Evaluation of the Elderly Patient With an Abnormal

Moe R. Lim, MD Abstract Russel C. Huang, MD Distinguishing between the normal gait of the elderly and Anita Wu, MD pathologic gaits is often difficult. Pathologic gaits with neurologic Federico P. Girardi, MD causes include frontal gait, spastic hemiparetic gait, parkinsonian Frank P. Cammisa, Jr, MD gait, cerebellar ataxic gait, and sensory ataxic gait. Pathologic gaits with combined neurologic and musculoskeletal causes include myelopathic gait, stooped gait of lumbar spinal stenosis, and . Pathologic gaits with musculoskeletal causes include Dr. Lim is Assistant Professor of Orthopaedic Surgery, Department of , coxalgic gait, , knee Orthopaedics, University of North hyperextension gait, and other gaits caused by inadequate joint Carolina–Chapel Hill, Chapel Hill, NC. mobility. A working knowledge of the characteristics of these gaits Dr. Huang is Assistant Professor of Orthopaedic Surgery, Weill Medical and a systematic approach to observational gait examination can College of Cornell University, New York, help identify the causes of abnormal gait. Patients with abnormal NY, and Assistant Attending gait can benefit from the treatment of the primary cause of the Orthopaedic Surgeon, Hospital for Special Surgery, New York. Dr. Wu is disorder as well as by general fall-prevention interventions. Assistant Professor of , Weill Treatable causes of gait disturbance are found in a substantial Medical College of Cornell University. proportion of patients and include normal-pressure hydrocephalus, Dr. Girardi is Assistant Attending vitamin B deficiency, Parkinson’s disease, alcoholism, medication Orthopaedic Surgeon, Hospital for 12 Special Surgery. Dr. Cammisa is toxicity, cervical spondylotic myelopathy, lumbar spinal stenosis, Associate Attending Orthopaedic joint contractures, and painful disorders of the lower extremity. Surgeon, Hospital for Special Surgery.

None of the following authors or the departments with which they are ait abnormalities exist in ap- The mere fear of falling contrib- affiliated has received anything of value Gproximately 15% of people old- utes to the loss of functional inde- from or owns stock in a commercial er than age 64 years. By age 85, the pendence in many elderly individu- company or institution related directly or prevalence increases to 40%.1 In the als.4 In one study, nearly 20% of the indirectly to the subject of this article: elderly, gait disorders contribute to elderly acknowledged limiting their Dr. Lim, Dr. Huang, Dr. Wu, Dr. Girardi, the risk of falls and subsequent inju- activities because of the fear of fall- and Dr. Cammisa. ry. In a study of 1,103 community- ing.5 Falls also contribute to perma- Reprint requests: Dr. Lim, Department living persons older than age 72 nent institutionalization of elderly of Orthopaedics, University of North years, nearly 50% of the partici- individuals, with concomitant de- Carolina–Chapel Hill, 3152 pants experienced at least one fall cline in functional status and social/ Bioinformatics Bldg, CB #7055, during a 2.5-year period.2 Approxi- physical activities.6,7 Chapel Hill, NC 27599-7055. mately 25% of the elderly who fall Although patients rarely present experience a serious injury, and ap- to the orthopaedic surgeon with gait J Am Acad Orthop Surg 2007;15:107- proximately 5% have a fracture. Bal- abnormality as a chief complaint, 117 ance and gait impairment nearly difficulty walking is a very common Copyright 2007 by the American double the risk of falling and the risk secondary symptom. The primary Academy of Orthopaedic Surgeons. of experiencing a subsequent serious clinical focus of orthopaedic sur- injury.3 geons has been on the injuries conse-

Volume 15, Number 2, February 2007 107 Evaluation of the Elderly Patient With an Abnormal Gait

Table 1 Classification of Gait Disorders

Neurologic Combined Neurologic/Musculoskeletal Musculoskeletal

Frontal gait Myelopathic gait Antalgic gait Dementias (Alzheimer’s disease) Cervical spondylotic myelopathy Knee

Normal-pressure hydrocephalus Vitamin B12 deficiency Other painful disorders of the lower Binswanger’s disease (subcortical extremity dementia) Thoracic disk herniation Coxalgic gait Spastic hemiparetic gait Stooped gait of lumbar spinal Hip osteoarthritis Cerebrovascular accident stenosis Other painful hip disorders Steppage gait () Mild hip abductor insufficiency Parkinson’s disease Acquired or hereditary peripheral Trendelenburg gait Drug-induced parkinsonism neuropathy Severe hip abductor insufficiency Progressive supranuclear palsy Sciatic/peroneal neuropathy Knee hyperextension gait Cerebellar ataxic gait Lumbar radiculopathy Ankle equinus contracture Alcoholism Quadriceps deficiency Phenytoin toxicity Inadequate knee extension gait Paraneoplastic syndromes Knee flexion contracture Hereditary Inadequate knee flexion gait Sensory ataxic gait Knee extension contracture or Tabes dorsalis (syphilis) fusion

Vitamin B12 deficiency Inadequate hip extension gait Polyneuropathy (diabetes, HIV, Hip flexion contracture neurotoxic medications)

