Symptoms of walking disorders

Disturbance of walking with dysfunction of afferent systems

Disorders of walking can be caused by a disorder of deep sensitivity (sensory ataxia), vestibular disorders (vestibular ataxia), and visual impairment.

• Sensitive ataxia is caused by the lack of information about the position of the body in space and the features of the plane through which the person walks. This variant of ataxia can be associated with polyneuropathies that cause a diffuse lesion of peripheral nerve fibers bearing a proprioceptive afferentation to the spinal cord or back columns of the spinal cord in which the fibers of deep sensitivity go back to the brain. A patient with a sensitive ataxia is cautious, slowly, with several legs apart, trying to control each step with his eyesight, raises his legs high and, feeling under the feet of a "cotton pad", forces his foot down all the way to the floor ("stamping gait"). Distinctive characteristics of a sensitive ataxia include deterioration of walking in the dark, detection of violations of deep sensitivity during examination, strengthening of shakiness in Romberg's posture when closing eyes.
• Vestibular ataxia usually accompanies the defeat of the vestibular apparatus of the inner ear or vestibular nerve (peripheral vestibulopathy), less often - of the stem vestibular structures. It is usually accompanied by systemic dizziness, lightheadedness, nausea or vomiting, nystagmus, a decrease in hearing and noise in the ears. The severity of ataxia increases with a change in the position of the head and trunk, eye movements. Patients avoid sudden movements of the head and carefully change the position of the body. In a number of cases, there is a tendency to fall in the direction of the affected labyrinth.
• Disorder of walking with visual impairment (visual ataxia) is not specific. The walk in this case can be called cautious, insecure.
• Sometimes the lesions of different senses are combined, and if the disorder of each of them is too small to cause significant disturbances in walking, then, combining with each other and sometimes with musculoskeletal disorders, they can cause combined walking disorder (multisensory insufficiency).

Disturbance of walking in motor disorders

Disturbances of walking can accompany motor disorders that occur in diseases of muscles, peripheral nerves, spinal roots, pyramidal tracts, cerebellum, basal ganglia. Immediate causes of walking disorders may be muscle weakness (for example, in myopathies), flaccid paralysis (with polyneuropathies, radiculopathies, spinal cord injuries), rigidity due to pathological activity of peripheral motor neurons (with non-myomotonia, rigid body syndrome, etc.), pyramidal syndrome (spastic paralyzes), cerebellar ataxia, hypokinesia and rigidity (for parkinsonism), extrapyramidal hyperkinesis.

Disturbances of walking with muscle weakness and flaccid paralysis

Primary muscle lesions usually cause symmetrical weakness in the proximal parts of the limbs, with the gait becoming overturned ("duck"), which is directly related to the weakness of the gluteus muscles, unable to fix the pelvis when moving the opposite leg forward. For the defeat of the peripheral nervous system (for example, with polyneuropathy), the paresis of the distal parts of the extremities is more characteristic, as a result of which the feet hang down and the patient is forced to lift them high so as not to catch on the floor. When the foot is lowered, the foot splashes against the floor (steppe, or "cock" gait). With the defeat of the lumbar spinal cord thickening, upper lumbar spines, lumbar plexus and some nerves, weakness in the proximal part of the limbs is also possible, which will also be manifested by the transient gait.

Disabilities of walking with spastic paralysis

The gait in spastic paresis (spasmodic gait) caused by the defeat of pyramidal tracts at the level of the brain or spinal cord is explained by the predominance of the tone of the extensor muscles, as a result of which the leg is bent at the knee and ankle joints and therefore elongated. In case of hemiparesis, because of the extensor set-up of the leg, the patient is forced to move his foot forward in order to make a swing motion in the form of a semicircle, while the body tilts slightly in the opposite direction (Wernicke-Mann's walk). With the lower spastic parapareza, the patient walks slowly, on toes, crossing the legs (due to an increase in the tone of the adductor hip muscles). He has to swing himself to do one step after another. The gait becomes strained, slow. The violation of gait in spastic paralysis depends both on the severity of the paresis, and on the degree of spasticity. One of the common causes of spastic gait in the elderly is spondylogenous cervical myelopathy. In addition, it is possible with strokes, tumors, craniocerebral trauma, infantile cerebral paralysis, demyelinating diseases, hereditary spastic paraparesis, funicular myelosis.

