Use of Gait Patterns to Reveal Possible Disorders in the Geriatric Patient

Abstract

Changes in gait occur frequently with advancing age and are often associated with falls, loss of independence, morbidity, and even mortality. Gait changes may occur as part of the natural process of aging or may be associated with underlying pathology. Careful observation of gait can provide insight into the patient’s overall state of health. This article discusses the various types of gait changes that can occur with aging and the significance of these gait abnormalities.

Walking is the result of complex interaction between the basal ganglia, mesencephalon, cerebellum, and spinal cord of the central nervous system and the joints, muscles, and ligaments of the musculoskeletal system. Such interaction between the two systems is critical for normal functioning and is accomplished through proprioception.

The normal, healthy adult propels the body forward with the help of gravity and inertia. Walking consists of “falling forward” and recapturing balance at the proper moment. The function of muscles during gait is typically to decelerate joint motion; thus their primary role is to restrain rather than to propel. Muscle activity is significant in maintaining the body’s balance at heel strike. This is accomplished through the deceleration function of back extensors, hip extensors, and knee flexors and is assisted by the mobile adapter function of the joints of the foot. In addition, muscles help maintain the body’s center of gravity in a relatively stable position by resisting ground-reaction force during midstance.

The posterior muscles actively contract at the end of the stance phase in order to propel the limb forward into the swing phase. The only “stabilizing” period of gait is during double-support stance. Even in this “stabilizing” period, however, the feet are not flat on the ground. The weight-accepting foot is at heel strike, and the contralateral foot is at toe-off. Thus, as the body is attempting to shift the weight from one foot to the other, it is inherently unstable. Therefore, the challenge for elderly patients is to precisely regulate their muscles while maintaining balance and propelling the body forward in gait.

The structures in the central nervous system responsible for standing and walking are the basal ganglia, mesencephalon, cerebellum, and spinal cord. Animal experiments have demonstrated that stance and locomotion are unaffected following complete removal of the cerebral cortex if the basal ganglia, thalamus, and brain stem are left intact. In addition, stimulation of the locomotor region in the mesencephalon evokes walking patterns of varying speeds and forms depending on the strength of the stimulus. However, coordination of the various muscle groups for locomotion is dependent on the neural circuits within the spinal cord. Finally, the cerebellum plays a vital role in maintaining proper posture and balance and in regulating trajectory, velocity, and acceleration of movement.

Evaluation of Gait

The “golden rule” of gait evaluation is that the clinician should always attempt to get a first impression of patients’ gait as they move from the waiting area to the treatment room. This gives the practitioner an unbiased view of the gait pattern, without the effects of patients’ nervousness or awareness that their gait is being analyzed. In the treatment area, the evaluation should proceed with patients seated in straightback, armless chairs. They should be asked to rise out of the chair without assistance, stand briefly, take several steps forward, turn around, and walk back. In addition, patients should be asked to walk sideways, walk backward, and sit down again. Romberg’s test should be employed to assess patients’ proprioceptive capabilities[1] and cerebellar function. In this test, patients stand with their feet together and without support. They are then asked to close their eyes while the clinician observes their ability to maintain balance. In addition, a nudge test should be performed. During the nudge test, the patient is asked to stand while the clinician stands behind the patient and wraps his or her arms loosely around the patient. The clinician then gently nudges the patient backward, checking the patient’s balance and position sense.

Normal Gait

Patients should be able to rise from straight-back, armless chairs without assistance. The initiation of normal gait is smooth and without hesitancy. During gait, the body should be erect with the head straight and arms hanging loosely to the sides while moving in rhythm with the opposite leg. Arm swings should be equal in length. The shoulders and hips should be level, and the knees should point forward. There should be no sign of head tilt, scoliosis, or lordosis. With each step, the hip and knee should flex smoothly, and the ankle should dorsiflex sufficiently to allow for toe clearance. Step length and height should be symmetrical. All periods of gait (heel contact, midstance, and propulsion) should be in normal sequence and flow smoothly. Patients should be walking in a straight line, without staggering or waddling. In addition, turning should be smooth and continuous, with a limited number of steps needed to make a 360° turn. Patients should be able to walk in all directions, with their eyes open as well as with them closed. There should be only slight swaying during Romberg’s test, and patients should not fall backward during a nudge test.

