What causes gait disturbances in an elderly person and what to do about it

Sudden dizziness, loss of balance - probably every adult has experienced these sensations. In most cases, no one attaches importance to these phenomena, although they may signal the onset of the development of a neurological or other disease. If you experience systematic dizziness and loss of balance, you should consult a neurologist to clarify the situation.

In Moscow, patients with dizziness are examined at the Yusupov Hospital. The clinic is a modern medical center, where the following areas are represented: neurology, rehabilitation, oncology, a scientific and practical center, a surgical department, and an addiction treatment clinic. The Yusupov Hospital provides examination, treatment and rehabilitation of various neurological pathologies, including dizziness and loss of balance. Highly qualified neurologists who have extensive experience in the treatment and diagnosis of diseases of any complexity work with the patient.

Causes of gait disturbances in older people

There are many health problems that change your gait or affect your balance. Often changes do not occur due to one specific disease. Some causes are treatable, while others can last a lifetime.

Problems with gait, balance and coordination in older adults are most often caused by:

• osteoarthritis of the hip and knee joints;
• multiple sclerosis;
• diseases of the inner ear;
• high blood pressure;
• cerebral hemorrhage;
• Parkinson's disease;
• peripheral neuropathy;
• muscular dystrophy;
• curvature of the spine;
• obesity;
• chronic alcohol abuse;
• vitamin B12 deficiency;
• stroke;
• dizziness, etc.

If an older person has difficulty walking due to a medical condition, the gait should correct itself after treatment. In some cases, physical therapy will be needed.

Taking four or more medications at once is also associated with an increased risk of unsteady gait. For example, this occurs with a combination of diuretics, antidepressants, anticonvulsants and antiarrhythmic drugs.

Walking disorders are often observed in patients in neurological clinics and in hospitals, being one of the most disabling manifestations in this category of patients.

Disturbances in walking and postural stability are most common in Parkinson's disease (PD), often leading to immobility of the patient and dependence on outside help. They do not respond well to antiparkinsonian therapy, which forces doctors and researchers to look for new approaches to the treatment of these disorders.

In the early stages of PD, gait disturbances are manifested by slower walking speed, shortened step length, and decreased step height, causing the gait to take on a “shuffling” appearance [1, 2]. There is a decrease in the range of motion in all joints of the lower extremities (dorsiflexion in the ankle and flexion in the hip joints are especially affected), which leads to a shortening of the step length [1]. At any given speed, its arbitrary increase occurs due to an increase in the frequency of steps, while in most cases the shortened step length is maintained [3]. This makes gait akinesia more dependent on a deficit in the internal generation of step length than on a violation of the ability to increase step frequency (cadence). At the same time, an increase in cadence can be considered as a compensatory mechanism. In this regard, visual stimulation contributes to an increase in step length, indicating a violation of the internal program for the formation of step amplitude. These data are consistent with the general understanding of hypokinesia [4, 5]. In the early stages of PD, no significant increase in step cycle variability is observed [6], but postural disorders due to increased tone may be observed. This may be due to the appearance of a hunched posture and rigidity of the trunk muscles, which persist regardless of the phase of the step cycle. All described changes are reduced by the action of levodopa [2].

In the advanced and late stages of PD, there is a violation of anticipatory and especially reactive postural synergies, which often manifests itself as instability when walking conditions become more difficult, as well as falls.

The aggravation of existing walking disorders is accompanied by the appearance of qualitatively new signs in the form of propulsions, mincing gait, variability of the step cycle, and episodes of freezing, which is associated with the development of postural instability and de-automation of the act of walking. From a neurochemical point of view, gait disturbances in the later stages of PD are caused by the involvement of non-dopaminergic, primarily noradrenergic and cholinergic mechanisms. This is associated with the resistance of walking disorders and postural stability to traditional dopaminergic therapy. In addition, cognitive impairment may negatively affect gait control and postural stability. These features are often noted in advanced and late stages of PD and are associated with more widespread deposits of Lewy bodies and β-amyloid in the cerebral cortex [7]. The period between the onset of the disease and the onset of falls and mobility impairment is shortened in patients with a later age of onset and a lower response to levodopa therapy [8].