Disorders of walking with parkinsonism

Disorders of walking in Parkinsonism are mainly associated with hypokinesia and postural instability. Parkinsonism is particularly characterized by difficulty in initiating walking, reducing its speed, reducing the length of the step (microbasia). Reducing the step height leads to shuffling. The foot area often remains normal when walking, but sometimes it decreases or slightly increases. In Parkinson's disease, due to the predominance of the tone in the pro- gravitational (flexor) muscles, a characteristic "supplicant's posture" is formed, characterized by the inclination of the head and trunk forward, slight bending in the knee and hip joints, and the bringing of hands and thighs. Hands are pressed to the trunk and do not participate in walking (aheyrokinesis).

In the expanded stage of Parkinson's disease, the phenomenon of congestion is often noted - a sudden short-term (most often from 1 to 10 s) blockade of the movement. Freezing can be absolute or relative. Absolute freezing is characterized by the cessation of movement of the lower extremities (the feet "stick to the floor"), as a result, the patient can not move. Relative congealing is characterized by a sudden shortening of the length of the step with the transition to a very short, shuffling step or trampling movements of the feet in place. If the torso continues to move forward by inertia, there is a threat of falling. Freezing occurs most often at the time of switching from one walking program to another: at the beginning of the walk ("start delay"), when cornering, overcoming an obstacle, for example, a threshold, passing through a door or narrow aperture, in front of the elevator door, upon entering the escalator, sudden shouting, etc. Most of the congestion develops against the background of a weakening effect of levodopa preparations (in the "turn-off" period), but eventually they begin to appear in some patients during the "on" period, sometimes increasing under the influence of an excessive dose of levodopa. Patients are able to overcome the congealing, crossing an obstacle, having made an unusual movement (for example, dancing), or simply taking a step to the side. Nevertheless, many patients with freezing appear fear of falls, which makes them sharply limit their daily activities.

At a late stage of Parkinson's disease, another variant of episodic walking disorder may develop - seizure walking. In this case, the ability to hold the center of gravity of the body within the area of the support is impaired, as a result the trunk is displaced forward, and in order to maintain balance and avoid falling, patients, trying to "catch up" the center of gravity of the body, are forced to accelerate (propulsion) and can involuntarily move to a fast short running step. Propensity to freezing, seeding walking, propulsions, falls correlates with increased variability in the length of the step and the severity of cognitive impairment, especially the frontal type.

Performing cognitive tasks and even just talking while walking (double task), especially at a late stage of the disease in patients with cognitive impairments, leads to a stoppage of motion - this indicates not only a certain deficiency of cognitive functions, but also that they are involved in Compensation of the stator-motor defect (in addition, this reflects the general pattern inherent in Parkinson's disease: from the two simultaneously implemented actions, the more automated one is performed worse). Stopping walking while trying to perform a second action predicts an increased risk of falls.

In most patients with Parkinson's disease, walking can be improved with visual landmarks (for example, cross-strips painted on the floor) or auditory signals (rhythmic commands or the sound of a metronome). At the same time, a significant increase in the length of the step is noted with its approach to normal parameters, but the walking speed increases only by 10-30%, mainly due to the reduction in the frequency of steps, which reflects the defectiveness of motor programming. Improving walking with external stimuli may depend on the activation of systems involving the cerebellum and premotor cortex and compensating for the dysfunction of the basal ganglia and the associated accessory motor cortex.

In multi-systemic degenerations (multisystem atrophy, progressive supranuclear paralysis, corticobasal degeneration, etc.), severe walking discomfort with congealing and falling occurs at an earlier stage than in Parkinson's disease. In these diseases, as well as in the late stage of Parkinson's disease (possibly as degeneration of the cholinergic neurons in the pedunculopontine nucleus), walking disorders associated with parkinsonism syndrome are often supplemented with signs of frontal dysbasia, and with progressing supranuclear paralysis, subcortical astasia.