HIV = human immunodeficiency virus

quent to falling. However, by identi- Parkinson’s disease, and cerebellar must coordinate the maintenance of fying causes of gait disorders, or- degeneration9,10 (Table 1). balance. Once motor activity is thopaedic surgeons can play an im- generated, feedback and modulation portant role in a multidisciplinary Normal Gait are relayed through the cerebellum. effort to prevent falls and improve As the support shifts from one leg the quality of life in the elderly. Normal gait is an unconsciously co- to the other in a dynamic equilib- The identification of the cause of ordinated activity resulting from rium, reflexive adjustments of the a can be challeng- the interaction between the muscu- legs and trunk must occur. These re- ing because many abnormal gaits in loskeletal and nervous systems. In flexive adjustments are based on sen- the elderly look similar. Common animals, the center of walking coor- sory information from the visual, compensatory patterns of gait often dination lies in the pattern genera- vestibular, and proprioceptive sys- mask the helpful characteristic fea- tor of the spine. Lower order animals tems.11,12 tures. For example, the cautious gait have the capacity for stepping when of the elderly, with short wide steps this spinal pattern generator is stim- Gait Cycle and increased time in double-limb ulated. In contrast, walking in support, is entirely nonspecific.8 Fol- higher order primates depends on To begin walking, one foot is raised lowing an exhaustive diagnostic supraspinal activity. Locomotion and accelerated forward. The hip and workup, many gait disturbances are centers have been identified in the knee flex and the ankle dorsiflexes found to be nonspecific and multi- brainstem. Spontaneous walking re- as the foot clears the ground. Muscle factorial. However, potentially treat- quires the basal ganglia and thala- action on the supporting contralater- able causes of gait impairment can mus, as well, but not the cerebral al leg accelerates the body’s center of be found in nearly one third of pa- cortex. Clearly, however, the higher gravity forward. The moving foot is tients. The most common causes of centers in the cerebral cortex are im- then placed on the ground, and gait disorder in the elderly are portant in initiating and directing weight is subsequently transferred cerebral infarcts, painful arthritic ambulation.11,12 to that leg. The heel strikes the disorders of the lower extremities, In addition to generating motor ac- ground first, followed by gradual cervical spondylotic myelopathy, tivity, the central also transfer of weight to the sole and

108 Journal of the American Academy of Orthopaedic Surgeons MoeR.Lim,MD,etal

Figure 1

Phases Stance Swing

Initial Second Single-limb Initial Mid- Terminal Periods Double-limb Double-limb Stance Swing Swing Swing Support Support

Foot Strike Opposite (Reversal of Opposite Toe-Off Foot Tibia Foot Strike Toe-Off Fore-Aft Foot Clearance Vertical Shear) Strike % of Cycle 0% 62% 100%

The normal gait cycle. (Adapted with permission from Sutherland DH, Kaufman KR, Moitoza JR: Kinematics of normal human walking, in Rose J, Gamble JG [eds]: Human Walking, ed 2. Baltimore, MD: Williams and Wilkins, 1994, pp 23-44.) then to the toes. The other foot is vice versa. Stance takes up about distance between the two feet), and then raised and accelerated forward. 60% of the time of the gait cycle and stride length (longitudinal distance The body is held erect, with the head the swing phase, about 40%. Both covered during a complete gait cycle, facing forward and the arms swing- feet are on the ground for two peri- representing the sum of the left and ing equally, smoothly, and loosely. ods during each cycle. Each of these right step lengths).12 The and shoulders remain rel- double-support periods lasts for atively level. As the body passes over about 10% of the cycle. Normal Gait of Elderly the weight-bearing leg, it displaces The gait cycle can be further char- the center of gravity toward the acterized by subdividing each of the The globally degenerative changes of weight-bearing side, causing a slight phases. The stance phase is subdi- aging have deleterious effects on side-to-side movement with each vided into initial double-limb sup- gait. Therefore, it may be challeng- step. In addition, the body rises and port, single-limb stance, and second ing to distinguish between “normal” falls with each step. double-limb support, or, more com- and pathologic gaits in the elderly. In Thus, a full gait cycle begins monly, initial contact, loading re- general, the elderly use a shorter, when one foot strikes the ground, sponse, midstance, terminal stance, broader-based stride. There is an ap- and it ends when the same foot and preswing. The swing phase is proximately 10% to 20% decrease in strikes the ground again. The cycle subdivided into initial swing, mid- walking velocity. This is caused by a is divided into the stance phase and swing, and terminal swing (Figure 1). decrease in step length rather than the swing phase. The stance phase Gait is also described in terms of by a change in cadence.13 Pelvic rota- begins with the initial contact of the walking velocity (distance per time), tion and lower extremity joint ex- heel on the ground and ends with cadence (steps per time), step length cursions are also reduced.8 Elderly toe-lift. The swing phase begins (longitudinal distance between the men tend to walk with a slightly when the stance phase ends, and two feet), step width (side-to-side flexed posture, with slightly flexed