A decrease in walking speed both in the early and in the advanced and late stages of PD is predominantly associated with a decrease in step length, while the step frequency does not change significantly. A voluntary increase in walking speed occurs due to an increase in the frequency of steps. Perhaps an increase in step frequency is a compensatory mechanism for a significant decrease in step length [3]. However, a disproportionate increase in step frequency may be considered an erroneous response, reflecting a defect in motor programming rather than a compensatory strategy [9]. In advanced and late stages of PD, step cycle variability appears, which worsens as the disease progresses [5]. At later stages, there is an increase in the duration of the double support period in the structure of the step cycle, which is inversely related to the length of steps and tends to increase as postural instability increases, suggesting the compensatory nature of these changes.

Solidification

Freezing while walking is a unique phenomenon characterized by sudden, brief episodes of impairment of the ability to initiate or continue walking. Alternative names for this phenomenon are paradoxical akinesia or motor block [9–16].

Freezing when walking occurs mainly in advanced and late stages of BP. If freezing is observed in the first year of the disease, it is necessary to exclude other possible causes (atypical and secondary parkinsonism).

During a freezing episode, the patient's feet literally “grow” to the floor, and he cannot move from his place (so-called absolute freezing

according to the classification of Thompson and Marsden, 1995). In addition, situations are possible when the patient takes ineffective small steps ranging from a few millimeters to several centimeters in length or marks time (partial freezing). Freezing may be manifested by trembling of the lower extremities when trying to start or continue movement.

Freezes, as a rule, occur spontaneously, at the moment of switching from one movement to another, for example, at the beginning of walking (the so-called starting freezes), when turning, overcoming obstacles, passing through a narrow space (for example, a doorway), when reaching a goal, for example chairs at home. In some cases, freezing occurs without any provoking factor, when walking in a straight line in an open space. In addition, the environment and emotional situations may have an effect on their occurrence. Circumstances that provoke freezing include simultaneous performance of a dual task, usually involving cognitive activity (for example, counting while walking or reciting poetry), being in a confined space (in a crowd), performing a motor task with a time limit (for example, crossing the road when the traffic light is green) [9-12, 14-16].

Depending on the phase of action of levodopa drugs, there are solidification periods of the off period, observed during the period when their action ends; freezing of the inclusion period, when, despite a decrease in the main symptoms of parkinsonism, the frequency and duration of freezing increase; in some cases, freezing is not associated with the period of action of levodopa drugs [9-16].

In the DATATOP study [16], the onset of freezing was noted on average after 5 years from the onset of the first symptoms. With increasing duration and stage of PD, the duration of episodes of freezing increases, often leading to impaired stability and falls [1, 13, 16]. The DATATOP study identified the main risk factors for freezing: progression of PD with the addition of gait and postural stability disorders. Tremor is not a risk factor; on the contrary, it delays the onset of freezing [1, 9, 13, 14, 16]. The role of hypokinesia and rigidity in the occurrence of freezing remains controversial. According to some authors [14, 16], the presence and severity of freezing correlates with speech impairment and dysuric manifestations [13, 16]. There has been a connection between freezing and cognitive impairment, primarily with regulatory disorders [1, 9–12, 16].

Currently, there is no single theory that explains all the features and heterogeneity of solidification. Disautomatization of walking and disruption of non-dopaminergic mechanisms (primarily noradrenergic) are considered as the main theories. There is also no doubt about the connection between freezing and dysfunction of the frontal lobes, since freezing more often occurs when the motor program changes (switches) and requires intense attention to overcome them [9-12, 14-16].

