awkwardness, and note that daily activities, such as getting dressed or eating, take longer than usual. The performance of fine movements of the limbs suffers the most: patients cannot fasten buttons, and writing becomes difficult. When writing, the patient begins a line with relatively large letters, but towards the end of the line they become increasingly smaller (micrography). As the disease progresses, other movements become more difficult. Many people complain that it is difficult for them to get up and out of the car, as well as perform movements that require torso mobility or maintaining a difficult posture. In extreme cases, these changes can lead to limited mobility and even complete inability to move. Wanting to make a movement, patients can freeze in a certain position.
Rigidity is manifested by increased resistance when performing passive movements of the involved limb. It is felt both during flexion and extension. Unlike spasticity, rigidity is present throughout the entire range of motion, from its beginning to its end. Symptoms spread from the prosimal to the distal parts, i.e. The muscles that operate the large proximal joints are the first and most severely affected.
Postural instability appears in the later stages of Parkinson's disease, on average approximately 5 years after its onset. This symptom leads to severe functional impairment and is practically untreatable. One of the reasons is an increase in the tone of the trunk muscles, especially the flexors, which leads to a constant forward tilt of the trunk. Due to the inability to quickly regain balance, patients often fall. There is often a need to use a cane, walker, or ask someone to accompany them, which leads to a pronounced limitation of the patients’ independence.
Difficulty moving and walking problems appear in the later stages of Parkinson's disease. Walking impairments increase slowly, with initial difficulty lifting the foot off the floor and limited swinging of the arms when walking. As the disease progresses, patients note difficulty in starting to move and a shuffling gait appears. It is characterized by a small, fast, uncontrolled step with the inability to stop. A shuffling gait usually occurs when walking on a level surface, but there is no difficulty when climbing stairs. At the moment of starting to move, before turning, when passing through a narrow opening (corridor, door), or when an obstacle suddenly arises, a patient with Parkinson's disease may suddenly experience freezing.
Urinary disorders. Patients with Parkinson's disease often have urinary problems, such as urinary frequency (pollakiuria), urination more often at night (nocturia), or urinary urgency. Possible causes of these disorders are detrusor hyperreflexia and bladder overactivity.
Urinary incontinence. In the later stages of Parkinson's disease, urinary incontinence may occur, accompanied by bowel dysfunction such as constipation or pseudo-obstruction. These symptoms arise due to damage to the autonomic nervous system, but the pathogenesis remains unclear. The development of these symptoms is associated with the presence of Lewy bodies in the neurons of the sympathetic ganglia and the hypothalamus.
Depression. 20-40% of people with Parkinson's disease develop depression during the course of the disease. In 20-30% it is the first symptom, ahead of movement disorders. One of the causes of depression is considered to be decreased activity of the dopaminergic mesolimbic system, but lesions of the noradrenergic and serotonergic systems also play a certain role in its development.
Anxiety states. Approximately 50% of patients with Parkinson's disease experience anxiety, mainly in the form of panic attacks. Often, anxiety states are associated with motor fluctuations, occurring during the “off” period.
Dementia (dementia) develops in 15-30% of patients with Parkinson's disease; in patients over 80 years of age, this figure can reach 70-80%. dementia is an unfavorable prognostic factor, indicating rapid progression of the disease. Risk factors for dementia: older age, low sensitivity to levodopa, akinetic-rigid form of the disease, the presence of psychotic episodes during antiparkinsonian therapy, the presence of dementia in relatives. Characteristic symptoms: memory loss, impaired attention, slow mental activity, impaired visuospatial functions. The mechanisms of development of dementia remain completely unclear, however, autopsy data indicate the role of degenerative pathology with the formation of Lewy bodies and amyloid deposition in the limbic structures and cerebral cortex, as well as weakening the activity of the cholinergic system.
Sleep disorders. The majority of patients with Parkinson's disease have sleep disorders, mainly related to its maintenance. Sleep becomes intermittent and incomplete, and does not bring a feeling of freshness. Falling asleep is also often disrupted. In the later stages of the disease, increased daytime sleepiness is observed, accompanied by sudden attacks of falling asleep. The most common parasomnias are nightmares, vivid dreams, night terrors, snoozing, and sleepwalking. Particularly characteristic is sleep behavior disorder with rapid eye movements, in which muscle atonia is lost in this phase of sleep and the patient begins to respond to dreams. Sometimes this disorder precedes other symptoms of Parkinson's disease by many years. Some patients have difficulty falling asleep due to restless legs syndrome. Although there are many reasons for the occurrence of these disorders, the main reason is damage to the centers of the brain that regulate sleep.

Modern man is constantly in blissful ignorance of his fate, not having the habit of calculating every step throughout his more or less long life.

But if at the beginning of life’s journey this has a purely rhetorical meaning, then closer to its end the time comes to save energy and literally think through each of your movements: a step, a gesture, a turn of the head. As the famous satirist said, old age is the time to bend down to tie your shoelaces and think about what you can do along the way.

A person reaches a point when some structures of his brain are either almost completely unusable, or their resources are extremely depleted.

This is what's happening to me

But becoming deliberate both in your desires and in your movements can be forced not only by reaching old age, but also by Parkinson’s disease, the manifestations of which are possible at an age that is far from ancient.

Parkinson's disease (idiopathic parkinsonism) is a degeneration of the extrapyramidal system due to an acute lack of dopamine due to the death of its producing neurons, primarily in the substantia nigra, as well as activation of the influence of the basal ganglia on the cerebral cortex. Changes occur in the subthalamic nucleus, parts of the midbrain and brain stem, leading to the formation of Lewy bodies in the cells of the latter.

