Gait is the most integrated test in the neurological examination. To walk normally, a patient needs intact strength, intact tone, intact sensation, intact cerebellar coordination, intact basal ganglia automaticity, intact vestibular function, intact attention and motor planning, and intact musculoskeletal structure. A disturbance at any one level disturbs the gait, often in a distinctive way. The examiner who watches a patient walk from the doorway to the chair has performed a coordinated test of the entire nervous system in fifteen seconds.

This page is a catalog of gait abnormalities organized by phenomenology, with the localization and differential each pattern implies. The principle throughout: the gait is the diagnosis in many neurological diseases, and the bedside exam consists of watching the patient walk before, during, and after the rest of the testing.

The Components of Normal Gait

Normal walking has several mechanical components, each of which can fail independently:

• Initiation: starting from a standstill, the patient leans slightly forward, the center of mass shifts, and the first step is taken. Initiation can fail in frontal disease and in parkinsonism (start hesitation, freezing).
• Stance and swing: each leg alternates between supporting the body weight (stance) and swinging forward (swing). The swing phase requires hip flexion, knee flexion, ankle dorsiflexion, and adequate clearance of the foot from the floor.
• Stride length and cadence: distance per step and steps per minute. Either can be reduced in different patterns of disease.
• Base width: the distance between the feet during gait. Narrow base is normal; widening of the base reflects compensation for instability.
• Arm swing: reciprocal arm swing accompanies the contralateral leg movement, providing rotational balance. Reduced arm swing is one of the earliest signs of unilateral parkinsonism.
• Turning: smooth turning requires coordinated stepping and trunk rotation. Many gait disorders affect turning before they affect straight-line walking.
• Postural reflexes: rapid corrective responses to perturbation, tested by the pull test (see Pyramidal vs Extrapyramidal).

How to Observe Gait

The gait exam should include:

1. Watching the patient walk normally across the room. Observe stance, posture, base width, stride, arm swing, and the symmetry of all of these.
2. Watching the patient turn — typically by asking them to stop and turn around. Many gait disorders show abnormality on turning that is absent on straight walking.
3. Asking the patient to walk on the toes and on the heels. Toe walking tests gastrocnemius-soleus function (and S1); heel walking tests tibialis anterior function (and L5).
4. Tandem gait: heel-to-toe walking along an imaginary line. Sensitive to mild cerebellar disease, sensory ataxia, and vestibular dysfunction.
5. The pull test for postural reflexes. Stand behind the patient, warn them, then pull firmly backward at the shoulders. Normal: one or two backward steps with rapid recovery. Abnormal: multiple uncontrolled backward steps (retropulsion) or a fall.
6. Romberg: standing with feet together, eyes open then closed. Sensory and vestibular contributions to balance.

Catalog of Gait Patterns

Hemiplegic Gait

The patient with a hemiparetic stroke develops a characteristic gait. The affected arm is held flexed at the elbow and the wrist, often pressed against the chest. The affected leg is held in extension, with the knee unbent and the foot in plantar flexion. To advance the affected leg, the patient swings it outward in an arc (circumduction) — flexion is not possible, so the leg is moved laterally around the body, and the foot is dragged along the floor. The classical posture combined with the circumducting gait is unmistakable.

The localization is contralateral upper motor neuron lesion — most often a stroke involving the motor cortex or its corticospinal projections.

Spastic Paraparetic Gait (Scissoring Gait)

Bilateral leg spasticity, most commonly from cord disease (hereditary spastic paraplegia, MS, cervical myelopathy, traumatic injury, vascular myelopathy), produces a stiff, narrow-based gait with each leg crossing over the midline of the body — the “scissoring” pattern. The toes scrape the floor, the feet are turned inward (equinovarus), and progress is slow. The classical gait of advanced bilateral upper motor neuron disease.

Parkinsonian Gait

Several features together make the parkinsonian gait one of the most recognizable in neurology:

• Stooped posture: trunk and head flexed forward; arms slightly flexed and held closer to the body.
• Reduced arm swing: classically asymmetric, with the side that first developed parkinsonism showing less swing.
• Short, shuffling steps: stride length is reduced; the feet barely clear the floor.
• Festination: a peculiar acceleration in which the patient takes progressively shorter and faster steps as if chasing their center of gravity — the upper body leans forward and the legs hurry to catch up.
• Start hesitation and freezing: the patient cannot initiate the first step (start hesitation), or stops abruptly mid-gait, often at doorways, on turning, or when crossing a marked line on the floor (freezing of gait). Sometimes the patient is “magnetically” stuck to the floor.
• En bloc turning: the patient turns by taking many small steps, with the head and body moving as a unit rather than the head leading the body.

Asymmetric reduction in arm swing is often the earliest gait sign and may be present years before formal parkinsonism is recognized.

