INTRODUCTION — Walking (gait) is a complex and unique motor behavior consisting of three primary components: locomotion, balance, and ability to adapt to the environment. Normal gait requires a delicate balance among multiple interacting systems, including three major afferent sensory systems (visual, vestibular, and proprioceptive senses), a locomotor efferent system (including nerves and muscles), and the strict surveillance by several structures of the central nervous system .
In older adults, gait disorders are a major cause of functional impairment, diminished quality of life, morbidity, and even mortality due to their connection with falls and resulting major fractures or head trauma. In any adult, a gait disorder may be the initial presentation of a wide range of neurologic disorders.
Most gait disorders are multifactorial and have both neurologic and non-neurologic components. Outside of the nervous system, other structures that play an important role in gait physiology include bones, joints, tendons, and the cardiovascular system (providing hemodynamic stability while standing). A defect at any level of control can result in a gait disorder.
This topic will review the causes and evaluation of 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 adults, and the prevalence increases with age. Approximately 30 percent of community-dwelling adults age 60 years and older have a gait disorder . 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].
In a population-based study of 488 community-dwelling older adults, neurologic, non-neurologic, and combined gait disorders were present in 24, 17, and 9 percent, respectively . 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 [3,7].
It is estimated that approximately 15 percent of falls in older adults can be attributed to balance or gait disorders, including leg weakness . Other contributing factors are reviewed separately. (See "Falls in older persons: Risk factors and patient evaluation".)
CLINICAL GAIT PATTERNS — Several classifications of neurologic gait disorders have been proposed. An early classification grouped disorders hierarchically into lower-level (eg, neuromuscular conditions), middle-level (eg, parkinsonian gait), and higher-level disorders (eg, gait apraxia) . Other classifications have been based on anatomy (eg, cerebellar), etiology (eg, vascular), or dominant clinical phenomenology .
The gait patterns below are organized primarily by clinical phenomenology. An alternative, partially overlapping organization based on the most prominent abnormal sign can be particularly useful in guiding the differential diagnosis at initial presentation . (See 'Sign-based diagnosis' below.)
Predominant motor dysfunction
Spasticity with weakness — Spasticity (increased velocity-dependent tone) is usually accompanied by some degree of weakness resulting from upper motor neuron (UMN) dysfunction in the spinal cord and/or higher central motor pathways in the brain. The combination of UMN leg weakness and increased tone produces a recognizable gait pattern.
●Gait pattern – The spastic gait is typically slow; when there is unilateral UMN involvement, the gait is slow and asymmetric. In subclinical cases, asking the patient to walk faster can elicit the typical stiff appearance of one or both legs.
Patients with bilateral spasticity in the legs often have a narrow, scissoring gait in which the thighs and knees are pulled close together by increased adductor tone, sometimes to the point of crossing. The toes turn in and scrape on the floor with each step, producing a scuffing sound and asymmetric wearing of the shoe soles at the tips. This may be more prominent because the hip flexors are weak, preventing compensatory lifting of the feet to clear the ground. 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.
●Other examination findings – 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. Hyperreflexia and extensor plantar responses are typically present.
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.
●Localization and causes – Unilateral UMN weakness and spasticity usually indicate involvement of higher motor pathways in the 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.
In adults, bilateral UMN leg weakness and spasticity usually localize 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 disorders (eg, adrenomyeloneuropathy, hereditary spastic paraplegia), vascular disease, copper deficiency, demyelinating disease, and intramedullary tumors, are less common. (See "Disorders affecting the spinal cord" and "Cervical spondylotic myelopathy".)
Other nonspinal causes for bilateral UMN leg weakness are neurodegeneration of the UMN (eg, primary lateral sclerosis), falcine meningiomas, and the long-term sequelae of cerebral palsy (so-called "diplegic gait"). (See "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Primary lateral sclerosis' and "Epidemiology, pathology, clinical features, and diagnosis of meningioma" and "Cerebral palsy: Classification and clinical features", section on 'Spastic subtypes'.)
Stiffness without weakness — While spasticity is usually accompanied by weakness, rarer conditions can cause a stiff gait in the absence of weakness. Such walking patterns may be mistaken for spasticity.
