Shaky (atactic) gait is observed with damage to the cerebellum and thalamus, sometimes occurs with pathology of the frontal lobes associated with the cerebellum. It is provoked by tumors, traumas, encephalitis, multiple sclerosis, purulent processes, intoxications, vascular formations, circulatory disorders. It is found in some hereditary diseases. It is diagnosed on the basis of anamnesis data, gait studies, neurological examination, EEG, CT, MRI, laboratory tests. Treatment includes antibacterial, vascular, detoxification therapy, restorative agents, exercise therapy, and surgery.
Due to balance disorders, patients with pathological processes in the cerebellum try to increase the area of support, spread their legs wide, stagger randomly and sway when walking. The movements of the upper and lower extremities are out of sync. Instability persists in the standing position, does not depend on the presence or absence of visual control. With a unilateral lesion of the cerebellum, one half of the body suffers, falls to the affected side are possible.
With the involvement of cortical structures, the clinical picture resembles that of cerebellar ataxia. The instability increases when turning, the patient often "falls" in the direction of the lesion, the unsteadiness of the gait correlates with the severity of the damage to the cortex. In people with lesions of the ventrolateral thalamus, unsteadiness and unsteadiness occur on the opposite side, and there is a tendency to fall back or to the healthy side.
Atactic gait is a permanent or possible symptom of some hereditary pathologies:
The cause of atactic gait may be ischemia or hemorrhage. Possible provoking factors are atherosclerosis of cerebral vessels, arteriovenous malformations, and other vascular disorders. In most cases, the pathology develops acutely, the clinical picture of a stroke is revealed. Less commonly, for example, with Kimerli's anomaly, cerebellar symptoms progress gradually.
The involvement of the cerebellar structures is evidenced by a decrease in muscle tone on the side of the lesion, macrography, and extended chanted speech. With the defeat of the cortical structures, characteristic changes in the psyche, olfactory disorders are found. The grasping reflex is determined. Hypotonia of the muscles of the affected half of the body is absent.
Ataxia
Among oncological diseases, cerebellar tumors play the most significant role in the occurrence of atactic gait. The clinical picture is variable, including ataxia, cerebral symptoms, and signs of brainstem compression. The listed groups of signs can occur both simultaneously and sequentially. A shaky gait is combined with dizziness, cephalgia, and vomiting of central origin. Cerebral symptoms are especially pronounced when obstructing the outflow of cerebrospinal fluid.
Cerebellar disorders tend to increase and spread. When the tumor is located in one hemisphere of the cerebellum, difficulties in maintaining balance are observed on one side, as the neoplasia grows, bilateral coordination disorders begin to predominate. The involvement of the trunk is evidenced by strabismus, neuritis of the trigeminal and facial nerve, hearing loss, oculomotor disorders.
With neoplasms of the cerebral hemispheres, dizziness occurs later than with neoplasia of the cerebellum. During an ophthalmological examination, congestive optic discs are detected on both sides. There is a high prevalence of mental pathologies - from mnestic and emotional disorders to delusions and hallucinations.
A wobbly gait is the result of intracranial hematomas of the corresponding localization, compression of the frontal lobes by subdural and epidural hematomas. In acute hematomas, symptoms develop within a few hours or days, in chronic hematomas - for weeks, months or years. Headaches, dizziness, vomiting not associated with eating, epileptic seizures, "frontal" mental disorders with elevated mood, ridiculous behavior and reduced criticism are possible.
The clinical picture of the abscess corresponds to other volume lesions of the cortex or cerebellum, there are no specific symptoms. The infectious nature of the process is indicated by the presence of injuries and operations on the brain structures, purulent-inflammatory lesions of the ENT organs, an acute onset with signs of intoxication, the rapid formation of a shaky gait, followed by stabilization of neurological disorders after the formation of a capsule that prevents the spread of pus to neighboring structures.
Balance disorders with the development of atactic gait are more characteristic of secondary encephalitis: influenza, measles, post-vaccination. The risk of developing ataxia increases with severe encephalitis with severe neurological disorders. In some cases, a wobbly gait is detected in patients who have had an encephalitic form of tick-borne encephalitis.
A wobbly gait can be observed already at the onset of the disease, but is not detected in all patients, which is explained by the polymorphism of symptoms, especially at the initial stages. Subsequently, cerebellar pyramidal and sensory disorders form a typical clinical picture of multiple sclerosis. Asynergy of movements, atactic gait and other symptoms of cerebellar damage are combined with intentional tremor, hyperkinesis. Paresis, optic neuritis, ophthalmoplegia are often determined.
Other pathologies associated with atactic gait include:
Establishing the causes of a shaky gait is carried out by neurologists. Due to the diverse etiology of cerebellar, cortical and stem disorders, genetics, oncologists, endocrinologists and other specialists may be involved in the examination. The list of diagnostic procedures includes:
Tests for ataxia
Therapeutic tactics is determined taking into account the underlying disease. In infectious-inflammatory genesis of atactic gait, antibiotic therapy or antiviral therapy is indicated. Patients with vascular diseases, depending on the nature of the pathology, may be recommended anticoagulants, antiplatelet agents, thrombolytics, angioprotectors, vasodilators. Patients with ataxia, staggering gait due to intoxication need detoxification therapy.
Pathogenetic therapy of hereditary ataxias has not been developed. Produce the same symptomatic measures as in ataxia of another etiology. Assign B vitamins, anticholinesterase drugs, ATP, piracetam, meldonium. Exercise therapy is carried out to improve the general condition and strength of the muscles, to reduce the severity of discoordination. Patients are referred for massage.
Surgical interventions are required for volumetric processes and circulatory disorders. Taking into account the etiology of atactic gait, the following techniques are used: