Violation of gait (dysbasia)

In humans, ordinary "bipedal" walking is the most complexly organized motor act, which, along with speech ability, distinguishes a person from his predecessors. Walking is optimally realized only under the condition of a normal functioning of a large number of physiological systems. Walking, as an arbitrary motor act, requires unhindered passage of motor impulses through the pyramid system, as well as the active participation of extrapyramidal and cerebellar control systems that perform 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 well as the preservation of the mechanical structure of bones, joints and muscles.

Since many levels of the nervous system participate in the exercise of a normal gait, there are therefore a large number of causes that can disrupt the normal act of walking. Some diseases and damage to the nervous system are accompanied by characteristic and even pathognomonic disabilities of the gait. The pathological gait pattern imposed by the disease erases its normal sexual differences and determines this or that type of dysbasia. Therefore, careful monitoring of walking is often very valuable for differential diagnosis and should be performed at the beginning of a neurological examination.

During the clinical study of gait, the patient walks with open and closed eyes; goes forward with his face and back; demonstrates flanking gait and walking around the chair; gait on toes and heels; along a narrow passage and along a line; slow and fast walking; run; turns during walking; climbing the stairs.

There is no generally accepted unified classification of types of dysbasia, In addition, sometimes the patient has a complex gait, since several types of dysbasia are present simultaneously. The physician should see all the components from which the dysbasia is composed 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 very different gait disorders complain of "dizziness".

Disorders of walking are a frequent syndrome in the population, especially among the elderly. Up to 15% of people older than 60 years experience some disturbance of walking and periodic falls. Among older people, this percentage is even higher.

Gait with diseases of the musculoskeletal system

The consequences of ankylosing spondylitis and other forms of spondylitis, atroses of large joints, tendon retractions on the foot, congenital anomalies, etc. Can lead to a variety of gait disorders, the causes of which are not always associated with pain (clubfoot, deformations like halux valgus, etc.) Diagnosis requires an orthopedic consultation.

The main types of abnormalities of gait (dysbasia)

1. Atactic gait:
   1. cerebellar;
   2. stamping ("tabetic");
   3. with the vestibular symptom complex.
2. "Hemiparetic" ("mowing" or by the type of "triple shortening").
3. Paraspastic.
4. Spastic-atactic.
5. Hypokinetic.
6. Apraxia walking.
7. Idiopathic senile dysbasia.
8. Idiopathic progressing "frising-dysbasia."
9. Gait in the "skater's pose" with idiopathic orthostatic hypotension.
10. "Peroneal" gait - one-sided or two-sided stepping.
11. Walking with perezhbibaniem in the knee joint.
12. "Duck" walk.
13. Walking with a pronounced lordosis in the lumbar region.
14. Gait in diseases of the musculoskeletal system (ankylosis, arthrosis, tendon retraction, etc.).
15. Hyperkinetic gait.
16. Dysbasia with mental retardation.
17. Gait (and other psychomotorics) with severe dementia.
18. Psychogenic disorders of gait of different types.
19. Dysbasia of mixed origin: complex dysbasia in the form of gait disorders against the background of certain combinations of neurological syndromes: ataxia, pyramidal syndrome, apraxia, dementia, etc.
20. Iatrogenic dysbasia (unstable or "drunk" gait) with drug intoxication.
21. Dysbasia caused by pain (antalgic).
22. Paroxysmal abnormalities of gait with epilepsy and paroxysmal dyskinesia.

Atactic gait

Movement in cerebellar ataxia is poorly commensurate with the features of the surface on which the patient is going. The equilibrium is disrupted to a greater or lesser degree, which leads to corrective movements, giving the gait a randomly chaotic character. It is characteristic, especially for the defeat of the cerebellar worm, walking on a wide base as a result of instability and staggering.