Volume 15, Number 2, February 2007 109 Evaluation of the Elderly Patient With an Abnormal Gait and knees and decreased arm Binswanger’s disease, also known shuffle results. Forward movement swing. Elderly women tend to walk as subcortical dementia, is another may lead to successively more rapid with a slight waddling quality.11 cause of frontal gait. It is character- steps (ie, festination). Walking may ized by multiple cerebrovascular le- then suddenly stop involuntarily. Neurologic Gait sions in the deep hemispheric white These patients also may freeze in an Disorders matter. The clinical syndrome con- attempt to pass through a doorway or sists of hypertension, loss of memo- over an obstacle. The body tends to Frontal Gait ry and cognition, dysarthria, lack of turn en bloc, as a single unit. Frontal gait associated with de- facial expression, increased tone in Parkinson’s disease results from mentia is common in the elderly and the lower extremities, and frontal the idiopathic degeneration of do- has a variety of causes.14 Patients gait. There is no specific treatment. pamine-producing neurons in the with this gait stand with their feet substantia nigra of the midbrain. It widely apart. The feet appear to be Spastic Hemiparetic Gait affects approximately 1.5% of the stuck to the floor (the so-called mag- A hemorrhagic or ischemic lesion population older than age 65 years. netic foot response). There is diffi- of the corticospinal tract in the con- In addition to the poor balance and culty in initiating ambulation and tralateral cerebrum or brainstem difficulty walking, are char- picking the feet off the floor. Sever- causes a spastic hemiparetic gait. acteristic. However, some elderly al small shuffling steps are taken for Characteristically, the affected arm is present only with axial rigidity and a short distance, followed by a few adducted at the shoulder, flexed at gait disorder. Drug-induced parkin- moderate steps. The patient then the , and flexed at the wrist and sonism can be caused by use of neu- suddenly stops, and the cycle is re- fingers. The upper extremity does not roleptic drugs (eg, droperidol), partic- peated. The neurologic examination swing and is held up against the ularly in nursing home patients. is often normal because patients chest or abdomen. Because of spastic- Progressive supranuclear palsy, a usually lack muscle weakness, re- ity, it is difficult to flex the hip and rare, rapidly progressive degenera- flex abnormalities, or sensory chang- knee and to dorsiflex the ankle. The tive disorder, also can present with a es. Because the ability to perform co- affected stiff spastic leg is then swept parkinsonian gait. In contrast with ordinated movements is lost in the outward to avoid the foot dragging on patients with Parkinson’s disease, absence of motor or sensory impair- the floor (circumduction). The upper those with progressive supranuclear ment, this pattern is considered a body rocks slightly to the contralat- palsy have eye-movement form of gait apraxia. eral side during circumduction. and an extended neck posture, and Communicating normal-pressure Hypertension and hypercholes- they display gait disturbance early in hydrocephalus is a treatable cause of terolemia are the most common the course of disease. frontal gait and dementia. The diag- treatable risk factors for . The nostic triad is slowness of thought rate of recurrence is high but Cerebellar Ataxic Gait and action, incontinence, and un- can be lowered by aggressive treat- Patients with lesions of the cere- steady gait. The gait disturbance may ment with antihypertensives, stat- bellum present with an unsteady be the only symptom in the early ins, and/or antiplatelet drugs.15 gait and tendency to fall. In cerebel- stages. Brain magnetic resonance im- lar ataxic gait, the feet are placed far- aging (MRI) shows ventricular en- Parkinsonian Gait ther apart than normal (ie, wide largement, an enlarged flow void A flexed posture and shuffling gait base) and tend to be externally rotat- about the cerebral aqueduct, and a are distinctive and readily identifi- ed. This foot positioning is thought variable degree of periventricular able features of parkinsonian gait. Pa- to be a compensatory strategy to im- white matter changes. However, tients stand immobile with a lack of prove balance. The patients stagger many elderly with or without gait spontaneous movements. They as- from side to side and often search for impairment have enlarged ventricles. sume a flexed posture with the spine a form of mechanical support. There To confirm the diagnosis of normal- flexed; head bent down; and elbows, is an accompanying fore-and-aft pressure hydrocephalus, a neurologic hips, and knees flexed. Initiating am- of the head and/or trunk (ie, consultation should be obtained for bulation from a standing or sitting titubation). The steps are of varying a dynamic lumbar puncture. The position is difficult. When the patient length, and the feet are placed errat- cerebrospinal fluid pressure should begins ambulation, the trunk bends ically. Tandem gait exhibits the be <180 mm Hg, and the patient’s further forward, and the lower ex- most striking abnormalities in even symptoms should improve after the tremities remain flexed. The upper mild cases of cerebellar . Pa- removal of 40 to 50 mL of cerebrospi- extremities do not swing. Step length tients quickly lose balance and must nal fluid. The treatment is ventricu- is reduced to the point that the feet place the foot to the side to prevent loperitoneal shunt implantation. barely clear the floor and a distinctive falling. Whether the eyes are open or

110 Journal of the American Academy of Orthopaedic Surgeons MoeR.Lim,MD,etal closed, patients with cerebellar atax- imbalance from bilateral vestibular In addition to cervical spondylotic ia cannot stand with their feet to- loss. myelopathy, vitamin B12 deficiency gether. Compared with normal con- is another cause of myelopathy in the trol subjects, there is no difference in Combined Neurologic/ elderly. Vitamin B12 deficiency is easy spontaneous gait velocity and stride Musculoskeletal Gait to identify and is readily treatable. length. The mean Disorders Thoracic disk herniations or demyeli- (ROM) of the hip, knee, and ankle nating disease (eg, multiple sclerosis) are also the same. However, stance Myelopathic Gait are other causes of myelopathy. and double-limb support phases are Cervical spondylotic myelopathy 16 prolonged. is one of the most common identifi- Stooped Gait of Lumbar The most common cause of cere- able causes of gait disturbance in the Spinal Stenosis bellar ataxia is alcoholism. In alco- elderly. Degenerative osteophytes Lumbar spinal stenosis is a com- holic cerebellar degeneration, the and ligamentous hypertrophy nar- mon cause of difficulty in ambula- gait disorder may be present without row the cervical spinal canal, caus- tion. Degenerative osteophytes and other signs of cerebellar dysfunction ing mechanical compression of the ligamentous hypertrophy narrow (eg, nystagmus, dysarthria). Other spinal cord. The primary clinical the lumbar spinal canal, causing me- causes of cerebellar dysfunction in- manifestations are gait/balance dis- clude toxins (eg, phenytoin), para- turbance with spasticity and hyper- chanical compression of the cauda neoplastic syndromes, vitamin E de- reflexia. Most patients have neck equina. Patients primarily present ficiency, and hereditary ataxias. pain, but 15% do not.17 Compression with a long history of back pain with of the cervical spinal cord causes a progression to leg pain. A feeling of Sensory Ataxic Gait lower motor neuron lesion at the tightness, heaviness, pain, and sub- Balance during ambulation de- level of the compression and upper jective weakness in the legs (ie, neu- pends on afferent input from the vi- motor neuron lesions below that rogenic claudication) is exacerbated sual, vestibular, and proprioceptive level. Patients often have numbness by standing, walking, and exercising systems. results from and in the upper ex- in an erect posture. This symptom a disruption anywhere along the af- tremities and report loss of fine mo- complex is rapidly relieved by sitting ferent pathways. In patients with tor skills, such as a change in their down or leaning forward (such as on sensory ataxia, proprioception is handwriting or the inability to han- a shopping cart). lost, and patients become unaware dle coins. Lower extremity weakness On examination, patients tend to of limb position. Strength is pre- affects the proximal musculature. assume a “simian” posture, with served. Patients stand and walk with There is loss of position and vibra- shoulders translated anterior to the their feet set widely apart, keeping tion sense because of dorsal column pelvis.20 Thigh pain can be elicited their eyes on the ground. They are dysfunction. In severe cases, changes following 30 seconds of lumbar ex- able to stand with eyes open but be- in bowel and bladder function (pri- tension.21 Patients walk slowly in a come unstable when their eyes are marily, urinary urgency) occur. stooped gait with decreased velocity, closed (Romberg’s test). In ambula- The spastic paraparetic gait in shortened stride, and the lumbar tion, the legs are lifted high in the air cervical spondylotic myelopathy is spine bent forward. The stooped gait and allowed to slap on the ground to described as stiff-legged, wide-based, is apparent as soon as gait is initiated, increase sensory feedback. The gait and jerky. Movements at the hip and before the onset of pain. Factors re- disturbance becomes worse when knee are slow and stiff, requiring lated to the style of walking, such as other sensory modalities become considerable effort. Toe clearance in symmetry, smoothness, and rhythm, compromised, such as in the dark the swing phase is compromised by also are abnormal.22 when vision is impaired. the reduced knee flexion and spastic In lumbar spinal stenosis, epidu- Sensory ataxia of tabes dorsalis is plantar flexion of the ankle. Conse- ral pressure rises intermittently dur- a classic example. Today, the most quently, there is a tendency to cir- ing ambulation. The severity of this common cause of sensory ataxia cumduct or scuff the feet. Patients rise in pressure has been shown to likely is diabetes, with polyneurop- also may move from side to side to depend on the posture, speed, and athy and combined deficits in vision, compensate for the slow and stiff stride of ambulation. The stooped proprioception, and vestibular func- movements of the leg. Walking gait observed in spinal stenosis is tion. Human immunodeficiency vi- speed is reduced because of a de- thought to be an adaptive mecha- rus and neurotoxic medications (eg, crease in step length. Normal ca- nism to minimize lumbar epidural cisplatin, isoniazid) are other causes dence is preserved. The time of pressure.22 Proprioceptive loss and of polyneuropathy. Ototoxic medica- double-limb support and the step bowel/bladder dysfunction are un- tions (eg, gentamicin) also can cause width are increased.18,19 common.

Volume 15, Number 2, February 2007 111 Evaluation of the Elderly Patient With an Abnormal Gait

Figure 2 be similar to that of sensory ataxia. sults from an unconscious adaptive However, the two problems are dis- response to decrease the joint reac- tinguishable on further physical ex- tion force on the painful hip. amination. In sensory ataxia, pa- A simplified free body diagram il- tients may report gait worsening in lustrates this adaptive response (Fig- the dark, and they will have preser- ure 3). During single-limb stance vation of ankle dorsiflexion strength phase on the affected hip, the hip and an abnormal Romberg test. In joint is a fulcrum, with the pull of contrast, patients with steppage gait the abductors on one side and the or foot drop demonstrate weakness weight of the body on the other. The of ankle dorsiflexion. joint reaction force is the sum of these two forces. To maintain a stat- Musculoskeletal Gait ic equilibrium during single-limb Disorders stance, the sum of the moments about the hip fulcrum must equal Antalgic Gait zero. Therefore, the distance from Antalgic gait is characterized by a the body’s center of gravity to the decreased time in the stance phase hip joint multiplied by body weight on the affected limb. The affected equals the distance from abductors limb is placed on the ground just to the hip joint multiplied by the long enough to quickly swing the force of the abductors. When the tor- unaffected limb to stance. This gait so is shifted toward the affected hip, Coxalgic gait. The gait caused by a allows the patient to diminish pain the moment arm of the body of grav- painful hip is characterized by shifting by minimizing the weight-bearing ity is decreased. Less abductor force of the upper torso toward the painful time on that limb. Antalgic gait can is then required to maintain a static side during the single-limb stance be caused by any painful condition equilibrium. The decrease in abduc- phase on the affected hip. This coxalgic of the lower extremity, such as knee tor force leads to a decrease in the gait pattern results from an osteoarthritis, ankle sprains, and joint reaction force. unconscious adaptive response to stress fractures of the foot. A common cause of coxalgic gait decrease the joint reaction force on the In knee osteoarthritis, the antal- in the elderly is hip osteoarthritis. painful hip. (Adapted with permission gic gait is accompanied by a de- Aside from the characteristic coxal- from Hoppenfeld S: Physical creased walking velocity and a short- gic gait, most of the other gait chang- Examination of the Spine and ened step length. Normal cadence is es associated with hip osteoarthritis Extremities. Upper Saddle, NJ: Pearson Education, 1976, p 139.) preserved. In addition to the de- are subtle and not easily detectable creased dynamic knee flexion ROM, by visual inspection alone. There patients with knee osteoarthritis may be an antalgic component to Steppage Gait also have less ROM at the hip and the coxalgic gait (ie, a minimization Steppage gait results from weak- ankle joints.23 Avoidance of forceful of weight bearing on the affected ness in ankle dorsiflexion (ie, foot quadriceps contraction also is ob- limb). There is also a decrease in dy- drop). Patients drag their feet and/or served and is thought to help reduce namic ROM of the hip during ambu- compensate by lifting the foot as articular loads. These subtle abnor- lation and an increase in anterior high as possible, with increased flex- mal knee kinematics are exaggerat- pelvic tilt and lumbar lordosis. This ion of the hips and knees. The gait ed during paced walking.24,25 increased extension of the spine and may be unilateral or bilateral. The pelvis is believed to compensate for toe of the affected leg hits the ground Coxalgic Gait the loss of hip extension.26 before the heel or sole of the foot, Patients with hip pain present The appearance of a coxalgic gait and the heel tends to strike the with a characteristic coxalgic gait. also can be caused by painless, mild ground with a characteristic slap- This gait is characterized by shifting hip abductor insufficiency. In mild ping sound. of the upper torso toward the painful abductor insufficiency, the compen- A foot drop can be caused by ac- hip during the single-limb stance satory trunk lurch decreases the quired and hereditary peripheral phase on the affected hip (Figure 2). force required by the abductors to neuropathies, sciatic or peroneal This shifting of the torso in ambula- maintain a level pelvis during single- neuropathy, or lumbar radiculopa- tion is often referred to as an abduc- limb stance. Abductor weakness thy. Initially, the slapping-foot pat- tor lurch, lurch, or that can follow an anterolateral tern of steppage gait may appear to the Duchenne sign. Coxalgic gait re- approach to total hip replacement is

112 Journal of the American Academy of Orthopaedic Surgeons MoeR.Lim,MD,etal associated with a postoperative pain- Figure 3 less “coxalgic” gait.27 L5 radiculopa- thy also can cause abductor weak- ness with a subsequent coxalgic gait pattern.

Trendelenburg Gait A Trendelenburg gait is very sim- ilar in appearance to a coxalgic gait, with one main distinguishing fea- ture—the tilt of the pelvis. With Trendelenburg gait, the contralateral hemipelvis drops during the single- limb stance phase on the affected side (Figure 4). As the contralateral hemipelvis drops, greater knee flex- ion is required to clear the swing- phase foot off the ground. Similar to the coxalgic gait pattern, the torso also lurches toward the affected side. However, in the coxalgic gait pat- tern, the pelvis remains level. A Trendelenburg gait is caused by Free body diagram of the hip in single-limb stance. A, Assume that the distance severe abductor insufficiency and is from the hip to the abductors is 5 cm and that the distance from the hip to the body most commonly seen in patients center of gravity is 15 cm. If the weight of the body is 500 N, the abductors must with . In the painless “coxal- exert 1,500 N of force to maintain the static equilibrium. (The sum of the moments about the hip fulcrum must equal zero, ie, 1,500N×5cm=500N×15cm.)In gic” gait pattern caused by mild ab- this case, the joint reaction force (JRF) is the sum of the abductor force and the ductor insufficiency, the torso lurch- body weight, totaling 2,000 N. B, When the upper body is lurched toward the es toward the affected hip during affected hip, the body center of gravity is effectively shifted in the same direction. single-limb stance. This compensa- Thus, if the distance from the hip to the body center of gravity is decreased to 10 tion brings the body’s center of grav- cm, the abductors need exert only 1,000 N to maintain static equilibrium: 1,000 N × ity closer to the hip joint, decreasing 5cm=500N×10cm.Therefore, the lurch reduces the JRF to 1,500 N. the required abductor force neces- sary to maintain a level pelvis in static equilibrium. Although the ab- single-limb stance of ambulation, The patient is then asked to stand on ductors are weak, the compensatory and a coxalgic gait will result. How- one leg. As one limb leaves the lurch permits the weak abductors to ever, if the abductors are severely ground, the abductors on the con- maintain a level pelvis. In severe ab- weak and unable to generate 1,000 N tralateral stance phase limb should ductor insufficiency, however, even of force, the contralateral hemipelvis contract and the pelvis should re- with the compensatory lurch, the will drop during the single-limb main level (a negative Trendelenburg abductors are unable to generate suf- stance of ambulation, and a Trende- test or sign). If, however, the hemi- ficient force to keep the pelvis level. lenburg gait will result. pelvis contralateral to the stance Therefore, during single-limb stance, The Trendelenburg gait also limb drops, the abductors on the the hemipelvis contralateral to the should be distinguished from the stance limb are severely insufficient severely weak abductor drops, re- Trendelenburg test. The presence of (a positive Trendelenburg test).30 A sulting in the characteristic Trende- a Trendelenburg gait indicates dy- Trendelenburg gait pattern and a pos- lenburg gait.28,29 namic abductor insufficiency. In con- itive Trendelenburg test usually co- For example, in Figure 3, B, with trast, the Trendelenburg test is a exist because they indicate the same the torso lurched toward the affect- static test, also used to demonstrate pathology. ed hip, 1,000 N of abductor force is abductor insufficiency. In the Tren- necessary to maintain a level pelvis delenburg test, the patient is first Knee Hyperextension Gait in single-limb stance. If the abduc- asked to stand in double-limb stance. Knee hyperextension gait can re- tors are only mildly weak and still The dimples of the posterior superior sult from an ankle equinus contrac- able to generate 1,000 N of force, the iliac spine are observed as a landmark ture or from quadriceps deficiency. pelvis will remain level during the for the pelvis and should be level. With an ankle equinus contracture,

Volume 15, Number 2, February 2007 113 Evaluation of the Elderly Patient With an Abnormal Gait

Figure 4 places the GRF closer to the knee joint, and the knee flexion moment is additionally reduced. These com- pensatory mechanisms all contribute to hyperextension of the knee ob- served during stance in a patient with a deficient quadriceps mechanism.31

Inadequate Knee Extension Gait (Flexion Contracture) Knee flexion contractures lead to inadequate knee extension during gait. Inadequate extension primarily affects the stance phase of the gait cy- cle. The flexed knee during mid- stance interferes with the normal mechanisms used to realign the body vector over the supporting foot. Without compensation, the flexed knee would place the body behind the foot. Compensatory increased an- kle dorsiflexion and/or premature heel rise allows the body to be Trendelenburg gait. The Trendelenburg gait is very similar in appearance to a aligned directly over the foot during coxalgic gait, with one main distinguishing feature—the tilt of the pelvis. In the midstance. Also, stance-phase weight Trendelenburg gait (A), the contralateral hemipelvis drops during the single-limb bearing on an excessively flexed knee stance phase on the affected side because of severe abductor insufficiency. In the requires greater extension forces coxalgic gait (B), the pelvis remains level. (Adapted with permission from from the quadriceps to preserve joint Hoppenfeld S: Physical Examination of the Spine and Extremities. Upper Saddle, NJ: Pearson Education, 1976, p 164.) stability. The increased functional demands placed on the quadriceps explain early ambulation fatigue in increased ipsilateral knee and hip the ground reaction force (GRF) is patients with knee flexion contrac- flexion are required to help the foot posterior to the ankle, anterior to the tures.31 clear the floor. Therefore, during the hip, and posterior to the knee. The initial contact portion of the stance posterior force gives the knee joint a Inadequate Knee Flexion phase, the combination of the plan- flexion moment. In normal gait, the Gait (Extension tarflexed ankle and the flexed knee quadriceps counteracts this flexion Contracture) directs the forefoot to the floor in- moment to preserve joint stability. Inadequate knee flexion primarily stead of the heel. Therefore, the heel However, when the quadriceps is de- affects the swing phase of the gait cy- rocker action of the stance phase is ficient, other compensatory mecha- cle. In patients with a severe exten- lost. In addition, during midstance nisms must be used to achieve sion contracture or a knee fused in and terminal stance, the contact of joint stability. These compensatory excessive extension, the swing-phase the plantarflexed foot on the ground mechanisms include increasing hip limb cannot be shortened sufficiently leads to an extension moment on extension and ankle plantar-flexion to clear the foot. In compensation, the knee, resulting in knee hyperex- forces to provide an extension mo- the ipsilateral hip may be abducted to tension. ment to the knee. The trunk may circumduct the limb. Circumduction The quadriceps-deficient knee hy- lean forward to move the GRF ante- may be accompanied by elevation of perextension gait results when the riorly, closer to the center of the the ipsilateral hemipelvis (ie, hip hik- quadriceps fails to perform its usual knee, and thus reduce the flexion ing) and leaning of the trunk to the stabilizing function during the load- moment. Also, initial contact may contralateral side. In addition, the ing response of gait. The loading re- occur with a flatfoot instead of with contralateral stance phase ankle may sponse occurs immediately after ini- the heel. Using the entire foot for ini- be plantarflexed to elevate the entire tial contact in the stance phase. tial contact moves the point of appli- body and clear the swing-phase foot During the normal loading response, cation of the GRF anteriorly. This (ie, vaulting).31

114 Journal of the American Academy of Orthopaedic Surgeons MoeR.Lim,MD,etal

Inadequate Hip Extension lishing a diagnosis. Benzodiazepines, indicate a bony spinal deformity. Gait phenytoin, and neuroleptic drugs are The width of the feet during stance Inadequate hip extension caused known to affect, respectively, the can be a sign of imbalance, seen in by a flexion contracture reduces vestibular system, cerebellum, and , sensory ataxia, stride length and the duration of basal ganglia. Toxic/metabolic caus- frontal lobe disease, and cervical single-limb support during gait. Inad- es of gait abnormality are important spondylotic myelopathy. Also, equate hip extension keeps the thigh to identify because they are general- standing balance in single-limb forward and prevents the body from ly reversible. Symptoms of depres- stance and in tandem stance should advancing over the supporting foot. sion also should be elicited because be observed. Next, with the patient Exaggerated lumbar lordosis is used depressed patients may exhibit slow- comfortably standing, ask the pa- to compensate for the lack of hip ex- ness from psychomotor retardation, tient to close his or her eyes (Rom- tension. The pelvis is tilted anteriorly manifesting as a lack of purpose in berg’s test). The clinician should re- to accommodate the flexed hips to stride and a lifting action of the legs main close to the patient in case he extend the while the trunk is during gait.32 or she begins to fall. Patients with tilted posteriorly to balance the body In the setting of a gait disorder sensory ataxia caused by propriocep- directly over the feet. In patients and recent fall, the nature of the fall tive loss will have dramatic stance with limited lumbar mobility, a should be carefully detailed. Crum- instability with eye closure. In con- forward-leaning trunk posture may pling at the knees suggests syncope trast, standing stability is unaffected be seen. This posture requires a form or loss of strength from a transient by eye closure in cerebellar ataxia. of external support such as a cane or ischemic attack. Falling stiffly back- The patient is then asked to walk a walker to support ambulation. Al- ward is common in Parkinson’s dis- at a normal pace. Difficulty in initi- ternatively, hip flexion contractures ease. The location and activity of the ating the first step can be indicative can be compensated for during gait patient during the fall may point to of Parkinson’s or frontal lobe disease. by knee flexion using a crouched gait. environmental or patient-related Once the walking is under way, the A crouched gait allows the femur to causes. If the fall occurred shortly af- patient is observed from the side, roll forward, but this adaptive mech- ter the patient had just arisen from front, and back. The overall pattern anism can result in concomitant sitting or lying down, orthostatic hy- of body movement should first be knee flexion contractures and early potension may have resulted. Re- noted. Next, the patient should be ambulation fatigue resulting from cently adjusted cardiac medications, observed from the feet upward, with the increased functional demands on especially antihypertensive diuretics the observer relating the action of the the quadriceps.31 or vasodilators, should be reviewed. two limbs, the torso, and then the Falls that occur shortly after meals upper extremities. The observer Approach to the Elderly may reveal postprandial hypoten- should now be able to differentiate a Patient With a Gait sion as a cause. Recurrent tripping focal problem in an extremity to a Abnormality may be caused by a foot drop or in- generalized . The creased tone from spasticity.33 velocity, step length, step width, History rhythm, and cadence all should be The presenting history can pro- Physical Examination noted. The fluidity and symmetry of vide many diagnostic clues. An in- Although the modern gait analy- arm swing should be noted, as should sidious nature of onset suggests a de- sis laboratory can provide a multi- the use of any mechanical assistive generative disorder, whereas sudden tude of objective measurements, the devices. Asking the patient to walk stepwise progressions suggest cere- most revealing features of a patient’s at a faster pace may elicit more sub- brovascular disease. Accompanying gait often can be garnered by careful tle characteristics of abnormal gait. reports of pain in the neck, low back, systematic observation alone. Some The patient then is asked to walk in or lower extremities suggest degen- gaits readily suggest a specific disor- a straight line heel to toe (tandem erative conditions in, respectively, der, as in Parkinson’s disease, cere- gait) and to perform the heel-to-shin the cervical spine, lumbar spine, and bellar ataxia, or hip osteoarthritis. test. In the heel-to-shin test, the su- lower extremities. Gait abnormality The gait examination begins by pine patient is asked to touch the with urinary urgency and inconti- observing the undressed patient as heel of one foot to the contralateral nence suggests multiple cerebral in- he or she rises from the chair to knee and drag it in a straight line farcts, Binswanger’s disease, normal- stand. The ease of the transition and down the shin and up again. These pressure hydrocephalus, or severe the standing posture should be not- two tests often bring out subtle cer- cervical spondylotic myelopathy.1 A ed. A flexed posture can be a sign of ebellar and sensory ataxias. history of alcohol and medication in- Parkinson’s disease or lumbar spinal The remaining routine neurolog- take also may be helpful in estab- stenosis. A rigid spinal posture may ic and musculoskeletal examina-

