Symptoms of impaired walking

Gait disturbance in dysfunction of afferent systems

Gait disorders can be caused by deep sensitivity disorders (sensory ataxia), vestibular disorders (vestibular ataxia), and visual impairment.

• Sensory ataxia is caused by the lack of information about the body's position in space and the features of the plane on which a person is walking. This type of ataxia may be associated with polyneuropathies causing diffuse damage to the peripheral nerve fibers that carry proprioceptive afferentation to the spinal cord, or to the posterior columns of the spinal cord, in which deep sensitivity fibers ascend to the brain. A patient with sensory ataxia walks carefully, slowly, with his legs slightly apart, trying to control each step with his vision, lifts his legs high and, feeling a "cotton pad" under his feet, forcefully lowers his foot with the entire sole to the floor ("stamping gait"). Distinctive characteristics of sensory ataxia include deterioration of walking in the dark, detection of deep sensitivity disorders during examination, and increased unsteadiness in the Romberg pose when closing the eyes.
• Vestibular ataxia usually accompanies damage to the vestibular apparatus of the inner ear or vestibular nerve (peripheral vestibulopathies), less often - stem vestibular structures. It is usually accompanied by systemic dizziness, lightheadedness, nausea or vomiting, nystagmus, hearing loss and tinnitus. The severity of ataxia increases with changes in the position of the head and body, turning the eyes. Patients avoid sudden head movements and carefully change body position. In some cases, a tendency to fall towards the affected labyrinth is noted.
• Gait disorder in visual impairment (visual ataxia) is not specific. The gait in this case can be described as cautious and uncertain.
• Sometimes, lesions of different sense organs are combined, and if the disorder of each of them is too minor to cause significant walking disorders, then, combined with each other, and sometimes with musculoskeletal disorders, they can cause a combined walking disorder (multisensory deficiency).

Gait disturbance in movement disorders

Gait disorders may accompany movement disorders that occur in diseases of muscles, peripheral nerves, spinal roots, pyramidal tracts, cerebellum, and basal ganglia. Direct causes of gait disorders may be muscle weakness (for example, in myopathies), flaccid paralysis (in polyneuropathies, radiculopathies, spinal cord lesions), rigidity due to pathological activity of peripheral motor neurons (in neuromyotonia, rigid person syndrome, etc.), pyramidal syndrome (spastic paralysis), cerebellar ataxia, hypokinesia and rigidity (in Parkinsonism), and extrapyramidal hyperkinesis.

Gait disturbances in muscle weakness and flaccid paralysis

Primary muscle lesions usually cause symmetrical weakness in the proximal parts of the limbs, with a waddling gait ("duck-like"), which is directly related to the weakness of the gluteal muscles, which are unable to fix the pelvis when the opposite leg moves forward. For lesions of the peripheral nervous system (for example, with polyneuropathy), paresis of the distal parts of the limbs is more typical, 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 lowering the leg, the foot slaps the floor (steppage, or "cock" gait). With lesions of the lumbar thickening of the spinal cord, upper lumbar roots, lumbar plexus and some nerves, weakness is also possible in the proximal part of the limbs, which will also manifest itself as a waddling gait.

Gait disturbances in spastic paralysis

The gait characteristics of spastic paresis (spastic gait) caused by damage to the pyramidal tracts at the level of the brain or spinal cord are explained by the predominance of the tone of the extensor muscles, as a result of which the leg is extended at the knee and ankle joints and therefore elongated. In hemiparesis, due to the extension position of the leg, the patient is forced to swing the leg forward in a semicircle, while the body is slightly tilted in the opposite direction (Wernicke-Mann gait). In lower spastic paraparesis, the patient walks slowly, on tiptoes, crossing his legs (due to increased tone of the adductor muscles of the thighs). He is forced to swing himself to take one step after another. The gait becomes tense and slow. Gait disturbance in spastic paralysis depends on both the severity of the paresis and the degree of spasticity. One of the common causes of spastic gait in the elderly is spondylogenic cervical myelopathy. In addition, it is possible with strokes, tumors, traumatic brain injury, cerebral palsy, demyelinating diseases, hereditary spastic paraparesis, funicular myelosis.