Mincing gait

A shuffling gait is another characteristic and unique gait pattern in BP. It is characterized by the appearance of short, quick steps that occur when trying to maintain the center of pressure within the area of ​​​​support, when the body involuntarily moves forward. A shuffling gait may precede an episode of freezing, in which steps become increasingly shorter and more frequent, eventually leading to the development of motor block (freezing). The mechanisms of the mincing gait and its connection with freezing are not fully understood. Most likely, the mincing gait is an independent episodic gait disorder that occurs in PD.

Falls

Falls are associated with an increased risk of death and injury, primarily due to traumatic brain injury and hip fracture. In addition, falls are a leading cause of disability, leading to dependence on assistance, hospitalization, deterioration in quality of life, and fear of falls. The incidence of falls in PD, according to various studies [9, 17, 18], varies. There is evidence that 51-68% of patients experience at least one fall per year, and the incidence of recurrent falls is approximately 50% of patients per year. From the moment of the first fall, life expectancy approaches that of atypical parkinsonism syndromes, which, as a rule, have a more severe course and a shorter duration of the disease [19]. Predictors of falls are considered to be a history of falls, fear of falling, duration and severity of the disease, changes in tone in the axial muscles and postural disorders, cognitive impairment, limitation of arm movements when walking (acheirokinesis), the presence of dyskinesias and taking antiparkinsonian drugs [20]. Most falls are not caused by external factors such as slips or trips, but are influenced by internal deficits in balance control. Falls occur mainly during postural changes, especially during turns, and also during dual tasks (cognitive or motor). The more difficult the dual task, the more balance control is impaired and the risk of falls increases.

Methods for assessing gait impairment

In routine practice, postural stability is assessed using the Thévenard test, where the patient is asked to maintain balance while pushing backward (UPDRS III). However, it should be noted the high variability of results during its implementation and repetition, as well as the low sensitivity of the test for early detection of fallers.

In the new validated version of the MDS-UPDRS, detailed assessment instructions may reduce the variability of the test [21]. However, in most studies, clinical assessment of postural instability is not associated with the risk of falls.

Non-specific scales (Berg Balance Scale, Timed Up and Go - TUG test and Tinetti scale) assess balance and risk of falls in patients with parkinsonism. They are characterized by fairly good sensitivity for identifying patients prone to falls in PD [20]. In addition, there is the Functional Gait Assessment (FGA), the Balance Evaluation System Test (BES Test), and the Rapid Assessment of Postural Stability in PD (RAPID), which have sufficient sensitivity [22].

Stabilometry is a quantitative measurement of oscillations of the center of pressure (CP) of the feet in a static and dynamic state using mobile platforms. Evaluation of the results includes measuring the support area and the speed of movement of the CP using touch sensors [23]. Despite the presence of significant differences in the results of measurements between patients with PD and in the control group, in most studies there are no correlations between stabilometric parameters and clinical data or the risk of falls. However, it is possible to use stabilometric platforms to individualize therapy, especially to evaluate therapeutic effects on postural instability in patients with PD [24]. One study [25] noted that changes in the vertical velocity of the CoP may be a sensitive method for identifying postural instability and the effect of therapy in individual patients. However, the feasibility of using stabilometry in clinical practice and assessing predictors of falls using this method requires further research.

General organization of structures providing stability and locomotion

The structures that support locomotion have been well studied in animals. They are hierarchically organized and include: 1) the lower level, consisting of the musculoskeletal and peripheral nervous systems; 2) a central gait generator, consisting of organized groups of spinal cord interneurons that generate rhythmic and alternating movements of the limbs; 3) several locomotor zones located in different areas of the trunk, which control the central gait generator and are characterized by the ability to provide locomotor activity under electrical and pharmacological stimulation. These include the subthalamic locomotor region, the mesencephalic locomotor area, consisting of the pedunculopontine nucleus (PPN) and the cuneate nucleus (CN); 4) the highest level of the gait control system, including the dopaminergic and other neurotransmitter systems, the basal ganglia and the prefrontal cortex. These locomotor circuits are modulated by a sensory feedback system through sensory afferent systems (somatosensory, vestibular and visual).