Disturbances of walking with muscular dystonia

Dystonic gait is especially often observed in patients with idiopathic generalized dystonia. The first symptom of generalized dystonia, as a rule, is the dystonia of the foot, characterized by plantar flexion, podvorachivaniem foot and tonic extension of the thumb, which arise and intensify when walking. Subsequently, hyperkinesis gradually generalizes, extending to axial muscles and upper limbs. The cases of segmental dystonia, mainly involving muscles of the trunk and proximal parts of the extremities, are described, which is manifested by a sharp torso inclination forward (dystonic camptocormia). When using corrective gestures, as well as running, swimming, walking backwards or other unusual walking conditions, dystonic hyperkinesis may decrease. The choice and initiation of postural and locomotor synergies in patients with dystonia are preserved, but their realization is defective due to a violation of selectivity of muscle involvement.

Disorders of walking with trochee

At chorea, normal movements are often interrupted by a stream of rapid chaotic twitchings involving the trunk and limbs. During walking, the legs may suddenly bend at the knees or climb up. Attempt of the patient to give to the chorean twitching the appearance of arbitrary expedient movements leads to a fanciful, "dancing" gait. Trying to keep the balance, the patients sometimes walk more slowly, widely spreading their legs. The choice and initiation of postural and locomotor synergies in most patients are preserved, but their implementation is difficult due to superposition of involuntary movements. In Huntington's disease, in addition, identify the components of parkinsonism and frontal dysfunction, leading to a violation of postural synergy, reducing the length of the step, walking speed, discoordination.

Disturbances of walking in other hyperkinesis

With active myoclonia, balance and walking are severely disturbed due to massive twitchings or short-term muscle tone turn-offs that occur when trying to rest on your legs. In orthostatic tremor in the vertical position, high-frequency oscillations in the muscles of the trunk and lower extremities are noted, which disturb the maintenance of equilibrium, but disappear when walking, however, the initiation of walking can be difficult. Approximately one third of patients with essential tremor exhibit instability in tandem walking, which limits daily activity and can reflect cerebellar dysfunction. Bizarre changes in walking are described with late dyskinesia, which complicates the administration of neuroleptics.

Disorders of walking in cerebellar ataxia

A characteristic feature of cerebellar ataxia is an increase in the area of support both during standing and walking. Often observed swings in the lateral and anteroposterior directions. In severe cases, when walking, and often at rest, rhythmic fluctuations of the head and trunk (tituration) are observed. Steps are uneven both in length and in direction, but on average the length and frequency of steps decrease. Elimination of eye control (closing eyes) has little effect on the severity of the coordination disorders. Postural synergies have a normal latent period and a temporal organization, but their amplitude is excessive, so patients may fall in the direction opposite to where they originally deviated. An easy cerebellar ataxia can be identified by tandem walking. Disorders of walking and postural synergy are most pronounced when the median structures of the cerebellum are affected, while discoordination in the extremities can be expressed minimally.

The cause of cerebellar ataxia can be cerebellar degenerations, tumors, paraneoplastic syndrome, hypothyroidism, etc.

Spasticity in the legs and cerebellar ataxia can be combined (spastico-atactic gait), which is often observed with multiple sclerosis or craniovertebral anomalies.

Integrative (primary) disorders of walking

Integrative (primary) walking disorders (violations of higher level walking) most often occur in old age and are not associated with other motor or sensory disorders. They can be caused by the defeat of various parts of the cortical-subcortical motor cycle (frontal cortex, basal ganglia, thalamus), fronto-cerebellar connections, as well as the functionally conjugated stem-spinal systems and limbic structures. The defeat of different parts of these circles in some cases can lead to a predominance of imbalance with the absence or inadequacy of postural synergy, in other cases to the predominance of disorders of initiation and maintenance of walking. However, most often observed a combination of both types of disorders in different ratios. In connection with this, the isolation of individual syndromes within the framework of violations of higher level walking is conditional, since the boundaries between them are not clear enough, and as one of the syndromes progresses, one of the syndromes may pass into another. Moreover, in many diseases, higher level walking disorders are layered into lower and middle-level syndromes, which greatly complicates the overall picture of motor disorders. Nevertheless, such isolation of individual syndromes is justified from a practical point of view, since it allows one to emphasize the leading mechanism of walking disorders.