Gait disturbances in Parkinsonism

Gait disorders in Parkinsonism are associated primarily with hypokinesia and postural instability. Parkinsonism is particularly characterized by difficulty initiating walking, decreased speed, and decreased step length (microbasia). A decrease in step height leads to shuffling. The support area during walking often remains normal, but sometimes decreases or increases slightly. In Parkinson's disease, due to the predominance of tone in the progravitational (flexor) muscles, a characteristic "supplicant pose" is formed, which is characterized by a forward tilt of the head and body, slight flexion in the knee and hip joints, and adduction of the arms and thighs. The arms are pressed to the body and do not participate in walking (acheirokinesis).

In the advanced stage of Parkinson's disease, the phenomenon of freezing is often noted - a sudden short-term (usually from 1 to 10 seconds) blockade of the movement being performed. Freezing can be absolute or relative. Absolute freezing is characterized by the cessation of movement of the lower limbs (the feet are "glued to the floor"), as a result of which the patient cannot move. Relative freezing is characterized by a sudden reduction in the length of the step with a transition to a very short, shuffling step or stamping movements of the legs in place. If the body continues to move forward by inertia, there is a risk of falling. Freezing most often occurs at the moment of switching from one walking program to another: at the beginning of walking ("start delay"), when turning, overcoming an obstacle, for example, a threshold, passing through a door or a narrow opening, in front of an elevator door, when stepping onto an escalator, a sudden shout, etc. Most often, freezing develops against the background of weakening of the effect of levodopa drugs (in the "off" period), but over time, in some patients, they begin to occur in the "on" period, sometimes intensifying under the influence of an excessive dose of levodopa. Patients are able to overcome freezing by stepping over an obstacle, making an unusual movement (for example, dancing), or simply taking a step to the side. However, many patients with freezing develop a fear of falling, which forces them to sharply limit their daily activities.

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

Performing cognitive tasks and even just talking while walking (dual task), especially in the late stage of the disease in patients with cognitive impairment, leads to a cessation of movement - this indicates not only a certain deficit of cognitive functions, but also that they are involved in compensating for the statolocomotor defect (in addition, this reflects a general pattern inherent in Parkinson's disease: of two simultaneously performed actions, the more automated one is performed worse). Stopping walking while trying to simultaneously perform a second action predicts an increased risk of falls.

In most patients with Parkinson's disease, walking can be improved by visual cues (e.g., contrasting transverse stripes painted on the floor) or auditory cues (rhythmic commands or the sound of a metronome). In this case, a significant increase in step length is noted, approaching normal values, but walking speed increases by only 10-30%, mainly due to a decrease in step frequency, which reflects a defect in motor programming. Improvement of walking with external stimuli may depend on the activation of systems involving the cerebellum and premotor cortex and compensating for dysfunction of the basal ganglia and the associated supplementary motor cortex.

In multisystem degenerations (multisystem atrophy, progressive supranuclear palsy, corticobasal degeneration, etc.), pronounced gait disturbances with freezing and falls occur 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 cholinergic neurons in the pedunculopontine nucleus degenerate), gait disturbances associated with parkinsonism syndrome are often supplemented by signs of frontal dysbasia, and in progressive supranuclear palsy - subcortical astasia.

Gait disturbances in muscular dystonia

Dystonic gait is especially common in patients with idiopathic generalized dystonia. The first symptom of generalized dystonia is usually dystonia of the foot, characterized by plantar flexion, inversion of the foot, and tonic extension of the big toe, which occur and intensify during walking. Subsequently, hyperkinesis gradually generalizes, spreading to the axial muscles and upper limbs. Cases of segmental dystonia have been described, primarily involving the muscles of the trunk and proximal parts of the limbs, which is manifested by a sharp forward bend of the trunk (dystonic camptocormia). Dystonic hyperkinesis may decrease with the use of corrective gestures, as well as running, swimming, walking backwards, or other unusual walking conditions. The selection and initiation of postural and locomotor synergies in patients with dystonia are preserved, but their implementation is defective due to impaired selectivity of muscle involvement.