The patient often staggers not only when walking, but also in a standing or sitting position. Occasionally tituration is revealed - a characteristic cerebellar tremor of the upper half of the trunk and head. As accompanying signs, dysmetry, adiadochokinesis, intentional tremor, postural instability are revealed. Other characteristic signs (chanted speech, nystagmus, muscle hypotension, etc.) can also be detected.

The main reasons: cerebellar ataxia accompanies a large number of hereditary and acquired diseases that occur with the defeat of the cerebellum and its connections (spin-cerebellar degenerations, malabsorption syndrome, cerebellar alcoholic degeneration, multiple systemic atrophy, late cerebellar atrophy, hereditary ataxia, OPCA, tumors, paraneoplastic degeneration cerebellum and many other diseases).

With the defeat of the conductors of deep muscular sensation (most often at the level of the posterior columns), a sensitive ataxia develops. It is particularly pronounced when walking and is manifested by characteristic movements of the legs, which are often referred to as "stamping" gait (the leg is forcefully lowered all over the sole to the floor); in extreme cases, walking is impossible at all because of the loss of deep sensitivity, which is easily revealed in the study of the musculo-articular feeling. A characteristic feature of a sensitive ataxia is the correction of its vision. This is the basis of the Romberg test: when closing the eyes, sensitive ataxia increases dramatically. Sometimes, with closed eyes, pseudoathetosis is detected in the arms extended forward.

The main reasons: Sensitive ataxia is characteristic not only of hitting the posterior columns, but also of other levels of deep sensitivity (peripheral nerve, posterior spine, brain stem, etc.). Therefore, sensitive ataxia is observed in the picture of such diseases as polyneuropathy ("peripheral pseudotubes"), funicular myelosis, spinal dryness, complications of vincristine treatment; paraproteinemia; paranesplastic syndrome, etc.)

With vestibular disorders, ataxia is less pronounced and more apparent in the legs (staggering when walking and standing), especially at dusk. A gross lesion of the vestibular system is accompanied by an expanded picture of the vestibular symptom complex (systemic dizziness, spontaneous nystagmus, vestibular ataxia, vegetative disorders). Light vestibular disorders (vestibulopathy) is manifested only by intolerance to vestibular loads, which often accompanies neurotic disorders. With vestibular ataxia, there are no cerebellar signs and a violation of the musculo-articular feeling.

The main causes: the vestibular symptom complex is characteristic for the lesion of vestibular conductors at any level (sulfur plugs in the external auditory canal, labyrinthitis, Meniere's disease, neurinoma of the auditory nerve, multiple sclerosis, degenerative lesions of the brainstem, syringobulbia, vascular diseases, intoxications , craniocerebral trauma, epilepsy, etc.). Peculiar vestibulopathy usually accompanies psychogenic chronic neurotic states. For diagnosis, it is important to analyze complaints of dizziness and related neurologic manifestations.

[1], [2], [3], [4]

The "hemiperetic" gait

The hemiparetic gait is manifested by the extension and circumcism of the leg (the arm is bent at the elbow joint) in the form of a "mowing" gait. The paretic leg when walking is exposed to body weight for a shorter period than a healthy leg. Circumduction (circular motion of the leg) is observed: the leg is unbent at the knee joint with a slight plantar flexion of the foot and performs a circular movement outward, with the trunk slightly deflected in the opposite direction; The homolateral hand loses some of its functions: it is bent in all joints and pressed against the trunk. If a stick is used when walking, it is used on the healthy side of the body (for which the patient bends and transfers her weight to it). At each step the patient raises the pelvis to tear his straightened leg off the floor and hardly carries it forward. Less often the gait is upset by the type of "triple shortening" (flexion in the three joints of the leg) with a characteristic rise and lowering of the pelvis on the side of paralysis at each step. Concomitant symptoms: weakness in the affected limbs, hyperreflexia, pathological stop signs.

The main reasons: hemiparetic gait occurs with a variety of organic lesions of the brain and spinal cord, such as strokes of various origin, encephalitis, brain abscess, trauma (including birth), 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 unbent in the knee and ankle joints. The gait is slow, the legs "shuffle" on the floor (the outsole of shoes is accordingly worn out), sometimes they move like a pair of scissors with their crossing (due to an increase in the tonus of the leading hamstrings), on the toes and with a slight turn of the fingers ("pigeon" fingers). This type of gait disturbance is usually due to a more or less symmetrical bilateral defeat of pyramidal pathways at any level.

The main reasons: the parasastic gait is most often observed under the following circumstances:

• Multiple sclerosis (characteristic spastico-atactic gait)
• Lacunar condition (in elderly patients with arterial hypertension or other risk factors of vascular disease, often preceded by episodes of small ischemic vascular strokes, accompanied by pseudobulbar symptoms with speech disorders and bright reflexes of oral automatism, gait with small steps, pyramidal signs).
• After a spinal cord injury (history, level of sensitive disorders, urination disorders). Illnesses of Little (special form of infantile cerebral palsy, the symptoms of the disease are from birth, there is a delay in motor development, but normal intellectual development, often only selective involvement of the extremities, especially the lower ones, with scissor movements with crossing legs during walking). Family spastic paralysis (a hereditary slowly progressing disease, symptoms often appear in the third decade of life). With cervical myelopathy in the elderly, mechanical compression and vascular insufficiency of the cervical spinal cord often cause a paraspastic (or spastic-atactic) gait.

As a result of rare, partially reversible conditions, such as hyperthyroidism, portocaval anastomosis, lathirism, damage to the posterior columns (with vitamin B12 deficiency or paraneoplastic syndrome), adrenoleukodystrophy.

Intermittent paras- tic gait is rarely seen in the picture of "intermittent claudication of the spinal cord".

Paraspastic gait sometimes imitates the dystonia of the lower limbs (especially with the so-called dopa-responsive dystonia), which requires a syndromic differential diagnosis.

Spastic-atactic gait

In this violation of the gait, a distinctive atactic component is attached to the characteristic parasastic gait: unbalanced movements of the body, slight overdistension in the knee joint, instability. This picture is characteristic, almost pathognomonic for multiple sclerosis.

The main reasons: it can be observed also in subacute combined degeneration of the spinal cord (funicular myelosis), Friedreich disease and other diseases involving the cerebellar and pyramidal pathways.

Hypokinetic gait

This type of gait is characterized by slow, constrained movements of the legs with a decrease or lack of friendly hand movements and a strained posture; difficulty in initiating walking, shortening a step, "shuffling", difficult turns, trampling on the spot before the movement, sometimes - "pulsion" phenomena.

The most common etiological factors of this type of gait include:

1. Hypokinetics-hypertensive extrapyramidal syndromes, especially parkinsonism syndrome (which is characterized by a slight flexor posture, there are no friendly hand movements during walking, stiffness, masklike face, quiet monotone speech and other manifestations of hypokinesia, tremor of rest, the phenomenon of cogwheel, gait slow, "Shuffling", rigid, with a shortened step, "pulsatile" phenomena are possible when walking).
2. Other hypokinetic extrapyramidal and mixed syndromes, including progressive supranuclear palsy, olive-ponto-cerebellar atrophy, Shay-Draeger syndrome, strigo-nigral degeneration (parkinsonism-plus syndromes), Binswanger's disease, vascular "parkinsonism of the lower half of the body." In the lacunar state, there may also be a gait like "marche a petits pas" (small short irregular shuffling steps) against the background of pseudobulbar paralysis with swallowing disorders, verbal disorders and parkinsonian-like motility. "Marche a petits pas" can also be observed in the picture of normotensive hydrocephalus.
3. Akinetic-rigid syndrome and associated gait are possible with Pick's disease, cortico-basal degeneration, Creutzfeldt-Jakob disease, hydrocephalus, frontal lobe tumor, Huntington's juvenile disease, Wilson-Konovalov's disease, posthypoxic encephalopathy, neurosyphilis and some other more rare diseases.

In young patients, torsion dystonia can sometimes make its debut with an unusual tightly-bound gait due to dystonic hypertension in the legs.

Syndrome of constant activity of muscle fibers (Isaacs syndrome) is most often observed in young patients. Unusual tension of all muscles (mostly distal), including antagonists, blocks the gait, like all other movements (gait armadillo)

Depression and catatonia may be accompanied by hypokinetic gait.

Apraxia walk

Apraxia walking is characterized by a loss or a decrease in the ability to properly use the legs in the act of walking in the absence of sensory, cerebellar and paretic manifestations. This type of gait occurs in patients with extensive cerebral lesions, especially frontal lobes. The patient can not imitate certain movements with his legs, although certain automatic movements are preserved. The ability to consecutive composition of movements in "bipedal" walking is reduced. This type of gait is often accompanied by perseverations, hypokinesia, rigidity and, sometimes, hegenhalten, as well as dementia or urinary incontinence.

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

[5], [6], [7], [8], [9]

Idiopathic senile dysbasia

This form of dysbasia ("gait of the elderly", "senile gait") is manifested by a slightly shortened slow pace, mild postural instability, a decrease in friendly hand movements in the absence of any other neurological disorders in the elderly and old people. At the heart of such a dysbasia is a complex of factors: multiple sensory deficiency, age changes in the joints and spine, worsening of vestibular and postural functions, etc.

Idiopathic progressive "frising-dysbasia"

"Friction-dysbasia" is usually observed in the picture of Parkinson's disease; rarely it occurs in a multi-infarction (lacunar) state, multisystem atrophy, and normotensive hydrocephalus. But elderly patients are described, in whom "frisbings-dysbasia" is the only neurological manifestation. The degree of "congealing" varies from sudden motor blocks when walking to total inability to begin walking. Biochemical analyzes of blood, CSF, and CT and MRI show a normal picture, with the exception of mild cortical atrophy in some cases.

Gait in the "Skater's Pose" with idiopathic orthostatic hypotension

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

Peroneal gait

Peroneal gait - one-sided (more often) or two-sided stepping. Gait by the type of steppe develops with the so-called hanging stop and is caused by weakness or paralysis of the dorsophleksis (back folding) of the foot and / or fingers. The patient either "drags" the foot when walking, or, trying to compensate for the dangling of the foot, raises it as high as possible to tear it off the floor. Thus, there is increased flexion in the hip and knee joints; The foot is thrown forward and falls down on the heel or the entire foot with a characteristic spanking sound. The support phase during walking is shortened. The patient is not able to stand on his heels, but can stand and walk on his toes.

The most common cause of unilateral paresis of the extensor of the foot is a violation of the function of the peroneal nerve (compression neuropathy), lumbar plexopathy, rarely lesions of the roots of L4 and, especially, L5, as in the hernia of the intervertebral disc (vertebral peroneal paralysis). Two-sided paresis of the extensor of the foot with a bilateral "stepping" is often observed with polyneuropathy (paresthesia is noted, sensitive disorders such as stockings, absence or decrease of achilles reflexes), with peroneal muscular atrophy of Charcot-Marie-Toot - a hereditary disease of three types (high arch of foot, atrophy of the leg muscles ("stork" legs), absence of achilles reflexes, sensitive disorders are minor or absent), with spinal muscular atrophy - (in which paresis is accompanied by atrophy of the other muscle growth, slow progression, fasciculations, absence of sensitive disorders) and in some distal myopathies (scapulo-peroneal syndromes), especially in the dystrophic myotonia of Steinert-strong atten-Gibb.

A similar pattern of gait disturbance develops when both distal branches of the sciatic nerve are affected ("hanging stop").

Walking with overextension in the knee joint

Walking with a one- or two-sided perezbibaniem in the knee joint is observed with paralysis of extensors of the knee. Paralysis of the extensor of the knee (quadriceps femoris muscle) leads to overextension with support on the leg. When the weakness is bilateral, both legs are dislocated in the knee joints while walking; otherwise carrying weight from foot to foot can cause changes in the knee joints. Descending the stairs begins with the paretic leg.

Causes of unilateral paresis include defeat of the femoral nerve (prolapse of the knee reflex, impaired sensation in the innervation region of n. Saphenous)) and lumbar plexus lesion (symptoms similar to those in femoral nerve injury, but the abductors and ilio-lumbar muscles are also involved). Most often, the cause of bilateral paresis is myopathy, especially progressive Duchenne muscular dystrophy in boys, as well as polymyositis.

«Duck» gait

The paresis (or mechanical failure) of the hip abductor muscles, that is, the femoral abductors (mm gluteus medius, gluteus minimus, tensor fasciae latae) leads to inability to keep the pelvis horizontally with respect to the leg carrying the load. If the insufficiency is only partial, then the over-extension of the trunk towards the supporting leg can be sufficient to transfer the center of gravity and prevent the pelvis from tilting. This is the so-called dumbling Duchenne, when there are bilateral violations, this leads to an unusual gait "in the mess" (the patient, as it were, is shifted from foot to foot, "duck" gait). With complete paralysis of the abductor of the hip, the transfer of the center of gravity described above is already insufficient, which leads to the skewing of the pelvis at each step towards the movement of the leg - the so-called Trendelenburg's lameness.

One-sided paresis or deficiency of the abductor of the femur can be caused by damage to the upper gluteal nerve, sometimes as a result of intramuscular injection. Even in an inclined position, there is a lack of strength for external removal of the affected leg, but there are no sensitive disorders. Such a deficiency is detected with unilateral congenital or posttraumatic hip dislocation or postoperative (prosthetics) damage to the abductor of the femur. Bilateral paresis (or failure) is usually a consequence of myopathy, especially progressive muscular dystrophy, or bilateral congenital dislocation of the hip.

[10], [11]

Walking with pronounced lordosis in the lumbar region

If extensor femurs are involved, especially m. Gluteus maximus, then climbing the stairs becomes possible only at the beginning of movement with a healthy leg, but when you descend the stairs first comes the affected leg. Walking on a flat surface is broken, as a rule, only with the bilateral weakness m. Gluteus maximus; such patients go with a ventral inclined pelvis and with an enlarged lumbar lordosis. For one-sided paresis, m. Gluteus maximus it is impossible to lead the affected leg to the back, even in the position of pronation.

The cause is always a (rare) lesion of the lower gluteal nerve, for example, due to intramuscular injection. Double sided paresis m. Gluteus maximus is most often seen with a progressive form of muscular dystrophy of the pelvic girdle and Duchenne's form.

Occasionally, the literature mentions the so-called syndrome of femoral-lumbar extensic rigidity, 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, indistinctly pronounced lordosis, sometimes with lateral curvature. The main symptom of the "board" or "shield": in the position lying on the back with passive lifting for both stops of elongated legs, the patient does not have flexion in the hip joints. Walking, which is jerky in nature, is accompanied by compensatory thoracic kyphosis and a tilt of the head forward in the presence of rigidity of the neck muscles of extensors. Pain syndrome is not leading in the clinical picture and is often blurred, abortive. A common cause of the syndrome is the fixation of the dural sac and the end thread by a cicatrical-adhesive process in combination with osteochondrosis against a background of dysplasia of the lumbar spine or with a spinal tumor at the cervical, thoracic or lumbar level. The symptom regression occurs after surgical mobilization of the dural sac.