Stiff-person syndrome is an autoimmune condition characterized by impairment of inhibitory transmission within the spinal cord. Stiff leg syndrome is a milder variant where only legs, even asymmetrically, are involved. (See "Stiff-person syndrome".)
Dystonia, a movement disorder characterized by involuntary twisting postures and movements of different body parts, can also involve the lower limbs (generalized dystonia) and thus cause a stiff gait. The triggering/worsening during specific movements (task specificity) or movements in general (overflow) as well as the transient amelioration with certain other actions (sensory tricks) are specific to dystonia. As an example, some patients might have a transient resolution of the dystonic gait during motor activities other than straight normal walking, such as backwards walking, running, or climbing stairs. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Clinical features'.)
Neuropathic gait — 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.
●Gait pattern – 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 ("steppage").
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.
●Other examination findings – 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. Deep tendon reflex loss can be used to help localize LMN weakness.
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. Alternatively, a pattern similar to foot drop or knee buckling can be seen in patients with dystonia or chorea; normal power and reflexes argue against a LMN cause in such cases.
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.
●Localization and causes – 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. A common cause of bilateral LMN weakness is spinal stenosis, which can often cause neurogenic claudication manifested by back pain, paresthesias, and gait involvement brought on by prolonged standing and/or walking. 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: Etiology, 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.
●Gait pattern – The myopathic gait is classically described as waddling based on the way that hip girdle weakness causes an abnormal pelvic tilt with each step. To isolate 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).
●Other examination findings – 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 (Gower's maneuver). Neck flexor weakness is often present in myopathies. The history may reveal difficulty with other tasks that require proximal strength, such as descending and ascending stairs. 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), and lack of sensory symptoms, as well as relative preservation of reflexes. (See "Muscle examination in the evaluation of weakness".)
●Localization and causes – 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. Drug-induced myopathies (eg, statins, glucocorticoids) and endocrinopathies (eg, Cushing syndrome, hypothyroidism) are among the treatable causes in older adults. (See "Approach to the patient with muscle weakness".)
Disorders of the neuromuscular junction can also present with a gait characterized by proximal weakness. 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. Proximal leg weakness is also common in Lambert-Eaton syndrome, a rare paraneoplastic myasthenic syndrome characterized by progressive improvement of strength with movement, the opposite of what seen in myasthenia gravis. (See "Clinical manifestations of myasthenia gravis" and "Lambert-Eaton myasthenic syndrome: Clinical features and diagnosis".)
Parkinsonian gait — Parkinsonism refers to a clinical syndrome of various combinations of bradykinesia, rest tremor, rigidity, and postural instability. Parkinson disease (PD) and other causes of parkinsonism are a significant cause of gait and posture dysfunction and balance problems in older adults.
●Gait pattern – The parkinsonian gait is slow and narrow-based. It is classically described as shuffling because the stride length is reduced, and the feet barely clear the floor. Cadence might be increased to compensate for the reduced stride length. There is a stooped posture, and the natural arm swing that occurs with casual walking is reduced or absent. In PD, the disease process almost always begins asymmetrically, and a difference in arm swing (one side reduced, one side moving freely) can often be observed.
In more severe cases, flexion at the elbows becomes prominent. The center of gravity is thrown forwards, and the patient takes increasingly faster, short (petits pas) steps that give the appearance of hurrying or "festinating." Some have described it as "chasing one's shadow."
Freezing of gait is a common feature of PD and other causes of parkinsonism. Freezing is defined as paroxysmal episodes in which the person cannot step effectively, despite attempting to do so. Manifestations of freezing range from start/turn/destination hesitation to complete akinesia . Start hesitation is observed when a patient has difficulty initiating gait and takes a few preliminary steps in place before takeoff. When patients step through a doorway or initiate a sudden turn, walking may stop altogether . Visual or auditory cues can transiently ameliorate freezing of gait.
When patients are asked to turn rapidly, turning is accomplished by making a series of small steps while keeping the neck and trunk rigid ("en bloc" turning). Importantly, patients tend to always turn in the same direction, pivoting on the most affected leg. Asking the patient to make a 360° turn in one direction and then the other is a useful test to elicit freezing of gait in the clinic.