Gait disturbances in chorea

In chorea, normal movements are often interrupted by a stream of rapid, chaotic twitching involving the trunk and limbs. During walking, the legs may suddenly bend at the knees or rise upward. The patient's attempt to give the choreic twitching the appearance of voluntary, purposeful movements leads to an elaborate, "dancing" gait. Trying to maintain balance, patients sometimes walk more slowly, placing their legs wide apart. The selection and initiation of postural and locomotor synergies are preserved in most patients, but their implementation is hindered by the superposition of involuntary movements. In addition, Huntington's disease reveals components of parkinsonism and frontal dysfunction, leading to a violation of postural synergies, a decrease in step length, walking speed, and discoordination.

Gait disturbances in other hyperkinesis

In action myoclonus, balance and gait are severely impaired by massive twitching or brief loss of muscle tone that occurs when attempting to support the legs. In orthostatic tremor, high-frequency oscillations in the trunk and lower extremity muscles are noted in the upright position, which disrupt balance but disappear during walking; however, initiation of walking may be difficult. About one-third of patients with essential tremor exhibit instability during tandem walking, which limits daily activities and may reflect cerebellar dysfunction. Bizarre gait changes have been described in tardive dyskinesia, which complicates the use of neuroleptics.

Gait disturbances in cerebellar ataxia

A characteristic feature of cerebellar ataxia is an increase in the support area both when standing and when walking. Lateral and anteroposterior swaying is often observed. In severe cases, rhythmic oscillations of the head and trunk (titubation) are observed when walking and often at rest. Steps are uneven in both length and direction, but on average, the length and frequency of steps decrease. Elimination of visual control (closing the eyes) has little effect on the severity of coordination disorders. Postural synergies have a normal latent period and temporal organization, but their amplitude can be excessive, so patients can fall in the direction opposite to the direction they initially deviated. Mild cerebellar ataxia can be detected using tandem walking. Impairments in gait and postural synergies are most pronounced in cases of damage to the midline structures of the cerebellum, while discoordination in the limbs may be minimal.

Cerebellar ataxia can be caused by cerebellar degeneration, tumors, paraneoplastic syndrome, hypothyroidism, etc.

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

Integrative (primary) gait disorders

Integrative (primary) gait disorders (higher-level gait disorders) most often occur in old age and are not associated with other motor or sensory disorders. They can be caused by damage to various links of the cortical-subcortical motor circle (frontal cortex, basal ganglia, thalamus), frontal-cerebellar connections, as well as functionally associated with them brainstem-spinal systems and limbic structures. Damage to different links of these circles in some cases can lead to the prevalence of balance disorders with the absence or inadequacy of postural synergies, in other cases - to the prevalence of disorders of initiation and maintenance of walking. However, most often a combination of both types of disorders in various proportions is observed. In this regard, the allocation of individual syndromes within the framework of higher-level gait disorders is conditional, since the boundaries between them are not clear enough, and as the disease progresses, one of the syndromes can turn into another. Moreover, in many diseases, higher-level gait disorders are superimposed on lower and middle-level syndromes, which significantly complicates the overall picture of movement disorders. Nevertheless, such a selection of individual syndromes is justified from a practical point of view, since it allows us to emphasize the leading mechanism of gait disorders.

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

Group of diseases	Nosology
Vascular lesions of the brain	Ischemic and hemorrhagic strokes with damage to the frontal lobes, basal ganglia, midbrain or their connections. Dyscirculatory encephalopathy (diffuse ischemic damage to white matter, lacunar status)
Neurodegenerative diseases	Progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration, dementia with Lewy bodies, Parkinson's disease (late stage), frontotemporal dementia, Alzheimer's disease, juvenile Huntington's disease, hepatolenticular degeneration. Idiopathic dysbasias
Infectious diseases of the central nervous system	Creutzfeldt-Jakob disease, neurosyphilis, HIV encephalopathy
Other diseases	Normal pressure hydrocephalus. Hypoxic encephalopathy. Tumors of the frontal and deep localization

Cases of higher-level gait disorders have been described in the past under various names - "gait apraxia", "astasia-abasia", "frontal ataxia", "magnetic gait", "lower-body parkinsonism", etc. JG Nutt et al. (1993) identified 5 main syndromes of higher-level gait disorders: cautious gait, frontal gait disorder, frontal balance disorder, subcortical balance disorder, isolated gait initiation disorder. There are 4 variants of integrative gait disorders.

• Senile dysbasia (corresponds to “cautious gait” according to the classification of JG Nutt et al.).
• Subcortical astasia (corresponds to "subcortical imbalance"),
• Frontal (subcortical-frontal) dysbasia (corresponds to “isolated gait initiation disorder” and “frontal gait disorder”),
• Frontal astasia (corresponds to "frontal imbalance").

Senile dysbasia

Senile dysbasia is the most common type of gait disorder in the elderly. It is characterized by a shortened and slowed stride, uncertainty when turning, some increase in the support area, mild or moderate postural instability, which is clearly visible only when turning, pushing the patient or standing on one leg, as well as when sensory afferentation is limited (for example, when closing the eyes). When turning, the natural sequence of movements is disrupted, as a result of which they can be performed by the entire body (en block). When walking, the legs are slightly bent at the hip and knee joints, the body is tilted forward, which increases stability.

In general, senile dysbasia should be considered as an adequate response to a perceived or real risk of falling. For example, a healthy person walks on a slippery road or in absolute darkness, fearing to slip and lose balance. In old age, dysbasia occurs as a response to an age-related decrease in the ability to maintain balance or adapt synergies to the characteristics of the surface. The main postural and locomotor synergies remain intact, but due to limited physical capabilities, they are not used as effectively as before. As a compensatory phenomenon, this type of gait disorder can be observed in a variety of diseases that limit mobility or increase the risk of falls: joint damage, severe heart failure, cerebrovascular insufficiency, degenerative dementias, vestibular or multisensory insufficiency, as well as obsessive fear of losing balance (astasobasophobia). In most cases, focal symptoms are not detected during a neurological examination. Since senile dysbasia is often observed in healthy elderly people, it can be considered an age norm if it does not lead to limitation of the patient's daily activity or falls. At the same time, it should be taken into account that the degree of limitation of daily activity often depends not so much on the actual neurological defect as on the severity of the fear of falling.

Given the compensatory nature of senile dysbasia, attributing this type of gait changes to a higher level, which is characterized by a limitation of adaptation capabilities, is conditional. Senile dysbasia reflects an increase in the role of conscious control and higher brain functions, in particular attention, in regulating gait. With the development of dementia and weakening of attention, further slowing of gait and loss of stability may occur, even in the absence of primary motor and sensory disorders. 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 severe disorder of postural synergies caused by damage to the basal ganglia, midbrain, or thalamus. Due to inadequate postural synergies, walking and standing are difficult or impossible. When trying to stand up, the center of gravity does not shift to a new center of support, instead, the body deviates backward, which leads to a fall on the back. When thrown off balance without support, the patient falls like a sawed-off tree. The syndrome may be based on a violation of the orientation of the body in space, due to which postural reflexes are not activated in time. Initiation of walking is not difficult in patients. Even if severe postural instability makes independent walking impossible, with support the patient is able to step over and even walk, while the direction and rhythm of the steps remain normal, which indicates the relative preservation of locomotor synergies. When the patient is lying or sitting and the demands on postural control are less, he can perform normal movements of the limbs.

Subcortical astasia occurs acutely with unilateral or bilateral ischemic or hemorrhagic lesions of the outer sections of the midbrain tegmentum and upper sections of the pons, the upper part of the posterolateral nucleus of the thalamus and adjacent white matter, basal ganglia, including the globus pallidus and putamen. With unilateral lesions of the thalamus or basal ganglia, when trying to stand up, and sometimes even in a sitting position, the patient may deviate and fall to the contralateral side or back. With unilateral lesions, the symptoms usually regress within a few weeks, but with bilateral lesions they are more persistent. Gradual development of the syndrome is observed in progressive supranuclear palsy, diffuse ischemic lesions of the white matter of the hemispheres, and normotensive hydrocephalus.

Frontal (frontal-subcortical) dysbasia

Primary gait disorders with damage to subcortical structures (subcortical dysbasia) and frontal lobes (frontal dysbasia) are clinically and pathogenetically close. In essence, they can be considered as a single syndrome. This is explained by the fact that the frontal lobes, basal ganglia and some structures of the midbrain form a single regulatory circuit and when they are damaged or separated (due to the involvement of the connecting pathways in the white matter of the hemispheres), similar disorders can occur. Phenomenologically, subcortical and frontal dysbasia are diverse, which is explained by the involvement of different subsystems that ensure various aspects of walking and maintaining balance. In this regard, several main clinical variants of dysbasia can be distinguished.