In other diseases that make up the concept of “parkinsonism,” changes in the nervous system differ in some details, but this is always a degenerative process in the extrapyramidal (striopallidal) system, leading to the characteristic clinical picture of the disease. Including acheirokinesis.

Features of “parkinsonian” movements

The term "acheirokinesis" literally means: absence of movement in the hand. But in neurology this is the name given to the absence of marching, waving arm movements accompanying walking. Or their extremely weak expression.

The position of the arms when walking in a person suffering from Parkinsonism is very indicative: half-bent at the elbows with frozen tension and some elevation of the shoulders, they are adjacent to the body in the wrist area, the hands are half-bent and turned inward. And they are motionless or almost motionless when walking, justifying the term: oligokinesia of the limbs.

The gait itself is also significantly different from the gait of a healthy person.

These are the characteristic changes:

Against the background of general stiffness of the body with the body moving forward and motionless arms, the patient begins to move with a slow “start reflex”, trying to move his legs as if stuck to the floor. After a series of foot actions in the form of quick and shallow stomping in one place, he manages to initiate walking, most often having the character of a slow shuffle with a small step width (a symptom of microbasia). In the case of hemiparkinsonism, only one leg shuffles.

Marking time is repeated if it is necessary to go through the door or in the presence of outside observers. The patient seems to hesitate in choosing the leg with which to begin performing the important maneuver. At the moment of a hitch, the body continues to move forward, but the legs lag behind, and due to a shift in the center of gravity, a fall forward occurs (a symptom of propulsion).

The need to turn while moving leads to the same result - falling backward (retropulsion) or to the side (lateropulsion).

It is possible to move both naturally and parallel to each other with feet, or it is pseudo-stepping walking.

An increase in step width (symptom of macrobasia), like climbing stairs, for patients “catching up” with their own forward-shifted center of gravity, is a less severe test than walking on a flat surface.

Mobilization of attention at the command of the researcher leads to a short-term improvement in the situation, but it does not persist for long due to the increase in muscle tension in the patient’s body and usually ends with his fall.

As a result

In addition to the manifestation in Parkinson's disease, the symptom of acheirokinesis accompanies the course of pathologies designated by the concept of “Parkinson-plus” - multisystem degeneration with:

• Steele-Richardson and Shy-Dreiger syndromes;
• degenerations of striato-nigral, olivo-ponto-cerebral, cortico-basal;
• combination of parkinsonism with dementia and amyotrophic lateral sclerosis.

Acheirokinesis, which appeared long before the full development of the parkinsonism clinic, is one of the most important signs of the disease precisely because of its early appearance.

This section was created to take care of those who need a qualified specialist, without disturbing the usual rhythm of their own lives.

Ataxia, balance and gait disorders

When starting treatment of patients with neurological disorders, it is necessary first of all to establish whether there is a history of changes in posture and gait, and also to examine these functions during examination. Changes in posture and gait can occur as a result of damage to the nervous system at various levels, and often the type of clinical changes indicates the location of the damage.

Ataxia occurs as a result of dysmetria and disproportionality of movements. Dysmetry is a violation of the direction or position of a limb during active movement, in which the limb falls short of reaching the target (hypometry) or moves beyond the target (hypermetry). Disproportionality of movements means errors in the sequence and speed of individual components of the movement. The result is a loss of speed and dexterity in movements that require different muscles to work together smoothly. Movements that were previously smooth and precise become uneven and imprecise. Clinically, ataxia is presented in the form of disturbances in the tempo and volume of individual movements and usually occurs when the cerebellum is damaged or various types of sensitivity are impaired. Gait ataxia is characterized by uneven tempo, duration, and sequence of movements with side-to-side swaying.

How to determine the type of brain damage based on the nature of changes in gait and balance?

When starting to treat a patient with gait disorders, it is first necessary to find out when the disorders most often occur: in the dark or in the light; whether they are accompanied by systemic or non-systemic dizziness or a feeling of lightness in the head; whether there is pain or parasthesia in the limbs. The examination should clarify the presence of weakness, dysfunction of the pelvic organs, stiffness or rigidity in the limbs. The doctor must determine whether the patient has difficulty starting or finishing walking.

Normal gait

With unchanged gait:

• The torso must be kept in an upright position
• head - straight
• arms - hang freely at the sides, moving in time with the movements of the opposite leg

• Shoulders and hips should be aligned, arms swing should be uniform.
• The steps must be correct and equal in length.
• The head should not shake.
• There should be no noticeable scoliosis or lordosis.
• With each step, the hip and knee should bend smoothly, the ankle joint should bend backward, and the foot should easily lift off the ground.

It is necessary to place your foot first on the heel, and then subsequently transfer your body weight to the sole and toes. With each step, the head and torso turn slightly, but this does not lead to staggering or falling. Every person walks in a certain manner, which is often hereditary. When walking, some people place their feet with their toes inward, some with their toes outward. Some people walk with big steps, while others shuffle, taking small steps. A person’s gait often reflects the characteristics of his character and may indicate timidity and shyness or aggressiveness and self-confidence.

The study of posture and gait is best done in such a way that the doctor can see the patient from different sides. The patient must quickly get up from the chair, walk slowly, then quickly, and turn around his axis several times. Must see:

The patient must stand up straight, put his feet together and keep his head straight; first the patient performs this task with his eyes open, then with his eyes closed, to find out whether he can maintain his balance (Romberg test). It is often advisable to pay attention to the patient's walking style from the very beginning, when he enters the office and does not suspect that his gait is being observed.