Cerebellar (Ataxic) Gait

Wide-based, unsteady, irregular gait. Each step is variable in length and direction, and the patient sways from side to side. Turning is particularly impaired. The patient compensates with a wider base and often uses the walls or furniture for support.

Specific patterns within cerebellar gait reflect the cerebellar region involved:

• Midline cerebellar disease (vermis): predominant gait and truncal ataxia, with relatively preserved limb coordination. Classic alcoholic cerebellar degeneration.
• Cerebellar hemisphere disease: unilateral limb ataxia and a tendency to veer toward the side of the lesion.
• Pancerebellar disease: combined truncal, gait, and bilateral limb ataxia.

Sensory Ataxic Gait

Loss of proprioception produces a gait with two cardinal features:

• Wide base for stability without proprioceptive feedback.
• Slapping (steppage) quality: the patient lifts the foot high, throws it forward, and slaps it down, watching it land. The foot does not know where it is until contact with the ground.
• Eyes on the floor: vision substitutes for proprioception.
• Dramatic worsening in the dark or with eyes closed: the patient may be unable to walk at all.

The differential includes B12 deficiency (subacute combined degeneration), tabes dorsalis, large-fiber sensory neuropathy, sensory neuronopathy (paraneoplastic, Sjögren), and chronic dorsal column disease of any cause.

Steppage Gait (Foot Drop)

The patient with foot drop cannot dorsiflex the foot during the swing phase. To clear the foot from the floor, they lift the entire leg higher than normal (excessive hip and knee flexion). The foot slaps the floor as it lands because of weak dorsiflexion control. Foot drop can be unilateral (common peroneal nerve palsy, L5 radiculopathy) or bilateral (peripheral neuropathy, Charcot-Marie-Tooth disease, distal myopathy).

Steppage gait without sensory loss suggests a pure motor lesion (anterior horn cell disease, motor neuropathy); with sensory loss in L5 distribution, the cause is more likely radicular or peripheral.

Waddling (Trendelenburg) Gait

Bilateral proximal lower extremity weakness — typically from myopathy — produces a characteristic side-to-side waddling gait. The patient cannot stabilize the pelvis during the stance phase, so the contralateral hip drops with each step; the patient compensates by leaning the trunk over the weight-bearing leg. The result is a rolling, “duck-like” gait. The pattern is classic for hip girdle weakness from muscular dystrophy, polymyositis, and other proximal myopathies, and can also be seen in bilateral hip joint disease (where it is mechanical rather than neurological).

Frontal Gait (Gait Apraxia)

Bilateral frontal disease produces a distinctive gait pattern often called gait apraxia or “magnetic gait.” Features:

• Difficulty initiating gait: the patient stands ready to walk but cannot start. The feet feel “stuck” to the floor.
• Short, shuffling steps with a wide base (in contrast to the narrow-based parkinsonian gait).
• Freezing and start hesitation: similar to parkinsonism but with a wider base and often more dramatic.
• Preserved leg strength with the patient lying down: the patient can pedal a bicycle motion with the legs while supine, yet cannot walk.
• Often combined with apathy, urinary incontinence, and cognitive decline.

The combination of gait apraxia, dementia, and urinary incontinence is the classical triad of normal pressure hydrocephalus — a potentially reversible cause of dementia. Other causes of frontal gait include bilateral subcortical small-vessel disease (vascular dementia, “lower-half parkinsonism”) and frontal lobe tumor.

Antalgic Gait

Pain in a lower extremity produces a limping gait in which the stance phase on the painful leg is shortened. The patient appears to hurry off the painful leg as quickly as possible. The gait is mechanical, not neurological — it tells you the patient has pain (hip osteoarthritis, knee pain, plantar fasciitis, fracture) rather than weakness.

Functional (Non-Organic) Gait

Functional gait disorders have characteristic features:

• Astasia-abasia: dramatic difficulty standing and walking that is out of proportion to any apparent weakness on supine examination. The patient may stagger violently across the room without falling, displaying remarkable preserved balance through “near-fall” maneuvers.
• Variable severity: dramatic worsening when observed, improvement when distracted.
• Sudden buckling of the knees during gait, with rapid recovery before falling.
• Atypical patterns: tightrope walking, dragging a “weak” leg behind without true foot drop posture, walking with extreme effort that is not matched by signs of effort (no muscle bulging, no facial expression of strain).
• Inconsistency: a patient who cannot walk on examination may walk normally when leaving the office.

The diagnosis is made on positive features (the inconsistencies, the dramatic preserved balance) rather than exclusion. Functional gait disorders are common, often respond to physical therapy and education, and deserve specific recognition.