Common Gait Changes

Several changes in gait can occur as a patient ages. For instance, there are gender differences in geriatric gait patterns. While men tend to widen their base of gait,[1] women tend to narrow it while developing a waddling gait.[2,3]

Elderly patients have also been found to have shorter stride lengths, an increased double-support period, decreased push-off power, and a more flatfooted landing, even without any apparent gait or balance abnormalities.[4]

One study showed that elderly patients have decreased ankle plantarflexion power during the latestance phase of gait and concluded that appropriate training of the posterior muscle group in the leg may be important in maintaining step length in advanced age.[5,6] Another study, involving 112 female elderly patients during a 12-month period, found that exercise can significantly improve dynamic postural stability in older patients.[7] An adjunctive study of 160 women over 22 weeks also concluded that gait velocity and related parameters can be increased as a result of an exercise regimen and determined that the increase may be due in part to increased lower-limb muscle strength.[8] An additional study found a strong relationship between lower-extremity strength and balance, gait, and the tendency to fall.[9]

Pathologic Gait

The term “pathologic gait” refers to a change in the normal walking pattern that may be attributed to a specific etiology. These etiologies may be placed into six categories: idiopathic, neurosensory, arthritic, musculoskeletal, cardiovascular, and metabolic (

Table 1. Etiologies of Abnormal Gait.

).

Idiopathic Disorders. Idiopathic gait disorder of the elderly, also referred to as marche a petite pas, senile gait, and essential gait disorder of aging, was found to occur in 16% of patients with undiagnosed difficulty in walking.[10] As its name implies, this disorder tends to be diagnosed when there is no overt pathology, although many hypotheses have been proposed as to its etiology. These include an exaggeration of normal gait changes associated with aging,[11] the result of unilateral or bilateral frontal lobe lesions secondary to arteriosclerosis of the anterior cerebral arteries,[12] peripheral neuropathy,[13] increased apprehension that causes postural “overreaction,”[14] and the precursor to an as-yet-asymptomatic disease.[15]

The gait pattern of patients with idiopathic gait disorder of the elderly is described as head facing forward, kyphosis of the upper spine with flattening of the lumbar spine, and the hips and knees slightly bent. Gross rowing movements of the arms are present in an attempt to grope for support,[16] resulting in diminished swinging of the arms.[17] Patients exhibit broad-based gait[17] and small steps, while shuffling the feet along the ground. The steps become even smaller while the patient is turning, with minimal leg movements due to apprehension and stiffness.[17] This gait pattern may be present only when patients first set out to walk; the gait pattern may become normal after a few steps. However, as patients continue to age, the gait progressively worsens until only the small-step shuffling pattern is present.[16] The result of Romberg’s test is negative, although increased sway in stance has been noted as a general condition of aging.[11,18,19] Also, patients are easily displaced backward during a nudge test and are therefore at a heightened risk of falling.[11] In advanced cases of idiopathic gait disorder of the elderly, canes and walkers may be necessary for patients to safely remain mobile.

Neurosensory Disorders. Hemiplegia (post– cerebrovascular accident), bilateral frontal lobe disease, Parkinson’s disease, cerebellar disorders, sensory ataxia, posterior column lesions (such as tabes dorsalis), and peroneal nerve neuropathy are the most common neurosensory etiologies that can cause changes in gait patterns.

Hemiplegia or unilateral paralysis, as a result of a stroke or cerebrovascular accident, is typically due to occlusion of the middle cerebral artery or one of its deep penetrating branches. The severity of the gait abnormality produced by a stroke is proportional to the amount of functional mobility patients can attain. One study determined that the amount of gait deformity can be predicted by leukoaraiosis, a radiologic change of cerebral white matter thought to be caused by ischemia.[20] Elderly patients with complete flaccid paralysis of the affected lower extremity will probably not walk again. Patients who have retained or recovered partial function will typically still have weakness of the hip flexors, extensors, and abductors, as well as the knee flexors. Interestingly, one study showed that patients with right-hemisphere deficits had decreased ambulatory ability as compared with patients with left-hemisphere deficits.[21] Walking begins when the patient lifts the contralateral heel in order to generate the necessary energy to initiate the swing phase of the weakened limb. The hemiplegic leg circumducts through the swing phase and adducts just prior to contacting the supporting surface, resulting in a prolonged swing on the affected side and prolonged stance on the unaffected side. The foot of the weakened side remains in a plantarflexed and adducted position throughout the swing phase. Consequently, there is no longer a typical heel-to-toe strike pattern during the contact period, resulting in a steppage gait. A double-step gait has been described in which patients pause after every other step to regain their balance.[22] Proximally, the shoulder on the affected side adducts; the elbows, wrists, and fingers are held in a flexed position; and the arm swing is greatly reduced. Patients may also have deficits in proprioception, as well as vision. Specifically, patients may suffer from homonymous hemianopia.

Bilateral frontal lobe disease, as well as other disorders affecting the frontal lobe, impairs gait integration, resulting in frontal ataxia or gait apraxia.[11,23] Patients are unable to rise from a chair unaided. Both legs are involved, and the feet are placed wide apart during stance, while the body is flexed slightly forward. There is a long delay before the initiation of steps, and in an effort to begin, patients may sway from side to side or appear to shuffle in place, the “slipping-clutch syndrome.”[11,23] Gait will consist of shuffling steps with occasional moderate steps; however, the stride length will be shorter than normal owing to the loss of reciprocal movement. Any change in floor surface, such as the edge of a carpet, may cause the patient to stop and resume shuffling. When the patient tries to turn around, one foot may appear frozen while the other makes multiple tentative steps. Similarly, when trying to stop, decelerate, or accelerate, the patient may shuffle in place or fall before assuming the new gait pattern. Patients with bilateral frontal lobe disease have normal muscle strength, intact deep tendon reflexes, absence of Babinski’s sign, and normal sensory reflexes. Disuse atrophy may occur, especially of thigh muscles. Education or retraining programs to teach better and safer ways to walk are unsuccessful. Although a weighted walker may be of some benefit, canes and nonweighted walkers do not help these patients. A thorough evaluation of the patient should be performed, as this disease may be associated with reversible forms of dementia, such as normal-pressure hydrocephalus.[23]

Parkinson’s disease is a slowly progressive, degenerative disorder characterized by slowness and poverty of movement (dyskinesia), muscular rigidity, resting tremor, and postural instability. Parkinson’s disease typically spares the deep tendon reflexes, and begins with a resting, “pill-rolling” tremor of the hand. Patients are slow to rise from a chair. The knees, hips, and elbows are flexed in stance, and the trunk is likewise flexed forward, placing increased weight on the metatarsals. The head is lowered, and the face is expressionless, with infrequent blinking. A pathologic gait entity known as festination is typically seen as a result of Parkinson’s disease. Initiating gait may be difficult, and once started, the gait is slow, laborious, and shuffling, with a loss of arm swing. The center of gravity is displaced forward as a result of the flexed trunk position, and festination results when the patient accelerates the gait rather than extending the spine in an attempt to recapture the center of gravity and prevent falling forward. Individuals with Parkinson’s disease also have a tendency toward retropulsion, or falling backward.[11] In addition, patients will turn en bloc, moving their whole body while turning. One study found that, as compared with male patients, female patients of similar age tended to have fewer symptoms and less difficulty with motor skills.[24]

Care should be taken to note the time of the examination in relation to the patient’s medication cycle, as gait patterns can differ significantly at peak medication times from those at the end of the dose.[25] When deciding on treatment modalities, the physician should consider heel lifts and stretching exercises for tight muscles, which may be beneficial.[16] It should be noted that one study concluded that patients with mild-to-moderate Parkinson’s disease have the potential to maintain normal exercise capacity with regular aerobic exercise, despite their neurologic deficit.[26] Therefore, having these patients participate in regular exercise programs would be extremely beneficial in improving their overall health.

Gait disorders may also result from infarction or degeneration of the cerebellum; these disorders are characterized by ataxia, or a disturbance in the rate and extent of an individual movement. The gait is broad-based and staggering, with no shuffling. The steps are irregular, with an overstepping stride. Titubation, or a coarse forward and backward tremor of the trunk, is present, as well as side-to-side lurching. Loss of ipsilateral arm swing and an ipsilateral shoulder drop are also present, with or without scoliosis. Other signs of cerebellar dysfunction include pastpointing and an inability to perform rapid alternating movements. In addition, patients will have a positive Romberg’s test both with their eyes open and with them closed.

Sensory ataxia is the loss of the afferent limb of the various spinal and brain stem reflexes that control standing and walking.[23] The resulting loss of proprioception is very disabling and causes irregularity in the placement and direction of limbs. Consequently, the base of gait varies from step to step, and patients will typically walk at a slower rate, often slapping the ground owing to lack of sensory feedback. Compensation is obtained with visual cues, and this fact is extremely helpful when determining the diagnosis. Patients will have a positive Romberg’s test only when their eyes are closed. In addition, patients with sensory ataxia will become “disabled” when attempting to navigate in darkness and should always have a light source available when arising in the middle of the night. Patients typically have good muscle strength, and muscle tone is either normal or slack. Their toes may make small “piano playing” movements as the foot is handled.[23] Patients respond well to the use of a cane or walker, and may be taught to associate upper-body movements with those of their legs.