Ataxia with hemiparesis

A patient with unilateral hemiparesis with damage to the corticospinal tract usually develops characteristic gait changes. The severity of the disease in such patients depends on the degree of weakness and stiffness in the affected limbs. In a patient with severe hemiparesis, when standing and walking, there will be adduction in the shoulder, flexion in the elbow, wrist joints and fingers, and in the leg - extension in the hip, knee and ankle joints. Difficulty in flexing the hip joint and flexing the ankle joint backwards occurs. The paretic limb moves forward so that the foot barely touches the floor. The leg is held with difficulty and describes a semicircle, first away from the body, and then towards it, making a rotational movement. Often the movement of the leg causes a slight tilt of the upper half of the body in the opposite direction. Movement of the paretic arm during walking is usually limited. Loss of arm swing when walking may be an early sign of progression of hemiparesis. A patient with moderate hemiparesis experiences the same disorders, but they are less pronounced. In this case, a decrease in the amplitude of the arm swing during walking may be combined with a subtle arching movement of the leg, without significant rigidity or weakness in the affected limbs.

Ataxia with paraparesis

In diseases of the spinal cord that affect the motor pathways leading to the muscles of the lower extremities, characteristic gait changes occur due to a combination of spasticity and weakness in the legs. Walking requires a certain amount of tension and is carried out using slow, stiff movements in the hip and knee joints. The legs are usually tense, slightly bent at the hip and knee joints and abducted at the hip joint. In some patients, the legs may tangle at every step and resemble scissor movements. The stride is usually measured and short; the patient may sway from side to side, trying to compensate for stiffness in the legs. The legs make arched movements, the feet shuffle on the floor, and the soles of shoes in such patients are worn in socks.

Ataxia in parkinsonism (Parkinson's disease)

In Parkinson's disease, characteristic postures and gait develop. In severe condition, patients have a flexed posture, with a forward bend in the thoracic spine, a tilt of the head down, arms bent at the elbows and legs slightly bent at the hip and knee joints. The patient sits or stands motionless; poor facial expressions, rare blinking, and constant automatic movements in the limbs are noted. The patient rarely crosses his legs or otherwise adjusts his body position when sitting in a chair. Although the hands remain motionless, tremors of the fingers and wrist are often noted with a frequency of 4-5 contractions per 1 s. In some patients, the tremor spreads to the elbows and shoulders. In later stages, drooling and tremor of the lower jaw may be noted. The patient slowly begins to walk. While walking, the torso leans forward, the arms remain motionless or are even more bent and held slightly in front of the torso. There are no arm swings when walking. When moving forward, the legs remain bent at the hip, knee and ankle joints. It is characteristic that the steps become so short that the legs barely drag on the floor, the soles shuffle and touch the floor. If the forward movement continues, the steps become faster and faster and the patient may fall if there is no support (mincing gait). If the patient is pushed forward or backward, compensatory flexion and extension movements of the torso will not occur and the patient will be forced to take a series of propulsive or retropulsive steps.

People with Parkinson's have significant difficulty getting up from a chair or moving after being immobile. The patient begins walking with several small steps, then the length of the step increases. When trying to pass through a doorway or enter an elevator, the patient may involuntarily stop. At times they can walk quite quickly for short periods of time. Sometimes in emergency situations, such as a fire, patients who were previously immobilized can walk quickly or even run for a while.

Cerebellar lesions, cerebellar ataxia

Lesions of the cerebellum and its connections lead to significant difficulties when the patient stands and walks without assistance. The difficulties are compounded when trying to walk a narrow line. Patients usually stand with their legs spread wide apart; standing itself can cause staggering and large-scale movements of the body back and forth. Trying to place your feet together leads to staggering or falling. Instability persists with eyes open and closed. The patient walks carefully, taking steps of varying lengths and swaying from side to side; complains of poor balance, is afraid to walk without support and leans on objects, such as a bed or chair, carefully moving between them. Often, simply touching a wall or some object allows you to walk quite confidently. In mild gait disorders, difficulty occurs when trying to walk in a straight line. This leads to loss of stability; the patient is forced to make a sharp movement with one leg to the side to prevent falling. With unilateral lesions of the cerebellum, the patient falls in the direction of the lesion.

When the lesion is limited to the midline cerebellum (vermis), as in alcoholic cerebellar degeneration, changes in posture and gait may occur without other cerebellar disorders such as ataxia or nystagmus. In contrast, with damage to the cerebellar hemispheres, unilateral or bilateral, gait disturbances often occur in combination with ataxia and nystagmus. When one hemisphere of the cerebellum is affected, changes in gait are often accompanied by disturbances in postures and movements on the affected side. Typically, in a patient who is in a standing position, the shoulder on the affected side is lowered, which can lead to scoliosis. On the affected side, a decrease in the resistance of the limb in response to passive movements (hypotonia) is detected. When walking, the patient staggers and deviates in the direction of the lesion. This can be verified by asking the patient to walk around an object, such as a chair. Turning in the direction of the lesion will cause the patient to fall into a chair, and turning in the healthy direction will cause a spiral movement away from him. When performing coordination tests, clear ataxia is revealed in the upper and lower extremities on the affected side. For example, the patient cannot touch the tip of his own nose or the doctor’s finger with his finger, or run the heel of the affected leg along the shin of the opposite leg.

Sensitive ataxia

A characteristic change in gait develops with loss of sensation in the legs, resulting from damage to the peripheral nerves, dorsal roots, dorsal columns of the spinal cord, or the medial lemniscus. The greatest difficulties arise when the sense of passive movements in the joints is lost; a certain contribution is also made by the interruption of afferent signals from muscle spindle receptors, vibration and skin receptors. Patients with sensitive ataxia do not feel the position of their legs, and therefore experience difficulty both when standing and when walking; they usually stand with their legs spread wide apart; can maintain balance if asked to put their feet together and keep their eyes closed, but with their eyes closed they will sway and often fall (a positive Romberg sign). The Romberg test cannot be performed if the patient, even with his eyes open, is unable to put his legs together, as is often the case with lesions of the cerebellum.