Mesencephalic locomotor region and gait control

Among the various locomotor areas with direct effects on the spinal cord, the mesencephalic locomotor area is the most important in the physiology and pathophysiology of gait. It is located in the reticular formation and consists of the PPN and the CN [26]. Both of these structures are groups of neurons located in the reticular formation. The presence of cholinergic neurons defines the boundaries of the PPN in primates. In addition to cholinergic neurons, the PPN contains GABAergic and glutamatergic neurons. In monkeys, 40% of cholinergic neurons produce glutamate [27]. The CN is located dorsal to the PPN and contains glutamatergic and GABAergic neurons. The PPN and CN have reciprocal connections with the basal ganglia and main projections to the descending reticulospinal and ascending thalamocortical pathways [28]. Ascending projections from the PPN are primarily directed to dopaminergic neurons of the substantia nigra pars compacta, subthalamic nucleus, globus pallidus, and thalamus. The descending tracts project to the pontobulbar reticular formation, where the reticulospinal tracts originate. A recent study [29] showed that the pars reticularis of the substantia nigra projects to both the PPN and the CN, whereas projections from the internal segment of the globus pallidus project primarily to the PPN. Other QW projections have not been studied enough.

Involvement of the mesocephalic-locomotor zone in normal and pathological walking in humans

Neuroimaging studies in humans confirm the role of this area in the organization of walking. According to positron emission tomography (PET) data performed in healthy people, the frontoparietal cortex and basal ganglia are activated during obstacle walking [30]. Functional MRI studies have shown activation of circuits including the frontal and parietal cortices, basal ganglia, cerebellum, tegmentum, and pons during a mental image of walking task [31]. Interestingly, midbrain activation was also detected during the task of mentally imagining running. The mesencephalo-locomotor area was particularly activated during the mental representation of fast walking, indicating that this region may be involved in the control of step frequency (gait cadence) [32]. During a mental representation of walking, patients with PD and freezing showed greater activity in this area than patients without freezing. In patients with PD and freezing, gray matter atrophy was noted in part of the mesencephalic-locomotor area [33]. The involvement of cholinergic neurons in this area in gait and postural stability has recently been confirmed. However, pathological studies [34] have shown that the degree of loss of cholinergic neurons in the PPN in PD correlates with the level of loss of dopaminergic neurons and, importantly, with the occurrence of falls. The same study found that there was no statistically significant difference in the decrease in the number of cells in the CN between PD patients with and without falls. In addition, another study [35] found a decrease in cholinergic terminals in the thalamus in patients with PD who experienced falls compared with patients without falls.

Involvement of other structures associated with gait impairment in PD

Brain stem.

Evidence of a connection between gait impairment and the noradrenergic and serotonergic systems of the brain has been repeatedly presented. It has recently been hypothesized that noradrenergic neurons of the locus coeruleus, which are susceptible to degeneration in PD [36], may contribute to gait and postural stability impairments in PD and other neurodegenerative diseases [37]. Noradrenergic neurons, primarily located in the locus coeruleus, innervate large areas of the central nervous system, including the cortex, cerebellum, and spinal cord. Since the ceruleocerebellar and ceruleospinal tracts are involved in the autonomic regulation of postural reflexes, their degeneration may explain postural instability in PD [38]. Serotonin, secreted by neurons of the raphe nuclei in the brainstem, is thought to modulate the rhythm and pattern of movements, especially the accuracy of load redistribution between antagonist muscles [39]. The level of serotonin in the CSF is reduced in patients with PD and especially in such patients with severe walking and balance impairments [40].

Cerebral cortex and cerebellum.

