The Parkinsonian Gait & Freezing of Gait: A Bedside Clinical Review

Diagnosing Parkinson's Disease and Its Mimics Through Observation of Ambulation

Dr Neeraj Manikath , claude.ai

Introduction

Parkinson's disease (PD) remains a fundamentally clinical diagnosis, requiring astute bedside observation and examination skills. While neuroimaging has revolutionized the diagnosis of many neurological conditions, magnetic resonance imaging (MRI) is characteristically normal in early PD, and dopamine transporter (DAT) scanning, though useful, is not universally available or necessary for diagnosis. The cornerstone of PD diagnosis rests on recognizing the cardinal motor features: bradykinesia, rigidity, resting tremor, and postural instability. Among these, gait abnormalities are often the most visible and diagnostically revealing manifestations, making them an invaluable tool for the astute clinician.

This review focuses on the detailed bedside assessment of parkinsonian gait and the phenomenon of freezing of gait (FOG), providing practical guidance for postgraduate trainees in internal medicine to confidently diagnose PD and differentiate it from its mimics through careful observation of ambulation.

Why Diagnosis is Clinical: The Primacy of Bedside Assessment

The diagnosis of PD is established using the UK Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria, which require the presence of bradykinesia plus at least one of the following: muscular rigidity, 4-6 Hz resting tremor, or postural instability not caused by primary visual, vestibular, cerebellar, or proprioceptive dysfunction. Notably, these criteria are entirely clinical, with no requirement for laboratory or imaging confirmation.

Structural neuroimaging (CT or MRI) in PD is typically normal or may show only age-appropriate changes. Its primary utility lies in excluding alternative diagnoses such as normal pressure hydrocephalus, vascular parkinsonism, or structural lesions. Functional imaging with DAT scanning can support the diagnosis by demonstrating reduced dopaminergic uptake in the striatum, but it cannot distinguish PD from atypical parkinsonian syndromes. Therefore, the bedside examination remains the gold standard, and mastery of gait observation is essential.

The Parkinsonian Gait: Key Features

1. Bradykinesia in Ambulation

Bradykinesia, defined as slowness of movement with progressive decrement in amplitude and speed during repetitive actions, is the sine qua non of parkinsonism. During ambulation, this manifests as:

• Reduced stride length: Steps become progressively shorter, creating a characteristic shuffling pattern
• Decreased velocity: Overall walking speed is markedly reduced
• Lack of automatic movements: The normal rhythmic, coordinated quality of gait is lost

Pearl: Bradykinesia is not merely slowness—it is the combination of slowness plus amplitude decrement. Ask the patient to walk faster; a parkinsonian patient will increase cadence but not stride length, resulting in rapid, tiny steps.

2. Shuffling Steps and Reduced Ground Clearance

Patients with PD exhibit reduced foot clearance during the swing phase of gait, leading to a shuffling quality where the feet barely leave the ground. This increases fall risk and produces the characteristic "scraping" sound of parkinsonian gait. The steps are not only short but also lack the normal heel-strike pattern, instead showing a flat-footed or forefoot contact.

3. Reduced Arm Swing (Often Asymmetric)

Healthy individuals display automatic, reciprocal arm swing during walking, which is lost early in PD. This reduction is often asymmetric, affecting the side ipsilateral to the more severely affected limbs.

Hack: Observe the patient walking toward you and away from you. The asymmetric reduction in arm swing is often more apparent when viewing from behind. The arm may appear "glued" to the side or may show only minimal movement at the shoulder with the elbow held in slight flexion.

Oyster: Unilateral reduction in arm swing may be the earliest motor sign of PD, appearing months to years before other symptoms become apparent. Always ask about the side with reduced arm swing—patients often report symptoms began on that side.

4. Stooped Posture (Flexed Posture)

Patients with PD characteristically adopt a flexed posture with:

• Forward flexion of the trunk (camptocormia in severe cases)
• Flexion at the hips and knees
• Head held in forward flexion
• Shoulders rounded forward

This posture shifts the center of gravity anteriorly, contributing to festination (see below) and fall risk.