Patients with sensitive ataxia spread their legs wide apart when walking, lift them higher than necessary, and impulsively sway back and forth. Steps vary in length, and the feet make characteristic clapping sounds when they touch the floor. The patient usually bends his torso somewhat at the hip joints and often uses a stick for support when walking. Visual defects aggravate gait disturbances. Often, patients lose stability and fall when washing, because by closing their eyes, they temporarily lose visual control.

Ataxia in cerebral palsy (spinocerebral)

This term refers to many different movement disorders, most of which arise as a result of hypoxia or ischemic damage to the central nervous system in the perinatal period. The severity of gait changes varies depending on the nature and severity of the lesion. Mild localized lesions may cause increased tendon reflexes and Babinski's sign with moderate equinovarus foot deformity without significant gait disturbance. More pronounced and extensive lesions usually lead to bilateral hemiparesis. There are changes in posture and gait characteristic of paraparesis; arms are abducted at the shoulders and bent at the elbows and wrists.

Cerebral palsy causes movement disorders in patients, which can lead to changes in gait. Athetosis often develops, characterized by slow or moderately fast serpentine movements in the arms and legs, varying postures from extreme flexion and supination to pronounced extension and pronation. When walking, such patients experience involuntary movements in the limbs, accompanied by rotational movements of the neck or grimaces on the face. The arms are usually bent and the legs are extended, but this asymmetry of the limbs can only appear when observing the patient. For example, one arm may be flexed and supinated while the other is extended and pronated. Asymmetrical position of the limbs usually occurs when the head turns to the sides. Typically, when you turn your chin to one side, the arm on that side extends and the opposite arm bends.

Ataxia with chorea

Patients with choreiform hyperkinesis often experience gait disturbances. Chorea most often occurs in children with Sydenham's disease, in adults with Huntington's disease, and in rare cases in patients with Parkinson's disease receiving excessive doses of dopamine antagonists. Choreiform hyperkinesis is manifested by rapid movements of the muscles of the face, trunk, neck and limbs. Flexion, extension and rotational movements of the neck occur, grimaces appear on the face, rotating movements of the torso and limbs, movements of the fingers become fast, as when playing the piano. Often with early chorea, flexion and extension movements appear in the hip joints, so that it seems that the patient is constantly crossing and straightening his legs. The patient may involuntarily frown, look angry, or smile. When walking, choreic hyperkinesis usually intensifies. Sudden jerking movements of the pelvis forward and to the sides and rapid movements of the torso and limbs lead to a dancing gait. Steps are usually uneven, and it is difficult for the patient to walk in a straight line. The speed of movement varies depending on the speed and amplitude of each step.

Dystonia

Dystonia is called involuntary changes in postures and movements that develop in children (deforming muscular dystonia, or torsion dystonia) and in adults (late dystonia). It can occur sporadically, be hereditary, or appear as part of another pathological process, such as Wilson's disease. With deforming muscular dystonia, which usually manifests itself in childhood, the first symptom is often a gait disturbance. A characteristic gait is with the foot slightly inverted, when the patient puts his weight on the outer edge of the foot. As the disease progresses, these difficulties are aggravated and posture disorders often develop: elevated position of one shoulder and hip, curvature of the torso and excessive flexion in the wrist joint and fingers. Intermittent muscle tension in the trunk and limbs makes walking difficult; in some cases, torticollis, pelvic curvature, lordosis and scoliosis may develop. In the most severe cases, the patient loses the ability to move. Tardive dystonia, as a rule, leads to a similar increase in movement disorders.

Muscular dystrophy

Severe weakness of the muscles of the trunk and proximal legs leads to characteristic changes in posture and gait. When trying to get up from a sitting position, the patient leans forward, bends his torso at the hip joints, puts his hands on his knees and pushes his torso up, resting his hands on his hips. In a standing position, a strong degree of lordosis of the lumbar spine and protrusion of the abdomen due to weakness of the abdominal and paravertebral muscles are noted. The patient walks with his legs wide apart, weakness of the gluteal muscles leads to the development of a “duck gait”. The shoulders are usually tilted forward, so that when walking you can see the movement of the wings of the scapula.

Frontal lobe lesion

Bilateral frontal lobe damage results in a characteristic gait change, often associated with dementia and frontal lobe relief symptoms such as grasping, sucking, and proboscis reflexes. The patient stands with his legs wide apart and takes the first step after a rather long preliminary delay. After these doubts, the patient walks with very small shuffling steps, then several steps of moderate amplitude, after which the patient freezes, unable to continue moving, then the cycle repeats. These patients usually do not exhibit muscle weakness, changes in tendon reflexes, tenderness, or Babinski signs. Usually the patient can perform the individual movements necessary for walking if he is asked to reproduce the walking movements in the supine position. Gait disturbance with damage to the frontal lobes is a type of apraxia, i.e., a disturbance in the performance of motor functions in the absence of weakness of the muscles involved in movement.

Aging of the body

With age, certain changes in gait develop and difficulty maintaining balance arises. In older people, the upper body leans slightly forward, the shoulders drop, the knees bend, the arm span when walking decreases, and the stride becomes shorter. Older women develop a waddling gait. Gait and stability problems predispose older adults to falls. About half of falls in older adults result from environmental factors, including poor lighting, steps, and uneven or slippery surfaces. Other causes of falling include fainting, orthostatic hypotension, turning the head, and dizziness.

