Gait disturbance (dysphasia)

In humans, regular "bipedal" walking is the most complexly organized motor act, which, along with speech ability, distinguishes humans from their predecessors. Walking is optimally realized only under the condition of normal functioning of a large number of physiological systems. Walking, as a voluntary motor act, requires unimpeded passage of motor impulses through the pyramidal system, as well as active participation of the extrapyramidal and cerebellar control systems, which carry out fine coordination of movements. The spinal cord and peripheral nerves ensure the passage of this impulse to the corresponding muscles. Sensory feedback from the periphery and orientation in space through the visual and vestibular systems are also necessary for normal walking, as is the preservation of the mechanical structure of bones, joints and muscles.

Since many levels of the nervous system are involved in the implementation of normal gait, there are, accordingly, a large number of causes that can disrupt the normal act of walking. Some diseases and injuries of the nervous system are accompanied by characteristic and even pathognomonic gait disturbances. The pathological gait pattern imposed by the disease erases its normal gender differences and determines one or another type of dysbasia. Therefore, careful observation of gait is often very valuable for differential diagnosis and should be performed at the beginning of the neurological examination.

During the clinical study of gait, the patient walks with open and closed eyes; walks forward facing and backwards; demonstrates a flank gait and walking around a chair; gait on toes and heels is examined; along a narrow passage and along a line; slow and fast walking; running; turns while walking; climbing stairs.

There is no generally accepted unified classification of types of dysbasia. In addition, sometimes a patient's gait is complex, since several of the below-listed types of dysbasia are present at the same time. The doctor must see all the components that make up the dysbasia and describe them separately. Many types of dysbasia are accompanied by symptoms of involvement of certain levels of the nervous system, the recognition of which is also important for diagnosis. It should be noted that many patients with a wide variety of gait disorders complain of "dizziness".

Gait disorders are a common syndrome in the population, especially among older people. Up to 15% of people over 60 experience some form of gait disorders and occasional falls. Among older people, this percentage is even higher.

Gait in diseases of the musculoskeletal system

The consequences of ankylosing spondylitis and other forms of spondylitis, arthrosis of large joints, tendon retractions on the foot, congenital anomalies, etc. can lead to various gait disorders, the causes of which are not always associated with pain (clubfoot, deformities such as halux valgus, etc.). The diagnosis requires consultation with an orthopedist.

Main types of gait disorders (dysbasia)

1. Ataxic gait:
   1. cerebellar;
   2. stamping ("tabetic");
   3. with vestibular symptom complex.
2. "Hemiparetic" ("skewed" or "triple shortening" type).
3. Paraspastic.
4. Spastic-ataxic.
5. Hypokinetic.
6. Apraxia of gait.
7. Idiopathic senile dysbasia.
8. Idiopathic progressive "freezing dysbasia".
9. Skater's gait in idiopathic orthostatic hypotension.
10. "Peroneal" gait - unilateral or bilateral steppage.
11. Walking with hyperextension of the knee joint.
12. "Duck" gait.
13. Walking with a pronounced lordosis in the lumbar region.
14. Gait in diseases of the musculoskeletal system (ankylosis, arthrosis, tendon retractions, etc.).
15. Hyperkinetic gait.
16. Dysbasia in mental retardation.
17. Gait (and other psychomotor skills) in severe dementia.
18. Psychogenic gait disorders of various types.
19. Dysbasia of mixed origin: complex dysbasia in the form of gait disturbances against the background of certain combinations of neurological syndromes: ataxia, pyramidal syndrome, apraxia, dementia, etc.
20. Iatrogenic dysbasia (unsteady or “drunk” gait) due to drug intoxication.
21. Dysbasia caused by pain (antalgic).
22. Paroxysmal gait disturbances in epilepsy and paroxysmal dyskinesias.

Ataxic gait

Movements in cerebellar ataxia are poorly proportionate to the characteristics of the surface on which the patient walks. Balance is disturbed to a greater or lesser extent, which leads to corrective movements that give the gait a disorderly-chaotic character. Characteristic, especially for lesions of the cerebellar vermis, is walking on a wide base as a result of instability and staggering.