The motor cortex and cerebellum are known to be involved in locomotor control. Although there is no direct evidence of their involvement in the pathophysiology of gait and balance disorders in PD, functional neuroimaging work reveals interesting relationships. Gait impairments have been associated with decreased perfusion in various brain regions, including the bilateral orbitofrontal cortex, parietofrontal regions, including the dorsomedial cortex [41]. SPECT was used to investigate the mechanisms underlying improvements in hypokinetic walking in patients with PD when visual stimuli (“paradoxical walking”) were presented. In patients with PD, activation of the lateral premotor cortex was found to be significantly greater than in the control group. It is assumed that the premotor cortex compensates for the impaired function of the dorsomedial cortex in patients with PD [42]. A more pronounced decrease in metabolism in several cortical areas, including the parietal region, detected using 18-[F]fluorodeoxyglucose PET, was observed in PD patients with freezing compared with patients without freezing [43].

In addition, patients with PD show increased activation of the cerebellum, which can be considered as compensation for dysfunction of the basal ganglia and brainstem [44].

Therapy and rehabilitation of walking disorders

Optimizing the dopaminergic treatment regimen remains a major challenge [14], especially in patients with early stages of PD. However, the positive effect of levodopa drugs on walking impairment and postural stability in patients even with early stages of PD is inconsistent and decreases over time [45], as nondopaminergic mediator systems are involved in the neurodegenerative process.

Several studies have investigated drugs that act on nondopaminergic systems during freezing and postural instability in BP. Thus, a randomized placebo-controlled trial [46] showed that central cholinesterase inhibitors (donepezil at a dose of 10 mg per day) reduce the number of falls compared with placebo, but these data were obtained in a group of patients with frequent falls. Further identification of cholinergic receptor subtypes that influence gait and balance function in PD may help select targets for therapy of these disorders and screen for new drugs [47]. Similar developments may also apply to drugs with noradrenergic effects. Although improvements in walking in PD following administration of a 5-HT2 serotonin receptor antagonist have been reported [48], the effect of serotonergic drugs on walking has not been systematically assessed.

The freezing period of the off period can be reduced by prescribing MAO-B inhibitors (selegiline, rasagiline) to patients with early and late stages of PD [49]. It is believed that drugs in this group have a symptomatic effect and may have a neuroprotective effect, delaying the onset of gait and postural stability disorders. It is possible that in this case, freezing is reduced not only as a result of blocking MAO-B receptors, but also due to amphetamine metabolites. This same hypothesis underlies the use of methylphenidate, an amphetamine precursor that acts as a potential catecholamine reuptake inhibitor, increasing norepinephrine levels in the brain. D. Devos et al. [50] noted an improvement in walking and a decrease in the severity of freezing in patients with advanced and late stages of PD while taking methylphenidate. In addition, methylphenidate may help reduce the severity of freezing, improving regulatory functions and attention. However, the results of one randomized placebo-controlled trial [51] of patients with PD with freezing did not confirm improvement in walking and reduction in the severity of freezing while taking methylphenidate.

A small placebo-controlled study conducted and recently published by J. Lee et al. [52] showed a positive effect of intravenously administered amantadine at a dose of 400 mg per day for 5 days on the freezing period of the off period.

Gait disturbances in PD can be reduced by using various external stimuli. Increasing attention, using visual (contrasting transverse stripes drawn on the floor, canes and walkers with a crossbar or laser beam, etc.) and audio stimulation (counting steps, metronome sounds) help improve walking and are an important part of the rehabilitation program for patients with stiffening. Two mechanisms underlie the improvement in gait with external stimulation: first, the need for internal planning and preparation of movements is reduced; second, external stimuli focus attention, especially during a more complex task, and thus help walking become a higher priority activity. In addition, the use of rhythmic audio stimulation helps reduce step cycle variability and step desynchronization, important factors in the occurrence of freezing. From a neuroanatomical point of view, under the influence of external stimuli, additional pathways are activated, including cerebellar-parietal-premotor connections, which makes it possible to “unload” the basal ganglia and the associated additional motor cortex [53, 54].

Rehabilitation programs aimed at improving gait and balance in PD are widely used in clinical practice, although scientific evidence for choosing the optimal technique is still insufficient. Almost all rehabilitation methods have a positive effect (compared to their absence). Thus, exercises carried out at home have been effective in reducing the risk of dangerous falls leading to injury and repeated falls [55].