1 comment on “Ataxia, balance and gait disorders”

My gait has changed, I read it on the Internet. looks like anatexia. How can I recover? Maybe there is some kind of gymnastics?

Parkinson's disease: causes, manifestations, stages, treatment

This disease was called shaking paralysis by James Parkinson, a doctor from London who, in addition to medicine, was actively involved in politics, geology, paleontology, chemistry and literature. Oddly enough, D. Parkinson did not study this pathological condition in a hospital or laboratory; he “recognized” it in old people with trembling hands and a shuffling gait in the park, in shops, on the street.

As is customary in medical circles, the disease was soon associated with the name of its author, and it began to be called Parkinson’s disease or simply parkinsonism, although “parkinsonism” is a broader concept that includes several forms, including shaking palsy (idiopathic syndrome parkinsonism).

Parkinson's disease has actually existed since time immemorial, its symptoms were noted by the Egyptian pharaohs long before the beginning of our era. Many famous figures of science and culture, statesmen and politicians, whose names are still widely known today, suffered from it. People of different nationalities, religions, occupations and professions: the legendary surrealist artist Salvador Dali, the leader of the Chinese Communist Party Mao Tse Tung, the writer Artoire Koestler, the mathematician Andrei Nikolaevich Kolmogorov, the poet Andrei Voznesensky, the actor Mikhail Ulyanov, the boxer Mohammed Ali, Pope John Paul II was united by one disease - parkinsonism. Often, Parkinson's disease influenced not only the personal life and career of a particular person, but also the history of an entire state, for example, it forced the resignation of the Spanish dictator Francisco Franco, who carefully monitored his health and intended to live 100 years.

Second after Alzheimer's disease

Idiopathic parkinsonism syndrome or Parkinson's disease is a degenerative disease of the brain, namely, damage to the structures of the extrapyramidal motor system, has a significant share (up to 80%) among all pathological conditions classified as parkinsonism syndrome. The disease has no geographical boundaries, is found in all corners of the globe and confidently holds 2nd place among neurodegenerative processes after the notorious Alzheimer's disease, which leads to complete loss of memory.

The first signs of shaking paralysis usually manifest themselves at the age of active mention of the word “pension”, that is, somewhere in the air. In rare cases, this “illness” can “happen” earlier – around 40 or even before 20 years of age (juvenile parkinsonism).

Parkinson's disease is a problem of old age, and if before the age of 60 it occurs with a frequency of 1 patient per 100 inhabitants of the planet approaching this age, then after the age of 60 one can already count 5 patients with this diagnosis among a hundred elderly people. Men are somewhat more “lucky” with regard to this pathology than women.

Study brought victory closer

Parkinson's disease was seriously studied in the 50s of the last century. Having studied the biochemical processes occurring in the brain of individuals with a characteristic clinical picture, scientists came to the conclusion that the cause of Parkinsonism syndrome is the death of neurons that are responsible for the production of a neurotransmitter called dopamine.

scheme: decreased dopamine transmission between affected neurons

Damaged neurons lose the ability to perform their tasks, resulting in a decrease in the synthesis of dopamine (dopamine) and the development of disease symptoms:

• Increased muscle tone (rigidity);
• Decreased motor activity (hypokinesia);
• Difficulty walking and maintaining balance;
• Trembling (tremor);
• Autonomic disorders and mental disorders.

The signs of Parkinson’s disease are very clearly visible not only to neurologists or doctors of other specializations; patients or their relatives are often the first to learn about changes in the head, because the difficulties in life that begin in connection with the onset of the disease are visible at every step: a person is deprived of the ability to make habitual movements (splashes, scatters, falls when walking...).

Nowadays, we have learned to treat Parkinson’s disease, but only to the point of alleviating symptoms, so defeating it still remains the cherished dream of modern neurologists. In any case, medical science has not taken upon itself the courage to announce to the whole world that someone has been completely cured. Or is this not Parkinson's disease?

Video: Parkinson's disease - medical animation

Why are neurons destroyed?

The causes of Parkinson's disease remain a mystery to this day, however, some factors, coming to the fore, still take on the leading function, and therefore are considered to be the culprits of this pathology. These include:

1. Aging of the body, when the number of neurons naturally decreases, and, therefore, the production of dopamine decreases;
2. Hereditary predisposition (the gene for the disease has not been identified, but the family pattern is indicated - 15% of patients have relatives suffering from parkinsonism);
3. Environmental factors: permanent residence in rural areas (treatment of plants with substances intended to destroy agricultural pests), near railways, highways (transportation of environmentally hazardous goods) and industrial enterprises (harmful production);
4. Poisoning with carbon monoxide and heavy metal salts;
5. Some medications used to treat various diseases and, as a side effect, have an effect on the extrapyramidal structures of the brain (aminazine, rauwolfia preparations);
6. Acute and chronic neuroinfections (for example, tick-borne encephalitis);
7. Vascular cerebral pathology;
8. Tumors and brain injuries.

At the same time, when considering the causes of Parkinson’s disease, it is worth noting an interesting fact that pleases smokers and coffee lovers. For those who smoke, the “chance” of getting sick is reduced by 3 times. It is said that tobacco smoke has such a “beneficial” effect because it contains substances resembling MAOIs (monoamine oxidase inhibitors), and nicotine stimulates the production of dopamine. As for caffeine, its positive effect lies in its ability to increase the production of dopamine and other neurotransmitters.

“Petitioner pose” and “doll walk”

Shaking paralysis, as mentioned above, has 4 leading (motor) symptoms, accompanied by disturbances in the functioning of the autonomic nervous system and mental activity, however, such laconic information will probably leave the reader with many questions, so it makes sense to describe the signs of the disease in more detail.

