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  • Gait disorders are common in older adults and are a predictor of functional decline.

  • The cause of gait impairment in older adults is usually multifactorial; therefore, a full assessment must include consideration of a number of different causes, as determined from a detailed physical examination and a functional performance evaluation.

  • Various interventions, ranging from medical to surgical to exercise, can reduce the degree of impairment, although some residual impairment is often present.


Limitations in walking increase with age. At least 20% of noninstitutionalized older adults admit to difficulty with walking or require the assistance of another person or special equipment to walk. In some samples of noninstitutionalized older adults ≥85 years old, the prevalence of walking limitations can be over 50%. Age-related gait changes such as slowed speed are most apparent after age 75 or 80, but most gait disorders appear in connection with underlying diseases, particularly as disease severity increases. For example, advanced age (>85 years old); three or more chronic conditions at baseline; and the occurrence of stroke, hip fracture, or cancer predict catastrophic loss of walking ability (SOE=B).

Determining that a gait is disordered is difficult, because there are no clearly accepted general standards of normal gait for older adults. Some believe that slowed gait speed suggests a disorder; others believe that deviations in smoothness, symmetry, and synchrony of movement patterns suggest a disorder. Regardless, a slowed and aesthetically abnormal gait can nevertheless provide an older adult with a safe, independent gait pattern. Attributing a gait disorder to one specific disease in older adults is particularly difficult, because similar gait abnormalities are common to many diseases.

Longitudinal observational studies suggest that certain gait-related mobility disorders progress with age and that this progression is associated with disability, morbidity and mortality. Community-dwelling older adults with gait disorders, particularly neurologically abnormal gaits, are at higher risk of institutionalization and death (SOE=B).


Impaired gait may not be an inevitable consequence of aging but rather a reflection of the increased prevalence and severity of age-associated diseases. These diseases, both neurologic and non-neurologic, are the major contributors to impaired gait. (For a glossary of gait abnormalities, see Table 1.)

Table 1—Glossary of Gait Abnormalities
Antalgic gait
Pain-induced limp with shortened stance phase of gait on painful side
Outward swing of leg in semicircle from the hip
Excessive plantar flexion and inversion of the ankle
Acceleration of gait
Foot drop
Loss of ankle dorsiflexion secondary to weakness of ankle dorsiflexors
Foot slap
Early, frequent audible foot–floor contact with steppage gait compensation
Freezing of gait
Sudden, short duration diminution or cessation of walking usually associated with shift in attention or movement circumstance or direction
Genu recurvatum
Hyperextension of knee
Tendency to fall forward
Tendency to fall backward
Hip adduction such that the knees cross in front of each other with each step
Shuffling Not lifting feet off ground when walking
Steppage gait
Exaggerated hip flexion, knee flexion, and foot lifting, usually accompanied by foot drop
Trendelenburg gait
Hip abductor weakness causes contralateral pelvis to drop, which may be compensated by trunk lean to affected side
Turn en bloc
Moving the whole body while turning

Patients in primary care report that pain, stiffness, dizziness, numbness, weakness, and sensations of abnormal movement are the most common causes of their walking difficulties. The most common conditions seen in primary care that are thought to contribute to gait disorders are degenerative joint disease, acquired musculoskeletal deformities, intermittent claudication, impairments after orthopedic surgery and stroke, and postural hypotension. Usually, more than one contributing condition is found. In a group of community-dwelling adults >88 years old, joint pain was by far the most common contributor, followed by multiple causes such as stroke and visual loss. Factors such as dementia and fear of falling also contribute to gait disorders. The disorders found in a neurologic referral population include frontal gait disorders (usually related to normal-pressure hydrocephalus [NPH] and cerebrovascular processes), sensory disorders (also involving vestibular and visual function), myelopathy, previously undiagnosed Parkinson disease or parkinsonian syndromes, and cerebellar disease. Known conditions causing severe gait impairment, such as hemiplegia and severe hip or knee disease, are commonly not mentioned in these neurologic referral populations. Thus, many gait disorders, particularly those that are classical and discrete (eg, those related to stroke and osteoarthritis) and those that are mild or may relate to irreversible disease (eg, vascular dementia), are presumably diagnosed in primary care and treated without a referral to a neurologist. Other less common contributors to gait disorders include metabolic disorders (related to renal or hepatic disease), CNS tumors or subdural hematoma, depression, and psychotropic medications. Case reports also document reversible gait disorders due to clinically overt hypo- or hyperthyroidism and B12 and folate deficiency.

Factors associated with slowed gait speed are also considered contributors to gait disorders. These factors are commonly disease associated (eg, cardiopulmonary or musculoskeletal disease) and include decreased leg strength, vision, aerobic function, standing balance, and physical activity, as well as joint impairment, previous falls, and fear of falling. Longitudinal data suggest that multiple organ system changes contribute to age-related changes in gait speed, but no single system is primarily associated with this decline. Combining factors can result in an effect greater than the sum of the single impairments (as when combining balance and strength impairments). Furthermore, the effect of improved strength and aerobic capacity on gait speed may be nonlinear; that is, for very impaired individuals, small improvements in strength or aerobic capacity yield relatively larger gains in gait speed, whereas these small improvements yield little gait speed change in healthy older adults.

Although older adults can maintain a relatively normal gait pattern well into their 80s, some slowing occurs, and decreased stride length thus becomes a common feature in descriptions of gait disorders of older adults. Some authors have proposed the emergence of an age-related gait disorder without accompanying clinical abnormalities, ie, essential “senile” gait disorder. This gait pattern is described as broad-based with small steps, diminished arm swing, stooped posture, flexion of the hips and knees, uncertainty and stiffness in turning, occasional difficulty initiating steps, and a tendency toward falling. These and other nonspecific findings (eg, the inability to perform tandem gait) are similar to gait patterns found in a number of other diseases, and yet the clinical abnormalities are insufficient to make a specific diagnosis. This “disorder” may be a precursor to an as-yet-undiagnosed disease (eg, related to subtle extrapyramidal symptoms) and is likely to be a manifestation of concurrent, progressive cognitive impairment (eg, Alzheimer disease or vascular dementia). Thus, “senile” gait disorder may reflect a number of potential diseases and is generally not useful in labeling gait disorders in older adults.

Subclinical as well as clinically evident cerebrovascular disease is increasingly recognized as a major contributor to causes of gait disorders (SOE=B). Individuals without a dementia diagnosis and with clinically abnormal gait (particularly unsteady, frontal, or hemiparetic gait) followed for approximately 7 years were found to be at higher risk of developing non-Alzheimer, particularly vascular, dementia. Of note, those with abnormal gait at baseline may not have met criteria for dementia but already had abnormalities in neuropsychologic function, such as in visual-perceptual processing and language skills. Gait disorders with no apparent cause (also termed “idiopathic” or “senile” gait disorder) are associated with a higher mortality rate, primarily from cardiovascular causes (SOE=B). These cardiovascular causes are likely linked to concomitant, possibly undetected, cerebrovascular disease.


Gait disorders can be assessed and categorized according to the sensorimotor levels that are affected.

Disorders that are the result of pathology of the low sensorimotor level can be divided into peripheral sensory and peripheral motor dysfunction, including myopathic or neuropathic disorders that cause weakness and musculoskeletal diseases. These disorders are generally distal to the CNS. With peripheral sensory impairment, unsteady and tentative gait is commonly caused by vestibular disorders, peripheral neuropathy, posterior column (proprioceptive) deficits, or visual impairment. With peripheral motor impairment, a number of classical gait patterns emerge. Examples of these patterns include Trendelenburg gait (ie, hip abductor weakness causes the contralateral pelvis to drop, which may be compensated by trunk lean to the affected side), antalgic gait (weight bearing is avoided and stance shortens on one side because of pain), and foot drop (due to ankle dorsiflexor weakness and characterized by a frequently audible foot-floor contact with steppage gait compensation, ie, excessive hip flexion). These gait impairments are the result of body segment and joint deformities, pain, and focal myopathic and neuropathic weakness. In general, if the gait disorder is limited to this low sensorimotor level (ie, the CNS is intact), the person can adapt well to the gait disorder, compensating with an assistive device or learning to negotiate the environment safely.