Integrative disorders of walking are much more variable and dependent on the situation, surface properties, emotional and cognitive factors, than violations of the lower and middle level. They are less amenable to correction due to compensatory mechanisms, the inadequacy of which is precisely their characteristic feature. Diseases manifested by integrative disorders of walking

Group of diseases	Nosology
Vascular lesions of the brain	Ischemic and hemorrhagic strokes with lesions of frontal lobes, basal ganglia, midbrain or their connections. Dyscirculatory encephalopathy (diffuse ischemic white matter, lacunar status)
Neurodegenerative diseases	Progressive supranuclear palsy, multisystem atrophy, cortis-cobasal degeneration, dementia with Levy bodies, Parkinson's disease (late stage), fronto-temporal dementias, Alzheimer's disease, juvenile form of Huntington's disease, hepatolenticular degeneration. Idiopathic dysbasia
Infectious diseases of the central nervous system	Creutzfeldt-Jakob disease, neurosyphilis, HIV-encephalopathy
Other diseases	Normotensive hydrocephalus. Hypoxic encephalopathy. Tumors of the frontal and deep localization

Cases of high-level walking disorders in the past have been repeatedly described under various names - "apraxia walk", "astasia-abasia", "frontal ataxia", "magnetic gait," "parkinsonism of the lower half of the body," etc. JG Nutt et al. (1993) identified 5 major syndromes of high level walking disorders: cautious gait, frontal disability of walking, frontal imbalance, subcortical imbalance, isolated violation of initiation of walking. There are 4 variants of integrative walking disorders.

• Senile dysbasia (corresponds to the "careful walk" according to the classification of JG Nutt et al.).
• Subcortical astasia (corresponds to "subcortical imbalance"),
• Frontal (subcortical-frontal) dysbasia (corresponds to "isolated violation of the initiation of walking" and "frontal disruption of walking"),
• Frontal astasia (corresponds to "frontal imbalance").

Senile dysbasia

Senile dysbasia is the most common type of gait disorder in old age. It is characterized by a shortening and slowing of the step, uncertainty during bends, some increase in the area of the support, slight or moderate postural instability, which is clearly manifested only when bending, pushing the patient or standing on one leg, and limiting sensory afferentation (for example, closing eyes). When cornering, the natural sequence of movements is violated, as a result of which they can be committed by the whole body (en block). Legs when walking are somewhat bent in the hip and knee joints, the body tilted forward, which increases stability.

In general, senile dysbasia should be considered as an adequate response to the estimated or actual risk of falling. So, for example, there is a healthy person on a slippery road or in absolute darkness, afraid to slip and lose balance. In the elderly, dysbasia occurs as a reaction to the age-related decline in the ability to maintain equilibrium or to adapt synergies to surface features. The main postural and locomotor synergies remain intact, but due to the limitation of physical capabilities they are not used as effectively as before. As a compensatory phenomenon, a similar type of walking disorder can be observed in a variety of diseases that limit the mobility or increase the risk of falls: joint damage, severe heart failure, discirculatory encephalopathy, degenerative dementia, vestibular or multisensory deficiency, and obsessive fear of losing balance (astazobasophobia). When a neurologic examination of the focal symptomatology is not detected in most cases. Since senile dysbasia is often observed in healthy elderly people, it can be recognized as an age norm if it does not lead to a restriction of the patient's daily activity or falls. At the same time, it should be borne in mind that the degree of restriction of daily activity often depends not so much on a real neurological defect as on the degree of fear of falling.

Given the compensatory nature of senile dysbasia, the attribution of this type of change in walking to the highest level, for which the limitation of adaptation possibilities is typical, is conditional. Senile dysbasia reflects an increase in the role of conscious control and higher brain functions, in particular attention, in the regulation of walking. With the development of dementia and the weakening of attention, a further slowing of the gait and impaired stability may occur, even in the absence of primary motor and sensory impairments. Senile dysbasia is possible not only in old age, but also in younger people, many authors believe that it is preferable to use the term "careful walking".