1: Increased muscle tone and movement disorders

Hypokinesia (or akinesia) is the main clinical syndrome characterizing movement disorders - patients can be recognized from afar:

• The patient’s posture is peculiar – the upper body is leaned forward, the joints of the arms and legs are bent, which creates the impression of a person asking (this symptom is called the “suppliant pose”);

A sick person's movements are constrained, he can freeze in one position for a long time before starting to move, however, pushing him, you can see that he is not able to stop on his own. Postural instability prevents the patient from overcoming both the inertia of rest and the inertia of movement, so his motor activity quickly becomes extremely limited;

Movement disorders in a patient are almost always noticeable to others. Increased muscle tone does not allow areas of the body to quickly return to their original position, since sharp passive flexion during parkinsonism does not imply a rapid reverse process; for some time the muscles will remain in the same position that they were given. For people who know nothing at all about Parkinson’s disease, these symptoms cause genuine surprise: he pushed a person - he ran, as if he was running down a mountain, but was unable to “slow down” himself, put his hand under the patient’s head to lift and remove the pillow - head remained in the same position...and many other examples. Surprising, but sad, or laughter through tears, especially if the illness has knocked down a loved one.

2: The most obvious sign of Parkinson's disease

Tremor is considered one of the most striking signs of the disease:

1. Rhythmic, regular, independent of a person’s will, trembling of the limbs, facial muscles, head, lower jaw (the tongue, by the way, too, it’s just not always visible), even at a respectful distance indicates Parkinson’s disease - just watch the patient for a couple of minutes;
2. Characteristic movements of the fingers, as if a person is counting out money or twisting straws, further strengthens the suspicion of parkinsonism;
3. Writing is hard for a person (how can you write with a trembling hand?). The patient's handwriting changes noticeably: the letters become small and trembling (micrography), the line is uneven, there is no deep meaning in the text - such people write only out of extreme necessity.

The trembling of various parts of the body, which is characteristic of Parkinson’s disease and independent of the will of the patient, is considered, perhaps, to be the most obvious signs of Parkinsonism, because it is impossible to hide it or control it somehow. In addition, excitement and nervous tension only intensify the tremor; it can disappear only during sleep.

3: Autonomic disorders and mental disorders

In a patient with Parkinson's disease, disorders of the autonomic nervous system are noticeable, leading to metabolic disorders, as a result of which the person either quickly loses weight (to the point of exhaustion), or, having spoiled it, gains excessive weight (obesity). Signs of autonomic disorders are: increased salivation, hyperhidrosis (excessive sweating), oily skin, development of symptoms of autonomic paroxysms.

As for mental suffering in Parkinsonism, the signs of disorders are quite diverse and often depend on the cause of the disease. However, recognizing a patient with parkinsonism is not so difficult, especially considering the presence of tremors, muscle rigidity and postural instability. The following symptoms may indicate “disorders in the head”:

• Disappearance of initiative, interest in the world around us, narrowing of horizons, apathy, lack of vivid emotions, slowness of mental activity, lethargy.
• Communication with patients causes difficulties, they become intrusive, sticky, self-centered, they need to repeat and explain the same concepts many times so that they again begin to ask the same questions with which the conversation began (and so on in a circle...);
• Switching from one type of activity to another (or changing the topic of conversation) does not evoke much enthusiasm on the part of the patient, and therefore is difficult;
• Sick people suffering from this pathology often have problems sleeping, become fearful, confused, and have difficulty oriented in space and time.

Mental problems are somewhat reminiscent of those with senile dementia of the Alzheimer's type, however, the lesions from Parkinsonism are not so deep, intellectual abilities suffer to a much lesser extent, although it cannot be said that the patient is “of sound mind and solid memory.” In addition, the stiffness and stiffness characteristic of shaking palsy are mild in Alzheimer's disease, and trembling is most often absent altogether.

Video: early signs of Parkinson’s disease, “Live Healthy” program

Forms and stages

Parkinson's disease, being a representative of a large group of degenerative diseases of the extrapyramidal motor system, itself has several varieties. There are:

• Rigid-bradykinetic variant, which is most characterized by an increase in muscle tone and impaired motor activity. While they are walking, such patients can be easily recognized by their “petitioner pose,” but they quickly lose the ability to move actively, stop standing and sitting down, and instead become disabled and remain immobilized for the rest of their lives;
• Trembling-rigid form, the main signs of which are trembling and stiffness of movements;
• Trembling form. Its leading symptom is, of course, tremor. Rigidity is slightly expressed, motor activity is not particularly affected.

Parkinson's disease has the unfortunate tendency to progress steadily. There is a chance of reversing it only in people who received it as a result of taking medications, which caused the development of pathological changes (withdrawal of the drug leads to an improvement in the condition).

The progression of the process goes through several stages. Excluding the zero phase, where there are no signs of the disease yet, we will present to the reader five stages:

1. At the first stage, signs of the disease are noted on one limb (with transition to the torso);
2. The second stage is characterized by the manifestation of postural instability on both sides;
3. At the third stage, postural instability progresses, but the patient, although with difficulty, still overcomes the inertia of movement when he is pushed, and is able to serve himself;
4. Although the patient can still stand or walk, he begins to greatly need outside help;
5. Complete immobility. Disability. Constant outside care.

Ability to work and assignment of a disability group depend on how severe the movement disorders are, as well as on the patient’s professional activity (mental or physical work, does the work require precise movements or not?). Meanwhile, with all the efforts of doctors and the patient, disability does not pass by, the only difference is in the timing of its onset. Treatment started at an early stage can reduce the severity of clinical manifestations, but one should not think that the patient has been cured - the pathological process has simply slowed down for some time.