Posterior column and root ganglia destruction can result in tabes dorsalis (locomotor ataxia), a sequela of acquired syphilis. Patients experience a slow and insidious onset of pain, ataxia, sensory changes, and loss of tendon reflexes. They are likely to describe an intermittent lancinating pain in their legs, and less commonly in the back, thorax, abdomen, arms, and face. As the disease progresses, there may be unsteadiness of gait that is worse in the dark, and patients may begin to walk with a wide base of gait and experience foot slap. They may also present with hyperesthesia and paresthesia, and describe a feeling of walking on foam rubber. Urinary retention, incontinence, and recurrent urinary tract infections, as well as impotence, are common. On examination, the legs are hypotonic, with diminished or absent tendon reflexes, decreased vibratory sensation and proprioception, and absence of pain sensation. Romberg’s test is positive. In addition, there is ataxia during the heel-shin rapid-movement coordination test, as well as during walking.

Peroneal nerve neuropathy may be secondary to diabetes mellitus, alcoholism, vitamin B₁₂ deficiency, malignancy, Hansen’s disease, Guillain-Barré syndrome, porphyria, collagen vascular diseases, uremia, herniated disc, trauma, and certain medications. Anatomically, the common peroneal nerve branches off of the sciatic nerve in the distal one-third of the posterior thigh. It then passes between the biceps femoris and the lateral head of the gastrocnemius muscle to traverse the lateral surface of the neck of the fibula. Then it branches into the common peroneal nerve, which supplies the muscles in the anterior leg compartment, and the superficial peroneal nerve, which supplies the peroneus longus and brevis muscles as well as sensory innervation for the distal lateral and anterolateral leg. Common findings in peroneal nerve neuropathy include foot slapping and raising the feet higher than necessary for ground clearance. In addition, patients may have difficulty climbing stairs. In severe cases, patients may find it necessary to watch their legs and the floor, in order to determine their position. Romberg’s sign is found. Diagnosis is confirmed by electromyography and electrodiagnostic tests. An ankle-foot orthosis and a cane may make walking easier and safer.

Arthritic Disorders. Abnormal gait can be caused by arthritic pathologies, such as degenerative joint disease or osteoarthritis, rheumatoid arthritis, cervical spondylitis, Paget’s disease, and polymyalgia rheumatica. In addition, gout and osteoporosis may cause gait disturbances, alone or in conjunction with other disorders.

Cervical spondylitis, or degenerative arthritis of the spine, can cause progressive myelopathy owing to chronic spinal cord compression. The gait will be spastic and stiff-legged, with reduced toe clearance and a tendency toward circumduction.[27] In addition, the spinal cord compression will cause hyperreflexia in the limbs, while the jaw jerk reflex will be normal. Also, patients will present with increased tone, decreased vibratory sensation, and Babinski’s sign. A computed tomographic scan can allow the measurement of the diameter of the cervical canal. If the canal measures 10 mm or less, then cord compression is likely.

Lumbar spine osteoarthritis is characterized by the loss of lordotic curvature, which causes a shift in the center of gravity. As a result, patients walk with their hips and knees flexed, in order to keep their center of gravity over their feet. Hip and knee flexion may produce contracture or stretching of various muscles and ligaments, and the resulting strain on the sacrolumbar region may further aggravate the condition.

Arthritis of the lower extremity is probably the most common cause of gait problems.[11] It may occur in the hips, knees, feet, or ankles. Initially, arthritis may present as asymmetric differences in the joint ranges of motion. Patients may complain of pain or stiffness, usually deep and localized. Periarticular muscle atrophy, contractures, joint deformity, and edema may also be present.

Osteoarthritis in the hip is commonly associated with an antalgic gait, shortening of the leg, flexion contracture, or muscle weakness. In addition, loss of internal rotation, flexion, extension, or abduction can usually be demonstrated. Patients may also have secondary lumbar lordosis to compensate for reduced hip flexion, resulting in low-back pain. During normal gait, the body’s center of gravity is shifted away from the foot that is touching the ground, and falling is prevented by a strong contraction of the hip abductors. This contraction, however, places increased force on the hip. Therefore, patients experiencing coxalgia (hip pain) tilt their body toward the painful hip whenever that side of the body is bearing weight. Adductor spasms, and groin pain associated with bursitis below the iliopsoas tendon, are commonly present. Patients will typically walk with a “scissor gait,” which may be exacerbated by painful spasms of the adductor muscles.[16] The antalgic gait pattern associated with osteoarthritis of the hip attempts to reduce the loading force on the hip joint. Patients accomplish this by flexing their knees, raising their pelvis during the swing phase, replacing heel contact with toe contact, and decreasing the overall contact time for that limb.