Subcortical astasia

Subcortical astasia is characterized by a rough disorder of postural synergy caused by damage to the basal ganglia, midbrain or thalamus. Due to inadequate postural synergies, walking and standing are difficult or impossible. When you try to get up, the center of gravity is not shifted to the new center of support, instead the trunk is deflected backwards, which results in a fall on the back. When you remove from equilibrium without support, the patient falls like a saw-tree. At the heart of the syndrome may be a violation of the orientation of the trunk in space, because of which postural reflexes do not turn on in time. Initiation of walking in patients is not difficult. Even if severe postural instability makes independent walking impossible, with the support of the patient it is able to step over and even walk, while the direction and rhythm of the steps remain normal, which indicates the relative safety of locomotor synergy. When the patient lies or sits and the requirements for postural control are less, he can perform normal limb movements.

Subcortical astasia occurs sharply with single or bilateral ischemic or hemorrhagic lesions of the outer parts of the middle brain and upper bridge, the upper part of the posterolateral nucleus of the thalamus and the adjacent white matter, basal ganglia, including the pale sphere and the shell. In the unilateral defeat of the thalamus or basal ganglia, when trying to stand up, and sometimes in the sitting position, the patient may deviate and fall to the contralateral side or back. With unilateral lesion, the symptomatology usually regresses within a few weeks, but with bilateral damage it is more resistant. Gradual development of the syndrome is observed with progressive supranuclear palsy, diffuse ischemic involvement of the white matter of the hemispheres, normotensive hydrocephalus.

Frontal (frontal-subcortical) dysbasia

Primary disorders of walking with lesions of subcortical structures (subcortical dysbasia) and frontal lobes (frontal dysbasia) are clinically and pathogenetically close. In fact, they can be considered as a single syndrome. This is explained by the fact that frontal lobes, basal ganglia, and certain structures of the midbrain form a single contour of regulation, and similar disorders can arise when they are damaged or separated (due to the involvement of the pathways connecting them in the white matter of the hemispheres). Phenomenologically, the subcortical and frontal dysbasia are manifold, which is explained by the involvement of different subsystems that provide various aspects of walking and maintaining equilibrium. In connection with this, several basic clinical variants of dysbasia can be distinguished.

The first variant is characterized by the predominance of a violation of initiation and maintenance of the locomotion act in the absence of pronounced postural disorders. When you try to start walking, the patient's legs "grow" to the floor. In order to take the first step, they are forced to shift from foot to foot for a long time or to "swing" the trunk and legs. Synergies, which normally provide propulsion and movement of the center of gravity of the body to one leg (in order to free the other for swing), often prove ineffective. After the initial difficulties are overcome and the patient still moves, he makes a few small test shuffling steps or stumbles in place, but gradually his steps become more confident and long, and the feet are more and more easily separated from the floor. However, when turning, overcoming an obstacle, passing through a narrow aperture, requiring the switching of the motor program, again there may be relative (trampling) or absolute hardening, when the feet suddenly "grow" to the floor. As with Parkinson's disease, congestion can be overcome by stepping over a crutch or a stick, making a detour (for example, by moving to the side) or by using rhythmic commands, counting out loud or rhythmic music (for example, marching).

The second variant of the frontal-subcortical dysbasia corresponds to the classical description of marshe a petit pas and is characterized by a short shuffling step that remains constant throughout the entire walking period, and, as a rule, there is no pronounced starting delay and a tendency to congeal.

Both variants described can, as the disease progresses, transform into the third, most complete and unfolded version of frontal-subcortical dysbasia, in which a combination of a violation of the initiation of walking and congestion with more pronounced and persistent changes in the pattern of walking, moderate or pronounced postural instability is observed. Often, the asymmetry of walking is noted: the patient makes a step with the leading leg, and then pulls the second leg to it, sometimes in several ways, while the leading leg can change, and the length of the steps can be quite variable. When cornering and overcoming obstacles, walking difficulties increase dramatically, so that the patient can begin to trample or freeze again. The supporting leg can remain in place, and the other can make a series of small steps.

