Walking disorders

Gait impairment is one of the most frequent and severe manifestations of neurological diseases, which often causes disability and loss of independence in everyday life. Despite its clinical significance and widespread prevalence, gait impairments have not been the subject of special study until recently. Research in recent years has significantly complicated the understanding of the phenomenology, structure and mechanisms of gait impairments. Particularly close attention has been drawn to the so-called higher-level gait impairments that arise from damage to the frontal lobes and associated subcortical structures and are caused by damage to the gait regulation and balance maintenance system.

Epidemiology of gait impairment

Gait disorders are common in the population, especially among the elderly. Their prevalence increases exponentially with age. Gait disorders are found in 15% of people over 60 years of age and in 35% of people over 70 years of age. Clinically significant gait disorders are present in approximately half of people placed in nursing homes. Only 20% of people over 85 years of age have normal gait. Among hospitalized neurological patients, gait disorders are found in 60% of cases. Even relatively mild gait disorders are associated with an unfavorable survival prognosis, which is explained by the increased incidence of falls, dementia, cardiovascular and cerebrovascular diseases in this patient population, and the negative impact on survival naturally increases with the severity of the disorder.

Physiology and pathophysiology of walking

Walking is a complex automated rhythmic act, which is provided by synergies - synchronized, time- and space-coordinated contractions of various muscle groups, providing targeted coordinated friendly movements. Some synergies carry out human movement in space (locomotor synergies), others - maintain his balance (postural synergies). The upright posture characteristic of humans makes maintaining balance during walking especially difficult. Each step is essentially a controlled fall and is impossible without a short-term deviation from the state of equilibrium.

Walking is a motor skill acquired in the process of individual development. The basic mechanisms of walking are the same for all people, but their implementation in a specific person with certain biomechanical parameters requires a fine, improved training adjustment of various links of the motor system. Consequently, each person has his own, to a certain extent unique manner of walking. The set of features characterizing the originality, manner of walking of a given person or group of people, as well as the features of walking that are formed under special external conditions or certain diseases, are designated by the term "gait".

Walking consists of steps. Each step is an elementary locomotor cycle consisting of 2 main phases: 1 - the transfer phase, during which the foot is transferred in the air to the next position; 2 - the support phase, during which the foot contacts the surface. Normally, the support phase lasts 60%, the transfer phase - 40% of the time of each cycle. The support phases of both legs overlap in time, and for approximately 20% of the duration of each locomotor cycle, a person rests on both legs (double support phase).

The generation of locomotor and postural synergies and their adaptation to environmental conditions is provided by a complex, hierarchically organized system, in which three main levels can be conditionally distinguished: spinal, brainstem-cerebellar, higher (cortical-subcortical). The subsystems included in its composition solve four main problems: maintaining balance in an upright position, initiating walking, generating rhythmic stepping movements, changing walking parameters depending on the person's goal and external conditions. The mechanisms of walking and maintaining balance (postural control) closely interact with each other, but do not coincide with each other. Therefore, with different diseases involving certain structures of the central nervous system, they can suffer to varying degrees, which often predetermines the specifics of walking disorders and requires a special approach to rehabilitation.