The first variant is characterized by the prevalence of disturbances in the initiation and maintenance of the locomotor act in the absence of pronounced postural disturbances. When attempting 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 "swing" the body and legs. Synergies that normally provide propulsion and the shift of the body's center of gravity to one leg (in order to free the other for the swing) often prove ineffective. After the initial difficulties have been overcome and the patient has finally moved, he takes several trial small shuffling steps or stamps on the spot, but gradually his steps become more confident and longer, and his feet are more easily lifted off the floor. However, when turning, overcoming an obstacle, passing through a narrow opening, which require switching the motor program, relative (stamping) or absolute freezing may again occur, when the feet suddenly "grow" to the floor. As with Parkinson's disease, freezing can be overcome by stepping over a crutch or stick, making a detour (such as moving to the side), or using rhythmic commands, counting out loud, or rhythmic music (such as a march).

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

Both of the described variants can, as the disease progresses, transform into the third, most complete and extensive variant of frontal-subcortical dysbasia, in which a combination of gait initiation disorder and freezing with more pronounced and persistent changes in the gait pattern, moderate or pronounced postural instability is observed. Asymmetry of gait is often noted: the patient takes a step with the leading leg, and then drags the second leg to it, sometimes in several steps, while the leading leg can change, and the length of the steps can be quite variable. When turning and overcoming obstacles, walking difficulties increase sharply, due to which the patient can again begin to stamp or freeze. The supporting leg can remain in place, and the other takes a series of small steps.

Characterized by increased variability of step parameters, loss of the ability to voluntarily regulate walking speed, step length, and leg lift height depending on the nature of the surface or other circumstances. Fear of falling, which occurs in most of these 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 disorders may be absent, but in some cases of subcortical dysbasia, bradykinesia, dysarthria, regulatory cognitive impairment, affective disorders (emotional lability, dulling of affect, depression) are observed. In frontal dysbasia, in addition, dementia, frequent urination or urinary incontinence, pronounced pseudobulbar syndrome, frontal signs (paratonia, grasping reflex), pyramidal signs often develop.

Gait in frontal and subcortical dysbasia is very similar to parkinsonism. At the same time, there are no manifestations of parkinsonism in the upper body in dysbasia (facial expressions remain lively, only sometimes weakened by the accompanying supranuclear insufficiency of the facial nerves; arm movements during walking not only do not decrease, but sometimes even become more energetic, since with their help the patient tries to balance the body relative to its center of gravity or move the legs "fused" to the floor), therefore this syndrome is called "parkinsonism of the lower body". However, this is not true, but pseudoparkinsonism, since it occurs in the absence of its main symptoms - hypokinesia, rigidity, rest tremor. Despite a significant decrease in step length, the support area in dysbasia, unlike parkinsonism, does not decrease, but increases, the body does not lean forward, but remains straight. In addition, unlike Parkinsonism, external rotation of the feet is often observed, which helps to increase the stability of patients. At the same time, with dysbasia, pro-, retropulsion, and mincing step are much less common. Unlike patients with Parkinson's disease, patients with dysbasia are able to imitate fast walking in a sitting or lying position.

The mechanism of the disturbance of gait initiation and freezing in frontal and subcortical dysbasia remains unclear. DE Denny-Brown (1946) believed that the disturbance of gait initiation is caused by the disinhibition of the primitive "grasping" foot reflex. Modern neurophysiological data allow us to consider these disorders as a deautomatization of the motor act caused by the elimination of descending facilitating influences from the frontostriatal circle on the brainstem-spinal locomotor mechanisms and dysfunction of the pedunculopontine nucleus, while the decisive role can be played by disturbances in the control of trunk movements.

