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Propulsive gait is characterized by a stooped, rigid posture—the patient’s head and neck are bent forward; his flexed, stiffened arms are held away from the body; his fingers are extended; and his knees and hips are stiffly bent. During ambulation, this posture results in a forward shifting of the body’s center of gravity and consequent impairment of balance, causing increasingly rapid, short, shuffling steps with involuntary acceleration (festination) and lack of control over forward motion (propulsion) or backward motion (retropulsion). (See Identifying gait abnormalities.)
Propulsive gait is a cardinal sign of advanced Parkinson’s disease; it results from progressive degeneration of the ganglia, which are primarily responsible for smooth muscle movement. Because this sign develops gradually and its accompanying effects are often wrongly attributed to aging, propulsive gait commonly goes unnoticed or unreported until severe disability results.
Ask the patient when his gait impairment first developed and whether it has recently worsened. Because he may have difficulty remembering, having attributed the gait to “old age,” you may be able to gain information from family members or friends, especially those who see the patient only sporadically.
Obtain a thorough drug history, including dosages. Ask the patient if he has been taking any tranquilizers, especially phenothiazines. If he knows he has Parkinson’s disease and has been taking levodopa, pay particular attention to the dosage because an overdose can cause acute exacerbation of signs and symptoms. If Parkinson’s disease isn’t a known or suspected diagnosis, ask the patient if he has been acutely or routinely exposed to carbon monoxide or manganese.
Begin the physical examination by testing the patient’s reflexes and sensorimotor function, noting any abnormal response patterns.
The characteristic and permanent propulsive gait associated with Parkinson’s disease begins early as a shuffle. As the disease progresses, the gait slows. Cardinal signs of the disease are progressive muscle rigidity, which may be uniform (lead-pipe rigidity) or jerky (cogwheel rigidity); akinesia; and an insidious tremor that begins in the fingers, increases during stress or anxiety, and decreases with purposeful movement and sleep. Besides the gait, akinesia also typically produces a monotone voice; drooling; masklike facies; stooped posture; and dysarthria, dysphagia, or both. Occasionally, it also causes an oculogyric crisis or blepharospasm.
Propulsive gait commonly appears several weeks after acute carbon monoxide intoxication. Earlier effects include muscle rigidity, choreoathetoid movements, generalized seizures, myoclonic jerks, masklike facies, and dementia.
Propulsive gait and other extrapyramidal effects can result from the use of phenothiazines, other antipsychotics (notably haloperidol, thiothixene, and loxapine) and, infrequently, metoclopramide and metyrosine. Such effects are usually temporary, disappearing within a few weeks after therapy is discontinued.
Chronic overexposure to manganese can cause an insidious, usually permanent, propulsive gait. Typical early findings include fatigue, muscle weakness and rigidity, dystonia, resting tremor, choreoathetoid movements, masklike facies, and personality changes. Those at risk for manganese poisoning are welders, railroad workers, miners, steelworkers, and workers who handle pesticides.
Because of his gait and associated motor impairment, the patient may have problems performing activities of daily living. Assist him as appropriate, while at the same time encouraging his independence, self-reliance, and confidence. Advise the patient and his family to allow plenty of time for these activities, especially walking, because festination and poor balance make him particularly susceptible to falls. Encourage the patient to maintain ambulation; for safety reasons, remember to stay with him while he’s walking, especially if he’s on unfamiliar or uneven ground. You may need to refer him to a physical therapist for exercise therapy and gait retraining.
Propulsive gait, usually with severe tremors, typically occurs in juvenile parkinsonism, a rare form. Other rare causes include Hallervorden-Spatz disease and kernicterus.
Read excerpts from these other book chapters related to Ataxia:
Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2008 Williams & Wilkins.
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More About This Book:
Title: Professional Guide to Signs & Symptoms (Fifth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 1-58255-510-9 
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