5. Festination

Festination describes the phenomenon where the patient's steps become progressively faster and shorter as they walk, as if they are "chasing their center of gravity." This occurs because the forward-flexed posture places the center of mass ahead of the base of support, compelling the patient to take rapid, small steps to prevent falling. It is particularly evident when patients accelerate or walk down an incline.

Pearl: Festination is not voluntary acceleration—it represents a failure of postural control. Patients may appear unable to stop themselves and may collide with walls or furniture.

6. Turning "En Bloc"

Healthy individuals pivot smoothly when turning, with sequential rotation of the head, trunk, and lower body. Patients with PD turn "en bloc" (as a unit), requiring multiple small steps to complete a 180-degree turn. This takes longer and appears stiff and awkward.

Hack: Ask the patient to turn 360 degrees. Count the steps required—more than 4 steps suggests parkinsonism. This simple maneuver is both sensitive and specific for PD.

Freezing of Gait: Pathognomonic for Parkinsonism

Freezing of gait (FOG) is one of the most striking and diagnostically valuable phenomena in PD. It describes a sudden, transient inability to initiate or continue walking, during which the feet appear "glued to the floor." Patients may exhibit trembling or shuffling movements in place but cannot generate effective forward propulsion.

Clinical Characteristics of FOG

FOG episodes typically last seconds to minutes and occur in specific situations:

1. Start hesitation: Difficulty initiating the first step from standing
2. Turn hesitation: Freezing during turns, particularly in tight spaces
3. Destination hesitation: Freezing as the patient approaches a target (e.g., a chair or doorway)
4. Narrow spaces: Freezing when passing through doorways, between furniture, or in crowded areas

Pearl: During FOG, patients may demonstrate "trembling in place" with rapid, small-amplitude leg movements but no forward progression. The upper body may continue moving forward while the feet remain frozen, increasing fall risk.

The Doorway Test

Observing the patient walk through a doorway is perhaps the single most valuable maneuver for detecting FOG. Narrow spaces, particularly doorways, are powerful triggers for freezing.

Bedside Protocol:

1. Position yourself to observe the patient from the side
2. Ask them to walk through a standard doorway
3. Watch for hesitation, multiple attempts to step, or complete arrest of forward motion as they approach or enter the doorway
4. Note whether they can overcome the freeze spontaneously or require cueing

Hack: If no doorway is available, place two chairs 2-3 feet apart and ask the patient to walk between them. This simulates a narrow passage and may provoke freezing.

Cueing and FOG

A remarkable feature of FOG is its responsiveness to external cues. Patients who are frozen may suddenly begin walking in response to:

• Visual cues (stepping over a line or object)
• Auditory cues (marching to a rhythm or countdown)
• Tactile cues (touching their leg)
• Cognitive strategies (counting steps aloud)

This responsiveness to cueing helps differentiate FOG from weakness, apraxia, or musculoskeletal causes of gait difficulty.

Clinical Pearl: If you observe freezing, place your foot in front of the patient's foot as a visual target to step over. Many patients will immediately unfreeze and step over your foot. This dramatic response confirms the diagnosis and can be taught to caregivers.

The Pull Test: Assessing Postural Instability

Postural instability is a late feature of PD but is crucial for staging disease severity and fall risk assessment. The pull test is the standardized method for evaluating this feature.

Performing the Pull Test

1. Position: Stand behind the patient with your hands ready to catch them
2. Warn the patient: Explain that you will pull them backward and they should maintain balance
3. Execute: Give a quick, firm pull on both shoulders, sufficient to displace the center of mass
4. Observe the response:
   • Normal: Patient takes 1-2 steps backward or none, recovering balance
   • Abnormal: Patient takes >2 steps backward (retropulsion)
   • Severely abnormal: Patient would fall without being caught

Safety Warning: Always be prepared to catch the patient. Position yourself with a wide stance and ensure adequate space behind the patient.