At the middle sensorimotor level, the execution of centrally selected postural and locomotor responses is faulty, and the sensory and motor modulation of gait is disrupted. Gait may be initiated normally, but stepping patterns are abnormal. Diseases causing spasticity (eg, those related to myelopathy, B12 deficiency, and stroke), parkinsonism (idiopathic as well as medication induced), and cerebellar disease (eg, alcohol induced) are examples of those that cause this type of impairment. Gait abnormalities appear when the spasticity is sufficient to cause leg circumduction and fixed deformities (eg, equinovarus), when the Parkinson disease produces shuffling steps and reduced arm swing, and when the cerebellar ataxia increases trunk sway sufficiently to require a broad base of gait support. Freezing of gait is found commonly in parkinsonian syndromes.

At the high or central level, gait impairments become more nonspecific. Lesions in the frontal lobe account for most gait abnormalities at this level. The severity of the frontal-related disorders runs a spectrum from difficulty with initiation of gait to frontal dysequilibrium, in which unsupported stance is not possible. Cerebrovascular insults to the cortex, as well as to the basal ganglia and their interconnections, may contribute to difficulty with initiation of gait and to apraxia.

Dementia and depression are also thought to contribute to an abnormal gait at the high or central level. With increasing severity of the dementia, particularly in patients with Alzheimer disease, frontal-related symptoms also increase. Gait impairments in this category have been given a number of overlapping descriptions, including gait apraxia, marche a petits pas, and arteriosclerotic parkinsonism.

More than one disease or impairment is likely to contribute to a gait disorder; one example is the longstanding diabetic patient with peripheral neuropathy and a recent stroke who is now very fearful of falling. Certain disorders can actually involve multiple parts of the nervous system, such as Parkinson disease affecting cortical and subcortical structures. Drug and metabolic causes (eg, from sedatives, tranquilizers, and anticonvulsants) can involve both central and peripheral nervous systems (eg, phenothiazines can cause central sedation and extrapyramidal effects).

History and Physical Examination

A careful medical history can help elucidate the multiple factors contributing to gait impairments in older adults. A brief systemic evaluation for evidence of subacute metabolic disease (eg, thyroid disorders), acute cardiopulmonary disorders (eg, myocardial infarction), or other acute illness (eg, sepsis) is warranted because an acute gait disorder may be the presenting feature of acute systemic decompensation in older adults. The physical examination should include an attempt to identify motion-related factors, eg, by provoking both vestibular and orthostatic responses. A focused examination, based on symptoms, should include the Dix-Hallpike test to test for vestibular dysfunction, postural blood pressure measurements to exclude orthostatic hypotension, and vision screening at least for acuity. In addition, the neck, spine, extremities, and feet should be evaluated for pain, deformities, and limitations in range of motion, particularly regarding subtle hip or knee contractures. Leg-length discrepancies such as can occur with a hip prosthesis and either as an antecedent or subsequent to lower back pain can be measured simply as the distance from the anterior superior iliac spine to the medial malleolus. A formal neurologic assessment is critical and should include assessment of strength and tone, sensation (including proprioception), coordination (including cerebellar function), station, and gait. The Romberg test screens for simple postural control and whether the proprioceptive and vestibular systems are functional. Some investigators have proposed that one-legged stance time <5 seconds is a risk factor for injurious falls, although even relatively healthy adults ≥70 years old can have difficulty with one-legged stance. Given the importance of cognition as a risk factor, assessing cognitive function is also indicated.

Laboratory and Imaging Assessments

Depending on the history and physical examination, further laboratory and diagnostic imaging evaluation may be warranted. A CBC, serum chemistries, and other metabolic studies may be useful when systemic disease is suspected. Head or spine imaging, including radiography, CT, or MRI, are not indicated unless history and physical examination identifies neurologic abnormalities, either preceding or of recent onset, that are related to the gait disorder. In a recent review of multiple imaging modalities, a number of pathologies (white matter, hippocampal volume, ventricular enlargement, and amyloid and tau aggregation) were associated with poor gait performance, with grey matter atrophy having the most consistent link (SOE=A).Other pathologies associated with poor gait performance included white matter atrophy, hippocampal volume decline, ventricular enlargement, and amyloid and tau aggregation. Gait disruption was also associated with both under- and overactivation of neuronal activity. Beause of substantial methodologic heterogeneity for measuring both neuropathology and gait, a meta-analysis was not possible.

