The Parkinsonian Gait & Freezing of Gait: Diagnosing Parkinson's Disease and Its Mimics Through Bedside Observation

Dr Neeraj Manikath , claude.ai

Abstract

Parkinson's disease (PD) remains a clinical diagnosis, particularly in early stages when neuroimaging is characteristically normal. The astute clinician must rely on careful observation of ambulation and execution of simple bedside tests to identify cardinal motor features. This review focuses on the systematic approach to diagnosing PD and differentiating it from mimics through gait analysis, with particular emphasis on the pathognomonic freezing phenomenon. We provide practical pearls for postgraduate physicians to enhance diagnostic accuracy at the bedside.

Introduction

Parkinson's disease affects approximately 1% of individuals over age 60, making it the second most common neurodegenerative disorder after Alzheimer's disease. Despite advances in neuroimaging, the diagnosis of PD remains fundamentally clinical, based on the UK Parkinson's Disease Society Brain Bank criteria: bradykinesia plus either rest tremor, rigidity, or postural instability. Early in the disease course, MRI and CT scans are normal, as PD is a disease of neuronal function and neurochemistry rather than gross structural pathology. The substantia nigra pars compacta loses dopaminergic neurons, but this microscopic loss is not visible on conventional imaging until very advanced stages.

The gait examination provides a wealth of diagnostic information that can be obtained in minutes without expensive technology. This review systematically approaches the bedside evaluation of parkinsonian gait, offering clinical pearls and diagnostic hacks for the busy clinician.

The Neuroanatomical Basis of Parkinsonian Gait

Understanding the pathophysiology enhances clinical observation. The basal ganglia circuitry, particularly the dopamine-depleted striatum, fails to properly facilitate movement initiation and execution. The supplementary motor area receives inadequate input, resulting in:

• Bradykinesia: Slowness and progressive decrement in amplitude and speed of repetitive movements
• Hypokinesia: Reduced amplitude of movement
• Akinesia: Difficulty initiating movement

The pedunculopontine nucleus (PPN), which receives basal ganglia output and projects to the spinal cord locomotor centers, becomes dysfunctional. This disruption particularly affects gait rhythm generation and postural reflexes, explaining both the characteristic shuffling gait and freezing phenomenon.

The Systematic Gait Examination

Part 1: Observation of Spontaneous Walking

Pearl #1: Watch the patient from the moment they rise from the waiting room chair. The most natural gait is observed when the patient is unaware they are being formally assessed.

What to Look For:

1. Initiation of Gait

• Normal individuals begin walking fluidly within 1-2 seconds
• PD patients show hesitation, often requiring multiple small preparatory steps
• Hack: Count the number of steps taken before achieving steady-state walking

2. Step Length and Height

• Parkinsonian gait: Short, shuffling steps with reduced foot clearance
• Step length typically <12 inches in moderate PD
• The shuffle creates a characteristic "skating" or "sliding" appearance
• Pearl: Measure step length by counting steps over a known distance (e.g., 10 feet). Fewer than 7 steps suggests normal gait; >12 steps indicates significant hypokinesia

3. Arm Swing

• Critical diagnostic feature: Reduced or absent arm swing, typically asymmetric
• The affected side corresponds to the side of predominant motor symptoms
• Normal arm swing arc is approximately 15-20 degrees; in PD, this reduces to <5 degrees
• Oyster: Asymmetric arm swing reduction is one of the earliest and most reliable signs of PD, often present years before diagnosis

4. Posture

• Stooped, flexed posture affecting neck, trunk, and knees
• The center of gravity shifts forward (camptocormia in severe cases)
• "Simian posture": flexed elbows, wrists, and knees
• Differential: Cervical myelopathy causes stiff, extended posture, not flexion

5. Turning

• Normal turning involves 1-2 pivoting steps
• PD patients require multiple small steps ("en bloc" turning)
• Hack: Ask the patient to turn 180 degrees and count the steps. ≥4 steps suggests parkinsonism

6. Velocity and Festination

• Reduced walking speed (normal: 1.2-1.4 m/s; PD: often <0.8 m/s)
• Festination: Involuntary acceleration with progressively shorter, faster steps as the patient "chases" their forward-displaced center of gravity
• This creates fall risk and is a poor prognostic sign

Part 2: The Pull Test for Postural Instability

Why It Matters: Postural instability is a cardinal feature but typically emerges later in disease (usually after 5-8 years). Early presence suggests atypical parkinsonism.

Technique:

1. Stand behind the patient with your arms ready to catch them
2. Warn them: "I'm going to pull you backward. Try to keep your balance."
3. Give a quick, firm pull on the shoulders, sufficient to displace them backward
4. Normal response: 0-1 step backward with recovery
5. Abnormal: ≥2 steps backward or inability to recover without assistance (retropulsion)

Pearl #2: True retropulsion involves the patient taking multiple rapid backward steps or falling directly backward like a "wooden plank." This differs from mere unsteadiness.