When a person is practically bedridden, therapeutic measures, even the most intensive ones, do not give the desired effect. The famous levodopa is not particularly encouraging in terms of improving the condition; it only slows down the progression of the disease for a short time, and then everything returns to normal. It will not be possible to contain the disease for a long time at the stage of pronounced symptoms; the patient will no longer leave the bed and will not learn to take care of himself, therefore, he will need constant outside help for the rest of his days.

Diagnostics

As a rule, a diagnostic search does not create any special problems for the doctor. It is based mainly on the patient’s complaints and clinical manifestations of the disease (rest tremor, muscle rigidity, postural instability).

The patient undergoes traditional tests (general blood and urine tests, biochemistry), in some cases (the appearance of symptoms of parkinsonism after a traumatic brain injury) there is a need for a lumbar (spinal) puncture. In addition, for the purpose of differential diagnosis, the patient is sometimes prescribed electromyography (EMG) and electroencephalography (EEG).

Shaking paralysis is differentiated from parkinsonism syndrome and other pathologies with similar clinical signs (hydrocephalus, brain tumor, cerebellar damage, etc.), since their symptoms are very similar to Parkinson’s disease.

Parkinson's Treatment - Medicines to Control Symptoms

Parkinson's disease is incurable; folk remedies cannot cure it, but medications designed to replace the missing dopamine are still able, in some cases, to slow down the progression or at least alleviate the symptoms of the disease. Currently, conservative and surgical methods are used to treat parkinsonism. Long-term complex conservative therapy includes, first of all, drugs that can increase the content of dopamine in the brain.

Dopaminergic drugs. At the initial stage of the disease, when clinical manifestations are still absent or barely noticeable, patients are prescribed a drug that is simultaneously classified as both dopaminergic and antiviral drugs (indirect dopaminomimetic). This is midantan or amantadine.

The progression of the process and the severity of symptoms require more effective treatment that can compensate for the lack of dopamine. Due to the fact that dopamine itself, which is sorely lacking in Parkinson's disease, has difficulty crossing the blood-brain barrier, there is no point in administering it. This task is currently assigned to its predecessor, which is dioxyphenylalanine (dopa, dopa). A synthetic analogue of dioxyphenylalanine, the levorotatory isomer of levodopa (L-dopa), has become the main drug affecting the course of parkinsonism. This drug slows the progression of the disease, reduces the severity of rigidity and hypokinesia, but, like other pharmaceuticals, it produces side effects such as nausea, vomiting, loss of appetite, development of arrhythmias, psychosis, decreased blood pressure, etc. In this regard, the use of levodopa is tried to prevent postpone the initial stages, replacing it, for example, with the indirect dopaminomimetic midantan.

Dopamine agonists (bromocriptine, ropinirole). These drugs imitate the effect of a deficient substance (dopamine), but have side effects such as drowsiness, dizziness, swelling, hallucinations, and indigestion.

MAOIs (monoamine oxidase inhibitors), type B (segiline, Azilect), ICOMT - catecholamine-O-methyltransferase inhibitors (tolcapone, entacapone). These drugs provide an effect similar to L-dopa, but in terms of severity of action they are noticeably inferior to the synthetic levorotatory isomer. Meanwhile, when used together with levodopa, MAOIs and ICOMT enhance the effect of L-dopa and make it possible to reduce its dosage.

Central anticholinergic blockers (synthetic anticholinergic drugs) - cyclodol, tropacin, procyclidine. Anticholinergic drugs block M- and N-cholinergic receptors, relax muscles and thereby help reduce the severity of symptoms of Parkinson's disease.

The variety of drugs used for parkinsonism, of course, is not limited to the listed groups, but, unfortunately, specific and nonspecific drugs for the treatment of shaking paralysis are not able to provide a sufficient therapeutic effect. In addition, one cannot ignore the side effects caused by their use, as well as individual intolerance and rapid addiction to these drugs. What is new in the treatment of Parkinson's disease is, most likely, surgical methods of influencing this pathology.

Successes of surgical treatment

The successes of conservative treatment methods are undoubtedly significant and obvious, but their possibilities, as practice shows, are not limitless. The need to find something new in the treatment of Parkinson's disease has forced not only neurologists, but also surgical doctors to think about this issue. The results achieved, although they cannot be considered final, are already beginning to be encouraging and pleasing.

Currently, destructive operations are already well mastered. These include interventions such as thalamotomy, which is effective in cases where tremor is the main symptom, and pallidotomy, the main indication for which is movement disorders. Unfortunately, the presence of contraindications and a high risk of complications does not allow these operations to be widely used.

The introduction of radiosurgical treatment methods into practice led to a breakthrough in the fight against parkinsonism.

a neurostimulator for the brain resembles a pacemaker

Neurostimulation, which is a minimally invasive surgical procedure - the implantation of a stimulator (neurostimulator), similar to an artificial pacemaker (heart pacemaker, but only for the brain), which is so familiar to some patients, is carried out under the control of MRI (magnetic resonance imaging). Electric current stimulation of the deep brain structures responsible for motor activity gives hope and reason to expect the effectiveness of such treatment. However, it also identified its “pros” and “cons.”

The advantages of neurostimulation include:

• Safety;
• Quite high efficiency;
• Reversibility (as opposed to destructive operations, which are irreversible);
• Well tolerated by patients.