The patient often staggers not only when walking, but also when standing or sitting. Sometimes titubation is detected - a characteristic cerebellar tremor of the upper half of the body and head. As accompanying signs, dysmetria, adiadochokinesis, intention tremor, postural instability are detected. Other characteristic signs may also be detected (scanned speech, nystagmus, muscle hypotonia, etc.).

Main causes: cerebellar ataxia accompanies a large number of hereditary and acquired diseases that occur with damage to the cerebellum and its connections (spinocerebellar degenerations, malabsorption syndrome, alcoholic degeneration of the cerebellum, multiple system atrophy, late cerebellar atrophy, hereditary ataxias, OPCA, tumors, paraneoplastic degeneration of the cerebellum and many other diseases).

When the conductors of deep muscle sense are affected (most often at the level of the posterior columns), sensory ataxia develops. It is especially pronounced when walking and manifests itself in characteristic movements of the legs, which are often defined as a "stamping" gait (the foot is forcefully lowered with the entire sole to the floor); in extreme cases, walking is generally impossible due to the loss of deep sensitivity, which is easily detected when examining the muscle-joint sense. A characteristic feature of sensory ataxia is its correction by vision. This is the basis of the Romberg test: when the eyes are closed, sensory ataxia sharply increases. Sometimes, with closed eyes, pseudo-athetosis is detected in the arms extended forward.

Main reasons: sensory ataxia is characteristic not only for lesions of the posterior columns, but also for other levels of deep sensitivity (peripheral nerve, posterior root, brainstem, etc.). Therefore, sensory ataxia is observed in the picture of such diseases as polyneuropathy ("peripheral pseudotabes"), funicular myelosis, tabes dorsalis, complications of treatment with vincristine; paraproteinemia; paraneoplastic syndrome, etc.)

In vestibular disorders, ataxia is less pronounced and is more evident in the legs (staggering when walking and standing), especially at dusk. Severe damage to the vestibular system is accompanied by a detailed picture of the vestibular symptom complex (systemic dizziness, spontaneous nystagmus, vestibular ataxia, autonomic disorders). Mild vestibular disorders (vestibulopathy) are manifested only by intolerance to vestibular loads, which often accompanies neurotic disorders. With vestibular ataxia, there are no cerebellar signs and disturbances of the muscular-articular sense.

Main causes: vestibular symptom complex is typical for damage to vestibular conductors at any level (cerumen plugs in the external auditory canal, labyrinthitis, Meniere's disease, acoustic neuroma, multiple sclerosis, degenerative lesions of the brainstem, syringobulbia, vascular diseases, intoxications, including drug-induced, traumatic brain injury, epilepsy, etc.). A peculiar vestibulopathy usually accompanies psychogenic chronic neurotic conditions. For diagnosis, it is important to analyze complaints of dizziness and accompanying neurological manifestations.

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"Hemiparetic" gait

Hemiparetic gait is manifested by extension and circumduction of the leg (the arm is bent at the elbow) in the form of a "slanting" gait. The paretic leg is exposed to the body weight during walking for a shorter period than the healthy leg. Circumduction (circular movement of the leg) is observed: the leg is extended at the knee joint with slight plantar flexion of the foot and performs a circular movement outward, while the body deviates slightly in the opposite direction; the homolateral arm loses some of its functions: it is bent at all joints and pressed to the body. If a stick is used during walking, it is used on the healthy side of the body (for which the patient bends over and transfers his weight to it). With each step, the patient raises the pelvis to lift the straightened leg off the floor and moves it forward with difficulty. Less frequently, the gait is disturbed by the “triple shortening” type (flexion in three joints of the leg) with a characteristic rise and fall of the pelvis on the side of paralysis with each step. Associated symptoms: weakness in the affected limbs, hyperreflexia, pathological foot signs.

Main reasons: hemiparetic gait occurs with various organic lesions of the brain and spinal cord, such as strokes of various origins, encephalitis, brain abscesses, trauma (including birth trauma), toxic, demyelinating and degenerative-atrophic processes (including hereditary), tumors, parasites of the brain and spinal cord, leading to spastic hemiparesis.