• The alternating contraction of the flexors and extensors of the legs, which underlies walking, is apparently generated by a special polysynaptic mechanism embedded in the lumbar and sacral segments of the spinal cord in animals. The mechanism includes special circles of reciprocally connected intercalated neurons, some of which stimulate flexors, others - extensors (spinal generators of walking). Although the morphological presence of such structures in the human spinal cord has not yet been proven, there is indirect evidence of their existence. This is evidenced, for example, by observations of patients with paraplegia due to high spinal cord damage: when they are placed on a treadmill (with appropriate support), stepping movements are observed.
• Spinal generator mechanisms are under the control of descending corticospinal and brainstem-spinal pathways, which facilitate the initiation of walking, provide fine-tuning of its parameters, especially in complex situations, such as turns, overcoming obstacles, walking on uneven surfaces, etc. The initiation of walking and its speed largely depend on the activity of the mesencephalic locomotor zone, which is located in the dorsolateral part of the midbrain tegmentum and in humans, apparently corresponds to the pedunculopontine nucleus. This nucleus contains cholinergic and glutamatergic neurons, afferentation to which comes (via GABAergic projections) from the subthalamic nucleus, globus pallidus, reticular part of the substantia nigra, striatum, as well as the cerebellum and other brainstem nuclei. In turn, neurons of the pedunculopontine nucleus send impulses to the striatum, compact part of the substantia nigra, thalamus, brainstem and spinal structures. It is through the pedunculopontine nucleus that the influence of the basal ganglia on walking and maintaining balance is apparently mediated. Bilateral damage to this area (for example, due to a stroke) can cause slowness, difficulty initiating walking, freezing, and postural instability.
• The cerebellum corrects the speed and amplitude of movements, coordinates the movements of the trunk and limbs, as well as different segments of one limb. Regulation of walking is provided mainly by the median structures of the cerebellum. Receiving information via the spinocerebellar and corticopontocerebellar tracts, the cerebellum is able to compare the actual movements with the planned ones and, if the result deviates from the planned one, generate corrective signals. Afferentation from the median structures of the cerebellum, following through the nuclei of the tent and further through the reticulo-, vestibulo- and rubrospinal tracts, controls postural synergies, trunk movements, modulates the parameters of the locomotor cycle. Through the thalamus, the cerebellum is connected with the premotor cortex and participates in the highest level of walking regulation.
• The highest level of walking regulation is mainly provided by the cerebral cortex and related subcortical structures. Its main function is to adapt postural and locomotor synergies to specific environmental conditions, body position in space, and individual intentions. It can be divided into 2 main subsystems.
  • The first subsystem is formed by the links of the main motor cortical-subcortical circle. Starting from various sections of the cortex, it successively includes neurons of the striatum, pallidum, thalamus and returns to the additional motor cortex. The latter, interacting with other links of the circle, ensures the preparation and implementation of complex automated, strengthened locomotor and postural synergies, as well as the selection and switching of walking programs when conditions change.
  • The main component of the second subsystem of the higher level of walking regulation is the premotor cortex, through which less automated movements are realized, initiated and realized under the influence of external stimuli. By means of numerous cortical-cortical connections, the premotor cortex interacts with the associative zones of the parietal cortex, which form a diagram of the body and the surrounding space on the basis of the received visual, proprioceptive, tactile, vestibular, auditory information. The premotor cortex ensures the adaptation of locomotor synergies to specific surface conditions and other features of the external environment. This subsystem is especially important for new unusual movements or when performing learned movements, but in an unusual context. Normal walking and maintaining balance are impossible without feedback, which is provided by sensory information of 3 main modalities - somatosensory, vestibular and visual. Information about the body's position in space and the surrounding world is received at all levels of walking regulation, where it is processed and influences the choice and implementation of locomotor and postural synergies. The system of internal representations of the surrounding space is formed in the posterior sections of the parietal cortex, where the received sensory information is generalized in the form of spatial maps. These maps are "transmitted" to the premotor cortex, striatum, superior colliculi, where they serve as the basis for movement regulation.

When sensory pathways are damaged, spatial and temporal coordination of movements may be disrupted due to inadequate representations of the body's position in space and the external environment, and the choice of synergy becomes erroneous. The loss of sensory stimuli of only one modality usually does not lead to balance or gait disorders, but the loss of 2 modalities significantly disrupts balance, and the disruption of 3 modalities inevitably causes severe balance and gait disorders, usually accompanied by frequent falls. In the elderly, the ability to compensate is weakened, and gait disorders may be caused by the loss of sensory stimuli of only one modality or a combination of mild disorders of several modalities.

In the adaptation of locomotor and postural synergies to current conditions, regulatory cognitive functions (such as attention, planning, and activity control) are of great importance, which depend on the functioning of the prefrontal cortex. The hippocampus and parahippocampal gyrus play an important role in spatial navigation. The damage to each level of gait regulation is characterized not only by the defectiveness of certain mechanisms, but also by the specificity of compensatory strategies. Accordingly, gait disorders reflect not only the dysfunction of a particular structure, but also the inclusion of various compensatory mechanisms. As a rule, the higher the level of damage, the more limited the possibilities for compensating the defect.

Classification of gait disorders

The difficulties in classifying gait disorders are explained by the diversity of their causes, mechanisms of development and clinical manifestations. In addition, in many diseases gait disorders are of a combined nature, arising as a result of the interaction of several causes. In recent years, attempts have been made to classify gait and balance disorders by etiology, phenomenology, localization of damage, and pathophysiological mechanism. The most successful attempt was made by JG Nutt, CD Marsden and PD Thompson (1993) to classify gait disorders based on H. Jackson's ideas about the levels of nervous system damage. They correlated gait disorders with 3 levels of nervous system damage. Lower-level disorders include gait disorders caused by damage to the musculoskeletal system and peripheral nerves, as well as impaired sensory afferentation. Middle-level disorders include gait disorders caused by damage to the pyramidal tracts, cerebellum, and extrapyramidal structures. Higher-level disorders include complex, integrative motor control disorders that cannot be explained by damage to the lower and middle levels. These gait disorders can also be designated as primary, since they are directly caused by a disturbance in the selection and initiation of locomotor and postural synergies, rather than their implementation, and do not depend on any other neurological pathology. We propose a modification of the classification of JG Nutt et al. (1993), according to which 6 main categories of gait disorders are distinguished.