Typical findings associated with osteoarthritis of the knees include swelling, quadriceps muscle atrophy, and joint instability. The knee will be flexed and inwardly rotated. A varus deformity may also be present. The gait can be described as narrow-based waddling, although this gait pattern is more common in elderly women than in men.[3] In addition to flexing the knee, patients will walk on their toes in an attempt to decrease the overall force and contact time for the affected limb.

Arthritis in the foot and ankle causes a variety of gait changes, depending on the location of the joints involved and the mechanisms employed by the patient in an effort to off-load painful areas. The clinician should perform a careful evaluation of the patient in order to differentiate arthritis from other ailments, such as gout, corns or calluses, toe deformities, bunions, nail disorders, or atrophy of the plantar fat pad.

Patients suffering from osteoarthritis can be treated with analgesic agents, muscle relaxants, and local heat and rest. In addition, bracing, bandaging, and assistive devices such as canes and walkers can be beneficial. Weight loss is highly recommended in obese patients. Muscle strengthening is also recommended, as muscles provide important support for joints. To assist in treatment of spinal problems, back extensors and abdominal muscles should be strengthened. For hip joint arthritides, the abductors and extensors should be targeted, and for knee joint problems, the extensors of the knee should be strengthened.

Rheumatoid arthritis results in a slow and shuffling gait, with a loss of heel-to-toe pattern. In addition, double-support stance time is increased. Foot pain has been shown to limit ambulation and alter gait patterns, while structural deformities of the foot have less influence on mobility and gait.[28] Currently, many different treatment regimens exist for rheumatoid arthritis, and patients should be referred to a rheumatologist.

Paget’s disease of bone (osteitis deformans) is a chronic disorder, characterized by localized areas of hyperactive bone, in which normal bone is replaced with softened, enlarged osseous structures. The etiology is unknown; however, a familial incidence has been observed, and a viral infection has been suggested. Symptoms include aching, deep pain that may worsen at night, and stiffness, fatigability, and increased skull size. In addition, there is lateral bowing of the femur or anterior bowing of the tibia, and there is a tendency for dense bone to be deposited on the concave side of the bowed bone. There may also be warmth and periosteal tenderness associated with the bowing and markedly increased blood flow to the involved extremity. As a result of the deformities, patients are likely to have a hobbling gait. Pathologic fractures may occur in the tibia or femur. Patients may be treated with analgesic agents to reduce pain, orthoses to correct abnormal gait patterns, or surgery to replace diseased joints. In addition, chemotherapy has been shown to suppress bone cell activity.

Polymyalgia rheumatica is a disease characterized by severe pain and stiffness in proximal muscle groups, without associated muscle weakness or atrophy. Although symptoms of pain are localized to muscles, there is evidence that the disease includes a proximal, inflammatory arthritis. Patients complain of pain and stiffness in the neck, pectoral region, and pelvic girdle. The stiffness is worse in the morning and after periods of inactivity. There is no evidence of muscle weakness; there is, however, profound disuse atrophy of muscles. The erythrocyte sedimentation rate is usually elevated, and patients may also suffer from temporal arteritis. Patients respond well to treatment with nonsteroidal anti-inflammatory drugs. However, such drugs are not recommended if temporal arteritis is present, and prednisone should be used instead.

Musculoskeletal Disorders. Abnormal gait can be caused by such muscular pathologies as muscular dystrophy, polymyositis, immobility, and foot disorders, which can add to the existing changes associated with age, such as decreased muscle strength, increased fatigability, and reduced contraction strength.

Muscular dystrophy is a slowly progressive disease causing weakness of the proximal leg muscles as well as the muscles of the shoulder and pelvic girdles. The shoulders tend to slump forward, and winging of the scapulae may occur. Patients typically have lumbar lordosis and a protuberant abdomen secondary to proximal muscle weakness. A chair with arms is essential for these patients because of the difficulty they experience when rising from a seated position. Weakness of gluteal muscles, particularly the gluteus medius, leads to a waddling motion or Trendelenburg gait pattern, in which the pelvis sags on the nonweightbearing leg. In addition, the knees are unstable owing to atrophy of the knee extensors. In more advanced stages of the disease, patients tend to toe-walk. Individuals with muscular dystrophy will also have Gower’s sign, whereby on arising from the floor, patients use their hands to climb up their legs in order to stand up.