Characterized by increased variability in the parameters of the step, the loss of the ability to arbitrarily regulate the speed of walking, the length of the step, the height of raising the legs, depending on the nature of the surface or other circumstances. Fear of falls, which occurs in the majority of such patients, aggravates the limitation of mobility. At the same time, in a sitting or lying position, such patients are able to imitate walking. Other motor disturbances may be absent, but in some cases of subcortical dysbasia, bradykinesia, dysarthria, regulatory cognitive impairment, affective disorders (emotional lability, dullness of affect, depression) are observed. With frontal disbasion, in addition, often develop dementia, rapid urination or urinary incontinence, pronounced pseudobulbar syndrome, frontal signs (paratonia, grasping reflex), pyramidal signs.

Gait with frontal and subcortical dysbasia is very similar to Parkinson's. At the same time, there are no manifestations of parkinsonism in the upper part of the body (mimicry remains alive, only sometimes it is weakened by the concomitant supranuclear insufficiency of the facial nerves, the movements of the hands during walking not only do not decrease, but sometimes even become more vigorous, because with their help the patient tries to balance the body with respect to its center of gravity or to move the legs "attached" to the floor), so this syndrome is called "lower body parksonism." Nevertheless, this is not true, but pseudoparkinsonism, since it arises in the absence of its main symptoms - hypokinesia, rigidity, restless tremor. Despite a significant decrease in the length of the step, the area of the support for dysbasia, unlike parkinsonism, does not decrease, but increases, the trunk does not bend forward, but remains straight. In addition, unlike parkinsonism, external rotation of the feet is often observed, which contributes to the increase in the resistance of patients. At the same time, when dysbasia is much less marked pro, retropulsions, a seminal step. Unlike patients with Parkinson's disease, patients with dysbasia in sitting or lying position are able to simulate fast walking.

The mechanism of violation of the initiation of walking and congealing with frontal and subcortical dysbasia remains unclear. DE Denny-Brown (1946) believed that the violation of the initiation of walking is due to the disinhibition of the primitive "grasping" stop reflex. Modern neurophysiological data allow us to treat these disorders as a deautomatization of the motor act caused by the elimination of downward facilitating influences from the front-horizontal circle to the stem-spinal locomotor mechanisms and the dysfunction of the pedunculopontin nucleus, while the control disorders over the trunk movements play a decisive role.

Subcortical dysbasia can develop with multiple subcortical or single strokes involving "strategic" for the locomotor functions of the midbrain, pallid sphere or shell, diffuse white matter damage of the hemispheres, neurodegenerative diseases (progressive supernuclear paralysis, multisystem atrophy, etc.), posthypoxic encephalopathy , normotensive hydrocephalus, demyelinating diseases. Small infarcts on the border of the midbrain and bridge in the projection of the pedunculopontine nucleus can cause combined disorders that combine signs of subcortical dysbasia and subcortical astasia.

Frontal disbasia can occur with bilateral lesions of the medial parts of the frontal lobes, in particular, in infarctions caused by thrombosis of the anterior cerebral artery, tumors, subdural hematoma, degenerative lesions of the frontal lobe (eg, frontal-temporal dementias). The early development of walking disorders is more characteristic of vascular dementia than of Alzheimer's. Nevertheless, in the expanded stage of Alzheimer's disease, frontal dysbasia is detected in a significant proportion of patients. In general, frontal dysbasia often occurs not in focal, but in diffuse or multi-focal brain damage, which is explained by the excess of walking regulation systems that combine frontal lobes, basal ganglia, cerebellum and stem structures.