Volume 15, Number 2, February 2007 115 Evaluation of the Elderly Patient With an Abnormal Gait tions should focus on evaluating physical therapist may be made for Summary muscle bulk and strength, sensation, gait training, use of assistive devices, proprioception, deep tendon reflexes, high-intensity resistance strength Evaluation of an elderly patient with spinal deformity, limb-length ine- training, and sensory balance train- a gait disturbance is challenging. qualities, and joint motion. In- ing. The practice of tai chi also has Failing gaits resulting from most creased muscle tone and hyperre- been shown to be beneficial in fall causes often appear to be similar be- flexia indicate an upper motor prevention.35,36 cause adaptive changes mask the neuron lesion. Muscle weakness and Medications that adversely affect underlying unique characteristics. areflexia indicate a lower motor neu- gait may be eliminated or the dosage Also, it is often difficult to distin- ron lesion. Subtle ankle dorsiflexion changed in consultation with the guish between the normal, slow, or plantar-flexion weakness can be primary care physician. Benzodiaz- wide-based gait of the elderly and elicited by observing the patient epines affect postural control and in- many pathologic gaits. Despite this, walking on the heels and toes, re- crease the risk of falls and hip frac- treatable causes of gait disturbance spectively. Finally, brief screening tures. Serotonin-reuptake inhibitors, can be found in a substantial propor- examinations of vision and hearing tricyclic antidepressants, neurolep- tion of patients. Treatable neurolog- also should be performed.34 tic agents, anticonvulsants, and class ic causes include normal-pressure IA antiarrhythmics (eg, procain- hydrocephalus, vitamin B12 deficien- Imaging amide) are other medications known cy, Parkinson’s disease, alcoholism, Clinical suspicion of a neurologic to increase the risk of falling.35 and medication toxicity. Treatable cause of gait disturbance warrants a Neurologic causes of gait distur- musculoskeletal causes include cer- referral to a neurologist for evalua- bances are treated under the care of vical spondylotic myelopathy, lum- tion and possible brain imaging. MRI the neurologist. Levodopa is the bar spinal stenosis, joint contrac- and/or computed tomography of the tures, and painful disorders of the mainstay of therapy for Parkinson’s brain are sensitive for infarcts, de- lower extremity. Orthopaedic sur- disease, but gait and balance are not myelinating disease, mass lesions, geons should be a key component of always improved with the medica- hydrocephalus, and cerebellar atro- a multidisciplinary effort to identify tion.37 Because vitamin B supple- phy. A patient with a recent fall and 12 and treat these disorders and thereby mentation is inexpensive and has disturbance in alertness should be contribute to improving the quality very limited potential for harm, it imaged emergently to rule out a sub- of life of elderly patients. may be initiated in patients sus- dural hematoma. pected to have B -deficient myelo- Patients suspected to have cervi- 12 References pathic or ataxic gait.38 Ventriculo- cal spondylotic myelopathy or lum- peritoneal shunting is effective in Citation numbers printed in bold bar spinal stenosis should be imaged improving gait in 85% of patients type indicate references published with plain radiography and MRI. In with normal-pressure hydroceph- within the past 5 years. patients with coxalgic or Trendelen- alus.39 burg gait, antalgic gait, knee hyper- In cervical spondylotic myelop- 1. Sudarsky L: Geriatrics: Gait disorders extension gait, or other gaits related in the elderly. NEnglJMed1990; athy, multiple studies using objec- to limited joint mobility, plain radio- 322:1441-1446. tive gait analysis have demonstrated graphs of the involved regions 2. Tinetti ME, Doucette J, Claus E, Ma- improved walking velocity, step rottoli R: Risk factors for serious inju- should be obtained. length, balance, and an overall nor- ry during falls by older persons in the malization of ambulation after surgi- community. J Am Geriatr Soc 1995; Treatment 19,40-42 43:1214-1221. cal decompression. Surgical 3. Tinetti ME, Speechley M, Ginter SF: Even when no identifiable cause of decompression for lumbar spinal Risk factors for falls among elderly the disorder is found, many patients stenosis has been demonstrated to persons living in the community. N with a gait disorder and a history of improve speed, stride, cadence, and Engl J Med 1988;319:1701-1707. falls can benefit from evaluation for other factors related to the style of 4. Vellas BJ, Wayne SJ, Romero LJ, Baum- 22 gartner RN, Garry PJ: Fear of falling possible interventions to prevent walking. In the setting of radicu- and restriction of mobility in elderly falls. A home visit can be arranged to lopathy from lumbar spinal stenosis fallers. Age Ageing 1997;26:189-193. eliminate environmental hazards, or herniated nucleus pulposus, surgi- 5. Tinetti ME, Mendes de Leon CF, such as inadequate lighting, tripping cal decompression improves or elim- Doucette JT, Baker DI: Fear of falling obstacles, and slippery surfaces. inates foot drop in most patients.43 and fall-related efficacy in relationship to functioning among community- Consideration may be given to the For osteoarthritis of the hip and living elders. J Gerontol 1994;49: installation of grab bars and stair- knee, total joint can im- M140-M147. well modifications. A referral to a prove gait to nearly normal.44,45 6. Wolinsky FD, Johnson RJ, Fitzgerald