Paraspastic gait

The legs are usually straightened at the knees and ankles. The gait is slow, the legs "shuffle" along the floor (the soles of the shoes wear out accordingly), sometimes they move like scissors with their crossing (due to increased tone of the adductor muscles of the thigh), on the toes and with a slight twisting of the toes ("pigeon" toes). This type of gait disorder is usually caused by more or less symmetrical bilateral damage to the pyramidal tracts at any level.

Main causes: Paraspastic gait is most often observed under the following circumstances:

• Multiple sclerosis (characteristic spastic-ataxic gait)
• Lacunar state (in elderly patients with arterial hypertension or other risk factors for vascular disease; often preceded by episodes of minor ischemic vascular strokes, accompanied by pseudobulbar symptoms with speech disorders and pronounced reflexes of oral automatism, gait with small steps, pyramidal signs).
• After spinal cord injury (history, level of sensory disturbances, urinary disturbances). Little's disease (a special form of cerebral palsy; symptoms of the disease are present from birth, there is a delay in motor development, but normal intellectual development; often only selective involvement of the limbs, especially the lower ones, with scissor-like movements with crossing of the legs during walking). Familial spastic spinal palsy (hereditary slowly progressive disease, symptoms often appear in the third decade of life). In cervical myelopathy in the elderly, mechanical compression and vascular insufficiency of the cervical spinal cord often cause a paraspastic (or spastic-ataxic) gait.

As a result of rare, partially reversible conditions such as hyperthyroidism, portocaval anastomosis, lathyrism, posterior column disease (in vitamin B12 deficiency or as a paraneoplastic syndrome), adrenoleukodystrophy.

Intermittent paraspastic gait is rarely observed in the picture of "intermittent claudication of the spinal cord".

Paraspastic gait is sometimes imitated by dystonia of the lower extremities (especially in the so-called dopa-responsive dystonia), which requires a syndromic differential diagnosis.

Spastic-ataxic gait

In this gait disorder, a clear ataxic component is added to the characteristic paraspastic gait: unbalanced body movements, slight hyperextension in the knee joint, instability. This picture is characteristic, almost pathognomonic for multiple sclerosis.

Main causes: it can also be observed in subacute combined degeneration of the spinal cord (funicular myelosis), Friedreich's disease and other diseases involving the cerebellar and pyramidal tracts.

Hypokinetic gait

This type of gait is characterized by slow, constrained movements of the legs with a decrease or absence of associated movements of the arms and a tense posture; difficulty initiating walking, shortening of the step, “shuffling”, difficult turns, stamping on the spot before starting to move, and sometimes “pulsation” phenomena.

The most common etiologic factors for this type of gait include:

1. Hypokinetic-hypertonic extrapyramidal syndromes, especially Parkinsonism syndrome (in which a slight flexor posture is observed; there are no coordinated arm movements during walking; rigidity, a mask-like face, quiet monotonous speech and other manifestations of hypokinesia, resting tremor, the cogwheel phenomenon are also observed; the gait is slow, “shuffling”, rigid, with a shortened step; “pulsive” phenomena are possible during walking).
2. Other hypokinetic extrapyramidal and mixed syndromes include progressive supranuclear palsy, olivo-ponto-cerebellar atrophy, Shy-Drager syndrome, stria-nigral degeneration (Parkinsonism-plus syndromes), Binswanger disease, and vascular lower-body Parkinsonism. In the lacunar state, there may also be a "marche a petits pas" gait (small, short, irregular shuffling steps) against the background of pseudobulbar palsy with swallowing disorders, speech disorders, and Parkinson-like motility. "Marche a petits pas" may also be observed in the picture of normotensive hydrocephalus.
3. Akinetic-rigid syndrome and the corresponding gait are possible with Pick's disease, corticobasal degeneration, Creutzfeldt-Jakob disease, hydrocephalus, frontal lobe tumor, juvenile Huntington's disease, Wilson-Konovalov disease, post-hypoxic encephalopathy, neurosyphilis and some other rarer diseases.

In young patients, torsion dystonia can sometimes debut with an unusual tense, constrained gait due to dystonic hypertonicity in the legs.

The syndrome of constant muscle activity (Isaacs syndrome) is most often observed in young patients. Unusual tension of all muscles (mainly distal), including antagonists, blocks gait, as well as all other movements (armadillo gait)

Depression and catatonia may be accompanied by hypokinetic gait.