Comparison of the clinical features of changes in walking and balance with MRI data in patients with discirculatory encephalopathy showed that disabilities of walking are more dependent on the lesions of the anterior sections of the cerebral hemispheres (the vastness of the frontal leycoarrea, the degree of widening of the anterior horns), and the imbalance of the leucoareosis in the posterior regions of large hemispheres. Lesions of the posterior parts of the brain can involve not only the motor circle fibers that follow from the anterior part of the ventrolateral thalamus nucleus to the additional motor cortex, but also numerous fibers from the posterior part of the ventrolateral nucleus receiving afferentation from the cerebellum, spinotalamic and vestibular systems and projecting onto the premotor cortex.

Disturbances of walking often precede the development of dementia, reflect more pronounced changes in subcortical white matter, especially in the inferior parts of the frontal and parietal lobes, more rapid disability of the patient.

In some cases, even a thorough examination does not reveal obvious reasons for isolated walking disorders ("idiopathic" frontal dysbasia). Nevertheless, subsequent monitoring of such patients, as a rule, allows to diagnose a particular neurodegenerative disease. For example, described by A. Achiron et al. (1993) "primary progressive congealing gait," in which the initiation of walking and congealing was the dominant manifestation, there were no other symptoms, levodopa drugs were ineffective, and neuroimaging methods did not reveal any deviations, was part of a wider clinical syndrome of "pure akinesia with congestion in walking ", which also includes hypophonia and micrography. A pathomorphological study showed that this syndrome in most cases is a form of progressive supranuclear palsy.

Frontal astaxia

The frontal asthasia is dominated by imbalance. However, in frontal asthasia, both postural and locomotor synergies suffer crudely. When trying to get sick from the frontal astasia can not transfer the weight of the body to the feet, badly repelled by the feet from the floor, and if they are helped to get up, then they fall back because of the retropulse. When you try to walk, their legs cross or are too wide apart and do not restrain the body. In more light cases, due to the fact that the patient is unable to control the trunk, to coordinate the movements of the trunk and legs, to ensure in the walking process an effective displacement and balance of the center of gravity of the body, the gait becomes incongruous, bizarre. Many patients have difficulty in initiating walking, but sometimes it is not disturbed. At the turn, the legs may cross over due to the fact that one of them makes movement, and the second remains stationary, which can lead to a fall. In severe cases, due to incorrect torso positioning, patients are not only unable to walk and stand, but are also unable to sit without support or change their position in bed.

Parezy, sensitivity disorders, extrapyramidal disorders are absent or not so pronounced as to explain these disorders of walking and balance. As additional symptoms, asymmetric revival of tendon reflexes, pseudobulbar syndrome, mild hypokinesia, frontal signs, echopraxia, motor perseverations, incontinence are noted. All patients have a pronounced cognitive defect of the frontal-subcortical type, often reaching a degree of dementia, which can aggravate walking disorders. The cause of the syndrome may be severe hydrocephalus, multiple lacunar infarctions and diffuse white matter damage of the hemispheres (with discirculatory encephalopathy), ischemic or hemorrhagic foci in the frontal lobes, tumors, abscesses of the frontal lobes, neurodegenerative diseases affecting the frontal lobes.

Frontal astaxia is sometimes mistaken for cerebellar ataxia, but for the lesions of the cerebellum the crossing of the legs is uncharacteristic when trying to walk, retropulsions, the presence of inadequate or inefficient postural synergies, bizarre attempts to move forward, a shallow shuffling step. Differences between frontal dysbasia and frontal asthasia are determined primarily by the proportion of postural disorders. Moreover, in a number of patients with astasia, the ability to perform symbolic movements on command is disproportionally impaired (for example, in a lying or sitting position, twist your "bicycle" or describe with your feet a circle and other figures, stand in the pose of a boxer or swimmer, simulate a ball or crush stub), often there is no awareness of the defect and attempts to somehow correct it, which may indicate an apratic character of the motor impairment. These differences can be explained by the fact that frontal astasia is associated not only with damage to the cortical-subcortical motor circle and its connections with stem structures, primarily the pedunculopontin nucleus, but also with dysfunction of the parietal frontal lobes that regulate the performance of complex movements that are impossible without the reverse sensory afferentation. The rupture of the connections between the posterior sections of the upper parietal lobe and the premotor cortex, controlling the posture, axial movements and movements of the legs, can cause an apratic defect in the movements of the trunk and walking in the absence of apraxia in the hands. In some cases, frontal astaxia develops as a result of frontal dysbasia progression with a more extensive lesion of the frontal lobes or their connections to the basal ganglia and stem structures.