Oyster: The pull test assesses retropulsion (tendency to fall backward), but patients with PD may also exhibit propulsion (tendency to fall forward) or lateropulsion (tendency to fall sideways). Observe for these during normal walking as well.

Pearl: True retropulsion should be distinguished from taking backward steps intentionally. In true retropulsion, the patient appears unable to generate corrective forward movement and may continue stepping backward with increasing speed (analogous to festination but in reverse).

Differential Diagnosis: Parkinsonian Mimics

Several conditions can produce gait abnormalities that superficially resemble PD. Careful observation of specific features helps differentiate these mimics.

1. Vascular Parkinsonism (Lower Body Parkinsonism)

Key Features:

• Gait abnormality disproportionately affects the lower body
• Relatively preserved arm swing
• Wide-based gait (unlike PD)
• Magnetic gait: feet appear "stuck to the floor" throughout the gait cycle (not episodic like FOG)
• MRI shows extensive white matter disease or lacunar infarcts
• Poor or absent response to levodopa

Pearl: Think of vascular parkinsonism as "parkinsonism from the waist down." If arm swing is normal but gait is severely affected, consider this diagnosis.

2. Normal Pressure Hydrocephalus (NPH)

Key Features:

• Classic triad: gait apraxia, urinary incontinence, cognitive impairment ("wet, wacky, and wobbly")
• Magnetic gait with wide base
• Difficulty initiating gait (start hesitation)
• Preserved arm swing
• MRI shows ventriculomegaly out of proportion to sulcal atrophy
• May respond to large-volume lumbar puncture or shunting

Hack: Ask about urinary symptoms. While FOG and magnetic gait appear similar, the presence of urge incontinence or frequency strongly suggests NPH rather than PD.

3. Progressive Supranuclear Palsy (PSP)

Key Features:

• Vertical supranuclear gaze palsy (especially downgaze)
• Erect or extended posture (unlike PD's flexed posture)
• Prominent early falls (backward falls are characteristic)
• Axial > limb rigidity
• Absent or minimal tremor
• Poor response to levodopa

Pearl: The "applause sign" can help differentiate PSP from PD. Ask the patient to clap three times as quickly as possible. PSP patients often continue clapping beyond three times (perseveration), whereas PD patients may have difficulty initiating the movement but can accurately perform three claps.

4. Multiple System Atrophy (MSA)

Key Features:

• Prominent early autonomic dysfunction (orthostatic hypotension, urinary retention/incontinence)
• Cerebellar signs (ataxia, dysmetria)
• Stridor or inspiratory sighs
• Symmetrical parkinsonism (unlike PD's typical asymmetry)
• Poor or unsustained response to levodopa

Oyster: MSA patients may initially respond to levodopa but typically lose this response within 2-3 years. Always check orthostatic vital signs in patients with parkinsonism.

5. Drug-Induced Parkinsonism

Key Features:

• Symmetrical involvement (classic feature)
• History of exposure to dopamine-blocking agents (antipsychotics, metoclopramide, prochlorperazine)
• Absence of resting tremor (tremor, if present, is often postural)
• May improve with discontinuation of offending agent (may take months)

Common culprits: metoclopramide (Reglan), prochlorperazine (Compazine), haloperidol, risperidone, valproic acid, lithium

Hack: Always obtain a detailed medication history, including over-the-counter medications and recent exposures. Patients may not volunteer use of antiemetics received in urgent care or emergency settings.

Differentiating PD from Essential Tremor

This distinction is critical as the treatments and prognoses differ substantially.

Feature	Parkinson's Disease	Essential Tremor
Tremor Type	Resting, "pill-rolling"	Action/postural/kinetic
Symmetry	Asymmetric	Symmetric
Affected Areas	Hands, legs, chin; rarely head	Hands, head, voice
Response to Action	Decreases or disappears	Increases or persists
Response to Alcohol	None	Often dramatic improvement
Gait	Shuffling, reduced arm swing	Normal (may have mild ataxia)
Bradykinesia	Present	Absent
Family History	10-15%	50-70% (autosomal dominant)

Pearl: The finger-to-nose test is revealing. PD tremor diminishes or disappears during the movement (kinetic tremor absent), whereas essential tremor worsens as the finger approaches the nose (intention component). Additionally, having the patient hold their arms outstretched will reveal the postural tremor of essential tremor but not provoke significant tremor in early PD.