Performance-Based Functional Assessment

A number of timed and semiquantitative balance and gait scales have been proposed as a means to detect and quantify abnormalities and to direct interventions. Fall risk, for example, can be increased with more abnormal gait and balance scale scores, such as with the Berg Balance Scale or the Performance-Oriented Mobility Assessment. Perhaps the simplest battery in the clinical setting is the "Timed Up and Go" (TUG), a timed sequence of rising from a chair, walking 3 meters, turning, and returning to sit in the chair. One study suggests a TUG score of ≥12 seconds as an indicator of fall risk. Other investigators have found limitations in TUG in the presence of cognitive impairment and difficulty in completing the test because of immobility, safety concerns, or refusal. Another functional approach that can be useful clinically is the Functional Ambulation Classification scale, which rates the use of assistive devices, the degree of human assistance (either manual or verbal), the distance the person can walk, and the types of surfaces the person can negotiate.

Comfortable gait speed and related endurance measures (such as the 6-minute walk) are powerful predictors of a number of important outcomes, such as falls, disability, hospitalization, institutionalization, and mortality (SOE=B). Another endurance measure, the 400-meter walk, has been increasingly used in research settings and considered a marker of major mobility disability that was responsive to a physical activity intervention. Gait speed is faster in individuals who are taller, who have a lower disease burden, and who are more active and less functionally disabled. Usual gait speed is frequently tested from a standing start over a distance of 4 meters. Although speeds between 0.6 and 0.8 m/s are associated with poor outcomes, a speed of 0.6 m/s has been proposed as the cut point for dismobility, given the rapid rise in disability and poor health outcomes below this speed. As expected, in clinical settings, gait speed is slowest in the acute hospital versus in subacute or outpatient settings (0.46, 0.53, and 0.74 m/s respectively, in a review). Speeds of >1.0 m/s and perhaps 1.2 m/s are associated with better functional outcomes and increased life expectancy. Several studies have found age- and disease-associated deficits in the ability to walk and perform a simultaneous cognitive task (“dual tasking,” such as talking while walking), and also linked these deficits with increased fall risk (SOE=B), and include gait speed changes as well as gait variability. However, dual task changes in gait speed as well as variability may be equivalent to single task changes in discriminating fallers from non-fallers even when considering those who walk more slowly or who are cognitively impaired. The dual task effect may thus be most clinically useful in very high-risk groups who require extensive attentional resources to maintain safe gait. Although slower gait speed can predict decreased cognition in healthy older adults, the opposite is true as well, namely that decreased cognitive function, in multiple domains including executive function, is associated with slower speed.


Even if a condition can be diagnosed on evaluation, many conditions causing a gait disorder are, at best, only partially treatable. The patient is often left with at least some residual disability. However, other functional outcomes such as reduction in weight-bearing pain may be equally important in justifying treatment. Functional improvement becomes the treatment goal. Comorbidity, disease severity, and overall health status tend to strongly influence treatment outcome.

Achievement of premorbid gait patterns may be unrealistic, but improvement in measures such as gait speed is reasonable as long as gait remains safe. Recent studies have estimated the extent to which a change in gait performance, such as usual gait speed, is clinically meaningful. For example, in cohorts that include mobility-impaired individuals, estimates range from 0.05 m/s to 0.10 m/s for small and substantial change, respectively. Exercise interventions in more physically impaired older adults may have lower meaningful differences (eg, 0.07 m/s in one review). However, using a cut-off of even 0.10 m/s may not coincide with perceived change in mobility in certain patient populations, such as in patients with a previous hip fracture. The most striking changes in gait speed occur with strength or combined training (including aerobic exercise), especially with higher intensity or dosage. An innovative program using goal-oriented, progressively more difficult stepping and walking patterns to promote the timing and coordination of stepping in subclinically gait-impaired older adults may be more effective than treadmill walking training (SOE=B). Task-specific training may also improve dual-task performance, but the same training in impaired populations may also improve single-task performance. Finally, recent trials using exercise or combined exercise–cognitive training may improve dual task performance (mainly gait speed), but the results are mixed and the mechanism for improvement (eg, applying a different cognitive response strategy) is not clear.