"Apraxia walk"

The striking dissociation between impaired walking ability and the preservation of the motor abilities of the legs in the supine or sitting position, as well as the connection with cognitive disorders, served as a prerequisite for denoting violations of higher level walking as "apraxia walk". However, this concept, which has gained wide popularity, meets serious objections. In the vast majority of patients with "apraxia walking" classical neuropsychological tests usually do not reveal apraxia in the extremities. According to its functional organization, walking significantly differs from arbitrary, largely individualized, acquired in the process of learning motor skills, with the dissolution of which it is customary to associate apraxia of the extremities. Unlike these actions, whose program is formed on the cortical level, walking is a more automated motor act, which is a collection of repetitive relatively elementary movements generated by the spinal cord and modified by stem structures. Accordingly, violations of higher level walking are associated not so much with the decay of specific locomotor programs, but rather with their inadequate activation due to a lack of downward facilitating influences. In this connection, it seems unjustified to use the term "apraxia walk" to denote the entire spectrum of high level walking disorders, which are very phenomenologically different and may be associated with the defeat of various links in the higher (cortical-subcortical) level of walking regulation. Perhaps the true apraxia is approached by those walking disorders that are associated with the defeat of the parietal frontal lobes, the function of which is to use sensory afferentation to regulate movements. The defeat of these structures plays a decisive role in the development of apraxia of the extremities.

Psychogenic dysbasia

Psychogenic dysbasia is a kind of bizarre gait changes observed in hysteria. Patients can walk in a zigzag, slide like a skater on a rink, cross their legs like a plait braid, move on straightened and divorced (stilted gait) or on half-bent legs, tilt forward when walking (camptocarmy) or lean back, some patients swing or simulate jitter. Such a gait rather demonstrates good motor control, rather than a disorder of postural stability and coordination ("acrobatic gait"). Sometimes observed underlined slowness and congealing, imitating parkinsonism.

Recognition of psychogenic dysbasia can be extremely difficult. Some variants of hysterical disorders (for example, astasia-abasia) outwardly resemble frontal disorders of walking, others - dystonic gait, the third - hemiparetic or paraparetic. In all cases, inconsistency is characteristic, as well as discrepancy with the changes observed in organic syndromes (for example, patients can caricatured on a diseased leg, imitating hemiparesis, or trying to keep their balance by the movements of their hands, but without wide legs). When you change the task (for example, when walking back or flank walking), the nature of the gait disturbance may change unexpectedly. The gait can suddenly improve if the patient believes that he is not being observed, or when distracting his attention. Sometimes the patients demonstratively fall (usually in the direction of the doctor or from him), but they never do themselves serious damage. For psychogenic dysbasia, there is also a discrepancy between the severity of symptoms and the degree of restriction of daily activity, as well as sudden improvements under the influence of placebo.

At the same time, the diagnosis of psychogenic dysbasia should be made with great caution. Some cases of dystonia, paroxysmal dyskinesia, frontal astasia, tardive dyskinesia, frontal epilepsy, episodic ataxia may resemble psychogenic disorders. Carrying out differential diagnostics, one should pay attention to the presence of other hysterical symptoms (for example, selective inconsistency, gradual weakness, characteristic distribution of sensitivity disorders with the midline line, rough misapprehension in coordinator samples, peculiar dysphonia, etc.), and volatility and communication with psychological factors, a demonstrative personality, the availability of rental equipment.

Changes in walking are observed in other mental disorders. With depression, there is a slow monotonous gait with a shortened step. When astazobazofobii patients try to balance their hands, walk a short step, stick to the wall or lean on a crutch. In phobic postural dizziness, a dissociation is revealed between a pronounced subjective sense of instability and good postural control in objective research, and walking can suddenly deteriorate in specific situations (when crossing a bridge, getting into an empty room, in a store, etc.).