Apraxia of gait

Apraxia of gait is characterized by the loss or reduction of the ability to use the legs properly in the act of walking in the absence of sensory, cerebellar and paretic manifestations. This type of gait occurs in patients with extensive cerebral damage, especially to the frontal lobes. The patient cannot imitate some leg movements, although certain automatic movements are preserved. The ability to consistently compose movements during "bipedal" walking is reduced. This type of gait is often accompanied by perseverations, hypokinesia, rigidity and, sometimes, gegenhalten, as well as dementia or urinary incontinence.

A variant of gait apraxia is the so-called axial apraxia in Parkinson's disease and vascular parkinsonism; dysbasia in normotensive hydrocephalus and other diseases involving the frontal-subcortical connections. A syndrome of isolated gait apraxia has also been described.

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Idiopathic senile dysbasia

This form of dysbasia ("elderly gait", "senile gait") is manifested by a slightly shortened slow step, mild postural instability, a decrease in the associated movements of the arms in the absence of any other neurological disorders in elderly and old people. This dysbasia is based on a complex of factors: multiple sensory deficits, age-related changes in the joints and spine, deterioration of vestibular and postural functions, etc.

Idiopathic progressive "freezing dysbasia"

"Freezing dysbasia" is usually observed in the picture of Parkinson's disease; less often it occurs in multi-infarct (lacunar) condition, multiple system atrophy and normotensive hydrocephalus. However, elderly patients have been described in whom "freezing dysbasia" is the only neurological manifestation. The degree of "freezing" varies from sudden motor blocks during walking to total inability to start walking. Biochemical blood and cerebrospinal fluid tests, as well as CT and MRI, show a normal picture, with the exception of mild cortical atrophy in some cases.

Skater's gait in idiopathic orthostatic hypotension

This gait is also observed in Shy-Drager syndrome, in which peripheral autonomic failure (mainly orthostatic hypotension) becomes one of the leading clinical manifestations. The combination of parkinsonism symptoms, pyramidal and cerebellar signs affects the gait characteristics of these patients. In the absence of cerebellar ataxia and pronounced parkinsonism, patients try to adapt their gait and body posture to orthostatic changes in hemodynamics. They move with wide, slightly to the side, quick steps on slightly bent knees, leaning their torso forward and lowering their head ("skater's pose").

"Peroneal" gait

Peroneal gait is a unilateral (more common) or bilateral steppage. Steppage gait develops with the so-called drop foot and is caused by weakness or paralysis of dorsiflexion (dorsiflexion) of the foot and/or toes. The patient either "dragged" the foot while walking or, trying to compensate for the drop foot, lifted it as high as possible to lift it off the floor. Thus, there is increased flexion in the hip and knee joints; the foot is thrown forward and lowered down onto the heel or the entire foot with a characteristic slapping sound. The support phase of walking is shortened. The patient is unable to stand on the heels, but can stand and walk on the toes.

The most common cause of unilateral paresis of the extensors of the foot is dysfunction of the peroneal nerve (compression neuropathy), lumbar plexopathy, and rarely damage to the L4 and especially L5 roots, as in the case of a herniated intervertebral disc (“vertebral peroneal palsy”). Bilateral paresis of the extensors of the foot with bilateral "stepage" is often observed in polyneuropathy (paresthesia, stocking-type sensory disturbances, absence or decrease of Achilles reflexes are noted), in Charcot-Marie-Tooth peroneal muscular atrophy - a hereditary disease of three types (high arch of the foot, atrophy of the calf muscles ("stork legs"), absence of Achilles reflexes, sensory disturbances are minor or absent), in spinal muscular atrophy - (in which paresis is accompanied by atrophy of other muscles, slow progression, fasciculations, absence of sensory disturbances) and in some distal myopathies (scapuloperoneal syndromes), especially in Steinert-strong atten-Gibb dystrophic myotonia.

A similar picture of gait disturbance develops when both distal branches of the sciatic nerve are affected (“drop foot”).