Modest improvement with residual disability is also the result of surgical treatment for compressive cervical myelopathy, lumbar stenosis, and NPH. Few controlled prospective studies and no well-controlled randomized studies address the outcome of surgical versus nonsurgical treatment for these 3 conditions. A number of problems plague the available series: outcomes such as pain and walking disability are not reported separately, the source of the outcome rating is not clearly identified or blinded, the criteria for classifying outcomes differ, the outcomes may be subjective and subject to interpretation, the follow-up intervals are variable, the participants who are reported in follow-up may be a highly select group, the selection factors for conservative versus surgical treatment between studies differ or are unspecified, and there is publication bias (only positive results are published). Many of the surgical series include all ages, although the mean age is usually >60 years old. A few studies document equivalent surgical outcomes with conservative, nonsurgical treatment.

With regard to lumbar stenosis procedures, many older adults have reduced pain after laminectomies and lumbar fusion surgery, although they have continued residual disability and if there is improvement in walking ability, the improvement may wane long term (SOE=B). Nonoperative treatment (with a variety of interventions, including oral anti-inflammatory medications, heating modalities, exercise, mobilizations, and epidural injections) can also result in modest improvements such as in walking tolerance (SOE=B). A randomized trial found that physical therapy yielded similar effects to those of surgical decompression (no gait data shown). However, methodologic differences, such as a large percentage of physical therapy patients crossing over to surgery, undermine the outcome, and similar to results of other studies, long-term benefits of surgery diminish after 24 months. Part of the problem in determining long-term gait outcomes of surgery for lumbar stenosis is other comorbidity, such as cardiovascular or musculoskeletal disease, that influences mobility. Regarding cervical stenosis, studies involving postoperative gait outcomes in older adults are limited, but in one nonrandomized study, walking speed improved significantly in most of the postcervical myelopathy decompression patients whose mean age was 60 years old (SOE=B).

Outcomes for hip and knee replacement surgery for osteoarthritis are better, although some of the same study methodologic problems exist. Multidisciplinary rehabilitation (versus more limited rehabilitation) after hip or knee replacement results in improved global functioning beyond walking measures (SOE=A). Other advances include “total body preoperative exercise,” ie, “prehabilitation,” which may have positive effects on length of stay and possibly postoperative function, as noted in a review that included primarily orthopedic surgeries. Despite rehabilitation after joint replacement, some residual weakness, stiffness, and slowed/altered gait and balance may remain. Simple function may be maintained after knee replacement, such as maintaining the ability to safely clear an obstacle, but usually at the expense of additional compensation by the ipsilateral hip and foot. Other than pain relief, sizable gains in gait speed and joint motion occur, although residual walking disability continues for a number of reasons, including residual pathology on the operated side and symptoms on the nonoperated side. Controlled trials of specific exercise programs offered at least 2 months after total knee replacement (such as aquatic or general exercise) generally show retention of strength but varying retention of walking speed gains at 1-year follow-up. In patients undergoing total hip replacement for osteoarthritis versus patients with osteoarthritis who received medical therapy, self-reported walking-related function at 6 months was improved (SOE=B). Nevertheless, in a review of hip replacements, reduction in strength output continues compared with controls and the nonoperated hip, with reductions in walking speed at long term (eg, 2 year) follow-up.

Finally, the use of orthoses and other mobility aids can help reduce gait disorders (SOE=C). Although there are few data supporting their use, lifts (either internal or external) to correct for limb length inequality can be used in a conservative, gradually progressive manner. Other ankle braces, shoe inserts, shoe body and sole modifications, and their subsequent adjustments are part of standard care for foot and ankle weakness, deformities, and pain but are beyond the scope of this chapter. In general, well-fitting walking shoes with low heels, relatively thin firm soles, and if feasible, high, fixed heel collar support are recommended to maximize balance and improve gait. Mobility aids such as canes and walkers reduce load on a painful joint and increase stability. Note that light touch of any firm surface like walls or “furniture surfing” provide feedback and assist with balance.


Plummer P, Zukowski LA, Giuliani C, et al. Effects of physical exercise interventions on gait-related dual-task interference in older adults: a systematic review and meta-analysis. Gerontology. 2015;62(1):94–117.

Taylor JL, Parker LJ, Szanton SL, et al. The association of pain, race and slow gait speed in older adults. Geriatr Nurs. 2018;39(5):580‒583.

Wennberg AM, Savica R, Mielke MM. Association between various brain pathologies and gait disturbance. Dement Geriatr Cogn Disord. 2017;43(3-4):128–143.