INTRODUCTION — Gait disorders are a major cause of functional impairment and morbidity in older adults [1]. Most gait disorders in this population are multifactorial and have both neurologic and nonneurologic components.
The control of gait and posture is multifactorial, and a defect at any level of control can result in a gait disorder. This topic will review the causes and evaluation of age-related gait disorders, with an emphasis on neurologic causes. Falling in older adults is discussed separately. (See "Falls in older persons: Risk factors and patient evaluation" and "Falls: Prevention in community-dwelling older persons".)
EPIDEMIOLOGY — Gait disorders are common in older adults, and the prevalence increases with age. Approximately 30 percent of community-dwelling adults age 60 years and older have a gait disorder [2]. Among adults age 80 years and older, the prevalence is as high as 60 to 80 percent [2,3]. Gait disorders are more common in hospitalized older adults and in nursing home populations [4-6].
Gait disorders contribute to reduced mobility, fall risk, diminished quality of life, and serious injuries including major fractures and head trauma. It is estimated that approximately 15 percent of falls in older adults can be attributed to balance or gait disorders, including leg weakness [7].
In a population-based study of 488 community-dwelling older adults, neurologic, nonneurologic, and combined gait disorders were present in 24, 17, and 9 percent, respectively [2]. Among subjects classified as having neurologic gait disorders, the most common involved multiple neurologic causes, often labeled a "multifactorial gait disorder," followed by peripheral sensory neuropathy and parkinsonism. In other studies, myelopathy and a history of multiple strokes are also common neurologic culprits [3,8].
PATTERNS AND CAUSES
Predominant motor dysfunction — Motor system dysfunction results in a variety of abnormal gait patterns, depending on the cause and distribution of nervous system pathology.
Weak gait with spasticity — Weakness due to dysfunction of the spinal cord and/or higher central motor pathways in the brain, referred to as upper motor neuron (UMN) weakness, is usually accompanied by signs of increased tone (spasticity). The combination of UMN weakness and increased tone in the legs produces a recognizable gait pattern.
In patients with a UMN gait, the toes do not adequately clear the ground because the hip flexors are weak, and the toes scuff with each step. Inspection of the patient's shoes may show asymmetric wearing of the soles at the tips. Especially when weakness is unilateral (as in a hemiparetic gait), the strategy of circumduction at the hip helps with toe clearance, and weakness or posturing in the ipsilateral arm (flexion at the elbow) is often also evident. Patients with bilateral spasticity in the legs often have a narrow, scissoring gait. The toes turn in and scrape on the floor with each step, producing a scuffing sound and wearing of the tips of the soles.
On examination, the typical distribution of UMN leg weakness involves hip flexion, foot and toe dorsiflexion, leg flexion at the knee (hamstrings), and thigh abduction. The other muscles in the legs may be slightly weak, but not to the same extent as the UMN muscles. Spasticity, hyperreflexia, and extensor plantar responses may be present with or without weakness.
Bladder dysfunction may accompany a UMN gait due to spinal cord dysfunction in the form of frequency, urgency, and urgency incontinence (ie, a small-capacity, spastic, and overactive bladder). Hesitancy and retention suggest bladder dyssynergia. If urinary symptoms are due to the same cause as the gait disorder, localization is usually a thoracic cord lesion.
Bilateral UMN leg weakness usually localizes to the spinal cord (myelopathy). Most myelopathies in older adults are compressive, related to cervical spondylitic/degenerative changes, traumatic or insufficiency fractures, or tumors originating in bone or soft tissue. Intrinsic disorders of the spinal cord, including inherited or neurodegenerative conditions, vascular disease, demyelinating disease, and intramedullary tumors, are less common. (See "Disorders affecting the spinal cord" and "Cervical spondylotic myelopathy".)
Unilateral UMN weakness usually indicates involvement of higher motor pathways in brain or brainstem, although slowly progressive cervical spine stenosis can sometimes cause unilateral weakness. Common causes of a hemiparetic gait include prior focal brain injury due to ischemic stroke or intracranial hemorrhage.
Weak gait with neuropathic weakness — Weakness due to pathology in the spinal motor neurons, nerve roots, or peripheral nerves is referred to as lower motor neuron (LMN) weakness, or neuropathic weakness. LMN dysfunction often involves focal or asymmetric weakness (eg, ankle dorsiflexion weakness, or "foot drop") and normal or reduced tone.
In patients with LMN foot drop, the gait is high stepping because the hip flexors are strong and compensate for the weakness to allow foot clearance. There may be an audible slap as the foot hits the ground.
On examination, the pattern of leg weakness is variable depending on the particular roots or peripheral nerves involved. Predominant quadriceps weakness is often LMN in origin; the knee fails to lock and this causes falls. Toe flexion and foot plantar flexion weakness also usually suggest an LMN cause. Tone is normal or reduced. Reflex loss can be used to help localize LMN weakness.
Observation of the patient during toe and heel walking is an easy way to assess for dorsiflexion and plantar flexion weakness at the ankles. Patients can also be observed attempting to stand on toes or heels. It may be difficult to separate an LMN foot drop from a UMN lesion, as both can affect foot extension strength; wasting of extensor digitorum brevis, weakness of foot inversion, and sparing of iliopsoas argue for LMN pathology.
Bladder dysfunction is relatively uncommon with LMN leg weakness. An exception is with acute bilateral cauda equina lesions, which may cause urinary retention along with LMN weakness.
Among older adults, common causes of weak gait with evidence of an LMN weakness on examination include lumbar radiculopathy secondary to degenerative spine disease, hereditary or acquired sensorimotor polyneuropathies, and peroneal mononeuropathy due to compression, trauma, or diabetes. Distal weakness with mixed LMN and UMN signs may be seen in motor neuron disease. (See "Overview of lower extremity peripheral nerve syndromes" and "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis" and "Overview of polyneuropathy" and "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease".)
Myopathic gait — Most myopathies involve leg weakness that is symmetric and affects proximal more than distal muscle groups. Because of limb girdle weakness, the myopathic gait is classically described as waddling, and there is abnormal pelvic tilt with each step.
On examination, hip flexor weakness can be detected by testing straight leg raise against resistance. A common test of proximal leg strength is to ask the patient to stand up with arms crossed in front of them. Patients with proximal muscle weakness will have difficulty standing up from a seated position without using their arms to push off. The history may reveal difficulty with other tasks that require proximal strength, such as descending and ascending stairs. To examine hip girdle strength, patients may be asked to bear weight on one leg to detect the pelvis tilting down on the contralateral side because of weakness of gluteus medius (a positive Trendelenburg test). Tone in the legs is normal.
Myopathic weakness can be challenging to distinguish from LMN weakness at the bedside. Signs that favor myopathic weakness include symmetry, involvement of proximal muscles in the upper body (eg, neck, shoulders), lack of sensory symptoms, as well as relative preservation of reflexes. (See "Muscle examination in the evaluation of weakness".)
Among older adults, particularly those in nursing homes, the most common cause of muscle weakness and altered gait is deconditioning and loss of muscle mass. The major categories of primary muscle disease include inflammatory disorders, endocrinopathies, metabolic myopathies, drugs and toxins, infections, and various causes of rhabdomyolysis. Inclusion body myositis, drug-induced myopathies (eg, statins, glucocorticoids), and endocrinopathies (eg, Cushing syndrome, hypothyroidism) are among the more important causes in older adults. Myasthenia gravis is an uncommon but important cause of acquired proximal muscle weakness in older adults that may be suspected based on a fluctuating or fatigable pattern of weakness as well as diplopia, ptosis, dysarthria, and dysphagia. (See "Approach to the patient with muscle weakness" and "Clinical manifestations of myasthenia gravis".)
Parkinsonian gait — Parkinson disease (PD) and other disorders of the basal ganglia are a significant cause of gait dysfunction, posture, and balance problems in older adults.
The parkinsonian gait is narrow-based with reduced stride length, and the feet barely clear the floor. There is a stooped posture, and poor or no arm swing when walking. Flexion at the elbows becomes prominent; the hands are pronated and the fingers flexed at the metacarpophalangeal joints, a sign known as the "striatal hand." When tremor is a major feature, the arm is usually extended at the elbow with a flexion-extension finger/hand tremor. The center of gravity is thrown forwards and the patient takes increasingly faster, short (petit pas) steps that give the appearance of hurrying or "festinating." There may be difficulty initiating gait, and a few preliminary steps on the spot are taken before takeoff (start hesitation). When stepping through a doorway or when initiating a sudden turn, walking may stop altogether (freezing) [9].
On examination, when standing, the patient is easily displaced backwards and may take a few backwards steps (retropulsion). When asked to turn rapidly, turning is accomplished by making a number of small steps while keeping the neck and trunk rigid (en bloc turn), rather than by pivoting on the foot as in an "army about-face."
PD is the most common neurodegenerative cause of parkinsonism. Other causes include several related neurodegenerative diseases (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration), drug-induced parkinsonism, and vascular dementia due to small vessel cerebrovascular disease. In vascular dementia, parkinsonism may preferentially affect the lower body [10,11]. Mild parkinsonism can be observed in older adults who do not meet criteria for PD or related disorders, in which case it has been referred to as idiopathic gait disorder of old age [12]. (See "Diagnosis and differential diagnosis of Parkinson disease" and "Etiology, clinical manifestations, and diagnosis of vascular dementia", section on 'Neuropsychiatric and motor signs' and "Drug-induced parkinsonism".)
The gait disorder in PD typically responds to carbidopa-levodopa, at least in the early stages of the disease. Failure to respond may suggest the diagnosis of atypical parkinsonism, such as multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, parkinsonism secondary to cerebrovascular disease, or a metabolic/genetic disorder of the basal ganglia, although these disorders can be levodopa responsive, particularly in their early stages. (See "Diagnosis and differential diagnosis of Parkinson disease", section on 'Response to dopaminergic therapy'.)
Frontal (apraxic) gait — Bilateral frontal lobe dysfunction can result in a higher-level gait disorder, in which basic motor and sensory functions are intact but there is a failure of motor programming, or an apraxia. Patients with a frontal (apraxic) gait may have some or all of the following features [13]:
●Cautious, slow gait. The stride length is shortened on a normal or slightly wide base, and there may be hesitation, freezing, and en bloc turns. The gait can also appear "magnetic," as if the feet are stuck to the floor.
●Gait ignition failure, characterized by difficulty initiating locomotion. Patients may take three or four steps in place before a normal stride ensues.
●Frontal disequilibrium, characterized by inappropriate or counterproductive postural and locomotion responses. The patient may be easily displaced backwards, precipitating falls. Fear of falling and anxiety associated with walking are common.
●Frontal ataxia, with a wide-based and lurching gait that resembles cerebellar ataxia. Symptoms result from disruption of bilateral frontopontine connections.
In addition to an abnormal gait, many patients will have cognitive impairment with prominent executive dysfunction, which localizes to the frontal lobe. Although the classic frontal gait can appear very similar to a parkinsonian gait, patients with a frontal gait lack other typical signs of extrapyramidal dysfunction (eg, resting tremor, bradykinesia, masked facies). (See "Clinical manifestations of Parkinson disease" and "Diagnosis and differential diagnosis of Parkinson disease".)
A frontal gait can result from any process that affects fibers interconnecting bilateral frontal cortical regions, especially those involving prefrontal cortex, which is important in the cognitive control of motor performance. The most common causes in older adults are small vessel vascular disease (arguably overdiagnosed), other neurodegenerative disorders affecting the frontal lobes (eg, Alzheimer dementia, frontotemporal dementia, parkinsonian syndromes), and normal pressure hydrocephalus (NPH). Frontal lobe tumors occasionally present in this manner.
In patients with small vessel disease (subcortical arteriosclerotic encephalopathy), magnetic resonance tensor imaging studies demonstrate abnormalities in areas of white matter that may appear normal on conventional magnetic resonance imaging (MRI) [14-16]. Loss of white matter integrity in major anterior projection fibers (thalamic radiations, corticofugal motor tracts) and adjacent association fibers (corpus callosum, superior fronto-occipital fasciculus, short association fibers) shows the greatest covariance with poorer gait. White matter lesions probably contribute to age-related gait decline by disconnecting motor networks served by these tracts [14].
The triad of frontal gait disturbance, dementia, and urinary incontinence is suggestive of NPH, and a gait disorder is usually the first sign to appear in patients with NPH. On brain imaging with computed tomography (CT) or MRI, the characteristic feature of NPH is enlargement of the ventricular system out of proportion to the degree of cortical atrophy. This is in contrast to "hydrocephalus ex vacuo," in which the cerebral ventricles are enlarged more or less in proportion to the amount of cortical atrophy. The distinction may be difficult to establish. NPH is discussed in detail separately. (See "Normal pressure hydrocephalus".)