Polymyositis is a systemic connective tissue disease that results in inflammatory and degenerative changes in muscles and frequently in the skin (dermatomyositis). Patients will present with symmetric, proximal muscle weakness and atrophy. It occurs twice as frequently in women as in men and occurs mainly in the sixth and seventh decades. Although the etiology is unknown, an autoimmune reaction has been suggested. Dermatomyositis presents as dusky and erythematous skin lesions, which may be slightly elevated and smooth or scaly. They may be found on the forehead, neck, shoulders, chest, back, forearms, lower legs, elbows, knees, and medial malleoli. In addition, patients may present with the heliotrope sign on the eyelids (periorbital edema with a pinkish-violet hue), Raynaud’s phenomenon, polyarthralgias, arthritis, cardiac involvement, and malignancy. Patients will have difficulty rising from chairs, as well as climbing stairs and performing reaching activities. Muscles of the feet, hands, and face are typically not involved. Corticosteroids and immunosuppressive agents are the drugs of choice for treatment.

Immobility can result in muscle atrophy and loss of flexibility, as well as decreased balance. If the immobility is the result of the temporary use of a wheelchair, as often occurs after injuries, the patient can become dependent on the wheelchair. Patients feel safe while in their wheelchair and no longer fear falling or injuring themselves. Often, patients continue to use the wheelchair for the rest of their life, even though there is no physical reason for them to do so. If patients do attempt to walk without the wheelchair, they will walk with a gait similar to that seen in idiopathic gait disorder of the elderly owing to the decrease in balance, flexibility, and muscle strength.

Muscle disorders can benefit from strengthening weak muscles and stretching exercises to reduce contractures. Assistive devices, such as crutches and canes, may also be helpful. Also, it is extremely important to keep patients active and avoid immobility, because patients suffering from neuromuscular disorders cannot reverse the results from cast disease or disuse atrophy.

Foot disorders such as hallux abducto valgus, gout, or other problems, including corns and calluses, will result in an antalgic gait. Atrophy of the plantar fat pad, for example, leads to a loss of shock absorption and may result in metatarsalgia. Even apparently benign disorders such as onychogryphosis—overgrown, clawlike toenails—can cause discomfort during gait and may result in decreased mobility. In addition, ulcers secondary to diabetes mellitus or peripheral vascular disease can cause an antalgic gait and may lead to more serious complications, such as infection and amputation.

Cardiovascular Conditions. Although not frequently thought to cause gait disturbances, cardiovascular conditions, such as chronic ankle edema, intermittent claudication, atherosclerosis, orthostatic hypotension, and vertebrobasilar insufficiency, can alter a patient’s gait.

Chronic ankle edema, as associated with rightsided heart failure or obstruction of venous and lymphatic drainage of the limb, will cause discomfort, pain, and fatigue for patients. As a result, patients may reduce their activities, and disuse atrophy could occur. Patients should be advised to maintain or increase their level of activity and to elevate their legs when resting. Also, compressive stockings, reduction of salt intake, and diuretics have been useful to reduce the edema.

Intermittent claudication, a deficient blood supply in exercising muscle, will often present as pain, ache, cramp, numbness, or a tired feeling in the lower extremities, especially the calves, during walking. The symptoms are relieved quickly with rest (1 to 5 min), and patients are then able to walk the same distance before the symptoms recur. The pain may occur more readily when walking faster or uphill. Patients will never experience the symptoms while at rest. As the disease progresses, the symptoms will occur after shorter and shorter distances. In severe cases, ischemic pain may occur at rest. The extremity may appear normal; however, pulses are reduced or absent. If pulses are present, yet intermittent claudication is suspected, pulses should be rechecked after exertion. Patients should be instructed to increase activity, as no damage can result from walking while the symptoms are present, and doing so will increase the collateral circulation in the affected extremity, thereby increasing blood flow distally.

Atherosclerosis is a generalized hypertrophy of the media of arterial walls and subintimal fibrosis, resulting in weakening and disruption of the elasticity of the walls. Diffuse calcification may develop, leading to intimal injury and ulceration, followed by thrombus formation, embolism, or complete occlusion. Pulses may be decreased or absent distal to the obstruction; bruits may be present over the narrowed artery; and muscle atrophy may occur. Initially, symptoms reflect the decreased blood flow to affected tissues during activities, such as angina on exertion or intermittent claudication. As a result, patients may become less active or expend less energy during activities. Treatment is focused on the complications of the disease, such as myocardial infarction, kidney failure, stroke, angina, and peripheral arterial occlusion. However, treatment should also include regular exercise, cessation of cigarette smoking, a diet low in fat and cholesterol, and weight reduction. Supportive measures include attention to such aspects of foot care as thorough cleaning, drying, and moisturizing. In addition, well-fitting and protective shoes should be worn to prevent trauma; however, synthetic shoes that do not “breathe” should be avoided. Also, elastic support hosiery should be avoided, as it can reduce the blood flow to the skin.