Walking with hyperextension of the knee joint

Walking with unilateral or bilateral hyperextension of the knee joint is observed with paralysis of the knee extensors. Paralysis of the knee extensors (quadriceps femoris) leads to hyperextension when putting weight on the leg. When weakness is bilateral, both legs are hyperextended at the knee joints during walking; otherwise, shifting weight from one leg to another can cause changes in the knee joints. Descending stairs begins with the paretic leg.

Causes of unilateral paresis include femoral nerve damage (loss of knee reflex, sensory disturbance in the area of innervation of the n. saphenous]) and lumbar plexus damage (symptoms similar to those of femoral nerve damage, but the abductor and iliopsoas muscles are also involved). The most common cause of bilateral paresis is myopathy, especially progressive Duchenne muscular dystrophy in boys, and polymyositis.

"Duck" gait

Paresis (or mechanical insufficiency) of the hip abductors, i.e. the hip abductors (mm. gluteus medius, gluteus minimus, tensor fasciae latae) results in the inability to hold the pelvis horizontally relative to the weight-bearing leg. If the insufficiency is only partial, then hyperextension of the trunk toward the supporting leg may be sufficient to shift the center of gravity and prevent pelvic tilt. This is the so-called Duchenne lameness, and when there are bilateral disorders, this results in an unusual 'waddling' gait (the patient seems to waddle from one foot to the other, a 'duck' gait). With complete paralysis of the hip abductors, the shift in the center of gravity described above is no longer sufficient, which results in pelvic tilt with each step in the direction of the leg movement - the so-called Trendelenburg lameness.

Unilateral paresis or insufficiency of the hip abductors may be caused by damage to the superior gluteal nerve, sometimes as a result of an intramuscular injection. Even in a prone position, insufficient strength is found for external abduction of the affected leg, but there are no sensory disturbances. Such insufficiency is found in unilateral congenital or posttraumatic hip dislocation or postoperative (prosthetic) damage to the hip abductors. Bilateral paresis (or insufficiency) is usually a consequence of myopathy, especially progressive muscular dystrophy, or bilateral congenital hip dislocation.

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Walking with a pronounced lordosis in the lumbar region

If the hip extensors are involved, especially m. gluteus maximus, then climbing stairs becomes possible only when starting with the healthy leg, but when descending stairs, the affected leg goes first. Walking on a flat surface is usually impaired only with bilateral weakness of m. gluteus maximus; such patients walk with a ventrally tilted pelvis and with increased lumbar lordosis. With unilateral paresis of m. gluteus maximus, abduction of the affected leg backward is impossible, even in the pronation position.

The cause is always (rarely) a lesion of the inferior gluteal nerve, for example due to an intramuscular injection. Bilateral paresis of the m. gluteus maximus is most often found in the progressive form of muscular dystrophy of the pelvic girdle and the Duchenne form.

Occasionally, the so-called femoral-lumbar extension rigidity syndrome is mentioned in the literature, which manifests itself in reflex disorders of muscle tone in the extensors of the back and legs. In the vertical position, the patient has a fixed, mild lordosis, sometimes with lateral curvature. The main symptom is the "board" or "shield": in the supine position, with passive lifting of both feet of the outstretched legs, the patient does not flex in the hip joints. Walking, which is of a jerky nature, is accompanied by compensatory thoracic kyphosis and a forward tilt of the head in the presence of rigidity of the cervical extensor muscles. Pain syndrome is not the leading one in the clinical picture and is often vague and abortive. A common cause of the syndrome is fixation of the dural sac and the terminal thread by a cicatricial-adhesive process in combination with osteochondrosis against the background of dysplasia of the lumbar spine or with a spinal tumor at the cervical, thoracic or lumbar level. Regression of symptoms occurs after surgical mobilization of the dural sac.

Hyperkinetic gait

Hyperkinetic gait is observed in various types of hyperkinesis. These include diseases such as Sydenham's chorea, Huntington's chorea, generalized torsion dystonia (camel gait), axial dystonic syndromes, pseudo-expressive dystonia, and foot dystonia. Less common causes of gait disorders include myoclonus, truncal tremor, orthostatic tremor, Tourette's syndrome, and tardive dyskinesia. In these conditions, the movements necessary for normal walking are suddenly interrupted by involuntary, disordered movements. A strange or "dancing" gait develops. (Such gait in Huntington's chorea sometimes looks so strange that it can resemble psychogenic dysbasia). Patients must constantly fight these disorders in order to move purposefully.