• Gait disorders due to lesions of the musculoskeletal system (for example, arthrosis, arthritis, reflex syndromes of osteochondrosis of the spine, scoliosis, rheumatic polymyalgia, etc.), which are often antalgic in nature.
• Gait disorders due to dysfunction of internal organs and systems (severe respiratory and cardiac failure, obliterating lesion of the arteries of the lower extremities, orthostatic arterial hypotension, etc.).
• Gait disorders due to dysfunction of the afferent systems (sensory, vestibular, visual ataxia, multisensory insufficiency).
• Gait disorders caused by other movement disorders (muscle weakness, flaccid paralysis, pyramidal, cerebellar syndromes, parkinsonism, hyperkinesis).
• Gait disorders not associated with other neurological disorders (integrative, or primary, gait disorders - see the relevant section below).
• Psychogenic gait disorders (psychogenic dysbasia in hysteria, depression and other mental disorders).

Along with this classification, reflecting the nature of gait disorder, there is a need for a purely phenomenological classification, which would be based on the key features of gait and facilitate differential diagnostics. Various options for phenomenological classification of gait have been proposed. Thus, J. Jancovic (2008) identified 15 types of pathological gait: hemiparetic, paraparetic, "sensory" (in sensory ataxia), waddling, steppage, cautious, apraxic, propulsive (or retropulsive), ataxic (in cerebellar ataxia), astatic, dystonic, choreic, antalgic, vestibulopathic, psychogenic (hysterical). Such a classification, for all its exhaustiveness, seems overly complicated. The following types of pathological gait and their characteristics are distinguished.

• Antalgic gait is characterized by a shortening of the support phase on the affected limb (for example, in case of damage and limited mobility of the joints).
• Paralytic (hypotonic) gait is caused by weakness and decreased muscle tone (for example, waddling gait in myopathy, steppage gait in polyneuropathy).
• Spastic (rigid) gait is characterized by a decrease in amplitude and slowness of movements, the need for additional effort when performing stepping movements, and is associated with stiffness of the lower limbs due to increased muscle tone (with spasticity, rigidity, dystonia).
• Hypokinetic gait is characterized by a decrease in walking speed and a shortening of the step length; it is most typical for Parkinsonism, but its individual features are possible with depression, apathy, or psychogenic disorders.
• Ataxic gait is characterized by instability, compensated by an increase in the support area when walking, and is possible with disorders of deep sensitivity, vestibulopathy, cerebellar pathology, decreased vision, disorder of postural synergies, as well as psychogenic disorders.
• Dyskinetic gait is characterized by the presence of violent excessive movements of the legs, trunk, head when walking, it is observed in chorea, tics, dystonia, athetosis, ballism, myoclonus, and may include voluntary compensatory movements (parakinesia) aimed at maintaining balance when walking. In some cases, it also occurs in psychogenic disorders.
• Dysbasia is characterized by a disturbance in the initiation and maintenance of gait (e.g., in the form of freezing or mincing gait), which is often accompanied by a defect in postural synergies. This variant is observed in Parkinsonism or frontal dysbasia (e.g., in normotensive hydrocephalus, cerebrovascular insufficiency, or neurodegenerative diseases).
• Mixed gait includes features of 2 or more of the listed gait variants.

Symptoms of gait impairment

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.

Diagnosis of gait disorders

Diagnostics are carried out in 2 stages. At the stage of syndromic diagnostics, the features of gait disorders and accompanying clinical signs are identified and analyzed, allowing a conclusion to be made about the leading neurological syndrome. Subsequently, by analyzing the data of additional research methods during the disease, nosological diagnostics are carried out. Motor and sensory disorders characteristic of a particular disease of the nervous system and attempts to compensate for them often form a specific gait, which is a kind of calling card of the disease, allowing a diagnosis to be made at a distance. The ability to diagnose a disease by a patient's gait is one of the most important skills of a neurologist.

Treatment of gait disorders

In the treatment of gait disorders, measures aimed at treating the underlying disease are of crucial importance. It is important to identify and correct all additional factors that may affect gait, including orthopedic disorders, chronic pain syndromes, and affective disorders. It is necessary to limit the intake of medications that may worsen gait (e.g., sedatives).

Of great importance is therapeutic gymnastics aimed at training the skills of initiating walking, turning, maintaining balance, etc. Recognizing the main defect allows developing a method for compensating it by connecting the intact systems. For example, a set of special exercises of Chinese gymnastics "tai chi" can be recommended, developing postural stability. In case of multisensory insufficiency, correction of visual and auditory functions, training of the vestibular apparatus, as well as improvement of lighting, including at night, are effective.