Subcortical dysbasia may develop with multiple subcortical or single strokes involving the "strategic" areas of the midbrain, globus pallidus or putamen in relation to locomotor functions, diffuse damage to the white matter of the hemispheres, neurodegenerative diseases (progressive supranuclear palsy, multiple system atrophy, etc.), post-hypoxic encephalopathy, normotensive hydrocephalus, demyelinating diseases. Small infarctions on the border of the midbrain and pons in the projection of the pedunculopontine nucleus can cause combined disorders that combine the signs of subcortical dysbasia and subcortical astasia.

Frontal dysbasia may occur with bilateral lesions of the medial parts of the frontal lobes, in particular with infarctions caused by thrombosis of the anterior cerebral artery, tumors, subdural hematoma, degenerative lesions of the frontal lobe (for example, with frontotemporal dementia). Early development of gait disorders is more typical for vascular dementia than for Alzheimer's disease. Nevertheless, at the advanced stage of Alzheimer's disease, frontal dysbasia is detected in a significant proportion of patients. In general, frontal dysbasia most often occurs not with focal, but with diffuse or multifocal brain damage, which is explained by the redundancy of the gait regulation systems that combine the frontal lobes, basal ganglia, cerebellum and brainstem structures.

Comparison of clinical features of gait and balance changes with MRI data in patients with discirculatory encephalopathy showed that gait disorders depend more on the damage to the anterior parts of the cerebral hemispheres (extent of frontal leukoaraiosis, degree of expansion of the anterior horns), and balance disorders - on the severity of leukoaraiosis in the posterior parts of the cerebral hemispheres. Damage to the posterior parts of the brain can involve not only the fibers of the motor circle, following from the anterior part of the ventrolateral nucleus of the thalamus to the additional motor cortex, but also numerous fibers from the posterior part of the ventrolateral nucleus, receiving afferentation from the cerebellum, spinothalamic and vestibular systems and projecting to the premotor cortex.

Gait disturbances often precede the development of dementia, reflecting more pronounced changes in the subcortical white matter, especially in the deep parts of the frontal and parietal lobes, and more rapid patient disability.

In some cases, even a thorough examination does not reveal obvious causes for relatively isolated gait disorders (“idiopathic” frontal dysbasia). However, subsequent observation of such patients, as a rule, allows diagnosing one or another neurodegenerative disease. For example, the “primary progressive freezing gait” described by A. Achiron et al. (1993), in which the dominant manifestation was a disorder of gait initiation and freezing, other symptoms were absent, levodopa drugs were ineffective, and neuroimaging methods did not reveal any abnormalities, turned out to be part of a broader clinical syndrome of “pure akinesia with freezing of gait,” which also includes hypophonia and micrographia. Pathomorphological examination showed that this syndrome in most cases is a form of progressive supranuclear palsy.

Frontal astasia

In frontal astasia, balance disorders predominate. At the same time, in frontal astasia, both postural and locomotor synergies are severely impaired. When trying to stand up, patients with frontal astasia are unable to transfer body weight to their legs, push off the floor poorly with their legs, and if they are helped to stand up, they fall backwards due to retropulsion. When trying to walk, their legs cross or are too wide apart and do not support the body. In milder cases, due to the fact that the patient is unable to control the trunk, coordinate the movements of the trunk and legs, ensure effective displacement and balancing of the body's center of gravity during walking, the gait becomes incongruous and bizarre. Many patients have severely impaired initiation of walking, but sometimes it is not impaired. When turning, the legs may cross due to the fact that one of them moves, and the other remains motionless, which can lead to a fall. In severe cases, due to incorrect positioning of the torso, patients are not only unable to walk and stand, but are also unable to sit without support or change position in bed.

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

Frontal astasia is sometimes mistaken for cerebellar ataxia, but cerebellar lesions are not characterized by crossing of legs when trying to walk, retropulsions, the presence of inadequate or ineffective postural synergies, bizarre attempts to move forward, a small shuffling step. The differences between frontal dysbasia and frontal astasia are determined primarily by the proportion of postural disorders. Moreover, a number of patients with astasia have a disproportionately impaired ability to perform symbolic movements on command (for example, in a lying or sitting position, spinning a "bicycle" with their legs or describing a circle and other figures, getting into a boxer's or swimmer's pose, imitating a kick at a ball or crushing a cigarette butt), there is often no awareness of the defect and no attempts to somehow correct it, which may indicate an apraxic nature of the movement disorder. 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 brainstem structures, primarily the pedunculopontine nucleus, but also with dysfunction of the parietal-frontal circles, which regulate the execution of complex movements that are impossible without feedback sensory afferentation. Disruption of connections between the posterior sections of the superior parietal lobe and the premotor cortex, which control posture, axial movements, and leg movements, can cause an apraxic defect in trunk movements and walking in the absence of apraxia in the arms. In some cases, frontal astasia develops as a result of progression of frontal dysbasia with more extensive damage to the frontal lobes or their connections with the basal ganglia and brainstem structures.