Gait disturbances in mental retardation

This type of dysbasia is a problem that has not yet been sufficiently studied. Awkward standing with an excessively bent or straightened head, an odd position of the arms or legs, awkward or strange movements - all this is often found in children with mental retardation. At the same time, there are no proprioception disorders, as well as cerebellar, pyramidal and extrapyramidal symptoms. Many motor skills that develop in childhood are age-dependent. Apparently, unusual motor skills, including gait in mentally retarded children, are associated with a delay in the maturation of the psychomotor sphere. It is necessary to exclude comorbid conditions with mental retardation: cerebral palsy, autism, epilepsy, etc.

Gait (and other psychomotor skills) in severe dementia

Dysbasia in dementia reflects the total collapse of the ability for organized, purposeful and adequate action. Such patients begin to attract attention to themselves with their disorganized motor skills: the patient stands in an awkward position, stamps his feet, spins, being unable to purposefully walk, sit down and adequately gesticulate (the collapse of "body language"). Fussy, chaotic movements come to the fore; the patient looks helpless and confused.

Gait can change significantly in psychoses, in particular in schizophrenia (“shuttle” motor skills, circular movements, stamping and other stereotypes in the legs and arms while walking) and obsessive-compulsive disorders (rituals while walking).

Psychogenic gait disorders of different types

There are gait disturbances, often reminiscent of those described above, but developing (most often) in the absence of current organic damage to the nervous system. Psychogenic gait disturbances often begin acutely and are provoked by an emotional situation. They are variable in their manifestations. They may be accompanied by agoraphobia. The prevalence of women is characteristic.

This gait often looks strange and is difficult to describe. However, a careful analysis does not allow us to classify it as a known example of the above-mentioned types of dysbasia. Often the gait is very picturesque, expressive or extremely unusual. Sometimes it is dominated by the image of falling (astasia-abasia). The patient's entire body reflects a dramatic call for help. During these grotesque, uncoordinated movements, it seems that patients periodically lose their balance. However, they are always able to hold themselves and avoid falling from any uncomfortable position. When the patient is in public, his gait can even acquire acrobatic features. There are also quite characteristic elements of psychogenic dysbasia. For example, the patient, demonstrating ataxia, often walks, "braiding a braid" with his legs, or, presenting paresis, "dragging" the leg, "pulling" it along the floor (sometimes touching the floor with the dorsum of the big toe and foot). But psychogenic gait can sometimes outwardly resemble gait in hemiparesis, paraparesis, cerebellar diseases, and even Parkinsonism.

As a rule, there are other conversion manifestations, which are extremely important for diagnosis, and false neurological signs (hyperreflexia, pseudo-Babinski symptom, pseudo-ataxia, etc.). Clinical symptoms should be assessed comprehensively; it is very important to discuss in detail in each such case the probability of true dystonic, cerebellar or vestibular gait disorders. All of them can sometimes cause chaotic gait changes without sufficiently clear signs of an organic disease. Dystonic gait disorders can more often resemble psychogenic disorders. Many types of psychogenic dysbasia are known and even their classifications have been proposed. Diagnostics of psychogenic movement disorders should always be subject to the rule of their positive diagnosis and exclusion of an organic disease. It is useful to involve special tests (Hoover test, weakness of the sternocleidomastoid muscle, etc.). The diagnosis is confirmed by the placebo effect or psychotherapy. Clinical diagnostics of this type of dysbasia often requires special clinical experience.

Psychogenic gait disorders are rarely observed in children and the elderly.

Dysbasia of mixed origin

Cases of complex dysbasia against the background of certain combinations of neurological syndromes (ataxia, pyramidal syndrome, apraxia, dementia, etc.) are often encountered. Such diseases include cerebral palsy, multiple system atrophy, Wilson-Konovalov disease, progressive supranuclear palsy, toxic encephalopathies, some spinocerebellar degenerations, and others. In such patients, the gait has features of several neurological syndromes at the same time, and a careful clinical analysis is needed in each individual case to assess the contribution of each of them to the manifestations of dysbasia.