High-frequency stimulation of the globus pallidus may slightly improve gait disturbances and reduce levodopa-responsive freezing in patients with PD, but this effect disappears after 3–4 years [56]. Bilateral high-frequency stimulation of the subthalamic nucleus (STN) is also effective for levodopa-sensitive gait disorders in PD [57]. In most patients with long-term PD, gait and postural stability impairments become resistant to levodopa and STN stimulation and may even worsen after such stimulation. However, by changing stimulation parameters, it is possible to reduce gait and balance disturbances. Thus, low-frequency stimulation of the STN (60 Hz) significantly reduces freezing when walking, but is less effective in alleviating cardinal symptoms of parkinsonism and cannot be recommended for long-term therapy of patients with severe manifestations of PD [58].

High-frequency stimulation of the substantia nigra pars reticularis improves axial symptoms and postural stability during walking, but does not improve the core symptoms of parkinsonism [59]. The mechanism of action that explains this effect on postural control may be related to the modulation of descending nondopaminergic projections connecting the substantia nigra to the mesencephalo-locomotor area. Although deep stimulation of the substantia nigra cannot be considered as an independent method of therapy in advanced stages of PD, stimulation of this zone in combination with other types of therapy is possible [4, 59].

The PPN is hypothesized to control axial symptoms resistant to levodopa therapy and may therefore be a target for deep stimulation. Early work included patients with advanced PD with already placed electrodes in the STN, and therefore suggested that additional bilateral low-frequency stimulation of the PPN may be effective in reducing gait and postural stability. Two double-blind controlled studies have shown that freezing may be reduced after stimulation of the PPN, but overall the results were unsatisfactory [60]. However, unilateral PPN stimulation in patients without STN stimulation may be effective in reducing falls [61]. Such conflicting results indicate the need to clarify optimal inclusion criteria, as well as the optimal selection of surgical targets within the mesencephalo-locomotor zone.

When to see a doctor

If your gait changes, you will need to consult a neurologist, traumatologist, orthopedist, ENT specialist or other specialist.

You should immediately seek medical help if your gait changes as a result of a fall or along with other symptoms:

• speech problems;
• labored breathing;
• dizziness;
• facial asymmetry;
• involuntary urination;
• severe throbbing headache;
• sudden numbness in one or more parts of the body.

You also need to urgently consult a doctor if problems with gait in an elderly person occur suddenly.

Treatment methods

To correct dyspraxia, modern innovative techniques using kinesiotherapy are used:

• stabilometry method with bioactive connection;
• dynamic correction with reflex-loading devices “Gravistat”, “Adelie”, “Graviton”;
• passive vestibular training using a computer stand;
• electrical stimulation of muscles;
• computer video analysis of movements;
• transcranial polarization of the brain.

Simultaneously with similar methods, pharmacological therapy with cerebroprotectors of nootropic action is used: Cytoflavin, Actovegin, Cortexin, Lecithin, Glycine, Semax, Gliatilin.

General therapeutic measures are highly effective - physical therapy, psychological and speech therapy correction. Much attention is paid to restoring the function of balance and basic movements, for which mobile and finger games and elements of sports games are used.

When treating verbal dyspraxia, the speech therapist chooses a special system of exercises for the child, one part of which is aimed at developing the pronunciation of sounds, and the second at restoring articulation.

• The first option involves teaching the child accurate articulation of phonemes. Much attention is paid to sound patterns.
• The essence of the second option is to actively train the facial muscles responsible for articulation. At the beginning of therapy, the baby imitates the elementary movements of the lips and tongue, the description of which is wrapped in a fairy tale plot (“The Tale of the Merry Tongue”). Upon completion of the correction, he must independently reproduce a sequence of several movements.

Children with dyspraxia are encouraged to participate in group gymnastics classes. They perfectly develop the vestibular apparatus, and the child gains control over his movements. Games with musical accompaniment are very useful. While playing them, children will feel the rhythm, which allows them to improve body control and coordination.