●Other examination findings – When tremor is a component of the syndrome, the more affected arm is usually extended at the elbow, and the typical pill-rolling tremor in the hand becomes more prominent with walking.
Postural instability often accompanies other aspects of the parkinsonian gait. This can manifest as retropulsion, when a patient is easily displaced backwards with a tug of the shoulders and takes a few steps backwards to stabilize themselves. Interestingly, patients with PD have preserved medio-lateral stability, meaning that they can often have a normal tandem gait test (walking one foot in front of the other, as though on a tightrope) and have preserved ability to ride a bicycle .
●Localization and causes – Parkinsonism generally localizes to the dopaminergic pathways of the basal ganglia. PD is the most common cause of neurodegenerative parkinsonism; other degenerative causes include dementia with Lewy bodies, multiple system atrophy, progressive supranuclear palsy (PSP), and corticobasal syndrome (table 1). Early involvement of gait and balance is typical in all of these conditions. (See "Diagnosis and differential diagnosis of Parkinson disease".)
A parkinsonian gait can also be due to secondary causes, including drug-induced parkinsonism due to dopamine receptor-blocking agents (eg, first- or second-generation antipsychotic agents, metoclopramide) (table 2). (See "Drug-induced parkinsonism".)
Cerebrovascular disease in particular often preferentially affects the lower body and thereby the gait [15,16]. This has been referred to as lower-body parkinsonism, which can also be seen in patients with normal pressure hydrocephalus (NPH), although features overlap with higher-level gait disorders, as discussed below. (See 'Higher-level gait disorder' below.)
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 . Many such patients are likely better classified as having higher-level gait disorders. (See 'Higher-level gait disorder' below.)
Higher-level gait disorder — Higher-level gait disorder refers to a failure of motor programming, in which basic motor and sensory functions are intact. It has become the preferred term for conditions previously called frontal gait or gait apraxia .
●Gait pattern – Patients with a higher-level gait disorder have some or all of the following features :
•Slow gait with short stride length, normal or slightly wide base, and preserved arm swinging, as in lower-body parkinsonism.
•Freezing of gait in all its manifestations (eg, hesitation, en bloc turns, etc), a motor condition described in this context as "magnetic."
•Disequilibrium, characterized by inappropriate or counterproductive postural and locomotion responses. The patient may be easily displaced backwards, precipitating falls. Frontal ataxia is the term used to describe a wide-based and lurching gait that resembles cerebellar ataxia, in which symptoms are believed to result from disruption of bilateral frontopontine connections.
•Variability of stepping.
•Issues navigating obstacles and using walking aids.
•Fear of falling and anxiety, further reducing the gait speed ("cautious gait").
●Other examination findings – In addition to an abnormal gait, many patients will have cognitive impairment with prominent executive dysfunction, which localizes to the frontal lobe and its connections with the basal ganglia and cerebellum. Although the classic frontal gait can appear very similar to a parkinsonian gait, patients with a frontal gait lack other typical signs of basal ganglia involvement, such as resting tremor and bradykinesia.
●Localization and causes – The most common causes of higher-level gait disorder are small vessel vascular disease, other neurodegenerative disorders affecting the cortex (eg, Alzheimer disease, frontotemporal dementia, parkinsonian syndromes), and 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) [19-21]. 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 (once called "senile gait") by disconnecting motor networks served by these tracts .
In patients with NPH, the gait disorder is often the first sign to appear. The full triad of idiopathic NPH is characterized by broad-based shuffling gait, early frontal dysexecutive syndrome, and urge incontinence due to detrusor hyperactivity . NPH is discussed in detail separately. (See "Normal pressure hydrocephalus".)
Predominant imbalance or unsteadiness
Sensory ataxia — Severe loss of position sense (proprioception) in the feet can be as disabling as severe weakness , and the motor control abnormalities that arise from severe loss of proprioception are referred to as a sensory ataxia.
●Gait pattern – Sensory ataxia is classically 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. Gait may be slightly wide-based and stride length is normal or a little reduced. These features deteriorate markedly in the dark.