Hyperkinetic gait

Hyperkinetic gait occurs with different types of hyperkinesia. These include diseases such as Sydenham's chorea, Huntington's chorea, generalized torsion dystonia ("camel's walk"), axial dystonic syndromes, pseudo-expressive dystonia, and dystonia of the foot. More rare causes of walking disorders are myoclonus, trunk trunk, orthostatic tremor, Tourette syndrome, tardive dyskinesia. Under these conditions, the movements necessary for normal walking are unexpectedly interrupted by involuntary, disordered movements. Develops a strange or "dancing" gait. (This walk with Huntington's chorea sometimes looks so strange that it can resemble psychogenic dysbasia). Patients should constantly struggle with these disorders to move purposefully.

Gait disorders with mental retardation

This type of dysbasia is an insufficiently studied problem. A clumsy standing with an overly bent or unbent head, a fanciful position of hands or feet, awkward or strange movements - all this is often found in children with mental retardation. There are no violations of proprioception, as well as cerebellar, pyramidal and extrapyramidal symptoms. Many motor skills formed 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 with mental retardation states: infantile cerebral palsy, autism, epilepsy, etc.

Gait (and other psychomotorics) with severe dementia

Disbalance in dementia reflects the total disintegration of the ability to organize purposeful and adequate action. Such patients begin to attract attention with their disorganized motor skills: the patient stands in an awkward posture, stumbles on the spot, dizzy, unable to walk purposefully, sit down and adequately gesticulate (disintegration of the "body language"). Fussy, chaotic movements come to the fore; the patient looks helpless and confused.

The gait can change significantly in psychoses, in particular in schizophrenia (shuttle motility, circular motion, pratoptyvaniya and other stereotypes in the legs and hands during walking) and obsessive-compulsive disorders (rituals during walking).

Psychogenic disorders of gait of different types

There are violations of gait, often reminiscent of those described above, but developing (most often) in the absence of the current organic lesion of the nervous system. Psychogenic disorders of gait often begin acutely and are provoked by an emotiogenic situation. They are variable in their manifestations. They can be accompanied by agoraphobia. Characteristic of the predominance of women.

Such a gait often looks strange and poorly describes. However, careful analysis does not allow to attribute it to known patterns 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 the fall (astasia-abasia). The entire body of the patient reflects a dramatic appeal for help. During these grotesque, uncoordinated movements, it seems that patients periodically lose their balance. Nevertheless, they are always able to restrain themselves and avoid falling from any uncomfortable position. When the patient is in public, his gait can acquire even acrobatic features. There are also quite typical elements of psychogenic dysbasia. The patient, for example, demonstrating ataxia, often goes "braiding his scythe" with his feet, or, showing paresis, "drags" his leg, "dragging" her on the floor (sometimes touching the floor with the back surface of the thumb and foot). But the psychogenic gait can sometimes outwardly resemble the gait in hemiparesis, paraparesis, cerebellar diseases and even in parkinsonism.

As a rule, there are other conversion manifestations, which is extremely important for diagnosis, and false neurological signs (hyperreflexia, Babinsky pseudo-symptom, pseudo-ataxia, etc.). Clinical symptoms should be evaluated in a comprehensive manner, it is very important in every such case to discuss in detail the likelihood of true dystonic, cerebellar or vestibular walking disorders. All of them can cause sometimes erratic changes in gait without sufficiently clear signs of organic disease. Dystonic disorders of gait more often than others may resemble psychogenic disorders. Many types of psychogenic dysbasia are known and even their classifications are suggested. Diagnosis of psychogenic motor disorders should always obey the rule of their positive diagnosis and exclusion of organic disease. It is useful to attract special tests (Hoover test, weakness of the nodding muscle, and others). The diagnosis is confirmed by the effect of placebo or psychotherapy. Clinical diagnosis of this type of dysbasia often requires special clinical experience.

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

Dislocation of mixed origin

Often there are cases of complex dysbasia against a combination of neurological syndromes (ataxia, pyramidal syndrome, apraxia, dementia, etc.). These diseases include infantile cerebral palsy, multiple systemic atrophy, Wilson-Konovalov's disease, progressive supranuclear palsy, toxic encephalopathies, some spinocerebellar degenerations, and others. In such patients, the gait carries the features of several neurological syndromes simultaneously and needs careful clinical analysis in each individual case in order to assess the contribution of each of them to the manifestations of dysbasia.