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Iatrogenic dysbasia

Iatrogenic dysbasia is observed during drug intoxication and is often ataxic (“drunk”) in nature, mainly due to vestibular or (less commonly) cerebellar disorders.

Sometimes such dysbasia is accompanied by dizziness and nystagmus. Most often (but not exclusively) dysbasia is caused by psychotropic and anticonvulsant (especially diphenin) drugs.

Dysbasia caused by pain (antalgic)

When pain occurs during walking, the patient tries to avoid it by modifying or shortening the most painful phase of walking. When pain is unilateral, the affected leg bears weight for a shorter period. The pain may occur at a specific point in each step, but may be present throughout the entire act of walking or gradually decrease with continued walking. Gait disturbances caused by leg pain most often manifest externally as a "claudication."

Intermittent claudication is a term used to describe pain that occurs only when walking a certain distance. In this case, the pain is due to arterial insufficiency. This pain occurs regularly when walking after a certain distance, gradually increases in intensity, and occurs over shorter distances over time; it occurs sooner if the patient climbs uphill or walks quickly. The pain forces the patient to stop, but disappears after a short period of rest if the patient remains standing. The pain is most often localized in the calf. The typical cause is stenosis or occlusion of blood vessels in the upper thigh (typical history, vascular risk factors, absent pulse in the foot, bruit over the proximal blood vessels, no other cause for pain, sometimes sensory disturbances such as stockings). In such circumstances, pain in the perineum or thigh may additionally be observed, caused by occlusion of the pelvic arteries; such pain must be differentiated from sciatica or a process affecting the cauda equina.

Intermittent claudication with cauda equina lesions (caudogenic) is a term used to describe pain from root compression observed after walking various distances, especially when going downhill. The pain is a consequence of compression of the cauda equina roots in the narrow spinal canal at the lumbar level, when the addition of spondylotic changes causes an even greater narrowing of the canal (stenosis of the canal). Therefore, this type of pain is most often found in elderly patients, especially men, but can also occur in young people. Based on the pathogenesis of this type of pain, the disorders observed are usually bilateral, radicular in nature, predominantly in the posterior perineum, upper thigh and lower leg. Patients also complain of back pain and pain when sneezing (Naffziger's symptom). Pain during walking forces the patient to stop, but usually does not completely disappear if the patient is standing. Relief occurs when changing the position of the spine, for example, when sitting, bending forward sharply, or even squatting. The radicular nature of the disorder becomes especially obvious if there is a shooting pain. In this case, there are no vascular diseases; radiography reveals a decrease in the sagittal size of the spinal canal in the lumbar region; myelography shows a violation of the passage of contrast at several levels. Differential diagnosis is usually possible, taking into account the characteristic localization of pain and other features.

Pain in the lumbar region when walking may be a manifestation of spondylosis or intervertebral disc disease (history of acute back pain radiating along the sciatic nerve, sometimes absence of Achilles reflexes and paresis of the muscles innervated by this nerve). Pain may be a consequence of spondylolisthesis (partial dislocation and "slippage" of the lumbosacral segments). It may be caused by ankylosing spondylitis (Bechterew's disease), etc. X-ray examination of the lumbar spine or MRI often clarify the diagnosis. Pain due to spondylosis and intervertebral disc disease often increases with prolonged sitting or an uncomfortable position, but may decrease or even disappear with walking.

Pain in the hip and groin area is usually the result of hip arthrosis. The first few steps cause a sharp increase in pain, which gradually decreases with continued walking. Rarely, pseudoradicular irradiation of pain along the leg, a violation of internal rotation of the hip, causing pain, a feeling of deep pressure in the femoral triangle. When a cane is used during walking, it is placed on the side opposite to the pain to transfer the body weight to the healthy side.

Sometimes, during walking or after prolonged standing, pain in the groin area may be observed, associated with damage to the ilioinguinal nerve. The latter is rarely spontaneous and is more often associated with surgical interventions (lumbotomy, appendectomy), in which the nerve trunk is damaged or irritated by compression. This cause is confirmed by the history of surgical manipulations, improvement with hip flexion, the most severe pain in the area two finger widths medial to the anterior superior iliac spine, sensory disturbances in the iliac region and the area of the scrotum or labia majora.