Predominant sensory dysfunction
Sensory ataxia — Severe loss of position sense (proprioception) in the feet can be as disabling as severe weakness [17], and the motor control abnormalities that arise from severe loss of proprioception are referred to as a sensory ataxia. Patients with milder deficits may be clumsy and bump into things. They are always worse in the dark when the "crutch" of vision is lost.
Classically, the gait associated with disturbed proprioception is described as high stepping and stamping. The stamping is thought to be an attempt to increase sensory feedback. In practice, the patients often come down hard on their heels and then slap the sole of the foot on the floor, with the same objective. The gait may be slightly wide based. Stride length is normal or a little reduced, and the gait deteriorates markedly in the dark.
On examination, proprioception in the legs is examined by testing joint position sense in the toes, and then moving to more proximal joints (ankles, knees) if the distal joints are abnormal. Vibration sensation, which is transmitted by the same large, myelinated sensory nerves as proprioception, is tested in the same manner using a tuning fork. Small fiber sensory function (pain, temperature) is typically tested with pinprick and the cold metal of a tuning fork or reflex hammer. The Romberg test, in which patients are asked to stand upright with feet together and then close the eyes, is positive (meaning that the patient is markedly more unsteady with eyes closed compared with open). (See "Approach to the patient with sensory loss", section on 'Sensory examination'.)
When proprioception is disproportionately affected compared with other sensory modalities and motor function, the site of pathology will usually be the posterior columns in the spinal cord. In older adults, a common cause is cervical spondylotic myelopathy, but a serum B12 level and syphilis serology should always be checked. Copper deficiency can present like B12 deficiency and is also treatable. Spine imaging for cord compression is mandatory, along with careful investigation for UMN signs.
Occasionally, a very severe sensory neuronopathy can present in this way; the likely candidate in such cases is diabetes (diabetic pseudotabes), but paraneoplastic dorsal ganglionic neuropathy or Sjögren's syndrome may present like this. (See "Approach to the patient with sensory loss", section on 'Sensory neuronopathies' and "Paraneoplastic syndromes affecting spinal cord, peripheral nerve, and muscle".)
A cortical lesion can occasionally interfere with proprioception. Medial medullary and thalamic infarctions are rare causes of proprioceptive loss. Isolated small fiber neuropathy, common in older adults, does not typically affect gait.
Predominant imbalance or unsteadiness
Cerebellar ataxia — A cerebellar ataxic gait may be described as stumbling, lurching, staggering, slow, reduced step length, wide based, reeling, or drunken. These features are often coupled with other signs of ataxia, including scanning and slow speech, finger-nose and heel-shin dysmetria, dyssynergia, and dysdiadochokinesia.
The patient with cerebellar ataxia has difficulty changing voluntary force levels abruptly. Acceleration and braking are impaired [18]. This leads to overshoot in point-to-point movements (dysmetria). In multijoint movements, there is a breakdown of normal coordination of joint rotations, with trajectory abnormalities (dyssynergia) [19]. The rhythm of repetitive, alternating single movements, such as finger tapping, breaks down (dysrhythmia). Dysfunction in the midline vermis results in truncal and gait ataxia.
There are many causes of cerebellar ataxia, and the workup for these patients is extensive. The onset of ataxia (acute, subacute, or chronic) is a key clinical feature that directs the pace and scope of the evaluation [20]. Among older adults, common causes of acute cerebellar ataxia include ischemic or hemorrhagic stroke, Wernicke encephalopathy, and medication toxicity (table 1). Subacute causes include vitamin E deficiency (or that of its transporter protein), hypothyroidism, gliadin antibody syndrome (gluten allergy), trauma, anoxia, alcoholism, demyelination, mass lesions, and paraneoplastic degeneration. A variety of hereditary and sporadic neurodegenerative disorders can cause late-onset chronic, progressive cerebellar ataxia. The causes and evaluation of cerebellar ataxia are reviewed separately. (See "Overview of cerebellar ataxia in adults" and "The spinocerebellar ataxias".)
Vestibular gait — Patients with unilateral vestibular dysfunction classically deviate to the side of the affected ear when walking. The gait varies from an occasional stumble to frank veering. The legs are slightly spread (wide based), and stride length is slightly reduced. Marching in place with eyes closed can bring out the veering (Unterberger test).
Patients with acute unilateral vestibular dysfunction experience rotary vertigo and a feeling of body tilt. On examination, nystagmus is prominent and there is a subjective sense of self-motion in the direction of the fast phase. There is then a compensatory reaction that results in objective postural destabilization, gait deviation, and falling to the side opposite to the fast phase of nystagmus [21]. The most common causes of unilateral vestibular dysfunction in older adults are benign paroxysmal positional vertigo and vestibular neuritis. Cerebellar stroke is an important central cause of acute sustained vertigo. (See "Causes of vertigo" and "Vestibular neuritis and labyrinthitis", section on 'Differential diagnosis'.)
In patients with bilateral vestibular dysfunction, there is loss of the vestibuloocular reflex, leading to oscillopsia with head movement. Unsteadiness worsens notably when visual and somatosensory input is diminished, as in walking in the dark or on uneven ground. Because there is no marked vestibular asymmetry, frank vertigo does not occur. In some patients, the observation that running is easier than walking is a clue to a vestibulopathy [22]. Bilateral vestibulopathies are relatively uncommon but can be seen with drug toxicity (eg, aminoglycosides, certain chemotherapies), bilateral vestibular neuritis, and Meniere disease. (See "Evaluation of the patient with vertigo", section on 'Impaired balance without vertigo'.)
A practical problem in the dizzy patient is to distinguish central from peripheral vertigo. Other brainstem signs on examination are hard evidence for a central cause. Vertical and direction-changing nystagmus also support a central origin. One should also consider nonvestibulopathic dizziness as a cause of gait and postural instability. Postural hypotension is easily diagnosed at the bedside, but further study may be necessary to demonstrate a cardiac arrhythmia. (See "Approach to the patient with dizziness" and "Evaluation of the patient with vertigo".)
Functional symptoms (conversion) — Functional movement disorders are clinical syndromes defined by the occurrence of abnormal involuntary movements that are incongruent with a known neurologic cause and are significantly improved on neurologic examination with distraction or nonphysiologic maneuvers. (See "Functional movement disorders".)
On examination, walking often does not conform to any of the usual patterns observed with neurologic gait disorders. There may be excessive slowness and stiffness, or maintenance of postural control on a narrow base with flailing arms and excessive trunk sway. Knee dipping and near falls with recovery may be seen. Functional gaits may resemble walking on ice, walking on a sticky surface, walking through water (bringing to mind excessive slowness), tightrope walking, habitual limping, and bizarre, robotic, knock-kneed, trepidant, anxious, and cautious gaits. (See "Functional movement disorders", section on 'Functional gait'.)
In some older adults, a functional gait disorder may be associated with fear of falling and a history of recent falls [23]. Such fear can be invoked as an explanation for some patients with a type of cautious gait described as "space phobia" that is characterized by timid walking while holding on to furniture and walls [24]. Individuals with severe depression and psychomotor retardation may walk with reduced stride length and a lifting motion of the legs [25].
The cautious gait of Nutt is a legitimate psychological adaptation, based upon an appropriate response to real or perceived disequilibrium [13]. Thus, the mere presence of a cautious gait does not confirm a functional ("psychogenic") etiology; the differential includes higher-level gait disorders. (See 'Frontal (apraxic) gait' above.)
Antalgic gait and other nonneurologic causes — Gait disorders are frequently of multifactorial origin. Nonneurologic causes may be the sole problem, or mixed in with the neurologic causes [2].
Nonneurologic causes of gait disorders include the following [26]:
●Visual loss
●Hearing impairment
●Orthopedic disorders
●Rheumatologic disorders
●Pain
●Side effects of drugs
●Cardiorespiratory problems (particularly orthostasis)
These and other factors commonly affecting gait and fall risk in older adults are reviewed in detail separately. (See "Falls in older persons: Risk factors and patient evaluation".)
EVALUATION — The goal of the history and examination of an older adult with an abnormal gait is to identify and localize functions that are interfering with gait. Localization largely directs the evaluation and narrows the diagnostic possibilities (table 2).
History and examination — The history may initially be vague, or simply consist of one or more falls that have been labeled as "mechanical." Patients often complain of nebulous symptoms such as "weakness," "dizziness," or just plain "I can't walk." Many gait disorders have an insidious onset, making it difficult for patients to say when the problem started. Patients who use an assistive device should be asked when and why they began using it. It can sometimes be helpful to index major events by asking patients to recall what their walking was like last Christmas, or at the last family event, and ask family members to help corroborate.