The disadvantages include:

• Large material costs for the patient’s family (not everyone can afford the operation);
• Failure of electrodes, replacement of the generator after several years of operation;
• Risk of infection (small - up to 5%)

What is new in the treatment of Parkinson's disease is the transplantation of neurons into the brain that can replace destroyed cells that previously produced dopamine (neurons for transplantation are obtained after differentiation of stem cells).

It is too early to talk about the success of such treatment methods as the introduction of genetic vectors, melting the markers of Parkinson’s disease - Lewy bodies, research is ongoing, so let’s wait, perhaps in the coming years humanity will learn to completely control this hitherto invincible disease.

Prevention and folk remedies

What does it mean to prevent Parkinson's disease? After all, no one will take medication in advance, and besides, it will not give anything. It is difficult to predict traumatic brain injuries, neuroinfections or intoxications, and even arguing with genetics is difficult, if not useless. One can, of course, advise to beware of such situations, but a person rarely creates them intentionally, so prevention may include preventing the rapid development of the disease to the stage of severe symptoms. Having set such a goal, the patient takes all the medications prescribed to him, engages in physical therapy, periodically (courses) visits the physiotherapy room, and also treats concomitant pathologies.

As for prevention using folk remedies, it is unlikely that there will be a “home remedy” that will harmlessly increase the dopamine content in the brain for the body. For example, it is advised to drink a lot of coffee, which promotes the production of dopamine. But at the same time, this drink increases blood pressure and makes the heart work harder. Does this suit everyone?

In the 19th century, belladonna was used to treat parkinsonism; in general, it is still not excluded from the list of drugs affecting shaking paralysis, but it is already used in the form of drugs (atropine). It is not recommended to use belladonna or belladonna vulgaris, collected in places where it grows, on its own. Exactly like hemlock, fly agaric, aconite. Extreme caution must be exercised with these medicines (or better not to “get involved” at all), so we will not take the liberty of describing the technology for its preparation.

In mild cases (at stages 1-2), they say, a decoction of oats helps (1 glass of grains + 3 liters of water, boil over low heat for an hour). It is recommended to drink the prepared decoction (all 3 liters) 2 days in advance - instead of water.

Some people praise freshly squeezed cherry or spinach juice. It is taken, if the stomach allows, a third of a glass 2-3 times a day.

Physical therapy, evening foot baths, physiotherapeutic procedures and medications prescribed by the doctor help combat Parkinson's disease at home in the early stages. Folk remedies will be effective if used wisely, in accordance with other doctor’s instructions.

The gait seen in parkinsonism is called

In most people with Parkinson's disease, walking can be improved by using visual cues (such as wide, contrasting stripes on the floor) or auditory cues (rhythmic commands or the sound of a metronome). At the same time, there is a significant increase in step length (sometimes by more than 100%) as it approaches normal values, but walking speed increases only by 10-30%, which is explained by a decrease in step frequency and reflects defective motor programming and de-automation of movements.

Improvement in gait by external stimuli may depend on additional involvement of the cerebellar pathways and premotor cortex compensating for dysfunction of the basal ganglia and associated supplementary motor cortex. Moreover, according to J.P.Azulay et al. (1999), improvement in walking parameters is provided not by static visual perception of drawn stripes, but by dynamic visual afferentation due to their displacement in the visual field.

Taking neuropsychological tests while walking, especially at a late stage of the disease, impairs it to a much greater extent than normal - this indicates not only a certain deficit in cognitive functions, but also that they are involved in compensation for the statolocomotor defect (in addition, this reflects a general pattern characteristic of Parkinson’s disease - of two simultaneously implemented actions, the more automated one is performed worse).

Under the influence of levodopa, step length or walking speed may increase. But in general, walking disorders, especially those dependent on postural instability, are more resistant to levodopa than hypokinesia and rigidity, since they are more dependent on nondopaminergic mechanisms. In some cases, under the influence of levodopa drugs, the amplitude of postural reactions increases, but more often, taking levodopa does not have a significant effect on them.

In recent years, it has been demonstrated that it is possible to reduce the severity of gait disturbances in Parkinson's disease using stereotactic operations, in particular pallidotomy and stimulation of the subthalamic nucleus. Stimulation of the globus pallidus outer segment has also been shown to improve walking, whereas stimulation of the globus pallidus internal segment (usually improving other features of parkinsonism) may impair walking.

In multisystem atrophy, corticobasal degeneration and diffuse Lewy body disease, as well as in the late stage of Parkinson's disease (possibly as cholinergic neurons in the pedunculopontine nucleus degenerate), gait disturbances associated with Parkinsonism syndrome are often complemented by signs of frontal (subcortical-frontal) dysbasia, and with progressive supranuclear palsy - subcortical astasia.

Walking impairment due to dystonia

Dystonic gait is especially often detected in patients with idiopathic generalized torsion dystonia. A characteristic feature of dystonia is increased hyperkinesis when walking. The first symptom of generalized dystonia is usually foot dystonia, characterized by plantar flexion, plantar flexion, and tonic extension of the big toe that occur when walking. Subsequently, hyperkinesis covers the entire leg and gradually generalizes.

Cases of segmental dystonia have been described, predominantly involving the muscles of the trunk and proximal limbs, which is manifested by a sharp forward bending of the trunk (dystonic camptocormia) and is also induced by walking.

When using corrective gestures, as well as when running, swimming, walking backwards or other unusual walking conditions, dystonic hyperkinesis may decrease.

The selection and initiation of postural and locomotor synergies in patients with dystonia are preserved, but, as in parkinsonism, their implementation may be defective due to impaired selectivity of movement and additional involvement of unnecessary muscles.

It should be noted the amazing ability of some patients with generalized dystonia to adapt: ​​thanks to complex balancing, they can maintain the skill of movement, overcoming pretentious deforming pathological postures.

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