A burning pain along the outer surface of the thigh is characteristic of meralgia paresthetica, which rarely leads to a change in gait.

Local pain in the area of long tubular bones that occurs when walking should raise suspicion of a local tumor, osteoporosis, Paget's disease, pathological fractures, etc. Most of these conditions, which can be detected by palpation (pain on palpation) or radiography, are also characterized by back pain. Pain along the anterior surface of the shin may occur during or after prolonged walking or other excessive tension in the muscles of the shin, as well as after acute occlusion of the vessels of the leg, after surgery on the lower limb. The pain is a manifestation of arterial insufficiency of the muscles of the anterior region of the lower leg, known as anterior tibial arteriopathic syndrome (pronounced increasing painful swelling; pain from compression of the anterior parts of the lower leg; disappearance of pulsation in the dorsalis pedis artery; lack of sensitivity on the dorsum of the foot in the innervation zone of the deep branch of the peroneal nerve; paresis of the extensor muscles of the fingers and the short extensor of the big toe), which is a variant of the muscle bed syndrome.

Pain in the foot and toes is particularly common. Most cases are caused by foot deformities such as flat feet or wide feet. Such pain usually occurs after walking, after standing in hard-soled shoes, or after carrying heavy objects. Even after a short walk, a heel spur can cause heel pain and increased sensitivity to pressure on the plantar surface of the heel. Chronic Achilles tendonitis is manifested, in addition to local pain, by a palpable thickening of the tendon. Pain in the forefoot is observed in Morton's metatarsalgia. The cause is a pseudoneuroma of the interdigital nerve. At first, the pain appears only after long walking, but later it may appear after short episodes of walking and even at rest (the pain is localized distally between the heads of the III-IV or IV-V metatarsal bones; it also occurs with compression or displacement of the heads of the metatarsal bones relative to each other; lack of sensitivity on the contacting surfaces of the toes; disappearance of pain after local anesthesia in the proximal intertarsal space).

Quite intense pain on the plantar surface of the foot, which forces you to stop walking, can be observed with tarsal tunnel syndrome (usually with a dislocation or fracture of the ankle, pain occurs behind the medial malleolus, paresthesia or loss of sensitivity on the plantar surface of the foot, dry and thin skin, lack of sweating on the sole, inability to abduct the toes compared to the other foot). Sudden visceral pain (angina, pain with urolithiasis, etc.) can affect gait, significantly change it and even cause a stop in walking.

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Paroxysmal gait disturbances

Periodic dysbasia can be observed in epilepsy, paroxysmal dyskinesia, periodic ataxia, as well as pseudo-seizures, hyperekplexia, and psychogenic hyperventilation.

Some epileptic automatisms include not only gesticulation and certain actions, but also walking. Moreover, there are such forms of epileptic seizures that are provoked only by walking. These seizures sometimes resemble paroxysmal dyskinesia or gait apraxia.

Paroxysmal dyskinesias that begin during walking can cause dysbasia, stopping, falling of the patient, or additional (forced and compensatory) movements against the background of continued walking.

Periodic ataxia causes periodic cerebellar dysbasia.

Psychogenic hyperventilation often not only causes lipothymic states and fainting, but also provokes tetanic convulsions or demonstrative movement disorders, including periodic psychogenic dysbasia.

Hyperekplexia can cause gait disturbances and, in severe cases, falls.

Myasthenia gravis is sometimes the cause of periodic weakness in the legs and dysbasia.

Diagnostic tests for gait disorders

A large number of diseases that can lead to dysbasia require a wide range of diagnostic tests, in which clinical neurological examination is of primary importance. They use CT and MRI; myelography; evoked potentials of various modalities, including evoked motor potential, stabilography, EMG; muscle and peripheral nerve biopsy; cerebrospinal fluid examination; screening for metabolic disorders and identification of toxins and poisons; psychological examination; sometimes consultation with an ophthalmologist, otolaryngologist or endocrinologist is important. Other various tests are also used as indicated, including special methods for studying gait.

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