A fall is a sudden, unintentional change in position causing an individual to land at a lower level, on an object, or on the ground. Because most falls are not associated with syncope, most investigators exclude falls associated with loss of consciousness (e.g., as from a seizure), although loss of consciousness can occur after the fall. Other overwhelming events (e.g., sustaining a violent blow or sudden onset of paralysis) are also not as common as nonsyncopal falls. Annually, falls occur in approximately one third of community-dwelling older adults and one half of nursing home residents. The nursing home resident rate (1.5 falls per bed annually) is likely caused by the increased frailty of these residents and the increased reporting in this setting (30). Depending on the published series, although up to 2% of falls result in hip fractures, other fractures can occur in up to 5% of falls, and other serious injuries (e.g., head injury) can occur in up to 10%. Often, more than 50% of persons who fall sustain at least some minor injury (e.g., a laceration); more importantly, however, these and others who fall can develop fear of falling and restrict their activity. Those who fall, particularly repeat fallers, tend to have activities of daily living (ADL) and instrumental ADL disability and are at high risk for subsequent hospitalization, further disability, institutionalization, and death (19,40,41).

Determining that a gait is “disordered” is difficult because no clearly accepted standards are generally seen for “normal” gait in older adults. Some believe that slowed gait speed suggests a disorder, whereas others believe that deviations in smoothness, symmetry, and synchrony of movement patterns suggest a disorder. However, a slowed and aesthetically abnormal gait, in fact, can provide the older adult with a safe, independent gait pattern. Self-reports of difficulty walking are common. At least 20% of noninstitutionalized older adults admit to having difficulty walking or require the assistance of another person or special equipment to walk (23). Limitations in walking also increase with age. In some samples of noninstitutionalized older adults aged 85 years and older, the incidence of limitation in walking can be more than 54% (23). Although age-related gait changes (e.g., in speed) are most apparent past age 75 or 80, most gait disorders appear in connection with underlying diseases, particularly as disease severity increases. Attributing a gait disorder to one disease cause in older adults is particularly difficult because similar gait abnormalities are common to many diseases (2).

Disordered gait may not be an inevitable consequence of aging, but rather a reflection of the increased prevalence and severity of age-associated diseases.
These underlying diseases, both neurologic and nonneurologic, are the major contributors to disordered gait. In a primary care setting, patients consider pain, stiffness, dizziness, numbness, weakness, and sensations of abnormal movement to be the most common contributors to their walking difficulties (17). The most common diagnoses found in a primary care setting thought to contribute to gait disorders include degenerative joint disease, acquired musculoskeletal deformities, intermittent claudication, postorthopedic surgery and poststroke impairments, and postural hypotension (17). Usually, more than one contributing diagnosis is found. Factors such as dementia and fear of falling also contribute to gait disorders. The diagnoses found in a neurologic referral population are primarily neurologically oriented (12, 34): 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’s disease or parkinsonian syndromes; and cerebellar disease. Known conditions causing severe impairment (e.g., hemiplegia and severe hip or knee disease) are frequently not referred to a neurologist. Thus, many gait disorders, particularly those that are classical and discrete (e.g., related to stroke and osteoarthritis) and those that are mild or may relate to irreversible disease (e.g., multi-infarct dementia), are presumably diagnosed in a primary care setting and treated without a referral to a neurologist. Other less common contributors to gait disorders include metabolic disorders (related to renal or hepatic disease), central nervous system (CNS) tumors or subdural hematoma, depression, and psychotropic medications. Case reports also document reversible gait disorders caused by clinically overt hypo- or hyperthyroidism and vitamin B12 and folate deficiency [for detailed review, see Alexander (2)].

A potentially useful classification system [based on Nutt et al. (22) and elaborated in Alexander (1)] (Table 9-4) categorizes these diseases according to the sensorimotor levels that are affected. Diseases considered part of the low sensorimotor level can be divided into peripheral sensory and peripheral motor dysfunction, including musculoskeletal (arthritic) and myopathic or neuropathic disorders that cause weakness. These disorders are generally distal to the CNS. With peripheral sensory impairment, vestibular disorders, peripheral neuropathy, posterior column (proprioceptive) deficits, and visual impairment commonly cause unsteady and tentative gait. With peripheral motor impairment, a number of classical gait patterns emerge, including obvious compensatory maneuvers. These conditions involve extremity (both body segment and joint) deformities, painful weight bearing, and focal myopathic and neuropathic weakness. Note that, if the gait disorder is limited to this low sensorimotor level (i.e., the CNS is intact), the person adapts well to the gait disorder, compensating with an assistive device or learning to negotiate the environment safely. At the middle level, the execution of centrally selected postural and locomotor responses is faulty, and the sensory and motor modulation of gait is disrupted. Gait can be initiated normally, but stepping patterns are abnormal. Examples include diseases causing spasticity (e.g., related to myelopathy, vitamin B12 deficiency, and stroke), parkinsonism (idiopathic as well as drug induced), and cerebellar disease (e.g., alcohol induced). Classical gait patterns appear when the spasticity is sufficient to cause leg circumduction and fixed deformities (e.g., equinovarus), the parkinsonism produces shuffling steps and reduced arm swing, and the cerebellar ataxia increases trunk sway sufficiently to require a broad base of gait support. At the high level, the gait characteristics become more nonspecific, and cognitive dysfunction and slowed cognitive processing become more prominent. Behavioral aspects such as fear of falling are also important, particularly in cautious gait. Frontal-related gait disorders often have a cerebrovascular component and are not merely the result of frontal masses and NPH. The severity of the frontal-related disorders runs a spectrum from gait ignition failure (i.e., difficulty with initiation) to frontal disequilibrium, where unsupported stance is not possible. Cognitive, pyramidal, and urinary disturbances can also accompany a gait disorder. Gait disorders that might fall into this category have been given a number of overlapping descriptions, including gait apraxia, marche à petit pas, and arteriosclerotic parkinsonism.

Note that more than one disease or impairment is likely present that contributes to a gait disorder; one example could be the long-standing diabetic patient with peripheral neuropathy or a recent stroke who is now very fearful of falls. Certain disorders can actually involve multiple levels, such as Parkinson’s disease affecting high (cortical) and middle (subcortical) structures. Drug-metabolic causes (e.g., from sedatives, tranquilizers, and anticonvulsants) can involve more than one level; phenothiazines, for example, can cause high (sedation) and middle (extrapyramidal) level effects.

Other factors that contribute to gait disorders that are frequently disease associated (e.g., related to cardiopulmonary disease) but are often assessed separately include marked reductions in activity and aerobic fitness, reductions in joint strength and range of motion, and previous falls.

Although older adults may maintain a relatively normal gait pattern well into their 80s, some slowing occurs, and decreased stride length becomes a common feature described in older adult gait disorders
[reviewed by Alexander (2)]. Some authors have proposed the emergence of an age-related gait disorder without accompanying clinical abnormalities (i.e., essential “senile” gait disorder) (20). 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 (e.g., 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-asymptomatic disease (e.g., related to subtle extrapyramidal signs) and is likely to be a manifestation of concurrent, progressive cognitive impairment (e.g., Alzheimer’s disease or vascular dementia) (10). Thus, “senile” gait disorder potentially reflects a number of potential disease causes and is generally not useful in labeling gait disorders in older adults.