Orthostatic hypotension, also known as postural hypotension, is an abnormal decrease in blood pressure after assuming an upright posture (>20/10 mm Hg decrease, sustained for at least 3 min). It can be caused by hypovolemia, decreased baroreceptor responsiveness, and neurologic disorders that involve the autonomic nervous system. In addition, certain drugs such as antidepressants, insulin, narcotics, β-adrenergic and calcium channel blockers, and antihypertensive agents, as well as mixing multiple drugs, may cause this condition. Patients may present with a history of faintness, lightheadedness, dimming or loss of vision, diaphoresis, diminished hearing, pallor, weakness, dizziness, or confusion, as well as syncope and generalized seizures. Symptoms may be exacerbated by exercise or eating a large meal. Treatment consists of eliminating or reducing the cause. In addition, patients are advised to change posture slowly and avoid prolonged standing.

Vertebrobasilar insufficiency results in decreased blood flow to the brain stem, cerebellum, and posterior hemisphere where the visual center is located. Patients present with symptoms that reflect brainstem dysfunction, such as confusion, vertigo, binocular blindness, or diplopia. In addition, bilateral weakness, sensory loss, and paresthesia of the extremities may be present. Patients may experience hemiballismus, choreoathetosis, intention tremor, incoordination, and posturing of the hand and arm, particularly while walking. Drop attacks, in which patients’ legs buckle, are often attributed to this condition. Multiple ischemic attacks may occur daily or only two to three times during a period of several years. Treatment consists of addressing the underlying risk factors, such as hypertension, diabetes mellitus, obesity, hyperlipidemia, and smoking. Antiplatelet agents, anticoagulants, and occasionally vascular surgery may be indicated.

Metabolic Disorders. Endocrine disorders, side effects of medications, and psychological problems may also present as changes in gait.

Endocrine Disorders. Endocrine disorders such as hypothyroidism and vitamin B₁₂ deficiency are easily overlooked causes of gait disturbance. Although other systemic signs and symptoms that would help in the diagnosis may exist, they may be masked by fatigue or depression.

Hypothyroidism causes an insidious decline in the general health and mobility of the affected patient. It may be erroneously diagnosed as Parkinson’s disease, depression, or Alzheimer’s disease or attributed to aging itself. Patients will have fatigue, lethargy, constipation, dull facies, periorbital swelling, cold intolerance, sparse hair, dry and thick skin, and stiffness and cramping of muscles. In addition, patients may have carotenemia on the palms and soles, and paresthesia of the hands and feet is common. Reflexes will show a brisk contraction followed by slow relaxation. Some degree of ataxia will be present, which will improve with thyroid-replacement therapy.[29]

Vitamin B₁₂ deficiency or pernicious anemia is the most common megaloblastic anemia in the elderly. It may first present as low serum B₁₂ levels and neurologic abnormalities in the absence of anemia or macrocytosis. Manifestations include mental changes as well as such neurologic changes as peripheral neuropathy and subacute combined degeneration of the spinal cord. Patients may present with paresthesia and unsteadiness and may drag their feet during gait. Patients may also have accompanying sensory ataxia and paraplegia.[29]

Medications. The geriatric population consumes 30% of all medications prescribed in the United States, despite accounting for only 13% of the population.[30] In addition, because of changes in metabolism, older patients have an increased risk of side effects and overdosage. A common and overlooked side effect of these medications is disturbance of the patient’s normal gait pattern. Drugs that can cause gait abnormalities include benzodiazepines, tricyclic antidepressants, antihypertensive agents, salicylates, and antivertigo agents.

Benzodiazepines may cause disorientation and a progressive deterioration of gait. They also cause ataxia, delayed reaction time, increased body sway, and decreased proprioception,[31,32] as well as other kinds of motor impairment.[33] One study found a threefold increase of falls in elderly patients taking benzodiazepines.[29]

Tricyclic antidepressants, on the other hand, can cause Parkinson-like symptoms.[34] Patients taking tricyclic antidepressants have an increased risk of hip fractures owing to falls (with the original symptoms of depression and confusion for which the drugs were taken possibly contributing to the risk).[35] In addition, many antidepressants have anticholinergic properties that may result in orthostatic hypotension. Similar clinical findings may be caused by other agents such as reserpine, alpha-methyldopa, and butyrophenones.[27]

Antihypertensive agents may cause drug-related hypotension, which, combined with orthostatic and postprandial hypotension, has been shown to cause 3% to 23% of falls in the elderly.[36] One study of 1,358 patients found the following drugs to be associated with the occurrence of multiple falls: diazepam (odds ratio [OR], 3.7), laxatives (OR, 2.1), diuretics (OR, 1.8), and diltiazem (OR, 1.8).[37] These agents may often require dose adjustment.