Oyster: If postural instability is present within the first 3 years of disease, strongly consider:

• Progressive supranuclear palsy (PSP)
• Multiple system atrophy (MSA)
• Vascular parkinsonism
• Drug-induced parkinsonism

Part 3: The Freezing Phenomenon - Pathognomonic When Present

Freezing of gait (FOG) is one of the most distinctive features of PD and a major cause of falls. It typically appears in intermediate to advanced disease but can occur earlier.

Definition: A sudden, episodic inability to generate effective forward stepping despite the intention to walk.

Clinical Presentation:

• Feet appear "glued to the floor"
• Often described by patients as "my feet just won't move"
• Duration: Typically 3-30 seconds
• Trembling movements of the legs may be visible without forward progression

When and Where to Look for Freezing:

1. Start hesitation: When initiating gait from standing
2. Turn freezing: While turning (most common trigger)
3. Destination freezing: When approaching a target (chair, doorway)
4. Narrow space freezing: Navigating doorways, crowded spaces
5. Dual-task freezing: Walking while talking or carrying objects

The Doorway Test - Essential Clinical Maneuver:

• Have the patient walk through a standard doorway
• Watch for sudden arrest of forward motion at the threshold
• Hack: Place visual markers (tape on floor) before the doorway. Freezing disrupts the ability to step over these cues

Pearl #3: Ask about freezing during the history. Patients may not volunteer this symptom but will confirm when asked specifically: "Do your feet ever feel stuck to the floor when you're trying to walk?"

Sensory Tricks for FOG (valuable diagnostic and therapeutic information):

• Marching to a beat or counting
• Stepping over an object or line
• Using a laser pointer or walking stick
• These tricks engage alternative motor pathways, bypassing dysfunctional basal ganglia circuits

Differential Diagnosis of Freezing: While FOG is strongly associated with PD, consider:

• PSP: Freezing with prominent vertical gaze palsy and axial rigidity
• MSA: Freezing with cerebellar signs and autonomic failure
• Vascular parkinsonism: Lower-body predominant with step-to-step variability
• Normal pressure hydrocephalus: Magnetic gait (feet stick but can slide), incontinence, dementia

Differentiating Parkinson's Disease from Essential Tremor

This distinction is critical, as treatment and prognosis differ dramatically.

Tremor Characteristics

Parkinson's Disease Tremor:

• Rest tremor: 4-6 Hz, present when limb is completely at rest, disappears with action
• Asymmetric: Often begins unilaterally, may remain asymmetric for years
• "Pill-rolling": Classic thumb-finger opposition movement
• Re-emergent tremor: After holding arms extended (postural position), tremor reappears after 5-10 seconds
• Location: Typically hands, may involve chin, rarely head

Pearl #4: Have the patient walk while observing the hands. PD tremor is most prominent when arms hang at rest during walking.

Essential Tremor:

• Action/postural tremor: 6-12 Hz, present with sustained posture or movement
• Symmetric: Bilateral from onset
• Locations: Hands (bilateral), head (yes-yes or no-no movements), voice
• No pill-rolling: Simple flexion-extension or pronation-supination
• Alcohol responsive: Improves with alcohol consumption (60-70% of cases)
• Family history: Autosomal dominant pattern in ~50%

Gait in Essential Tremor

Critical Pearl #5: Gait is NORMAL in essential tremor. The presence of shuffling, reduced arm swing, or postural instability rules out pure essential tremor.

Oyster: Approximately 20% of ET patients eventually develop PD. If gait abnormalities emerge in someone with longstanding ET, consider evolving parkinsonism.

The Extended Bedside Examination

Additional maneuvers to enhance diagnostic accuracy:

1. Finger tapping test: Ask patient to tap thumb and index finger together as rapidly and widely as possible. Look for progressive decrement in amplitude and speed (characteristic of PD).

2. Observe facial expression: Hypomimia (reduced facial expression) or "masked facies" is present in 70% of PD patients at diagnosis.

3. Listen to speech: Hypophonic (soft), monotonous speech with reduced inflection suggests PD.

4. Check for cogwheel rigidity: Passive movement of the wrist reveals ratchet-like resistance, especially with reinforcement (have patient move opposite limb).

Atypical Parkinsonism: Red Flags

While PD is the most common cause of parkinsonism, recognizing atypical features prevents misdiagnosis:

Progressive Supranuclear Palsy (PSP)

• Hallmark: Vertical gaze palsy (especially downward gaze)
• Gait: Erect or extended posture (not flexed), freezing early, frequent falls
• Axial > limb rigidity
• Poor response to levodopa
• "Rocket sign": Suddenly standing from chair without using arms

Multiple System Atrophy (MSA)

• Autonomic failure: Severe orthostatic hypotension, urinary incontinence
• Cerebellar signs: Ataxia, dysarthria, nystagmus
• Symmetrical parkinsonism
• Anterocollis: Severe forward neck flexion
• Poor levodopa response