Vestibular (Drunken) Gait

Vestibular ataxia from acute peripheral or central vestibular dysfunction produces a gait that veers toward the side of the lesion. The patient may stagger, lurch, or refuse to walk at all if vertigo is severe. Unlike cerebellar ataxia, vestibular gait often improves with visual cues, and the Romberg may show falling toward the side of the lesion.

Special Gait Patterns to Recognize

Chorea-Related Gait

Patients with Huntington disease and other choreiform disorders develop a “dancing” gait — irregular, lurching steps with superimposed choreic movements. The patient may incorporate the chorea into apparent voluntary movements (parakinesia). Distinguishable from cerebellar ataxia by the presence of involuntary movements at rest and the irregular, non-rhythmic quality.

Dystonic Gait

Dystonia can produce striking gait abnormalities. Generalized dystonia produces twisted postures during walking, with the trunk and limbs assuming sustained abnormal positions. Lower extremity dystonia, particularly inverted foot posturing during gait (action-induced dystonia), can be the presenting feature of childhood-onset dystonia, especially dopa-responsive dystonia. Recognition is important because childhood-onset dystonia warrants a levodopa trial.

The Lower-Half Parkinsonism Pattern

Gait abnormality predominates over upper extremity bradykinesia in lower-half parkinsonism. The pattern often reflects bilateral subcortical disease: small vessel ischemic disease producing vascular parkinsonism, normal pressure hydrocephalus, or atypical parkinsonism. The arms swing relatively normally while the gait is shuffling and freezing. Levodopa is often less effective than in idiopathic Parkinson disease.

Marche à Petits Pas

“Walking with small steps” — a pattern of bilateral cerebrovascular disease in which the patient walks with very small, shuffling steps, often with a wide base and minimal arm swing. Closely related to vascular parkinsonism and lower-half parkinsonism.

Cautious Gait

Many patients with fear of falling, regardless of underlying disease, develop a cautious gait: wide base, slow speed, short steps, arms slightly abducted, looking at the floor. This is not a specific neurological pattern but rather a behavioral response to instability. Often present in older patients with multiple sensory deficits (presbyopia, presbycusis, mild peripheral neuropathy, mild cognitive impairment) — the “multifactorial gait disorder of aging.”

Summary Table

🔍 Did You Know?

Asymmetric reduction in arm swing during gait can precede the formal diagnosis of Parkinson disease by several years. It is one of the earliest motor signs and is often noticed by the patient’s spouse before any tremor, bradykinesia, or rigidity is apparent on examination. A patient whose left arm swings less than the right, who later develops unilateral hand tremor at rest, is showing the natural history of asymmetric Parkinson disease.

Pitfalls and Pearls

• Watch the patient walk into the room. Many gait diagnoses are obvious before the patient sits down.
• Always assess turning. Many gait disorders manifest on turning when straight-line walking looks normal.
• The pull test predicts falls. A patient who retropulses or falls on the pull test has substantially increased fall risk.
• Wide base + slapping + dramatic Romberg = sensory ataxia. Check vibration, joint position sense, and B12.
• Wide base + irregular + only mildly worse with eyes closed = cerebellar ataxia. Look for nystagmus, dysmetria, dysarthria.
• Narrow base + stooped + shuffling + freezing = parkinsonism. Check for tremor, cogwheeling, asymmetry.
• Wide base + shuffling + start hesitation + preserved strength supine = frontal gait apraxia. Look for the rest of the NPH triad (incontinence, cognitive decline).
• Asymmetric reduction in arm swing is the earliest sign of parkinsonism in many patients. Watch every patient walk past you.
• Functional gait has positive features. Astasia-abasia, dramatic balance preservation, inconsistency are positive signs, not exclusion.
• Childhood-onset dystonia with action-induced foot inversion deserves a levodopa trial (dopa-responsive dystonia).
• NPH gait is treatable. Always consider NPH in an older patient with gait apraxia, urinary incontinence, and cognitive decline; the response to lumbar puncture trial can be diagnostic and the response to shunting can be life-changing.

References

1. Campbell WW. DeJong’s The Neurologic Examination. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 44.
2. Nutt JG, Marsden CD, Thompson PD. Human walking and higher-level gait disorders, particularly in the elderly. Neurology. 1993;43(2):268-279.
3. Snijders AH, van de Warrenburg BP, Giladi N, Bloem BR. Neurological gait disorders in elderly people: clinical approach and classification. Lancet Neurol. 2007;6(1):63-74.
4. Stolze H, Klebe S, Zechlin C, et al. Falls in frequent neurological diseases: prevalence, risk factors and aetiology. J Neurol. 2004;251(1):79-84.
5. Stone J, Carson A. Functional neurological disorders: the neurological assessment as treatment. Pract Neurol. 2016;16(1):7-17.
6. Marsden CD, Thompson PD. The disorders of gait. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, eds. Neurology in Clinical Practice. 4th ed. Butterworth-Heinemann; 2004.