[12], [13], [14]

Iatrogenic dysbasia

Iatrogenic dysbasia is observed with drug intoxication and often has an atactic ("drunk") character mainly due to vestibular or (more rarely) cerebellar disorders.

Sometimes such a 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 there is pain during walking, the patient tries to avoid it by changing or shortening the most painful phase of walking. When the pain is one-sided, the affected leg transfers weight for a shorter period. Pain may occur at a certain point in each step, but may occur during the entire act of walking or gradually decrease with continuous walking. Gait disturbances, caused by pain in the legs, often appear externally as "lameness".

Intermittent claudication is a term that is used to refer to pain that appears only while walking a certain distance. In this case, the pain is due to arterial insufficiency. This pain appears regularly when walking after a certain distance, gradually increases in intensity, and over time appears at shorter distances; It will appear sooner if the patient rises or goes quickly. The pain causes the patient to stop, but disappears after a short rest period, if the patient remains standing. The pain is most often localized in the region of the shin. A typical cause is stenosis or occlusion of the blood vessels in the upper thigh (typical anamnesis, vascular risk factors, absence of pulsations on the foot, noise above the proximal blood vessels, absence of other causes for pain, sometimes sensitive disorders by the type of stockings). Under such circumstances, pain in the perineal or hip region caused by occlusion of the pelvic arteries may be observed in addition, such pain should be differentiated from sciatica or the process that attacks the ponytail.

Intermittent claudication in the defeat of the horse's tail (caudogenic) is the term used to refer to pain when compressing the roots, observed after walking to different distances, especially when going down. Pain is the result of compression of the roots of the horse tail in a narrow spinal canal at the lumbar level, when the attachment of spondyloid changes causes an even narrower canal (canal stenosis). Therefore, this type of pain is most often found in elderly patients, especially men, but can also occur at a young age. Based on the pathogenesis of this type of pain, the observed disorders are usually bilateral, radicular in nature, mainly in the posterior crotch, upper thigh and lower leg. Patients also complain of back pain and pain during sneezing (Nuffziger's symptom). Pain during walking causes the patient to stop, but usually does not completely disappear if the patient is standing. Relief occurs when the position of the spine changes, for example, when sitting, slanting forward, or even squatting. The radicular nature of the disturbances becomes especially obvious if there is a shooting character of the pain. At the same time there are no vascular diseases; X-ray reveals a decrease in the sagittal size of the vertebral canal in the lumbar region; Myelography shows a violation of the passage of contrast at several levels. Differential diagnosis is usually possible, given the characteristic localization of pain and other features.

Pain in the lumbar region when walking can be a manifestation of spondylosis or lesion of intervertebral discs (a history of acute back pain with irradiation on the sciatic nerve, sometimes the absence of achilles reflexes and paresis of the muscles innervated by this nerve). Pain can be a consequence of spondylolisthesis (partial dislocation and "slipping" of the lumbosacral segments). It can be caused by ankylosing spondylitis (Bekhterev's disease), etc. Radiographic examination of the lumbar spine or MRI often clears the diagnosis. Pain due to spondylosis and intervertebral disk pathology often increases with prolonged sitting or uncomfortable posture, but may decrease or even disappear when walking.

Pain in the hip and groin area is usually the result of arthrosis of the hip joint. The first few steps cause a sharp increase in pain, which gradually decreases with the continuation of walking. Rarely there is pseudo-radicular pain radiating on the leg, a violation of the inner rotation of the thigh, causing pain, a feeling of deep pressure in the region of the femoral triangle. When walking is used with a walking stick, it is located on the side of the opposite pain to transfer the body weight to the healthy side.