It is important to inquire about bladder dysfunction in patients with a gait disorder, since the pattern of urinary symptoms may be a clue to the anatomic localization and etiology of the gait disorder. In general, when central nervous system dysfunction affects the bladder, it results in detrusor hyperactivity that leads to symptoms of urgency and urge incontinence. Patients with frontal lobe impairment may be indifferent to or unconcerned about the incontinence. Patients with thoracic cord lesions may have dyssynergia, in which the detrusor contracts on a closed sphincter resulting in poor initiation of micturition.
A complete neurologic examination helps to identify the predominant function interfering with normal walking (eg, weakness, motor control, sensory loss, imbalance). Cognition and affect should be examined with an emphasis on frontal lobe function. Informative patterns of weakness may emerge on muscle strength testing (eg, a hemiparesis suggesting a central, contralateral brain lesion, or bilateral proximal leg weakness with increased tone suggestive of a myelopathy). The sensory examination should include tests of light touch/pinprick as well as position sensation and vibration. Close observation during the examination may reveal a resting tremor suggestive of parkinsonism.
To examine tone in the legs, patients should be lying supine with legs extended. The examiner first rotates the relaxed leg from side to side at or above the knee. If the foot moves en bloc with the leg, increased tone is present. The examiner then suddenly jerks the leg up at the popliteal fossa. The normal response is for the knee to flex and the heel to slide proximally along the table. If the leg jerks and the heel lifts upwards off the table before relaxing, spasticity is present.
Most examination rooms are too small for an adequate gait assessment, and patients should be observed while walking the length of a hallway, when possible. Some abnormalities are apparent with casual, undisturbed walking, while others are brought out by challenging tasks (eg, walking on heels and toes to bring out foot dorsiflexion weakness; marching in place with eyes closed to bring out rotation/deviation due to vestibular dysfunction; heel-toe walking to bring out cerebellar dysfunction). Asking the patient to do a cognitive task while walking (eg, reciting months of the year backwards), referred to as a dual-task gait test, can also help to identify motor phenotypes, especially in the setting of mild cognitive impairment [27].
Postural control and reactivity can be examined by a retropulsion test (standing in back of the patient and exerting a sudden tug on the shoulders, and watching for a corrective step backwards).
Further testing — Further evaluation and testing vary according to the examination findings and pattern of gait:
●Leg weakness – Patients with previously unrecognized lower extremity weakness generally require imaging to look for a structural cause of weakness. For patients with evidence of increased tone or spasticity in the lower limbs (with or without frank weakness), MRI of the cervical spine is a good first test to look for cervical spondylopathy or other causes of cervical myelopathy. Thoracic and lumbar MRI may be needed to exclude a compressive lesion if cervical spine imaging is unremarkable; in addition, patients with cervical spondylosis often have multilevel disease. Brain imaging should always be considered when weakness is asymmetric, when it involves the face and/or arm as well as leg, or when there are other cortical signs. (See "Cervical spondylotic myelopathy" and "Disorders affecting the spinal cord".)
●Foot drop – For patients with a foot drop or other signs of lower motor neuron (LMN) weakness, a lumbosacral spine MRI is useful to look for a structural cause of a radiculopathy. There should be a low threshold for brain MRI in patients with asymmetric weakness, as upper motor neuron (UMN) and LMN foot weakness can be difficult to distinguish. Electrophysiologic studies (nerve conduction studies [NCS] and electromyography [EMG]) can help delineate a radiculopathy or mononeuropathy. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis", section on 'Diagnosis' and "Overview of lower extremity peripheral nerve syndromes", section on 'Diagnostic testing'.)
●Myopathic gait – In patients suspected of having myopathic weakness, initial studies may include blood work to look for elevations of plasma muscle enzymes, serologic tests including antinuclear antibodies if an inflammatory myopathy is suspected, and electrophysiologic studies (NCS and EMG). (See "Approach to the patient with muscle weakness".)
●Frontal or parkinsonian gait – Patients suspected of having a frontal (apraxic) gait should have brain imaging to look for ventricular enlargement characteristic of normal pressure hydrocephalus (NPH) or other frontal pathology. The initial evaluation of patients with suspected Parkinson disease (PD) or other parkinsonian disorder generally includes a brain MRI to exclude structural abnormalities like hydrocephalus or lacunar infarcts in the basal ganglia. (See "Normal pressure hydrocephalus" and "Etiology, clinical manifestations, and diagnosis of vascular dementia" and "Diagnosis and differential diagnosis of Parkinson disease".)