Vascular Parkinsonism

• Lower body predominant: "Lower-body parkinsonism"
• Stepwise progression with clear relationship to vascular events
• Vascular risk factors: Hypertension, diabetes, smoking
• Gait: Wide-based, shuffling, "magnetic" (feet don't lift off ground)
• Upper extremity function relatively preserved
• MRI: Multiple lacunar infarcts, white matter changes

Drug-Induced Parkinsonism

• History is key: Typical culprits include:
  • Antipsychotics (especially typical neuroleptics)
  • Antiemetics (metoclopramide, prochlorperazine)
  • Calcium channel blockers (cinnarizine, flunarizine)
  • Valproate
• Symmetrical presentation (bilateral from onset)
• Rapid onset (weeks to months after drug initiation)
• Reversibility: Improves weeks to months after drug discontinuation (may take 6-12 months)

Pearl #6: In drug-induced parkinsonism, rest tremor is uncommon. Predominance of rigidity and bradykinesia suggests drug etiology.

Lewy Body Dementia: The Gait Connection

When parkinsonian gait is accompanied by cognitive fluctuations, visual hallucinations, and REM sleep behavior disorder, consider dementia with Lewy bodies (DLB). The gait features are identical to PD, but cognitive symptoms precede or occur within 1 year of motor symptoms (versus PD dementia where motor symptoms precede cognitive decline by >1 year).

Clinical Pearls and Diagnostic Hacks: Summary

1. The "Coat Test": Watch how the patient removes their coat in the examination room. Asymmetric slowness and reduced fluidity on one side suggests PD.

2. The "Smartphone Test": Observe how the patient retrieves and uses their phone. Fine motor slowing, tremor at rest, and difficulty with small buttons are revealing.

3. Quantify the turn: Count steps during 180-degree turn. Normal = 1-3 steps; PD = 4-8+ steps.

4. The "Two-Task Test": Have patient walk while performing a cognitive task (serial 7s, naming animals). Gait freezing or marked worsening suggests PD.

5. Asymmetry is your friend: PD begins asymmetrically in 75% of cases. Symmetric parkinsonism from onset suggests alternative diagnosis.

6. Response to levodopa: While not a bedside test per se, robust response to levodopa (>30% improvement in UPDRS motor score) strongly supports PD diagnosis. Atypical parkinsonism typically shows poor or absent response.

7. The "10-meter walk test": Time the patient walking 10 meters at their comfortable pace. <7 seconds = normal; >12 seconds = significant gait impairment.

8. Check for orthostatic hypotension: A drop of ≥20/10 mmHg suggests autonomic dysfunction, more common in MSA than PD.

Special Populations

Young-Onset PD (Age <50)

• More likely to have genetic forms (PINK1, Parkin, LRRK2)
• Prominent dystonia (sustained muscle contractions)
• Slower progression
• More levodopa-induced dyskinesias over time

Elderly Patients

• Distinguishing from "senile gait" (cautious, wide-based due to fear of falling)
• Vascular parkinsonism more common
• Polypharmacy increases risk of drug-induced parkinsonism

When Imaging IS Helpful

While structural MRI is normal in early PD, certain imaging can support diagnosis:

• DaTscan (Ioflupane I-123 SPECT): Shows reduced dopamine transporter uptake in PD, PSP, MSA, CBD but is NORMAL in essential tremor, drug-induced parkinsonism, and psychogenic parkinsonism. Useful in diagnostically uncertain cases.

• MRI in atypical parkinsonism:

  • PSP: Midbrain atrophy ("hummingbird sign")
  • MSA: Putaminal atrophy with T2 hyperintensity, "hot cross bun" sign in pons
  • Vascular: Lacunar infarcts, white matter disease

Prognosis and Natural History

Understanding disease trajectory helps interpret examination findings:

• Early PD (0-5 years): Asymmetric tremor, bradykinesia, good medication response
• Intermediate PD (5-10 years): Motor fluctuations, dyskinesias, freezing emerges, postural instability begins
• Advanced PD (>10 years): Axial symptoms dominate (freezing, falls, dysphagia, dysarthria), cognitive decline, medication becomes less effective

Oyster: Hoehn and Yahr staging based on gait and balance:

• Stage 1: Unilateral, no balance impairment
• Stage 2: Bilateral, no balance impairment
• Stage 3: Balance impairment, physically independent
• Stage 4: Severe disability, able to stand/walk unassisted
• Stage 5: Wheelchair-bound or bedridden

Conclusion

The bedside gait examination remains the cornerstone of PD diagnosis. Through systematic observation of step length, arm swing, posture, turning, and specific testing for postural instability and freezing, the skilled clinician can diagnose PD and distinguish it from mimics without advanced imaging. The asymmetric presentation, characteristic rest tremor, and freezing phenomenon are pathognomonic when present. As postgraduate physicians, developing expertise in these bedside skills enhances diagnostic accuracy and ensures early, appropriate management of this common and disabling disorder.

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