Sometimes during walking or after a long standing, there may be pain in the inguinal area associated with the defeat of the ilio-inguinal 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 reason is confirmed by anamnesis of surgical manipulations, improvement in flexion of the thigh, the most pronounced pain in the region by two fingers medial to the anterior superior iliac spine, sensitive disorders in the ileum and scrotum or large labia.

Burning pain over the external surface of the thigh is characteristic of the paresthetic meralgia, which rarely leads to a change in gait.

Local pain in the region of long tubular bones that occurs when walking should cause suspicion of a local tumor, osteoporosis, Paget's disease, pathological fractures, and the like. For most of these conditions, which can be detected by palpation (pain in palpation) or radiography, back pain is also characteristic. Pain along the front surface of the shin can appear during or after a long walk, or other excess tension of the calf muscles, and also after acute occlusion of the leg vessels, after surgical intervention on the lower limb. Pain is a manifestation of arterial insufficiency of the anterior calf muscles, known as anterior tibial arteriopathic syndrome (pronounced painful edema, pain from compression of the anterior calf, disappearance of pulsation on the back artery of the foot, lack of sensitivity on the back surface of the foot in the innervation zone of the deep branch of the peroneal nerve; paresis of the extensor muscles of the fingers and a short extensor of the thumb), which is a variant of the syndrome of the muscle bed.

Pain in the foot and fingers is especially frequent. The reason for most cases is a deformation of the foot, such as a flat foot or a wide foot. Such a pain usually appears after walking, after standing in the shoes on the hard soles, or after wearing the weight. Even after a short walk, the calcaneal spur can cause pain in the heel area and an increased sensitivity to the pressure of the plantar surface of the heel. Chronic tendonitis of the Achilles tendon is manifested, not counting local pain, with palpable thickening of the tendon. Pain in the forefoot of the foot is observed with Metatarsalgia Morton. The reason is the pseudoneuropath of the interdigital nerve. In the beginning, the pain appears only after a long walk, but later it can appear after short episodes of walking and even at rest (the pain is localized distally between the heads of III-IV or IV-V metatarsal bones, also occurs when the heads of metatarsal bones are compressed or displaced 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).

A fairly intense pain on the sole of the foot, which forces you to stop walking, can be observed with a tarsal tunnel syndrome (usually with a dislocation or fracture of the ankle, pain occurs behind the medial malleolus, paresthesia or loss of sensation on the plantar surface of the foot, dryness and thinning of the skin, no sweating on soles, the impossibility of removing the fingers in comparison with the other foot). Suddenly, visceral pain (angina pectoris, pain in urolithiasis, etc.) can affect the gait, significantly change it and even cause a stop in walking.

[15]

Paroxysmal gait disorders

Periodic dysbasia can be observed with epilepsy, paroxysmal dyskinesia, periodic ataxia, as well as with pseudo attacks, hyperexpension, psychogenic hyperventilation.

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

Paroxysmal dyskinesia that began during walking can cause dysbasia, stopping, falling sick or additional (violent and compensatory) movements against the backdrop of continuing walking.

Periodic ataxia causes periodically cerebellar dysbasia.

Psychogenic hyperventilation often not only causes lipotypic conditions and fainting, but also provokes tetanic cramps or demonstrative movement disorders, including periodic psychogenic dysbasia.

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

Myasthenia gravis sometimes causes periodic weakness in the legs and dysbasia.

Diagnostic tests for gait disorders

A large number of diseases that can lead to dysbasia, involves a wide range of diagnostic studies in which a clinical neurological examination is a priority. Use CT and MRI; myelography; evoked potentials of different modalities, including caused motor potential, stabilography, EMG; biopsy of muscles and peripheral nerves; investigation of cerebrospinal fluid; they screen metabolic disorders and identify toxins and poisons; carry out psychological research; Sometimes consultation of the oculist, the otolaryngologist or the endocrinologist is important. Other diverse studies, including special methods for studying gait, are also involved in the indications.

[16], [17], [18],