●Sensory loss – Patients with prominent sensory loss in the legs should be evaluated for common causes of peripheral neuropathy, including diabetes and B12 deficiency (when sensory loss is predominantly proprioceptive). Importantly, posterior column dysfunction in older adults can be a manifestation of a compressive myelopathy, and a spine MRI should be obtained to rule out compression, especially in the presence of increased tone/spasticity in the legs. (See "Overview of polyneuropathy" and "Cervical spondylotic myelopathy", section on 'Clinical presentation'.)
●Ataxia – The evaluation of patients with a wide-based gait and other cerebellar signs is guided largely by the acuity of symptoms (ie, acute, subacute, chronic). (See "Overview of cerebellar ataxia in adults", section on 'Etiologic evaluation'.)
SUMMARY
●Epidemiology – Gait disorders are a major cause of functional impairment and morbidity in older adults, affecting approximately one-third of people age 60 years and older. (See 'Epidemiology' above.)
●Motor dysfunction – Motor system dysfunction results in a variety of abnormal gait patterns, depending on the cause and distribution of nervous system pathology (table 2). Major patterns include the following:
•Upper motor neuron (UMN) weakness preferentially involves hip flexion, foot and toe dorsiflexion, and hamstring strength. It is usually accompanied by increased tone (spasticity). Bilateral UMN weakness in the lower extremities usually localizes to the spinal cord, whereas unilateral UMN weakness indicates involvement of motor pathways in the brain or brainstem. (See 'Weak gait with spasticity' above.)
•Lower motor neuron (LMN) dysfunction often involves focal or asymmetric weakness, muscle atrophy, normal or reduced tone, and loss of reflexes. The pattern of leg weakness is variable depending on the particular roots or peripheral nerves involved. Lumbar radiculopathy secondary to degenerative spine disease and peripheral neuropathy are common causes. (See 'Weak gait with neuropathic weakness' above.)
•Most myopathies cause lower extremity weakness that is symmetric and predominantly proximal. Patients with proximal muscle weakness have difficulty standing up from a seated position without using their arms to push off, and the gait may appear waddling as the pelvis tilts with each step. Deconditioning, primary muscle disease, and myasthenia gravis are important causes in older adults. (See 'Myopathic gait' above.)
•Extrapyramidal dysfunction results in a parkinsonian gait characterized by small steps, decreased arm swing, stooped posture, and retropulsion. Parkinson disease (PD), related neurodegenerative disorders, drug-induced parkinsonism, and vascular dementia are the most common causes of parkinsonism in older adults. (See 'Parkinsonian gait' above.)
•Bilateral frontal lobe dysfunction is associated with a failure of motor programming and a number of higher-level gait disorders. The usual causes are subcortical arteriosclerotic encephalopathy, normal pressure hydrocephalus (NPH), and neurodegenerative disease. (See 'Frontal (apraxic) gait' above.)
●Sensory ataxia – Severe loss of position sense (proprioception) in the feet can result in a disabling gait disorder that worsens markedly in the dark. When proprioception is disproportionately affected, the differential diagnosis includes myelopathy, B12 or copper deficiency, and sensory neuronopathy. (See 'Sensory ataxia' above.)
●Cerebellar ataxia – Cerebellar ataxia has many causes. The gait is characterized by a wide base and reduced step length; it is typically described as stumbling, lurching, staggering, slow, reeling, or drunken. These features are often coupled with other signs of ataxia. (See 'Cerebellar ataxia' above.)
●Vestibular dysfunction – Vestibular dysfunction impairs the ability of the brain to sense body position in space. The vestibular gait is characterized by deviation to the side of the affected ear, and varies from an occasional stumble to frank veering. The base is mildly wide, and stride length is slightly reduced. The presence of nystagmus supports the diagnosis. (See 'Vestibular gait' above.)
●Nonneurologic factors – Gait disorders are frequently multifactorial in origin. Nonneurologic causes include visual loss, orthopedic disorders, rheumatologic disorders, pain, side effects of drugs, and cardiorespiratory problems (particularly orthostasis). These may be the sole problem, but often coexist with neurologic causes. (See 'Antalgic gait and other nonneurologic causes' above.)
●Evaluation – The goal of the history and examination of an older adult with an abnormal gait is to identify and localize functions that are interfering with gait. Localization largely directs the evaluation and narrows the diagnostic possibilities (table 2). (See 'Evaluation' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Ryan R Walsh, MD, PhD, FAAN, who contributed to earlier versions of this topic review.
