Propulsive gait is characterized by a stooped, rigid posture with forward-flexed head and neck, stiffened arms held away from the body, extended fingers, and flexed knees and hips. This posture shifts the body’s center of gravity forward, causing short, rapid, shuffling steps (festination), with difficulty controlling forward (propulsion) or backward (retropulsion) motion.

It is a hallmark sign of advanced Parkinson’s disease, although it can also result from drug exposure, carbon monoxide poisoning, or manganese toxicity. Early identification is essential for fall prevention and management of underlying neurologic disorders.

Pathophysiology

Propulsive gait arises from degeneration of the basal ganglia, particularly the substantia nigra, leading to impaired dopamine-mediated motor control. Loss of smooth muscle coordination results in rigidity, akinesia, tremor, and postural instability, which collectively produce the characteristic forward-leaning, festinating gait. Drug- or toxin-induced propulsive gait is due to interference with dopaminergic neurotransmission or basal ganglia injury.

History and Physical Examination

History:

• Onset and progression of gait impairment; recent worsening.

• Exposure to medications (particularly phenothiazines or other antipsychotics) or environmental toxins (carbon monoxide, manganese).

• Parkinson’s disease history, including levodopa usage and dose changes.

• Family or caregiver reports of gait changes and falls.

Physical Examination:

• Assess posture: stooped, forward-flexed head and neck.

• Observe arm and leg positioning: stiffened arms, extended fingers, bent knees and hips.

• Examine for tremor, rigidity (lead-pipe or cogwheel), bradykinesia, and masklike facies.

• Test reflexes and motor strength; evaluate gait over short distances and on turns.

Medical Causes

Special Considerations

• Monitor falls risk due to festination and impaired balance.

• Encourage ambulation to prevent deconditioning; supervise walking on uneven or unfamiliar surfaces.

• Refer to physical therapy for gait retraining and balance exercises.

• Assess activities of daily living (ADLs); provide assistive devices if necessary.

Patient Counseling

• Allow extra time for walking and daily activities.

• Advise use of assistive devices (canes, walkers) as needed.

• Encourage adherence to prescribed medications and follow-up for neurologic evaluation.

• Educate about fall prevention strategies and home safety.

Pediatric Pointers

• Juvenile parkinsonism may present with propulsive gait and severe tremors.

• Rare causes include Hallervorden-Spatz disease and kernicterus.

• Early recognition is crucial to prevent complications and optimize therapy.

References

1. Jankovic, J. (2008). Parkinson’s disease: Clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry, 79(4), 368–376.

2. Lees, A. J., Hardy, J., & Revesz, T. (2009). Parkinson’s disease. The Lancet, 373(9680), 2055–2066.

3. Olanow, C. W., Stern, M. B., & Sethi, K. (2009). The scientific and clinical basis for the treatment of Parkinson’s disease. Neurology, 72(21 Suppl 4), S1–S136.

4. Koller, W. C., & Lang, A. E. (2011). Drug-induced parkinsonism. Advances in Neurology, 63, 1–9.

5. Guilarte, T. R. (2010). Manganese and Parkinson’s disease: Insights from nonhuman primates. Environmental Health Perspectives, 118(8), 1213–1218.

6. Weaver, L. K. (2009). Carbon monoxide poisoning. New England Journal of Medicine, 360(12), 1217–1225.

7. Rajput, A. H., & Rozdilsky, B. (2002). Juvenile parkinsonism: Clinical features and pathophysiology. Parkinsonism & Related Disorders, 8(4), 223–228.