Oyster: Some patients have both conditions. The coexistence of a resting tremor plus a postural tremor should raise suspicion for this scenario rather than defaulting to a single diagnosis.

Practical Bedside Examination Protocol

A systematic approach ensures no critical features are missed:

1. Observe from the waiting room: Watch the patient rise from the chair and walk toward the examination room. This "unguarded moment" often reveals the most natural gait pattern.

2. Formal gait assessment:

   • Ask the patient to walk at their normal pace down a hallway (at least 10 meters if possible)
   • Observe from multiple angles: front, side, and behind
   • Note: speed, stride length, arm swing, posture, foot clearance
   • Have them turn 360 degrees and count the steps

3. Test for freezing:

   • Walk through a doorway
   • Navigate around furniture or obstacles
   • Start and stop on command
   • Perform dual-tasking (count backward while walking)

4. Pull test: As described above

5. Assess other cardinal features:

   • Observe for resting tremor while the patient is distracted (e.g., counting backward)
   • Test rigidity at wrist and elbow (look for cogwheeling)
   • Assess finger-tapping, hand opening/closing, and rapid alternating movements for bradykinesia

6. Examine eye movements: Critical for identifying PSP and other mimics

7. Check orthostatic vital signs: Essential if considering MSA or vascular causes

Treatment Pearls for Gait Disturbances in PD

While a comprehensive discussion of PD treatment is beyond the scope of this review, several points are relevant to gait dysfunction:

Levodopa responsiveness: Classical PD features (bradykinesia, rigidity, resting tremor) typically respond well to levodopa. However, FOG and postural instability are often levodopa-resistant or may even worsen with treatment, particularly in advanced disease. This is a red flag distinguishing true PD from drug-induced parkinsonism or vascular parkinsonism.

Physical therapy: Gait training with cueing strategies is highly effective for FOG. Patients can be taught to use visual cues (laser canes, floor markers) or auditory cues (metronomes, rhythmic music) to overcome freezing.

Medication timing: FOG may be "off-period" freezing (occurring when medication wears off) or "on-period" freezing (occurring despite adequate medication). Off-period freezing may improve with medication optimization, whereas on-period freezing requires non-pharmacological strategies.

Conclusion

The parkinsonian gait and freezing of gait are rich sources of diagnostic information that can be fully appreciated through careful bedside observation. In an era increasingly dominated by advanced imaging and biomarkers, the clinical examination remains supreme in the diagnosis of PD. The ability to recognize subtle asymmetries in arm swing, identify FOG during doorway navigation, and properly perform and interpret the pull test separates the excellent clinician from the average one.

For the postgraduate trainee in internal medicine, mastery of these skills provides not only diagnostic confidence but also a foundation for understanding disease progression, fall risk assessment, and treatment response. The bedside remains the ultimate diagnostic tool, and the observant eye the most sophisticated technology available.

Key Clinical Pearls Summary

1. Asymmetric reduced arm swing may be the earliest sign of PD—always observe from behind
2. FOG is provoked by doorways—this is the single best bedside test
3. >4 steps to turn 360 degrees suggests parkinsonism
4. Retropulsion on pull test indicates significant postural instability and high fall risk
5. Symmetry suggests drug-induced or vascular parkinsonism, not idiopathic PD
6. Preserved arm swing with severe gait disturbance suggests lower body parkinsonism (vascular or NPH)
7. External cues can "break" freezing—teach this to patients and families
8. Erect posture with parkinsonism suggests PSP, not PD
9. Always obtain orthostatic vital signs—autonomic dysfunction helps identify MSA
10. The waiting room observation is often more revealing than the formal examination

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