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JF: Falling, health status, and the use generative lumbar spinal stenosis: Di- MA: Butterworth Heinemann, 2000, of health services by older adults: A agnostic value of the history and phys- pp 341-354. prospective study. Med Care 1992; ical examination. Rheum 35. Tinetti ME: Clinical practice: Pre- 30:587-597. 1995;38:1236-1241. venting falls in elderly persons. N 7. Stel VS, Smit JH, Pluijm SM, Lips P: 22. Suda Y, Saitou M, Shibasaki K, Engl J Med 2003;348:42-49. Consequences of falling in older men Yamazaki N, Chiba K, Toyama Y: Gait 36. Wolf SL, Barnhart HX, Kutner NG, et and women and risk factors for health analysis of patients with neurogenic in- al: Selected as the best paper in the service use and functional decline. termittent claudication. Spine 2002; 1990s: Reducing frailty and falls in Age Ageing 2004;33:58-65. 27:2509-2513. older persons. An investigation of tai 8. Sudarsky L, Simon S: Gait disorder in 23. Al-Zahrani KS, Bakheit AM: A study chi and computerized balance training. late-life hydrocephalus. Arch Neurol of the gait characteristics of patients J Am Geriatr Soc 2003;51:1794-1803. 1987;44:263-267. with chronic osteoarthritis of the 37. Suchowersky O: Parkinson’s disease: 9. Fuh JL, Lin KN, Wang SJ, Ju TH, knee. Disabil Rehabil 2002;24:275- Medical treatment of moderate to Chang R, Liu HC: Neurologic diseases 280. presenting with gait impairment in 24. Stauffer RN, Chao EY, Gyory AN: advanced disease. Curr Neurol the elderly. J Geriatr Psychiatry Biomechanical gait analysis of the dis- Neurosci Rep 2002;2:310-316. Neurol 1994;7:89-92. eased knee joint. Clin Orthop Relat 38. Johnson KA, Bernard MA, Funderburg 10. Sudarsky L, Ronthal M: Gait disorders Res 1977;126:246-255. K: Vitamin nutrition in older adults. among elderly patients: A survey 25. Kaufman KR, Hughes C, Morrey BF, Clin Geriatr Med 2002;18:773-799. study of 50 patients. 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Verghese J, Lipton RB, Hall CB, Kus- al: The effect of total hip arthroplasty changes after surgery for cervical lansky G, Katz MJ, Buschke H: Abnor- surgical approach on gait. J Orthop spondylotic myelopathy: A case re- mality of gait as a predictor of non- Res 2004;22:44-50. port. Spine 2003;28:E136-E139. Alzheimer’s dementia. N Engl J Med 28. Raney RB: Useful Orthopaedic Ep- 41. Kuhtz-Buschbeck JP, Johnk K, Mader 2002;347:1761-1768. onyms. New York, NY: Vantage Press, S, Stolze H, Mehdorn M: Analysis of 15. Muir KW: Secondary prevention for 1987, pp 170-171. gait in cervical myelopathy. Gait stroke and transient ischaemic at- 29. Trendelenburg F: Uber den Gang bei Posture 1999;9:184-189. tacks. BMJ 2004;328:297-298. angeborener Huftgelenksluxation. 42. Singh A, Crockard HA: Quantitative 16. Stolze H, Klebe S, Petersen G, et al: Deutsch Med Wschr 1895;21:21-24. assessment of cervical spondylotic Typical features of cerebellar ataxic 30. Hoppenfeld S: Physical Examination myelopathy by a simple walking test. gait. J Neurol Neurosurg Psychiatry of the Spine and Extremities. Nor- Lancet 1999;354:370-373. 2002;73:310-312. walk, CT: Appleton & Lange, 1976, p 43. Girardi FP, Cammisa FP Jr, Huang RC, 17. Emery SE: Cervical spondylotic my- 164. Parvataneni HK, Tsairis P: Improve- elopathy: Diagnosis and treatment. 31. Perry J: Pathologic gait. Instr Course ment of preoperative foot drop after J Am Acad Orthop Surg 2001;9:376- Lect 1990;39:325-331. lumbar surgery. J Spinal Disord Tech 388. 32. Sloman L, Berridge M, Homatidis S, 2002;15:490-494. 18. Clark CR: Cervical spondylotic my- Hunter D, Duck T: Gait patterns of 44. Miki H, Sugano N, Hagio K, et al: Re- elopathy: History and physical find- depressed patients and normal sub- covery of walking speed and symmet- ings. Spine 1988;13:847-849. jects. Am J Psychiatry 1982;139:94- rical movement of the pelvis and low- 19. Maezawa Y, Uchida K, Baba H: Gait 97. er extremity joints after unilateral analysis of spastic walking in patients 33. Nutt JG: Gait and balance, in Goetz THA. J Biomech 2004;37:443-455. with cervical compressive myelop- CG, Pappert EJ (eds): Textbook of 45. Lee TH, Tsuchida T, Kitahara H, athy. J Orthop Sci 2001;6:378-384. Clinical Neurology. Philadelphia, PA: Moriya H: Gait analysis before and af- 20. Hilibrand AS, Rand N: Degenerative WB Saunders, 1999, pp 301-313. ter unilateral total knee arthroplasty: lumbar stenosis: Diagnosis and man- 34. Thompson PD, Marsden CD: Walking Study using a linear regression model agement. J Am Acad Orthop Surg disorders, in Bradley WG, Daroff RB, of normal controls—women without 1999;7:239-249. Fenichel GM, Marsden CD (eds): Neu- arthropathy. J Orthop Sci 1999;4:13- 21. Katz JN, Dalgas M, Stucki G, et al: De- rology in Clinical Practice. Boston, 21.

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