Elderly patients may unknowingly experience salicylate intoxication from chronic ingestion of moderate doses of aspirin, and this may cause imbalance, tinnitus, and confusion.[27]

Surprisingly, antivertigo agents, such as meclizine hydrochloride, can actually aggravate imbalance[38] and may cause orthostatic hypotension and sedation.

The adverse effects of the practice of prescribing multiple medications cannot be emphasized enough. In long-term-care facilities, the average is between 6.6 and 7.7 prescriptions per patient, and it has been shown that the incidence of adverse drug reactions increases from 10% when a single medication is taken to nearly 100% when ten drugs are taken.[39]

Psychological Disorders. Gait disturbances may be the result of psychological disorders, such as psychogenic gait, fear of falling, and dementia.

Psychogenic or hysterical gait can be characterized by six features: 1) momentary fluctuations of stance and gait, often in response to suggestion; 2) excessive slowness or hesitation of locomotion incompatible with neurologic disease; 3) “psychogenic” Romberg’s sign with a buildup of sway amplitudes after a silent latency or with improvement by distraction; 4) uneconomic postures with waste of muscular energy; 5) the walking-on-ice gait pattern, which is characterized by small, cautious steps with fixed ankle joints; and 6) sudden buckling of the knees, usually without falls.[40] In addition, patients may present with factitious impairment of gait. In order to diagnose psychogenic gait, it is helpful to have patients perform unrehearsed tasks, such as walking backward and sideways and, while their eyes are closed, have them hop, skip, run, and crawl.[41] Patients will have normal muscle strength, tone, deep tendon reflexes, and sensation. It should be noted that actual conditions, such as dystonia and Huntington’s chorea, may be mistakenly diagnosed as psychogenic.[41]

Fear of falling may cause patients to lose confidence and reduce their activity, thereby decreasing their independence. In an effort to avoid falls, patients will walk inefficiently and frequently reach out for handholds. Although their balance is intact, their gait is irregular, unsteady, and abrupt, and they will turn en bloc. In addition, they will walk slowly, but are capable of increasing the speed on command. One study reported an association between fear of falling and reduced postural performance in spontaneous-sway and one-leg stance-balance tests.[42] The induced-sway tests were performed while having the subjects stand on a platform that moved either back and forth or from side to side, with subjects blindfolded or not. The strongest association occurred during the anterior/posterior induced-sway test, with the subjects blindfolded. Other studies found that stride-to-stride temporal variations of gait are significantly increased in elderly “fallers” (determined by history), as compared with nonfallers, and this may provide a useful quantitative measurement for assessing the risk of falls in the elderly.[43,44] Contrary to common belief, a wider stride does not necessarily increase stability, but rather seems to be associated with an increased risk of falls.[44]

Dementia incapacitates more than one million Americans and can occur at any age. Patients may present with depression, paranoia, or anxiety; the most common presentation is slow disintegration of personality and intellect. Patients may perform familiar tasks well, but have difficulty learning new skills. Eventually, patients will present with apraxia of gait and with advanced dementia, and their gait becomes slow and shuffling with short steps.[29] Demented patients with normal walking patterns still had impaired performance on tests of gait and balance.[29] Because dementia is occasionally secondary to a treatable condition, a detailed examination should be conducted.

Conclusion

As the baby-boomer generation ages, an increasing percentage of people will be in the “golden years” of life. Thus it is imperative that clinicians familiarize themselves with the pathologies and presentations that are unique to the geriatric population. A thorough history and physical examination should include a Romberg’s test, a nudge test, and careful gait observation so that the physician can assess possible underlying pathologies (

Table 2. atient Signs and Possible Underlying Disorders.

). Certainly, any patient complaining of falls, difficulty walking or balancing, or even lightheadedness should immediately be evaluated for the conditions discussed above.

In addition to discovering potential underlying causes of gait abnormalities, physicians should be aware of the importance of gait to the overall health of their patients. A physically active lifestyle, which includes walking, will improve the general health and well-being of patients while at the same time helping them maintain muscle strength and stimulating balance function. It is imperative to correct any gait abnormalities that patients may suffer from so that they can continue to lead an active life.