●Other examination findings – On examination, patients will have abnormal proprioception and vibration sensation in the feet. Small fiber sensory function (pain, temperature) may also be impaired. 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).
Unlike in patients with cerebellar causes of ataxia, patients with sensory ataxia have normal speech and eye movements.
●Localization and causes – 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 disease may also present like this.
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.
Cerebellar ataxia — Cerebellar ataxia refers to gait dysfunction and imbalance arising from pathology in the cerebellum and its connections.
●Gait pattern – A cerebellar ataxic gait is typically slow and wide-based with reduced step length. It may be described as stumbling, lurching, staggering, reeling, or drunken. Acceleration and braking are impaired . Dysfunction in the midline vermis results in truncal and gait ataxia.
●Other examination findings – Gait features are often coupled with other signs of ataxia, including scanning and slow speech, finger-nose and heel-shin dysmetria, dyssynergia, and dysdiadochokinesia. In multijoint movements, there is a breakdown of normal coordination of joint rotations, with trajectory abnormalities (dyssynergia) . The rhythm of repetitive, alternating single movements, such as finger tapping, breaks down (dysrhythmia).
●Localization and causes – 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 .
Among adults, common causes of acute and subacute cerebellar ataxia include potentially treatable or reversible causes. Acute ataxia may be caused by ischemic or hemorrhagic stroke, Wernicke encephalopathy, or medication toxicity. Subacute causes include vitamin E deficiency, hypothyroidism, gliadin antibody syndrome (gluten ataxia), trauma, anoxia, alcoholism, demyelination, mass lesions, and paraneoplastic degeneration (table 3). A variety of hereditary and sporadic neurodegenerative disorders can cause late-onset chronic, progressive cerebellar ataxia.
Vestibular gait — Dysfunction of the vestibular system commonly results in abnormalities in gait, balance, and postural stability.
●Gait pattern – The vestibular gait varies from an occasional stumble to frank veering. The legs might be slightly spread (wide-based) and stride length slightly reduced. Notably, gait speed is increased as a compensatory mechanism to reduce the stance time. In some patients, the observation that running is easier than walking is a clue to a vestibulopathy ; in fact, during running there is no stance phase. Unsteadiness worsens notably when visual and somatosensory input is diminished, as in walking in the dark or on uneven ground.
Patients with unilateral vestibular dysfunction classically deviate to the side of the affected ear when walking. Marching in place with eyes closed can bring out the veering (Unterberger test).
●Other examination findings – In patients with bilateral vestibular dysfunction, there is loss of the vestibulo-ocular reflex, demonstrated by the presence of a catch-up saccade on the head impulse test. Loss of the vestibulo-ocular reflex leads to nystagmus and oscillopsia with head movement. Because there is no marked vestibular asymmetry, frank vertigo does not occur. (See "Evaluation of the patient with vertigo", section on 'Head impulse 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 . Nausea and vomiting are also common.
●Causes – Bilateral vestibulopathies are relatively uncommon but can be seen with drug toxicity (eg, aminoglycosides, certain chemotherapies), bilateral vestibular neuritis, and Meniere disease. An important degenerative cause is CANVAS (cerebellar ataxia, neuropathy, and vestibular areflexia syndrome) due to repeat expansions in the replication factor C subunit 1 (RFC1) gene, which typically presents in middle life with progressive imbalance, oscillopsia, sensory disturbance, and a dry cough. (See "Evaluation of the patient with vertigo", section on 'Impaired balance without vertigo' and "Overview of cerebellar ataxia in adults", section on 'Autosomal recessive ataxias'.)
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'.)
Functional gait — Functional gait, like other functional movement disorders, is defined by the occurrence of abnormal involuntary movements with characteristic clinical features (table 4) and positive signs, including variability, motor inconsistency, and incongruency (table 5).
In patients with a functional gait, walking often does not conform to any of the usual patterns observed with neurologic gait disorders. There may be excessive slowness and stiffness, knee bucking and near falls, or maintenance of postural control on a narrow base with flailing arms and excessive trunk sway. These and other features are reviewed in more detail separately. (See "Functional movement disorders", section on 'Functional gait'.)
