Treatment of walking impairment

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).

Non-drug treatment of gait disorders

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.

In some patients, methods of step correction using visual cues or rhythmic auditory commands, walking training on a treadmill (with special support), etc. are effective. Regular feasible physical activity helps prevent the consequences of limited mobility (muscle atrophy due to inactivity, osteoporosis, decreased compensatory capabilities of the cardiovascular system), which close the vicious circle and complicate subsequent rehabilitation. Educational programs that teach patients how to move to avoid falls, injuries from falls, how to use orthopedic devices (various types of crutches, walkers, special shoes, devices that correct posture, etc.) can significantly improve the quality of life of patients.

Medicinal treatment of gait disorders

Drug therapy depends on the etiology of gait disorder. The best results are achieved when treating Parkinson's disease with dopaminergic agents. Under the influence of levodopa, the step length and walking speed in patients with Parkinson's disease increase significantly, especially in the early stages of the disease, when gait disorders are largely dependent on hypokinesia and rigidity in the limbs. As the disease progresses due to the increase in postural instability, axial motor disorders, which are largely dependent on non-dopaminergic mechanisms and are relatively resistant to levodopa, the effectiveness of treatment decreases. In case of freezing that occurs during the "off" period, measures aimed at increasing the duration of the "on" period are effective - dopamine receptor agonists, catechol-O-methyltransferase inhibitors. In case of relatively rare freezing during the "on" period, it may be necessary to reduce the levodopa dose, which can be compensated by increasing the dose of a dopamine receptor agonist, adding a MAO-B inhibitor or amantadine, teaching techniques to overcome freezing, walking training using visual cues and rhythmic auditory signals, and correction of concomitant psychopathological changes (primarily with antidepressants). Long-term observation of patients with Parkinson's disease who began treatment with levodopa or pramipexole showed that earlier use of levodopa is associated with a lower risk of freezing. It is also noted that early and long-term use of MAO-B inhibitors reduces the frequency of freezing and helps correct it if it has already developed. Correction of orthostatic hypotension may be of great importance. Levodopa preparations may also be useful in other diseases associated with parkinsonism (e.g., vascular parkinsonism or multiple system atrophy), but their effect is at best moderate and temporary. Isolated cases of improvement in freezing and other gait disorders resistant to levodopa have been described under the influence of MAO-B inhibitors (selegiline and rasagiline) and amantadine.

Correction of chorea, dystonia, myoclonus and other extrapyramidal hyperkinesis may improve walking, but appropriate antidyskinetic drugs should be prescribed with caution, given the possible negative effect. For example, in patients with Huntington's disease, neuroleptics may weaken hyperkinesis, but contribute to the deterioration of mobility due to the increase in bradykinesia and sedation - in this situation, amantadine is the drug of choice. In case of dystonia of the lower extremities, local treatment with botulinum toxin may be effective.

Reducing spasticity (using muscle relaxants or botulinum toxin injections), for example, in patients with cerebral palsy, can significantly facilitate walking. However, in patients who have suffered a stroke, increased tone in the calf muscles can have a compensatory effect and its elimination with the use of antispasmodics can make walking difficult. Therefore, the use of antispasmodics should be focused not so much on reducing muscle tone as on increasing the patient's mobility and be accompanied by physical rehabilitation methods. In patients with severe lower spastic paraparesis (for example, after a spinal injury) or severe spastic hemiparesis, continuous intrathecal administration of baclofen using a special pump can improve locomotor function.

Drug treatment of primary (integrative) gait disorders remains underdeveloped. According to Japanese neurologists, the severity of gait initiation disorders in vascular and some degenerative brain lesions can be reduced by using a norepinephrine precursor, L-threo-3,4-dihydroxyphenylserine (L-DOPS), which is consistent with experimental data on the activating effect of noradrenergic pathways on spinal generator mechanisms. A number of studies have shown the effectiveness of amantadine, which blocks NMDA-glutamate receptors, in patients with vascular encephalopathy with frontal dysbasia resistant to levodopa drugs. In the presence of signs of an apraxic defect, the drug was ineffective.

In patients with cognitive impairment and dementia, their correction can (primarily by increasing attention and concentration) improve mobility and increase the effectiveness of rehabilitation methods, but this aspect of the effectiveness of cognitive enhancers remains poorly understood. In the presence of an irrational fear of falls, selective serotonin reuptake inhibitors can be effective, especially in combination with therapeutic exercise and rational psychotherapy.

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Surgical treatment of gait disorders

Surgical treatment of gait disorders may include orthopedic interventions, spinal cord decompression in spondylotic cervical myelopathy, shunting operations in normotensive hydrocephalus, and stereotactic operations in patients with extrapyramidal syndromes. In patients with Parkinson's disease, improvement in gait can be achieved by deep brain stimulation with the introduction of electrodes into the subthalamic nucleus. It has also been shown that stimulation of the external segment of the globus pallidus improves gait, while stimulation of the internal segment of the globus pallidus (usually improving other manifestations of parkinsonism) can worsen it. Low-frequency stimulation of the pedunculopontine nucleus is the most promising in terms of improving gait, but to date its effectiveness has been demonstrated only in a small sample of patients with Parkinson's disease. In generalized and segmental muscular dystonia (both idiopathic and within the framework of multisystem degeneration, for example, in Hallervorden-Spatz disease), a pronounced effect with a significant improvement in walking can be achieved with the help of bilateral stimulation of the medial segment of the globus pallidus.