"Apraxia of walking"

The striking dissociation between the impairment of walking ability and the preservation of the motor capabilities of the legs in a lying or sitting position, as well as the connection with cognitive disorders, served as a prerequisite for designating higher-level walking disorders as "gait apraxia". However, this concept, which has gained wide popularity, encounters serious objections. In the overwhelming majority of patients with "gait apraxia", classical neuropsychological tests usually do not reveal apraxia in the limbs. In its functional organization, walking differs significantly from voluntary, largely individualized, motor skills acquired in the process of learning, with the disintegration of which limb apraxia is usually associated. Unlike these actions, the program of which is formed at the cortical level, walking is a more automated motor act, representing a set of repetitive, relatively elementary movements generated by the spinal cord and modified by the brainstem structures. Accordingly, higher-level gait disorders are associated not so much with the breakdown of specific locomotor programs as with their insufficient activation due to a deficit of descending facilitating influences. In this regard, it seems unjustified to use the term "gait apraxia" to designate the entire spectrum of higher-level gait disorders, which differ greatly phenomenologically and may be associated with damage to various links of the higher (cortical-subcortical) level of gait regulation. Perhaps, those gait disorders that are associated with damage to the parietal-frontal circles, whose function is to use sensory afferentation to regulate movements, are close to true apraxia. Damage to these structures plays a decisive role in the development of limb apraxia.

Psychogenic dysbasia

Psychogenic dysbasia - peculiar bizarre changes in gait observed in hysteria. Patients may walk in a zigzag, glide like a skater on a rink, cross their legs like a braid, move with straight and apart (stilted gait) or half-bent legs, lean their torso forward when walking (camptokarmia) or lean back, some patients sway or imitate trembling when walking. Such a gait is more likely to demonstrate good motor control than a disorder of postural stability and coordination ("acrobatic gait"). Sometimes, pronounced slowness and freezing, imitating Parkinsonism, are observed.

Recognizing psychogenic dysbasia can be extremely difficult. Some variants of hysterical disorders (e.g., astasia-abasia) outwardly resemble frontal gait disturbances, others - dystonic gait, and still others - hemiparetic or paraparetic. In all cases, inconsistency is characteristic, as well as discrepancy with changes observed in organic syndromes (for example, patients may limp on the affected leg, imitating hemiparesis, or try to maintain balance with arm movements, but not placing their feet wide). When the task changes (for example, when walking backwards or flank walking), the nature of the gait disturbance may suddenly change. The gait may suddenly improve if the patient believes that he is not being observed, or when his attention is distracted. Sometimes patients demonstratively fall (usually towards the doctor or away from him), but never cause themselves serious injuries. Psychogenic dysbasia is also characterized by a discrepancy between the severity of symptoms and the degree of limitation 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 dyskinesias, frontal astasia, tardive dyskinesias, frontal epilepsy, episodic ataxia may resemble psychogenic disorders. When conducting differential diagnostics, it is necessary to pay attention to the presence of other hysterical symptoms (for example, selective incompetence, graded weakness, characteristic distribution of sensitivity disorders with a border along the midline, gross misses in coordination tests, peculiar dysphonia, etc.), and inconstancy and connection with psychological factors, demonstrative personality, the presence of a rent-seeking attitude.

Changes in walking are also observed in other mental disorders. In depression, a slow monotonous gait with a shortened step is observed. In astasobasophobia, patients try to balance with their hands, walk with short steps, hold on to a wall or lean on a crutch. In phobic postural dizziness, a dissociation is revealed between a pronounced subjective feeling of instability and good postural control during an objective examination, and walking may suddenly worsen in specific situations (when crossing a bridge, entering an empty room, in a store, etc.).