Antalgic gait and other non-neurologic causes — Gait disorders are frequently of multifactorial origin. Non-neurologic causes may be the sole problem or mixed in with the neurologic causes .
An important non-neurologic cause of gait disorders is pain, often caused by orthopedic and rheumatologic disorders. Antalgic gait is slow and often asymmetric, as the affected individual tends to reduce the weight shift on the affected limb. A pain killer or local injection of an anesthetic agent can transiently normalize the gait, thus confirming the diagnosis.
Gait disorders can be caused by a variety of other non-neurologic conditions, including visual loss, hearing impairment, 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 goals of the history and examination are to characterize and localize the gait abnormality, understand whether it is primary or compensatory, and arrive at a gait pattern or main sign to narrow the differential diagnosis and direct further testing, if necessary (table 6).
●Chief complaint – The history may initially be vague or simply consist of one or more falls. Patients often complain of nebulous symptoms such as "weakness," "dizziness," or just plain "I can't walk."
●Time course – 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 at a major holiday the year before, or at the last family event, and ask family members to help corroborate.
●Associated symptoms – Patients should be asked about pain and fear of falling. It is also 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.
Examination — A complete neurologic examination helps to identify the predominant function interfering with normal walking (eg, weakness, motor control, sensory loss, imbalance) as well as signs of an associated neurologic disorder. Vision, hearing, and blood pressure should also be examined.
Key aspects of the gait examination include the following:
●Assess lower limbs – 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.
●Examine postural control – Postural control along the antero-posterior axis can be examined by a pull test (standing in back of the patient and exerting a sudden tug on the shoulders, and watching for a corrective step backwards). A variant of the test that is less prone to habituation and compensation is the "push-and-release" test.
●Observe walking – 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 .
Walking should be assessed at the preferred pace, but asking patients to walk faster can elicit freezing of gait or increased tone in case of spasticity. By contrast, asking patients to slow down can worsen vestibular imbalance or orthostatic tremor. If safe, gait should be assessed without walking aids as well. For example, using a walker narrows the base of support in the case of medio-lateral instability (eg, cerebellar ataxia).
Arm swing should be observed during casual walking, with attention paid to whether there is a symmetric or asymmetric reduction.
●Additional maneuvers – A variety of additional maneuvers during examination can help elicit and differentiate key features, as summarized in the table (table 7).
Recognizable gait pattern present — In some cases, a gait pattern is apparent from the neurologic examination, and further testing and diagnosis is guided by the pattern. As an example, the combination of reduced step height and length, slow walking speed, asymmetrically reduced arm swing, and stooped posture is recognized as a parkinsonian gait, and the diagnostic evaluation proceeds as it would for a patient with suspected Parkinson disease (PD). (See 'Parkinsonian gait' above.)
Further evaluation and testing vary according to the examination findings and pattern of gait (table 8):
●Leg weakness and/or spasticity – 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".)
●Higher-level gait disorder or parkinsonian gait – These patients 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 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'.)
Sign-based diagnosis — A fully recognizable gait pattern may not present at the time of initial evaluation, either because the patient is presenting early in the course, or because subtle accompanying features are overlooked due to time constraints or a superficial examination. In such cases, we suggest a sign-based approach to narrowing the differential diagnosis .
This approach can be particularly useful in patients presenting with early-stage disease. Although no single abnormal sign allows for diagnostic certainty in isolation, each comes with a specific differential diagnosis. The signs that follow are presented in the order in which they are typically observed during the neurologic examination.
●Sitting – Abnormalities observed during sitting include leaning sideways (figure 1), drifting backwards, forwards dropping of the head (disproportionate antecollis) (figure 2), and backwards dropping of the head (retrocollis). A refined differential diagnosis for each of these signs is presented in the table (table 9).
●Rising from a chair – Difficulty in rising from a chair can be further broken down into inappropriate motor strategies, needing to push off with arms, rising too quickly/recklessly, shaking of the legs upon standing, and needing to place the legs wide apart to stand. Each abnormality points to a particular differential diagnosis (table 9).