What does the gait of an elderly person tell you?

Peripheral neuropathy:

• too long, uneven steps;
• poorly controlled movements, legs “do not obey” when walking;
• noticeable sagging of the foot when walking;
• when walking, a person constantly looks at his feet;
• in poor lighting, gait becomes unstable.

Frontal lobe disease:

• a person walks bent over;
• has difficulty starting to move;
• moving forward, he often stops;
• the steps are short and shuffling.

Parkinson's disease:

• mincing gait;
• legs are bent and arms are bent;
• short shuffling steps;
• arm span is smaller than usual;
• When moving, the center of gravity is shifted forward.

Cerebellar diseases:

• uneven stride length;
• legs are wide apart when walking;
• a person loses balance when changing position.

What can be done for an elderly person with unsteady gait

Since unsteady gait increases the risk of falls, it is important to secure the elderly person's home:

• Remove all items from walkways (shoes, furnishings, extension cords, etc.).
• The corridors should be well lit (especially the path to the bathroom, toilet and kitchen).
• Place non-slip mats on the floor of the bathtub as well as at the exit of the bathtub.
• Buy comfortable house shoes with non-slip soles.
• You can keep a flashlight by your bed and use it if you need to get up at night.

According to doctors' recommendations, an elderly person needs:

• wear leg braces and orthoses;
• use a cane or walker for additional support and balance.

How to improve unsteady gait

Walking 30 minutes a day and maintaining a physically active lifestyle are the most important recommendations for maintaining mobility. But walking alone is not enough.

If your gait has changed due to problems with your lower extremities, exercises to strengthen your muscles and improve your balance will help. They are prescribed by neurologists, orthopedists or physiotherapists. Here are examples of popular exercises.

Balancing on one leg

Hold onto a chair and keep your weight on one leg only. Slowly release the chair. Try balancing for 30 seconds and then increase the time to a minute.

Leg raises

While leaning on a chair, slowly lift one leg in front of you at least 20cm off the ground. At the same time, hold it straight for 5-10 seconds. Repeat several times, then perform lifts with the other leg.

Heel raise

Stand with your feet shoulder-width apart. Slowly rise up onto your toes, then lower back down. Repeat ten or more times.

Diagnostics

Determining the causes of unsteady gait is carried out by neurologists. Due to the varied etiology of cerebellar, cortical and brainstem disorders, geneticists, oncologists, endocrinologists and other specialists may be involved in the examination. The list of diagnostic procedures includes:

• Gait and Balance Study
  . The doctor assesses the severity of instability and the symmetry of movements when walking in a straight line and during turns, taking into account the unilateral or bilateral nature of the disorders. Determines stability in the Romberg pose with eyes closed and open.
• Neurological examination
  . The specialist examines reflexes, sensitivity and muscle strength, and identifies focal symptoms. When examining patients with an unsteady gait, attention is paid to muscle hypotonia, nystagmus and dysarthria, indicating the localization of the pathological focus.
• Research of the vestibular analyzer
  . Includes vestibulography, stabilography, electronystagmography. They are carried out in the process of differential diagnosis to exclude vestibular disorders.
• Visualization techniques
  . EEG is informative for hereditary ataxias. MRI and CT of the brain make it possible to diagnose neoplasms, abscesses, hematomas, degenerative changes and congenital anomalies of the central nervous system, and detect prolapse of the cerebellum into the foramen magnum. For the vascular etiology of unsteady gait, Doppler sonography or MR angiography of cerebral vessels is recommended.
• Lab tests
  . Lumbar puncture followed by examination of cerebrospinal fluid is used to detect signs of intracranial hypertension, inflammation, neoplasia, and hemorrhage. To confirm the infectious nature of the pathology, PCR is performed. If a hereditary nature of the ataxic gait is suspected, DNA diagnostics and genetic tests are performed.

Tests for ataxia