●Quiet standing – Quiet standing with eyes open can reveal a wide range of abnormalities in patients with a gait disorder, including an abnormally narrow or wide stance, excessive spontaneous sway, abnormal leaning (figure 1), and excessive trunk flexion (figure 3). Differential considerations are summarized in the table (table 10).
●Gait initiation, maintenance, and termination – Difficulty starting, stopping, or maintaining walking is usually a sign of a parkinsonian gait pattern (table 11). (See 'Recognizable gait pattern present' above.)
●Step length, height, and cadence – Abnormalities in stepping can be broken down into reduced step height, abnormally small steps, irregularly sized steps or cadence, and limping (table 11).
●Arm swing – In addition to reduced arm swing, which is seen in parkinsonism as well as a limited number of other disorders, other abnormalities in this portion of the examination that may help point to a specific disorder include excessive movements, tremor that appears during walking, and posturing of an arm (table 11).
●Movement fluidity and speed – The fluidity of walking is affected in many gait disorders. The diagnostic approach can be further refined according to the specific problem, such as stiffness/spasticity, locking or giving way of the knees, focal weakness (eg, foot drop), and excessive pelvic tilting (table 11). A fast gait is seen in a relatively limited number of disorders and can be helpful in narrowing the differential diagnosis.
●Epidemiology – Gait disorders are a major cause of functional impairment and morbidity in older adults, affecting approximately one-third of people 60 years of age and older. (See 'Epidemiology' above.)
●Clinical gait patterns
•Spastic (stiff) gait – Spasticity of the lower extremities is usually accompanied by upper motor neuron (UMN) leg weakness affecting hip flexion, foot and toe dorsiflexion, and hamstring strength. Unilateral UMN weakness and spasticity results in a hemiparetic gait with stiffness and circumduction of the affected leg, whereas bilateral spasticity usually results in a narrow, scissoring gait. (See 'Spasticity with weakness' above and 'Stiffness without weakness' above.)
•Neuropathic gait – 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. (See 'Neuropathic gait' above.)
•Myopathic gait – 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. (See 'Myopathic gait' above.)
•Parkinsonian gait – Basal ganglia disorders result in a variety of movement disorders: Dystonia causes a stiff gait while parkinsonian gait is characterized by small steps, decreased arm swing, stooped posture, and retropulsion. Parkinson disease (PD) is one of the most common causes of parkinsonism in older adults (table 1). (See 'Parkinsonian gait' above.)
•Higher-level gait disorders – "Higher-level gait disorder" refers to a failure of motor programming, in which basic motor and sensory functions are intact. Patients often have a slow gait with short stride length, disequilibrium, issues navigating obstacles, and fear of falling. (See 'Higher-level gait disorder' above.)
•Predominant imbalance or unsteadiness – Disorders of the sensory, cerebellar, and vestibular system result in gait disorders marked by imbalance and unsteadiness (table 3). (See 'Sensory ataxia' above and 'Cerebellar ataxia' above and 'Vestibular gait' above.)
•Antalgic gait – Gait disorders are frequently multifactorial in origin. Pain and rheumatologic disorders commonly contribute to abnormal gait. Antalgic gait is slow and often asymmetric, as the affected individual tends to reduce the weight shift on the affected limb. (See 'Antalgic gait and other non-neurologic causes' above.)
●Evaluation and diagnosis – The goal of the history and examination is to characterize the clinical gait pattern or most prominent abnormal sign, which narrows the etiologic diagnosis and directs further investigations (table 6). (See 'History' above and 'Examination' above.)
•Recognizable pattern present – In some cases, a gait pattern is apparent from the neurologic examination, and further testing and diagnosis is guided by the pattern (table 8). (See 'Recognizable gait pattern present' above.)
•Sign-based diagnosis – A fully recognizable gait pattern may not present at the time of initial evaluation, either because the patient is presenting early in the course, or because subtle accompanying features are overlooked due to time constraints or a superficial examination. In such cases, a sign-based approach is helpful to narrow the differential diagnosis (table 7 and table 9 and table 10 and table 11).
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Ryan R Walsh, MD, PhD, FAAN, who contributed to earlier versions of this topic review.
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